Research Bibliography for Eye Conditions
and Other Diseases

Note, to see the newer, better organized research section click here.


1. Anti-acids (2012) & Clostridium difficile risk

Learn more about natural indigestion recommendations

The Canadian Health Ministry is warning people about the possible risk of potentially dangerous clostridium difficile-related diarrhea from use of prescription anti-acids, known as "protein-pumps". Protein-pumps are used to treat acid reflux, and stomach and small intestine ulcers.

While there is not yet conclusive evidence, a number of different studies strongly suggest a connection between prescription anti-acids and clostridium difficile problems, especially in vulnerable people: the elderly, those with severe underlying illness, hospitalization, or those taking antibiotics.

Symptoms include severe watery or bloody diarrhea, fever, loss of appetite, nausea, and abdominal pain or tenderness.

Here's a list of drugs (sold in Canada):

  • Dexlansoprazole (Dexilant)
  • Esomeprazole (Nexium and its generic equivalent)
  • Omeprazole (Losec and its generic equivalents)
  • Lansoprazole (Prevacid and its generic equivalents)
  • Pantoprazole (Pantoloc and Panto IV, and their generic equivalents)
  • Pantoprazole/magnesium (Tecta)
  • Rabeprazole (Pariet and its generic equivalents)
  • These products may also be found in combination with other drugs, for example: Vimovo contains esomeprazole

2. CoQ10 (2011) & Migraine Headaches

Learn more about migraine headaches.

Researchers, noting that CoQ10 has been shown to be effective in preventing adult migraines, wanted to examine its helpfulness in children and teens. They also noted that CoQ10 has been seen to be deficient in many children and teens who report headaches.

In a double-blind, placebo, crossover, random study researchers analyzed 120 children and teens with frequent migraines who were given either placebo or CoQ10 for 224 days. At the half way point, treatments were reversed (the crossover) so that all patients received either placebo or CoQ10.

Both groups reported fewer, less severe, and/or shorter-lasting migraines by the end of the 224 days.

3. Selenium (2012) & Cardiac Health

This study aimed to assess whether selenium deficiency played an important role in healthy cardiac function.

The researchers looked at selenoprotein P in cases of sudden cardiac death in 124 subjects. SePP levels were measured in all subjects, and glutathione peroxidase were measured in 119 people. They found that the correlation was statistically significant and concluded that selenium deficiency might play an important role in the disease.

Researchers: Li Q, Li XZ, Wang T, Zhou LW, Feng HQ, Gao L, Pei JR, Lin C, Jiang CX, Institute of Keshan Disease, Center for Endemic Disease Control, Harbin Medical University, 157 Baojian Road, Harbin, 150081, China.

Published: Biol Trace Elem Res. 2012 Oct 2

Editor's Note: Selenium deficiency is rare in the US. In China, there were many childhood deaths due to Keshan disease (selenium deficiency) which leads to an abnormality of the heart muscle. The link to selenium was discovered and supplements reversed the problem. Two other conditions, Kashin-Beck disease (joint/bone), and myxedematous endemic cretinism (mental retardation).

Therefore, selenium cannot be considered as a treatment for heart disease. Meta-analysis of the literature confirms this.
Flores-Mateo G, Navas-Acien A, Pastor-Barriuso R, Guallar E., Selenium and coronary heart disease: a meta-analysis, Am J Clin Nutr. 2006 Oct;84(4):762-73;
Ghaemian A, Salehifar E, Shiraj H, Babaee Z., A Comparison of Selenium Concentrations between Congestive Heart Failure Patients and Healthy Volunteers, J Tehran Heart Cent. 2012 Spring;7(2):53-7.

4. Vitamin D (2011) Boosts Immune Response

In this study the researchers wanted to know whether Vitamin D helped boost the bodies' immune response. In the lab, they found that gingival cells that were treated with Vitamin D displayed an improved ability to produce an endogenous antibiotic that was able to kill more bacteria than untreated cells.

Researchers: L. McMahon, K. Schwartz, O. Yilmaz, E. Brown, L. K. Ryan, G. Diamond.

Published: Vitamin D-Mediated Induction of Innate Immunity in Gingival Epithelial Cells. Infection and Immunity, 2011; 79 (6): 2250.

5. Allergies and Sensitivities Bibliography
Also see discussion of allergies & sensitivities research.

1. Breneman JC. Basics of Food Allergy. Springfield, IL: Charles C Thomas, 1978, 45–53.
2. Darlington LG, Ramsey NW, Mansfield JR. Placebo controlled, blind study of dietary manipulation therapy in rheumatoid arthritis. Lancet 1986;i:236–8.
3. Beri D, Malaviya AN, Shandilya R, Singh RR. Effect of dietary restrictions on disease activity in rheumatoid arthritis. Ann Rheum Dis 1988;47:69–72.
4. Panush RS. Possible role of food sensitivity in arthritis. Ann Allerg 1988;61(part 2):31–5.
5. Taylor MR. Food allergy as an etiological factor in arthropathies: a survey. J Internat Acad Prev Med 1983;8:28–38 [review].
6. Darlington LG, Ramsey NW. Diets for rheumatoid arthritis. Lancet 1991;338:1209 [letter].
7. Rowe AH, Young EJ. Bronchial asthma due to food allergy alone in ninety-five patients. JAMA 1959;169:1158.
8. Genton C, Frei PC, Pecoud A. Value of oral provocation tests to aspirin and food additives in the routine investigation of asthma and chronic urticaria. J Asthma 1985;76:40–5.
9. Townes SJ, Mellis CM. Role of acetyl salicylic acid and sodium metabisulfite in chronic childhood asthma. Pediatrics 1984;73:631–7.
10. Boris M, Mandel FS. Foods and additives are common causes of the attention deficit hyperactive disorder in children. Ann Allergy 1994;72:462–8.
11. Carter CM, Urbanowicz M, Hemsley R, et al. Effects of a few food diet in attention deficit disorder. Arch Dis Child 1993;69:564–8.
12. Egger J, Stolla A, McEwen LM. Controlled trial of hyposensitisation in children with food-induced hyperkinetic syndrome. Lancet 1992;339:1150–3.
13. Horesh AJ. Allergy and infection. Proof of infectious etiology. J Asthma Res 1967;4:269–82.
14. Rudolph JA. Allergy as a cause of frequent recurring colds and coughs in children. Dis Chest 1940;6:138.
15. Berman BA. Pseudomononucleosis of allergic origin: a new clinical entity. Ann Allergy 1964;22:403–9.
16. Kudelco N. Allergy in chronic monilial vaginitis. Ann Allergy 1971;29:266–7.
17. Crandall, M. Allergic predisposition and recurrent vulvovaginal candidiasis. J Advancement Med 1991;4:21–38 [review].
18. Hay KD, Reade PC. The use of an elimination diet in the treatment of recurrent aphthous ulceration of the oral cavity. Oral Surg Oral Med Oral Pathol 1984;57:504–7.
19. Wray D. Gluten-sensitive recurrent aphthous stomatitis. Dig Dis Sci 1981;26:737–40.
20. Wright A, Ryan FP, Willingham SE, et al. Food allergy or intolerance in severe recurrent aphthous ulceration of the mouth. BMJ 1986;292:1237.
21. Wray D, Vlagopoulos TP, Siraganian RP. Food allergens and basophil histamine release in recurrent aphthous stomatitis. Oral Surg Oral Med Oral Pathol 1982;54:338–95.
22. Faulkner-Hogg KB, Selby WS, Loblay RH. Dietary analysis in symptomatic patients with coeliac disease on a gluten-free diet: the role of trace amounts of gluten and non-gluten food intolerances. Scand J Gastroenterol 1999;34:784–9.
23. Sewell P, Cooke WT, Cox EV, Meynell MJ. Milk intolerance in gastrointestinal disorders. Lancet 1963;2:1132–5.
24. Haeney MR, Goodwin BJF, Barratt MEJ, et al. Soya protein antibodies in man: their occurrence and possible relevance in coeliac disease. J Clin Pathol 1982;35:319–22.
25. Mike N, Haeney M, Asquith P. Soya protein hypersensitivity in coeliac disease: evidence for cell mediated immunity. Gut 1983;24:A990.
26. Ament ME, Rubin CE. Soy protein—another cause of the flat intestinal lesion. Gastroenterology 1972;62:227–34.
27. Hill DJ, Hosking CS, Heine RG. Clinical spectrum of food allergy in children in Australia and South-East Asia: identification and targets for treatment. Ann Med 1999;31:272–81.
28. Jakobsson I, Lindberg T. Cow’s milk proteins cause infantile colic in breast-fed infants: a double-blind crossover study. Pediatr 1983;71(2):268–71.
29. Evans RW, Fergusson DM, Allardyce RA, et al. Maternal diet and infantile colic in breast-fed infants. Lancet 1981;49:1340–2.
30. Clyne PS, Kulczycki A. Human breast milk contains bovine IgG. Relationship to infant colic? Pediatr 1991;87:439–44.
31. Hill DJ, Hudson IL, Sheffield LJ, et al. A low allergen diet is a significant intervention in infantile colic: results of a community-based study. J Allergy Clin Immunol 1995;96:886–92.
32. Iacono G, Cavataio F, Montalto G, et al. Intolerance of cow’s milk and chronic constipation in children. N Engl J Med 1998;339:1100–4.
33. Daher S, Solé D, de Morias MB. Cow’s milk and chronic constipation in children. N Engl J Med 1999;340:891.
34. Shah N, Lindley K, Milla P. N Engl J Med 199918;340:891–2.
35. Riordan AM, Hunter JO, Cowan RE, et al. Treatment of active Crohn’s disease by exclusion diet: East Anglian Multicentre Controlled Trial. Lancet 1993;342:1131–4.
36. King DS. Can allergic exposure provoke psychological symptoms? A double-blind test. Biol Psychiatry 1981;16:3–19.
37. Brown M, Gibney M, Husband PR, Radcliffe M. Food allergy in polysymptomatic patients. Practitioner 1981;225:1651–4.
38. James JM, Burks AW. Food-associated gastrointestinal disease. Curr Opin Pediatr 1996;8:471–5 [review].
39. McMahan JT, Calenoff E, Croft J, et al. Chronic otitis media with effusion and allergy: modified RAST analysis of 119 cases. Otolaryngol Head Neck Surg 1981;89:427–31.
40. Nsouli TM, Nsouli SM, Linde RE, et al. Role of food allergy in serous otitis media. Ann Allerg 1994;73:215–9.
41. Juntti H, Tikkanen S, Kokkonen J, et al. Cow’s milk allergy is associated with recurrent otitis media during childhood. Acta Otolaryngol 1999;119:867–73.
42. Sampson HA, Scanlon SM. Natural history of food hypersensitivity in children with atopic dermatitis. J Pediatr 1989;115:23–7.
43. Burks AW, Mallory SB, Williams LW, Shirrell MA. Atopic dermatitis: clinical relevance of food hypersensitivity. J Pediatr 1988;113:447–51.
44. Niggemann B, Sielaff B, Beyer K, et al. Outcome of double-blind, placebo-controlled food challenge tests in 107 children with atopic dermatitis. Clin Exp Allergy 1999;29:91–6.
45. Atherton DJ. Diet and atopic eczema. Clin Allerg 1988;18:215–28 [review].
46. Worm M, Ehlers I, Sterry W, Zuberbier T. Clinical relevance of food additives in adult patients with atopic dermatitis. Clin Exp Allergy 2000;30:407–14.
47. Breneman JC. Allergy elimination diet as the most effective gallbladder diet. Ann Allerg 1968;26:83–7.
48. Moneret-Vautrin DA. Cow’s milk allergy. Allerg Immunol (Paris) 1999;31:201–10 [review].
49. McLain BI, Cameron DJ, Barnes GL. Is cow’s milk protein intolerance a cause of gastro-oesophageal reflux in infancy? J Paediatr Child Health 1994;30:316–8.
50. Forget P, Arends JW. Cow’s milk protein allergy and gastro-oesophageal reflux. Eur J Pediatr 1985;144:298–300.
51. Staiano A, Troncone R, Simeone D, et al. Differentiation of cow’s milk intolerance and gastro-oesophageal reflux. Arch Dis Child 1995;73:439–42.
52. Iacono G, Carroccio A, Cavataio F, et al. Gastroesophageal reflux and cow’s milk allergy in infants: a prospective study. J Allergy Clin Immunol 1996:97:822–7.
53. Forget P, Arends JW. Cow’s milk protein allergy and gastro-oesophageal reflux. Eur J Pediatr 1985;144:298–300.
54. Hill DJ, Cameron DS, Catto-Smith A, et al. Multiple food protein intolerance (MFPI) as a cause of reflux oesophagitis in infancy: results of a pilot study. J Allergy Clin Immunol 1998;101:S89 [abstract].
55. Hill DJ, Hosking CS, Heine RG. Clinical spectrum of food allergy in children in Australia and South-East Asia: identification and targets for treatment. Ann Med 1999;31:272–81 [review].
56. Berens C, et al. Allergy in glaucoma. Manifestations of allergy in three glaucoma patients as determined by the pulse-diet method of Coca. Ann Allergy 1947;5:526–35.
57. Raymond LF. Allergy and chronic simple glaucoma. Ann Allergy 1964;22:146–50.
58. Speer F. Multiple food allergy. Ann Allerg 1975;34:71–6.
59. Buczylko K, Kowalczyk J, Zeman K, et al. Allergy to food in children with pollinosis. Rocz Akad Med Bialymst 1995;40:568–72.
60. Ogle KA, Bullock JD. Children with allergic rhinitis and/or bronchial asthma treated with elimination diet. Ann Allergy 1977;39:8–11.
61. Grant ECG. Food Allergies and migraine. Lancet 1979;1:966–9.
62. Henz BM, Zuberbier T. Most chronic urticaria is food-dependent, not idiopathic. Exp Dermatol 1998;7:139–42. [review].
63. Winkelmann RK. Food sensitivity and urticaria or vasculitis. In: Brostoff J, Challacombe SJ (eds.) Food Allergy and Intolerance. Philadelphia: WB Saunders, 1987, 602–17 [review].
64. Lessof MH. Reactions to food additives. Clin Exp Allergy 1995;25 Suppl 1:27–8. [review].
65. Wraith DG, Merrett J, Roth A, et al. Recognition of food allergic patients and their allergens by the RAST technique and clinical investigation. Clin Allergy 1975;9:25–36.
66. Zuberbier T, Chantraine-Hess S, Hartmann K, et al. Pseudoallergen-free diet in the treatment of chronic urticaria. ACTA Dermatologica Venerol (Stockh) 1995;75:484–7.
67. Gibson A, Clancy R. Management of chronic idiopathic urticaria by the identification and exclusion of dietary factors. Clin Allergy 1980;10:699–704.
68. Meyer de Schmid JJ, Zeller J. Urticaria due to vitamin B 12 allergy verified by the lymphoblastic transformation test. Bull Soc Fr Dermatol Syphiligr 1969;76:670–1 [in French].
69. Rippere V. “A little something between meals”: masked addiction not low blood blood-sugar. Lancet 1979;1:1349 [letter].
70. Horesh AJ. Allergy and infection VII. Support from the literature. J Asthma Res 1968;6:3–55 [review].
71. Pang LQ. The importance of allergy in otolaryngology. Clin Ecology 1982;1(1):53.
72. Nsouli TM, Nsouli SM, Linde RE, et al. Role of food allergy in serous otitis media. Ann Allergy 1994;73:215–9.
73. Horesh AJ. Allergy and recurrent urinary tract infections in childhood. II. Ann Allergy 1976;36:174–9.
74. Crandall, M. Allergic predisposition and recurrent vulvovaginal candidiasis. J Advancement Med 1991;4:21–38 [review].
75. Kudelco N. Allergy in chronic monilial vaginitis. Ann Allergy 1971;29:266–7.
76. Paganelli R, Fagiolo U, Cancian M, et al. Intestinal permeability in irritable bowel syndrome. Effect of diet and sodium cromoglycate administration. Ann Allergy 1990;64:377–80.
77. Alun Jones V, McLaughlan P, Shorthouse M, et al. Food intolerance: A major factor in the pathogenesis of irritable bowel syndrome. Lancet 1982;ii:1115–7.
78. Grant EC. Food allergies and migraine. Lancet 1979;i:966–9.
79. Monro J, Brostoff J, Carini C, Zilkha K. Food allergy in migraine. Lancet 1980;ii:1–4.
80. Egger J, Carter CM, Wilson J, et al. Is migraine food allergy? A double-blind controlled trial of oligoantigenic diet treatment. Lancet 1983;ii:865–9.
81. Hughs EC, Gott PS, Weinstein RC, Binggeli R. Migraine: a diagnostic test for etiology of food sensitivity by a nutritionally supported fast and confirmed by long-term report. Ann Allergy 1985;55:28–32.
82. Schaumburg HH, Byck R, Gerstl R, Mashman JH. Monosodium L-glutamate: its pharmacology and role in the Chinese restaurant syndrome. Science 1969;163:826–8.
83. Rosenblum I, Bradley JD, Coulston F. Single and double blind studies with oral monosodium glutamate in man. Toxicol Appl Pharmacol 1971;18:367–73.
84. Kenney RA, Tidball CS. Human susceptibility to oral monosodium L-glutamate. Am J Clin Nutr 1972;25:140–6.
85. Randolph TG. Masked food allergy as a factor in the development and persistence of obesity. J Lab Clin Med 1947;32:1547.
86. Douglas JM. Psoriasis and diet. West J Med 1980;133:450 [letter].
87. Bullock C. Chronic infectious sinusitis linked to allergies. Med Trib 1995;Dec 7:1.
88. Derebery MJ. Otoplaryngic allergy. Otolaryngol Clin North Am 1993;26:593–611 [review].
89. Host A. Mechanisms in adverse reactions to food. Allergy 1995;50(20 suppl):60–3 [review].
90. Bucca C, Rolla G, Oliva A, Farina JC. Effect of vitamin C on histamine bronchial responsiveness of patients with allergic rhinitis. Ann Allergy 1990;65:311–4.
91. Bellioni P, Artuso A, Di Luzio Paparatti U, Salvinelli F. Histaminic provocation in allergy. The role of ascorbic acid. Riv Eur Sci Med Farmacol 1987;9:419–22 [in Italian].
92. Annesi-Maesano I, Oryszczyn MP, Neukirch F, Kauffmann F. Relationship of upper airway disease to tobacco smoking and allergic markers: a cohort study of men followed up for 5 years. Int Arch Allergy Immunol 1997;114:193–201.
93. Ogle KA, Bullock JD. Children with allergic rhinitis and/or bronchial asthma treated with elimination diet: a five-year follow-up. Ann Allergy 1980;44:273–8.
94. Rowe AH, Rowe A Jr. Perennial nasal allergy due to food sensitization. J Asthma Res 1965;3:141–54.
95. Derlacki EL. Food sensitization as a cause of perennial nasal allergy. Ann Allergy 1955;13:682–9.
96. Kern RA, Stewart G. Allergy in duodenal ulcer: incidence and significance of food hypersensitivities as observed in 32 patients. J Allergy 1931;3:51.
97. Reimann HJ, Lewin J. Gastric mucosal reactions in patients with food allergy. Am J Gastroenterol 1988;83:1212–9.
98. Breneman JC. Allergic cystitis: the cause of nocturnal enuresis. General Practice 1959;20:85–98.
99. Zaleski A, Shokeir MK, Garrard JW. Enuresis: familial incidence and relationship to allergic disorders. Can Med Assoc J 1972;106:30–1.
100. Lucarelli S, Corrado G, Pelliccia A, et al. Cyclic vomiting syndrome and food allergy/intolerance in seven children: a possible association. Eur J Pediatr 2000;159:360–3.
101. Abu-Arafeh I, Russell G. Cyclical vomiting syndrome in children: a population-based study. J Pediatr Gastroenterol Nutr 1995;21:454–8.
102. Pelto L, Salminen PL, Lilius E-M, et al. Milk hypersensitivity—key to poorly defined gastrointestinal symptoms in adults. Allergy 1998;53:307–10.
103. Bombardieri S, Ferri C. Low antigen content diet in the management of immunomediated diseases. Isr J Med Sci 1992;28:117–20 [review].
104. Hill DJ, Hosking CS, Heine RG. Clinical spectrum of food allergy in children in Australia and South-East Asia: identification and targets for treatment. Ann Med 1999;31:272–81.
105. AAAAI Board of Directors. Position statement. Idiopathic environmental intolerances. J Allergy Clin Immunol 1999;103:36–40.
106. Arnetz BB. Model development and research vision for the future of multiple chemical sensitivity. Scand J Work Environ Health 1999;25:569–73 [review].
107. Graveling RA, Pilkington A, George JP, et al. A review of multiple chemical sensitivity. Occup Environ Med 1999;56:73–85 [review].
108. Brown AE. Developing a pesticide policy for individuals with multiple chemical sensitivity: considerations for institutions. Toxicol Ind Health 1999;15:432–7 [review].
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110. Kaufman W. Food-induced, allergic musculoskeletal syndromes. Ann Allerg 1953;Mar/Apr:179–84.
111. Gaboardi F, Perlett L, Mihansch MJ. Dermatitis herpetiformis and nephrotic syndrome. Clin Nephrol 1983;20:49.
112. Meadow SR, Sarsfield JK. Steroid-responsive nephrotic syndrome and allergy: clinical studies. Arch Dis Childhood 1981;56:509–16.
113. Walker WA. Pathophysiology of intestinal uptake and absorption of antigens in food allergy. Ann Allergy 1987;59:7–16 [review].
114. Reinhardt MC. Macromolecular absorption of food antigens in health and disease. Ann Allergy 1984;53:597–601 [review].
115. Jalonen T. Identical intestinal permeability changes in children with different clinical manifestations of cow’s milk allergy. J Allergy Clin Immunol 1991;88:737–42.
116. Andre F, Andre C, Feknous M, et al. Digestive permeability to different-sized molecules and to sodium cromoglycate in food allergy. Allergy Proc 1991;12:293–8.
117. Bahna SL. Management of food allergies. Ann Allergy 1984;53:678–82 [review].
118. Crook WG. Detecting your hidden food allergies. Jackson, TN: Professional Books, 1988.
119. Mandell M. Dr. Mandell’s 5-Day Allergy Relief System. New York: Pocket Books, 1979.
120. Sampson HA. Food allergy. Part 2: diagnosis and management. J Allergy Clin Immunol 1999;103:981–9 [review].
121. Klein GL. Controlling allergies by controlling environment. A big help for your patients. Postgrad Med 1992;91:215–8, 221–4 [review].
122. Kirjavainen PV, Gibson GR. Healthy gut microflora and allergy: factors influencing development of the microbiota. Ann Med 1999;31:288–92 [review].
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126. Hunter JO. Food allergy—or enterometabolic disorder? Lancet 1991;24:495–6 [review].
127. Cavagni G, Piscopo E, Rigoli E, et al. Food allergy in children: an attempt to improve the effects of the elimination diet with an immunomodulating agent (thymomodulin). A double-blind clinical trial. Immunopharmacol Immunotoxicol 1989;11:131–42.
128. Genova R, Guerra A. Thymomodulin in management of food allergy in children. Int J Tissue React 1986;8:239–42.
129. Oelgoetz AW, Oelgoetz PA, Wittenkind J. The treatment of food allergy and indigestion of pancreatic origin with pancreatic enzymes. Am J Dig Dis Nutr 1935;2:422–6.
130. McCann M. Pancreatic enzyme supplement for treatment of multiple food allergies. Ann Allergy 1993;71:269 [abstract #17].
131. Kokkonen J, Simila S, Herva R. Impaired gastric function in children with cow’s milk intolerance. Eur J Pediatr 1979;132:1–6.
132. Kokkonen J, Simila S, Herva R. Gastrointestinal findings in atopic children. Eur J Pediatr 1980;134:249–54.
133. Gonzalez H, Ahmed T. Suppression of gastric H2-receptor mediated function in patients with bronchial asthma and ragweed allergy. Chest 1986;89:491–6.
134. Johnston CS, Retrum KR, Srilakshmi JC. Antihistamine effects and complications of supplemental vitamin C. J Am Diet Assoc 1992;92:988–9.
135. Johnston S, Martin LJ, Cai X. Antihistamine effect of supplemental ascorbic acid and neutrophil chemotaxis. J Am Coll Nutr 1992;11:172–6.
136. Gabor M. Anti-inflammatory and anti-allergic properties of flavonoids. Prog Clin Biol Res 1986;213:471–80 [review].
137. Middleton E, Drzewieki G. Naturally occurring flavonoids and human basophil histamine release. Int Arch Allergy Appl Immunol 1985;77:155–7.
138. Amella M, Bronner C, Briancon F, et al. Inhibition of mast cell histamine release by flavonoids and bioflavonoids. Planta Medica 1985;51:16–20.
139. Kasahara T, Amemiya M, Wu Y, Oguchi K. Involvement of central opioidergic and nonopioidergic neuroendocrine systems in the suppressive effect of acupuncture on delayed type hypersensitivity in mice. Int J Immunopharmacol 1993;15:501–8.
140. Kasahara T, Wu Y, Sakurai Y, Oguchi K. Suppressive effect of acupuncture on delayed type hypersensitivity to trinitrochlorobenzene and involvement of opiate receptors. Int J Immunopharmacol 1992;14:661–5.
141. Jian M. Influence of adrenergic antagonist and naloxone on the anti-allergic shock effect of electro-acupuncture in mice. Acupunct Electrother Res 1985;10:163–7.
142. Lau BH, Wong DS, Slater JM. Effect of acupuncture on allergic rhinitis: clinical and laboratory evaluations. Am J Chin Med 1975;3:263–70.
143. Lai X. Observation on the curative effect of acupuncture on type I allergic diseases. J Tradit Chin Med 1993;13:243–8.
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145. Miller JB. A double-blind study of food extract injection therapy: a preliminary report. Ann Allerg 1977:185–91.
146. Hosen H. Provocative testing for food allergy diagnosis. J Asthma Res 1976:45–51.
147. Rea WJ, Podell RN, Williams ML, et al. Elimination of oral food challenge reaction by injection of food extracts. A double-blind evaluation. Arch Otolaryngol 1984;110:248–52.
148. King WP, Fadal RG, Ward WA, et al. Provocation-neutralization: a two-part study. Part II. Subcutaneous neutralization therapy: a multi-center study. Otolaryngol Head Neck Surg 1988;99:272–7.
149. Jewett DL, Fein G, Greenberg MH. A double-blind study of symptom provocation to determine food sensitivity. New Engl J Med 1990;323:429–33.
150. Morris DL. Use of sublingual antigen in diagnosis and treatment of food allergy. Ann Allergy 1969;27:289–94.
151. Scadding GK, Brostoff J. Low dose sublingual therapy in patients with allergic rhinitis due to house dust mite. Clin Allergy 1986;16:483–91.
152. Tari MG, Mancino M, Monti G. Efficacy of sublingual immunotherapy in patients with rhinitis and asthma due to house dust mite. A double-blind study. Allergol Immunopathol (Madr) 1990;18:277–84.
153. Bousquet J, Scheinmann P, Guinnepain MT, et al. Sublingual-swallow immunotherapy (SLIT) in patients with asthma due to house-dust mites: a double-blind, placebo-controlled study. Allergy 1999;54:249–60.
154. Mungan D, Misirligil Z, Gurbuz L. Comparison of the efficacy of subcutaneous and sublingual immunotherapy in mite-sensitive patients with rhinitis and asthma—a placebo controlled study. Ann Allergy Asthma Immunol 1999;82:485–90.
155. Urbanek R, Gehl R. Efficacy of oral hyposensitization treatment in house dust mite allergy. Monatsschr Kinderheilkd 1982;130:150–2 [in German].
156. Guez S, Vatrinet C, Fadel R, Andre C. House-dust-mite sublingual-swallow immunotherapy (SLIT) in perennial rhinitis: a double-blind, placebo-controlled study. Allergy 2000;55:369–75.
157. Mastrandrea F, Serio G, Minelli M, et al. Specific sublingual immunotherapy in atopic dermatitis. Results of a 6-year follow-up of 35 consecutive patients. Allergol Immunopathol (Madr) 2000;28:54–62.
158. Passalacqua G, Albano M, Riccio A, et al. Clinical and immunologic effects of a rush sublingual immunotherapy to Parietaria species: A double-blind, placebo-controlled trial. J Allergy Clin Immunol 1999;104:964–8.
159. Pradalier A, Basset D, Claudel A, et al. Sublingual-swallow immunotherapy (SLIT) with a standardized five-grass-pollen extract (drops and sublingual tablets) versus placebo in seasonal rhinitis. Allergy 1999;54:819–28.
160. Sabbah A. Specific immunotherapy using allergens apropos of specific immunotherapy by the sublingual route. Allerg Immunol (Paris) 1998;30:221–8 [review; in French].
161. Patriarca C, Romano A, Venuti A, et al. Oral specific hyposensitization in the management of patients allergic to food. Allergol Immunopathol (Madr) 1984;12:275–81.
162. Patriarca G, Schiavino D, Nucera E, et al. Food allergy in children: results of a standardized protocol for oral desensitization. Hepatogastroenterology 1998;45:52–8.
163. Am Academy of Allergy. Position statements: controversial techniques. J Allergy Clin Immunol 1981:333–8.
164. Gleich G, Yunginger J. The radioallergosorbent test: its present place and likely future in the practice of allergy. Adv Asthma Allergy 1975(Spring):1.
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Alzheimer's Disease

1. Alzheimer's Disease Bilbiography
Also see discussion of alzheimer's research

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3. Rogers MA, Simon DG. A preliminary study of dietary aluminium intake and risk of Alzheimer’s disease. Age Ageing 1999;28:205–9.
4. Grant WB. Dietary links to Alzheimer’s disease. Alzheimer Dis Rev 1997;2:42–55.
5. Smith MA, Petot GJ, Perry G. Diet and oxidative stress: a novel synthesis of epidemiological data on Alzheimer’s disease. Alzheimer Dis Rev 1997;2:58–9.
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8. Pettegrew JW, Klunk WE, Panchalingam K, et al. Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer’s disease. Neurobiol Aging 1995;16:1–4.
9. Salvioli G, Neri M. L-acetylcarnitine treatment of mental decline in the elderly. Drugs Exp Clin Res 1994;20:169–76.
10. Rai G, Wright G, Scott L, et al. Double-blind, placebo controlled study of acetyl-l-carnitine in patients with Alzheimer’s dementia. Curr Med Res Opin 1990;11:638–47.
11. Sano M, Bell K, Cote L, et al. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer’s disease. Arch Neurol 1992;49:1137–41.
12. Cucinotta D et al. Multicenter clinical placebo-controlled study with acetyl-L-carnitine (LAC) in the treatment of mildly demented elderly patients. Drug Development Res 1988;14:213–6.
13. Bonavita E. Study of the efficacy and tolerability of L-acetylcarnitine therapy in the senile brain. Int J Clin Pharmacol Ther Toxicol 1986;24:511–6.
14. Thal LJ, Carta A, Clarke WR, et al. A 1-year multi-center placebo-controlled study of aceyl-L-carnitine in patients with Alzheimer’s disease. Neurology 1996;47:705–11.
15. Calvani M, Carta A, Caruso G, et al. Action of acetyl-L-carnitine in neurodegeneration and Alzheimer’s disease. Ann NY Acad Sci 1992;663:483–6.
16. Morris MC, Beckett LA, Scherr PA, et al. Vitamin E and vitamin C supplement use and risk of incident Alzheimer disease. Alzheimer Dis Assoc Disord 1998;12:121–6.
17. Schmidt R, Hayn M, Reinhart B, et al. Plasma antioxidants and cognitive performance in middle-aged and older adults: results of the Austrian Stroke Prevention Study. J Am Geriatr Soc 1998;46:1407–10.
18. Lethem R, Orrell M. Antioxidants and dementia. Lancet 1997;349:1189–90 [commentary].
19. Sano M, Ernesto C, Thomas RG, et al. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer’s disease. N Engl J Med 1997;336:1216–22.
20. Eder L, Hirt L, Dunant Y. Possible involvement of thiamine in acetylcholine release. Nature 1976;264:186–8.
21. Eder L, Dunant Y, Loctin F. Thiamine and cholinergic transmission in the electric organ of Torpedo. J Neurochem 1980;35:1278–96.
22. Gibson GE, Sheu KF, Blass JP, et al. Reduced activities of thiamine-dependent enzymes in the brains and peripheral tissues of patients with Alzheimer’s disease. Arch Neurol 1988;45:836–40.
23. Meador K, Loring D, Nichols M, et al. Preliminary findings of high-dose thiamine in dementia of Alzheimer’s type. J Geriatr Psychiatry Neurol 1993;6:222–9.
24. Blass JP, Gleason P, Brush D, et al. Thiamine and Alzheimer’s disease. A pilot study. Arch Neurol 1988;45:833–5.
25. Nolan KA, Black RS, Sheu KF, et al. A trial of thiamine in Alzheimer’s disease. Arch Neurol 1991;48:81–3.
26. Crook T, Petrie W, Wells C, Massari DC. Effects of phosphatidylserine in Alzheimer’s disease. Psychopharmacol Bull 1992;28:61–6.
27. Amaducci L. Phosphatidylserine in the treatment of Alzheimer’s disease: results of a multicenter study. Psychopharmacol Bull 1988;24:130–4.
28. Engel RR, Satzger W, Gunther W, et al. Double-blind cross-over study of phosphatidylserine vs. placebo in patients with early dementia of the Alzheimer type. Eur Neuropsychopharmacol 1992;2:149–55.
29. Heiss WD, Kessler J, Mielke R, et al. Long-term effects of phosphatidylserine, pyritinol, and cognitive training in Alzheimer’s disease. A neuropsychological, EEG, and PET investigation. Dementia 1994;5:88–98.
30. Gindin J, Novickov M, Kedar D, et al. The effect of plant phosphatidylserine on age-associated memory impairment and mood in the functioning elderly. Rehovot, Israel: Geriatric Institute for Education and Research, and Department of Geriatrics, Kaplan Hospital, 1995.
31. Little A, Levy R, Chuaqui-Kidd P, Hand D. A double-blind, placebo controlled trial of high-dose lecithin in Alzheimer’s disease. J Neurol Neurosurg Psychiatry 1985;48:736–42.
32. Gauthier S, Bouchard R, Lamontagne A, et al. Tetrahydroaminoacridine-lecithin combination treatment in patients with intermediate-stage Alzheimer’s disease. Results of a Canadian double-blind, crossover, multicenter study. N Engl J Med 1990;322:1272–6.
33. Chatellier G, Lacomblez L. Tacrine (tetrahydroaminoacridine; THA) and lecithin in senile dementia of the Alzheimer type: a multicentre trial. Groupe Francais d’Etude de la Tetrahydroaminoacridine. BMJ 1990;300:495–9.
34. Fitten LJ, Perryman KM, Gross PL, et al. Treatment of Alzheimer’s disease with short- and long-term oral THA and lecithin: a double-blind study. Am J Psychiatry 1990;147:239–42.
35. Eagger SA, Levy R, Sahakian BJ. Tacrine in Alzheimer’s disease. Lancet 1991;338:50–1 [letter; comment].
36. Ferris SH, Sathananthan G, Gershon S, et al. Senile dementia. Treatment with Deanol. J Am Geriatr Soc 1977;25:241–4.
37. Fisman M, Mersky H, Helmes E. Double-blind trial of 2-dimethylaminoethanol in Alzheimer’s disease. Am J Psychiatry 1981;138:970–2.
38. Imagawa M, Naruse S, Tsuji S, et al. Coenzyme Q10, iron, and vitamin B6 in genetically-confirmed Alzheimer’s disease. Lancet 1992;340:671 [letter].
39. Bush AI, Pettingell WH, Multhaup G, et al. Rapid induction of Alzheimer A8 amyloid formation by zinc. Science 1994;265:1464–5.
40. Potocnik FCV, van Rensburg SJ, Park C, et al. Zinc and platelet membrane microviscosity in Alzheimer’s disease. The in vivo effect of zinc on platelet membranes and cognition. S Afr Med J 1997;87:1116–9.
41. Prasad AS. Zinc in human health: an update. J Trace Elem Exp Med 1998;11:63–87.
42. Birkmayer JGD. Coenzyme nicotinamide adenine dinucleotide: New therapeutic approach for improving dementia of the Alzheimer type. Ann Clin Lab Sci 1996;26:1–9.
43. Clarke R, Smith D, Jobst KA, et al. Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease. Arch Neurol 1998;55:1449–55.
44. Snowdon DA, Tully CL, Smith CD, et al. Serum folate and the severity of atrophy of the neocortex in Alzheimer disease: findings from the Nun study. Am J Clin Nutr 2000;71:993–8.
45. Joosten E, Lesaffre E, Riezler R, et al. Is metabolic evidence for vitamin B-12 and folate deficiency more frequent in elderly patients with Alzheimer’s disease? J Gastroenterol 1997;52A:M76–M79.
46. Ebly EM, Schaefer JP, Campbell NR, Hogan DB. Folate status, vascular disease and cognition in elderly Canadians. Age Ageing 1998;27:485–91.
47. Hillen T, Lun A, Reischies FM, et al. DHEA-S plasma levels and incidence of Alzheimer’s disease. Biol Psychiatry 2000;47:161–3.
48. Nasman B, Olsson T, Backstrom T, et al. Serum dehydroepiandrosterone sulfate in Alzheimer’s disease and in multi-infarct dementia. Biol Psychiatry 1991;30:684–90.
49. Sunderland T, Merril CR, Harrington MG, et al. Reduced plasma dehydroepiandrosterone concentrations in Alzheimer’s disease. Lancet 1989;2:570.
50. Yanase T, Fukahori M, Taniguchi S, et al. Serum dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEA-S) in Alzheimer’s disease and in cerebrovascular dementia. Endocr J 1996;43:119–23.
51. Birkenhager-Gillesse EG, Derksen J, Lagaay AM. Dehydroepiandrosterone sulphate (DHEAS) in the oldest old, aged 85 and over. Ann N Y Acad Sci 1994;719:543–52.
52. Schneider LS, Hinsey M, Lyness S. Plasma dehydroepiandrosterone sulfate in Alzheimer’s disease. Biol Psychiatry 1992;31:205–8.
53. Wolkowitz OM, Kramer JH, Reus VI, et al. Dehydroepiandrosterone (NPI-34133) treatment of Alzheimer’s disease: a randomized, double-blind, placebo-controlled, parallel group study. Presented at the annual meeting of the American Psychiatric Association, Washington, DC, May 15–20, 1999.
54. Dukoff R, Molchan S, Putnam K, et al. Dehydroepiandrosterone administration in demented patients and non-demented elderly volunteers. Biol Psychiatry 1999;46:1533–41.
55. Le Bars PL, Katz MM, Berman N, et al. A placebo-controlled, double-blind, randomized trial of an extract of Ginkgo biloba for dementia. North American EGb Study Group. JAMA 1997;278:1327–32.
56. Hofferberth B. The efficacy of EGb 761 in patients with senile dementia of the Alzheimer type, a double-blind, placebo-controlled study on different levels of investigation. Hum Psychopharmacol 1994;9:215–22.
57. Kanowski S, Herrmann W, Stephan K, et al. Proof of efficacy of the Ginkgo biloba special extract EGb 761 in outpatients suffering from mild to moderate primary degenerative dementia of the Alzheimer type or multi-infarct dementia. Pharmacopsychiatry 1996;29:47–56.
58. Maurer K, Ihl R, Dierks T, Frolich L. Clinical efficacy of Ginkgo biloba special extract EGb 761 in dementia of the Alzheimer’s type. J Psychiatr Res 1997;31:645–55.
59. van Dongen M, van Rossum E, Kessels A, et al. The efficacy of ginkgo for elderly people with dementia and age-associated memory impairment: New results of a randomized clinical trial. J Am Geriatr Soc 2000;48:1183–94.
60. Wettstein A. Cholinesterase inhibitors and Ginkgo extracts–are they comparable in the treatment of dementia? Comparison of published placebo-controlled efficacy studies of at least six months’ duration. Phytomedicine 2000;6:393–401.
61. Xu SS, Gao ZX, Weng Z, et al. Efficacy of tablet huperzine-A on memory, cognition, and behavior in Alzheimer’s disease. Chung Kuo Yao Li Hsueh Pao 1995;16:391–5.
62. Zhang RW, Tang XC, Han YY, et al. Drug evaluation of huperzine A in the treatment of senile memory disorders. Chung Kuo Yao Li Hsueh Pao 1991;12:250–2 [in Chinese].
63. Wang Z, Ren G, Zhao Y, et al. A double-blind study of huperzine A and piracetam in patients with age-associated memory impairment and dementia. In: Kanba S, Richelson E, eds. Herbal Medicines for Nonpsychiatric Diseases. Tokyo: Seiwa Shoten Publishers, 1999, 39–50.
64. Thal LJ, Salmon DP, Lasker B, et al. The safety and lack of efficacy of vinpocetine in Alzheimer’s disease. J Am Geriatr Soc 1989;37:515–20.
65. Fischhof PK, Moslinger-Gehmayr R, Herrmann WM, et al. Therapeutic efficacy of vincamine in dementia.

2. Astaxanthin (2011) & Dementia

Learn more about Alzheimers Disease.

Phospholipid hydroperoxides (PLOOH) is an enzyme that abnormally accumulate abnormally in the red blood cells of patients with dementia. Scientists studied whehter powerful carotenoid antioxidants could be helpful. They conducted a double-blind, random, placebo-controlled trial in 30 patients to see whether astaxathin would be helpful as a supplement. Patients were give either 6mg or 12mg of astaxanthin daily for 12 weeks and looked at astaxanthin and PLOOH levels in the elderly and middle-aged patients.

They found that astaxanthin was higher in the red blood cells (erythrocytes) of both groups given that supplement than in the placebo group. At the same time they found that PLOOH levels decreased more strongly in the groups receiving astaxanthin. They also looked at plasma where PLOOH levels were also reduced, although less strongly.

The scientist felt that these results may indicate a valuable contribution to the prevention of dementia.

Researchers: Nakagawa K, Kiko T, Miyazawa T, Carpentero Burdeos G, Kimura F, Satoh A, Miyazawa T. Source Food and Biodynamic Chemistry Laboratory, Graduate School of Agricultural Science, Tohoku University, Sendai 981-8555, Japan

Published: British Journal of Nutrition, 2011 Jun;105(11):1563-71. Online Jan 31, 2011.

3. Ginkgo biloba (2003) and dementia

Ginkgo biloba has been extensively examined for its cognitive effects in patients with dementia. A a six-month double blind trial published in 2003 at UCLA found significant improvement in verbal recall among subjects with age-associated memory impairment1. Using positron-emission tomography (a 3D imaging technique), the researchers reported that improved recall correlated with better function in key brain memory centers of those taking ginkgo supplements.

The effects of ginkgo are attributed to its ability to enhance cerebral blood flow and provide antioxidant activity.

Reference: 1. Ercoli L et al. Society for Neuroscience Meeting, New Orleans, November, 2003

4. Magnesium-L-threonate, MgT (2010) & Memory Loss

Learn more about alzheimers and other related conditions.

Researchers have found that Magnesium-L-threonate, MgT is helpful for both long and short term memory loss. They point out that both learning and memory are impacted by diet considerations and found that, in animal models, this particular form of magnesium, which is more easily absorbed by the body than other forms, is exceptionally helpful.

They concluded that MgT helped make short-term synaptic functions more effective, and was helpful for long-term gains and stabilization in memory capacity.

Researchers: Slutsky I, Abumaria N, Wu LJ, Huang C, Zhang L, Li B, Zhao X, Govindarajan A, Zhao MG, Zhuo M, Tonegawa S, Liu G.: Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

Published: Neuron. 2010 Jan 28;65(2):165-77.

5. Omega-3 (2010) & Alzheimer's

Learn more about Alzheimer's disease.

Researchers substantiated earlier indications that a diet that is rich in Omega-3 fatty acids can help protect the brain against developing Alzheimers disease. The protective powers stem from an ability to regulate the brain's natural level of zinc, which can prove toxic at elevated levels, They found that when the level of DHA in neuronal cells drops, the level of zinc rises. Omega-3 fatty acids contain a combination of EPA, DHA and alpha linoleic acid.

Previous research had shown a reduced incidence of neurodegenerative diseases in populations with a diet rich in Omega-3 fatty acids.

Researchers: Leah Aukland, et al, Deakin University, Australia.

Published: Omega-3 fatty acid may help prevent brain cell death, FEBS Letters, volume 584, Issue 3, Pages 612-618, 5 February 2010

6. Vitamin D3 (2012) & Alzheimers

Learn more about Alzheimer's disease.

Researchers have looked into how vitamin D regulation of cell functioning may help clear the brain of the main component of plaque - amyloid beta. They found that vitamin D3 may activate key genes and cellular signal networks in order to stimulate the immune system to remove the problematic protein.

Earlier research had found that immune cells in Alzheimer's patients may respond with a combination of curcumin (tumeric) and vitamin D3, but researchers didn't know why it was effective.

In this study researchers took blood samples from Alzheimer patients and healthy control subjects and then separated the important immune cells from the blood. These cells are called macrophages and they remove waste products from the brain and body. They had known from previous research that there two types of macrophages - those that are improved by vitamin D3, and those that are improved by the combination of D3 and curcumin.

They found that both kinds of macrophages opened a specific channel called "chloride channel 3" which supports taking away amyloid beta. They identified additional steps in the gene regulation process.

Their conclusion was that active forms of D3 may be important in the regulation of functioning of the macrophages in clearing plaque by directly regulating gene expressions and cell functioning ... and thus helpful in preventing dementia.

They indicated that the next step would be a clinical trial using vitamin D3.

Researchers: Dr. Milan Fiala, et al, David Geffen School of Medicine at UCLA

Published: Journal of Alzheimer's Disease, March 6, 2012.

7. Vitamin D3, Curcumin (2009) & Alzheimers

Learn more about Alzheimer's disease.

Researchers investigated reports that a combination of vitamin D3 and curcumin (a chemical in tumeric) could help stimulate the immune system to clear the brain of amyloid beta, a component of plaque in the brains of Alzheimer's patients.

Note: Later research has discovered that there are two types of macrophages that remove waste, including amyloid beta, and that one type responds well to vitamin D3 and the other responds well to the combination of vitamin D3 and curcumin.

This small study involved three controls, nine Alzheimer patients, and one patient with mild mental impairment. The researchers took blood samples and isolated the cells that transform into macrophages. They incubated the macrophages with vitamin D3, synthetic or natural curcumin and amyloid beta.

They found that the naturally occurring curcumin was not as readily absorbed as the synthetic, rendering it less effective. Editor's note this may be because natural turmeric is less easily absorbed into the body when it is uncooked. It is always recommended to dry roast or cook turmeric in oil prior to adding it to food, or taking it as an herbal remedy.

They found that the curcumin caused amyloid beta to bind more readily to macrophages and that vitamin D3 strongly stimulated the taking up and absorption of amyloid beta.

Researchers: John Cashman, et al, Human BioMolecular Research Institute, Unviersity of California, UCLA.

Published: Journal of Alzheimer's Disease, July, 2009.


Anemia (Iron Deficiency)

1. Anemia (iron-deficiency) Bibliography

Also see more information about anemia and nutritional recommendations.

1. Sullivan JL. Stored iron and ischemic heart disease. Circulation 1992;86:1036 [editorial].
2. Morck TA, Lynch SR, Cook JD. Inhibition of food iron absorption by coffee. Am J Clin Nutr 1983;37:416–20.
3. Mehta SW, Pritchard ME, Stegman C. Contribution of coffee and tea to anemia among NHANES II participants. Nutr Res 1992;12:209–22.
4. Kaltwasser JP, Werner E, Schalk K, et al. Clinical trial on the effect of regular tea drinking on iron accumulation in genetic haemochromatosis. Gut 1998;43:699–704.
5. Cook JD, Noble NL, Morck TA, et al. Effect of fiber on nonheme iron absorption. Gastroenterology 1983;85:1354–8.
6. Mejia LA, Chew F. Hematological effect of supplementing anemic children with vitamin A alone and in combination with iron. Am J Clin Nutr 1988;48:595–600.
7. Ajayi OA, Nnaji UR. Effect of ascorbic acid supplementation on haematological response and ascorbic acid status of young female adults. Ann Nutr Metab 1990;34:32–6.
8. Hunt JR, Gallagher SK, Johnson LK. Effect of ascorbic acid on apparent iron absorption by women with low iron stores. Am J Clin Nutr 1994;59:1381–5.
9. Schade SG, Cohen RJ, Conrad ME. Effect of hydrochloric acid on iron absorption. N Engl J Med 1968;279:672–4.
10. Bezwoda W, Charlton R, Bothwell T, et al. The importance of gastric hydrochloric acid in the absorption of nonheme food iron. J Lab Clin Med 1978;92:108–16.
11. Grindulis H, Scott PH, Belton NR, Wharton BA. Combined deficiency of iron and vitamin D in Asian toddlers. Arch Dis Child 1986;61:843–8.
12. Lawson M, Thomas M. Vitamin D concentrations in Asian children


Asthenopia (eye fatigue)

1. Lutein, blackcurrant extract (2009) may reduce visual fatigue

Learn more about computer eye strain and asthenopia (eye fatigue).

Visual fatigue such as computer eye strain caused by staring at the computer for long hours, may be eased a daily supplement containing blackcurrant fruit extract (200 mg), lutein (5 mg), and zeaxanthin (1 mg), according to a randomized, double-blind, placebo-controlled cross-over trial.

The subjects were randomly assigned to receive either the lutein supplement, or placebo, for two weeks, followed by two weeks of washout, and a further two weeks with the opposite intervention.

After completing a two hour visual proof reading task, the researchers measured signs of visual fatigue, including so-called eye fixation related potentials (EFRP).

Published: Applied Ergonomics, Volume 40, Issue 6, Pages 1047-1054, “The effect of lutein supplementation on visual fatigue: A psychophysiological analysis”

Authors: A. Yagi, K. Fujimoto, K. Michihiro, B. Goh, D. Tsi, H. Nagai

2. Reducing Asthenopia (2002-2006 Studies) with Astaxanthin

A couple of randomized double blind placebo controlled pilot studies demonstrated the positive effects of astaxanthin supplementation on visual function. For example, a study by Nagaki et al., (2002), demonstrated that subjects (n=13) who received 5 mg astaxanthin per day for one month showed a 54% reduction of eye fatigue complaints. In a sports vision study led by Sawaki et al., they demonstrated that depth perception and critical flicker fusion had improved by 46% and 5% respectively on a daily dose of 6 mg (n=9). The effect of astaxanthin on visual performance prompted a number of other clinical studies to evaluate the optimum dose and identify the mechanism of action.


Atherosclerosis

1. Atheroscherosis research bibliography
These are earlier studies. Also see discussion of research for atherosclerosis

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5. De Lorgeril M, Renaud S, Mamelle N, et al. Mediterranean alpha-linolenic-rich diet in secondary prevention of coronary heart disease. Lancet 1994;343:1454–9.
6. De Lorgeril M, Salen P, Martin J-L, et al. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction. Final report of the Lyon Diet Heart Study. Circulation 1999;99:779–85.
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38. Leaf A, Jorgensen MB, Jacobs AK, et al. Do fish oils prevent restenosis after coronary angioplasty? Circulation 1994;90:2248–57.
39. Sacks FM, Stone PH, Gibson CM, et al. Controlled trial of fish oil for regression of human coronary atherosclerosis. HARP Research Group. J Am Coll Cardiol 1995;25:1492–8.
40. von Schacky C, Angerer P, Kothny W, et al. The effect of dietary omega-3 fatty acids on coronary atherosclerosis. A randomized, double-blind, placebo-controlled trial. Ann Intern Med 1999;130:554–62.
41. Sacks FM, Stone PH, Gibson CM, et al. Controlled trial of fish oil for regression of human coronary atherosclerosis. HARP Research Group. J Am Coll Cardiol 1995;25:1492–8.
42. Salonen JT et al. Association between cardiovascular death and myocardial infarction and serum selenium in a matched-pair longitudinal study. Lancet 1982;ii:175.
43. Shamberger RJ, Willis CE. Epidemiological studies on selenium and heart disease. Fed Proc 1976;35:578 [abstract #2061].
44. Korpela H, Kumpulainen J, Jussila E, et al. Effect of selenium supplementation after acute myocardial infarction. Res Comm Chem Pathol Pharmacol 1989; 65:249–52.
45. Chambers JC, McGregor A, Jean-Marie J, et al. Demonstration of rapid onset vascular endothelial dysfunction after hyperhomocysteinemia. An effect reversible with vitamin C therapy. Circulation 1999;99:1156–60.
46. Frei B. Ascorbic acid protects lipids in human plasma and low-density lipoprotein against oxidative damage. Am J Clin Nutr 1991;54:1113S–8S.
47. Balz F. Antioxidant Vitamins and Heart Disease. Presented at the 60th Annual Biology Colloquium, Oregon State University, February 25, 1999.
48. Salonen JT, Nyyssönen K, Salonen R, et al. Antioxidant supplementation in atherosclerosis prevention (ASAP) study: a randomized trial of the effect of vitamin E and C on 3-year progression of carotid atherosclerosis. J Intern Med 2000;248:177–86.
49. Belcher JD, Balla J, Balla G, et al. Vitamin E, LDL, and endothelium: Brief oral vitamin supplementation prevents oxidized LDL-mediated vascular injury in vitro. Arterioscler Thromb 1993;13:1779–89.
50. Stephens NG, Parsons A, Schofield PM, et al. Randomised controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study (CHAOS). Lancet 1996;347:781–6.
51. Rimm E. Micronutrients, Coronary Heart disease and cancer: Should we all be on supplements? Presented at the 60th Annual Biology Colloquium, Oregon State University, February 25, 1999.
52. Salonen JT, Nyyssönen K, Salonen R, et al. Antioxidant supplementation in atherosclerosis prevention (ASAP) study: a randomized trial of the effect of vitamin E and C on 3-year progression of carotid atherosclerosis. J Intern Med 2000;248:177–86.
53. Stampfer MJ, Malinow R, Willett WC, et al. A prospective study of plasma homocyst(e)ine and risk of myocardial infarction in US physicians. JAMA 1992;268:877–81.
54. Bostom AG, Silbershatz H, Rosenberg IH, et al. Nonfasting plasma total homocysteine levels and all-cause and cardiovascular disease mortality in elderly Framingham men and women. Arch Intern Med 1999;159:1077–80.
55. Folsom AR, Nieto FJ, McGovern PG, et al. Prospective study of coronary heart disease incidence in relation to fasting total homocysteine, related genetic polymorphisms, and B vitamins. Circulation 1998;98:204–10.
56. Kuller LH, Evans RW. Homocysteine, vitamins, and cardiovascular disease. Circulation 1998;98:196–9 [editorial/review].
57. Stolzen berg-Solomon RZ, Miller ER III, Maguire MG, et al. Association of dietary protein intake and coffee consumption with serum homocysteine concentrations in an older population. Am J Clin Nutr 1999;69:467–75.
58. Selhub J, Jacques PF, Wilson PW, et al. Vitamin status and intake as primary determinants of homocysteinemia in an elderly population. JAMA 1993;270:2693–8.
59. Ubbink JB, Hayward WJ, van der Merwe A, et al. Vitamin requirements for the treatment of hyperhomocysteinemia in humans. J Nutr 1994;124:1927–33.
60. Manson JB, Miller JW. The effects of vitamin B12, B6, and folate on blood homocysteine levels. Ann NY Acad Sci 1992;669:197–204 [review].
61. Folsom AR, Nieto FJ, McGovern PG, et al. Prospective study of coronary heart disease incidence in relation to fasting total homocysteine, related genetic polymorphisms, and B vitamins. Circulation 1998;98:204–10.
62. Hackam DG, Peterson JC, Spence JD. What level of plasma homocyst(e)ine should be treated? Am J Hypertens 2000;13:105–10.
63. Franken DG, Boers GHJ, Blom HJ, et al. Treatment of mild hyperhomocysteinemia in vascular disease patients. Arterioscler Thromb 1994;14:465–70.
64. Ubbink JB, Vermaak WJH, van der Merwe A, et al. Vitamin requirements for the treatment of hyperhomocysteinemia in humans. J Nutr 1994;124:1927–33.
65. Ubbink JB, van der Merwe A, Vermaak WJH, Delport R. Hyperhomocysteinemia and the response to vitamin supplementation. Clin Investig 1993;71:993–8.
66. Ronzio RA. Antioxidants, nutraceuticals and functional foods. Townsend Letter for Doctors and Patients 1996;Oct:34–5 [review].
67. Hertog MGL, Feskens EJM, Hollman PCH, et al. Dietary antioxidant flavonoids and risk of coronary heart disease: the Zutphen Elderly Study. Lancet 1993;342:1007–11.
68. Hertog MGL, Kromhout D, Aravanis C, et al. Flavonoid intake and long-term risk of coronary heart disease and cancer in the Seven Countries Study. Arch Intern Med 1995;155:381–6.
69. Knekt P, Jarvinen R, Reunanen A, Maatela J. Flavonoid intake and coronary mortality in Finland: a cohort study. BMJ 1996;312:478–81.
70. Rimm EB, Katan MB, Ascherio A, et al. Relation between intake of flavonoids and risk for coronary heart disease in male health professionals. Ann Intern Med 1996; 125:384–9.
71. Hertog MGL, Sweetnam PM, Fehily AM, et al. Antioxidant flavonols and ischemic heart disease in a Welsh population of men: the Caerphilly Study. Am J Clin Nutr 1997;65:1489–94.
72. Boberg M, Vessby B, Selinus I. Effects of dietary supplementation with n-6 and n-3 long-chain polyunsaturated fatty acids on serum lipoproteins and platelet function in hypertriglcyeridaemic patients. Acta Med Scand 1986;220:153–60.
73. Horrobin DF, Manku MS. How do polyunsaturated fatty acids lower plasma cholesterol levels? Lipids 1983;558–62.
74. Morrison LM, Branwood AW, Ershoff BH, et al. The prevention of coronary arteriosclerotic heart disease with chondroitin sulfate A: Preliminary report. Exp Med Surg 1969;27:278–89.
75. Morrison LM, Enrick NL. Coronary heart disease: Reduction of death rate by chondroitin sulfate A. Angiology 1973;24:269–82.
76. Bertelli AA, Giovanninni L, Bernini W, et al. Antiplatelet activity of cis-resveratrol. Drugs Exp Clin Res 1996;22(2):61–3.
77. Chen CK, Pace-Asciak. CR. Vasorelaxing activity of resveratrol and quercetin in isolated rat aorta. Gen Pharm 1996;27(2):363–6.
78. Pace-Asciak CR, Rounova O, Hahn SE, et al. Wines and grape juices as modulators of platelet aggregation in healthy human subjects. Clin Chim Acta 1996;246(1–2):163–82.
79. Salonen JT, Nyssönen K, Korpela H, et al. High stored iron levels are associated with excess risk of myocardial infarction in Eastern Finnish men.Circulation 1992;86:803–11.
80. Van Asperen IA, Feskens EJM, Bowles CH, Kromhout D. Body iron stores and mortality due to cancer and ischaemic heart disease: a 17-year follow-up study of elderly men and women. Int J Epidemiol 1995;24:665–70.
81. Iribarren C, Sempos CT, Eckfeldt JH, Folsom AR. Lack of association between ferritin level and measures of LDL oxidation: the ARIC study. Atherosclerosis 1998;139:189–95.
82. Corti M-C, Guralnik JM, Salive ME, et al. Serum iron level, coronary artery disease, and all-cause mortality in older men and women. Am J Cardiol 1997;79:120–7.
83. Tzonou A, Lagiou P, Trichopoulou A, et al. Dietary iron and coronary heart disease risk: a study from Greece. Am J Epidemiol 1998;147:161–6.
84. Kiechl S, Willeit J, Egger G, et al. Body iron stores and the risk of carotid atherosclerosis. Circulation 1997;96:3300–7.
85. Danesh J, Appleby P. Coronary heart disease and iron status. Meta-analyses of prospective studies. Circulation 1999;99:852–4.
86. de Valk B, Marx MMJ. Iron, atherosclerosis, and ischemic heart disease. Arch Intern Med 1999;159:1542–8 [review].
87. Klipstein-Grobusch K, Launer LJ, Geleijnse JM, et al. Serum carotenoids and atherosclerosis. The Rotterdam Study. Atherosclerosis 2000;148:49–56.
88. Koscienlny J, Klüßendorf D, Latza R, et al. The anti-atherosclerotic effect of Allium sativum. Atherosclerosis 1999;144:237–49.
89. Neil HAW, Silagy CA, Lancaster T, et al. Garlic powder in the treatment of moderate hyperlipidaemia: A controlled trial and a meta-analysis. J R Coll Phys 1996;30:329–34.
90. McCrindle BW, Helden E, Conner WT. Garlic extract therapy in children with hypercholesterolemia. Arch Pediatr Adolesc Med 1998;152:1089–94.
91. Isaacsohn JL, Moser M, Stein EA, et al. Garlic powder and plasma lipids and lipoproteins. Arch Intern Med 1998;158:1189–94.
92. Berthold HK, Sudhop T, von Bergmann K. Effect of a garlic oil preparation on serum lipoproteins and cholesterol metabolism. JAMA 1998;279:1900–2.
93. Lawson L. Garlic oil for hypercholesterolemia–negative results. Quart Rev Natural Med 1998;Fall:185–6.
94. Garlic powder for hyperlipidemia–analysis of recent negative results. Quart Rev Natural Med 1998;Fall:187–9.
95. Kiesewetter H, Jung F, Pindur G, et al. Effect of garlic on thrombocyte aggregation, microcirculation and other risk factors. Int J Pharm Ther Toxicol 1991;29(4):151–5.
96. Srivastava KC, Tyagi OD. Effect of a garlic derived principle (ajoene) on aggregation and arachidonic acid metabolism in human blood platelets. Prostagl Leukotr Ess Fatty Acids 1993;49:587–95.
97. Munday JS, James KA, Fray LM, et al. Daily supplementation with aged garlic extract, but not raw garlic, protects low density lipoprotein against in vitro oxidation. Atherosclerosis 1999;143:399–404.
98. Braquet P, Touqui L, Shen TS, Vargaftig BB. Perspectives in platelet activating factor research. Pharmacol Rev 1987;39:97–210.
99. Brown DJ. Herbal Prescriptions for Better Health. Rocklin, CA: Prima Publishing, 1996, 119–28.
100. Kiesewetter H, Jung F, Mrowietz C, et al. Effects of garlic on blood fluidity and fibrinolytic activity: A randomised, placebo-controlled, double-blind study. Br J Clin Pract Suppl 1990;69:24–9.
101. Jung F, Mrowietz C, Kiesewetter H, Wenzel E. Effect of Ginkgo biloba on fluidity of blood and peripheral microcirculation in volunteers. Arzneimittelforschung 1990;40:589–93.
102. Brown D, Austin S. Hyperlipidemia and Prevention of Coronary Heart Disease. Seattle: Natural Product Research Consultants, 1997, 4–6.
103. Phelps S, Harris WS. Garlic supplementation and lipoprotein oxidation susceptibility. Lipids 1993;28(5):475–7.
104. Yan LJ, Droy-Lefaix MT, Packer L. Ginkgo biloba extract (EGb 761) protects human low density lipoproteins against oxidative modification mediated by copper. Biochem Biophys Res Comm 1995;212:360–6.
105. Singh K, Chander R, Kapoor NK. Guggulsterone, a potent hypolipidaemic, prevents oxidation of low density lipoprotein. Phytother Res 1997;11:291–4.
106. Olson BH, Anderson SM, Becker MP, et al. Psyllium-enriched cereals lower blood total cholesterol and LDL cholesterol, but not HDL cholesterol, in hypercholesterolemic adults: Results of a meta-analysis. J Nutr 1997;127:1973–80.
107. Sharma RD, Raghuram TC, Dayasagar Rao V. Hypolipidaemic effect of fenugreek seeds. A clinical study. Phytother Res 1991;5:145–7.
108. Serafini M, Ghiselli A, Ferro-Luzzi A. In vivo antioxidant effect of green tea in man. Eur J Clin Nutr 1996;50:28–32.
109. van het Hof KH, de Boer HS, Wiseman SA, et al. Consumption of green or black tea does not increase resistance of low-density lipoprotein to oxidation in humans. Am J Clin Nutr 1997;66:1125–32.
110. Bordia A, Verma SK, Srivastava KC. Effect of ginger (Zingiber officinale Rosc) and fenugreek (Trigonella foenumgraceum L) on blood lipids, blood sugar, and platelet aggregation in patients with coronary artery disease. Prostagland Leukotrienes Essential Fatty Acids 1997;56:379–84.
111. Lumb AB. Effect of dried ginger on human platelet function. Thromb Haemost 1994;7:110–1.
112. Janssen PL, Meyboom S, van Staveren WA, et al. Consumption of ginger (Zingiber officinale Roscoe) does not affect ex vivo platelet thromboxane production in humans. Eur J Clin Nutr 1996;50:772–4.
113. Srivastava R, Dikshit M, Srimal RC, Dhawan BN. Anti-thrombotic action of curcumin. Throm Res 1985;404:413–7.
114. Srivastava KC, Bordia A, Verma SK. Curcumin, a major component of food spice turmeric (Curcuma longa) inhibits aggregation and alters eicosanoid metabolism in human blood platelets. Prost Leuk Essen Fat Acids. 1995;52:223–7.
115. Pulliero G, Montin S, et al. Ex vivo study of the inhibitory effects of Vaccinium myrtillus (bilberry) anthocyanosides on human platelet aggregation. Fitoterapia 1989;60:69–75.
116. Liu J. Effect of Paeonia obovata 801 on metabolism of thromboxane B2 and arachidonic acid and on platelet
aggregation in patients with coronary heart disease and cerebral thrombosis. Chin Med J 1983;63:477–81 [in Chinese]. 117. Felix W, Schmidt Y, Nieberle J. Protective effect of Ruscus extract against injury of vascular endothelium and vascular smooth muscle caused by ethracrynic acid. Int Angiol 1983;3:77.

2. Homocystein (2004) & Heart Disease

Learn more about atherosclerosis.

A number of studies have demonstrated that patients who have coronary heart disease have higher homocysteine levels in their blood plasma than controls without heart disease. The International Task Force for Prevention of Coronary Heart Disease reported:

  • A meta-analysis (an averaging of many studies, or a study of studies) verfied that increased homocysteine by 5 µmol/l doubled heart disease risk. (Boushey et al.; JAMA 1995; 274:1049-1057)
  • Heart disease patients with a level of homocysteine lower than 9 µmol/l had a much better life expectancy than those with levels above 20 µmol/l. (Nygard et al., NEJM 1997; 337:230-236)
  • Blood levels of vitamins B6 and B12 and folate are correlated with blood homocysteine concentration levels. (ARIC Study: Folsom et al.; Circulation 1998; 98: 204-210)
  • Low levels of vitamin B6 are a more important risk factor than high homocysteine levels and these high levels reflect the cardiovascular risk created by vitamin B6 deficiency. (ARIC Study: Folsom et al. Circulation, 1998, 98: 204-210)
  • High homocysteine levels may also be a risk factor for stroke, and that the higher the level the greater the risk. (British Regional Heart Study, Perry et al. Lancet, 1995, 346: 1395-1398)
  • Folic acid treatment appears to be effective in reducing homocysteine levels. (Homocysteine Lowering Trialist´s Collaboration. Br. Med J. 1998; 316:894-898)
  • Patients with homocysteine levels greater 12 µmol/l should increase and/or supplement their dietary intake of folic acid and those with homocysteine levels greater 30 µmol/l should receive daily doses of 400-800mg folic acid, 2-4mg vitamin B6 and 400mg vitamin B12. (Nutrition, Metabolism, and Cardiovascular Disease 1998, 8:212-271)
  • Mild homocystein elevation levels can be treated with attention to diet. See food sources for folic acid and vitamins B6 and B12.

See full report.

3. Homocysteine Levels (1998) Blocked Arteries & Stroke

Learn more about atherosclerosis.

Researchers have determined that higher homocysteine levels are tied to higher risk of strokes. The degree of heart blood vessel narrowing or blockage appears to be related to the level of homocysteine. Greater thicknesses of plaque thickness are connected to high homocysteine concentrations and low levels of vitamin B-12.

The reearchers examined studied both blood vessels both within and outside the skull using MR angiography and found that homocysteine levels were higher in patients with 2- or 3-vessel narrowings than in those with 1-vessel blockage.

Researchers: Yoo JH, Chung CS, Kang SS.

Published: Relation of plasma homocysteine to cerebral infarction and cerebral atherosclerosis. Stroke. Dec 1998;29


Attention Deficit Disorder (ADD)

1. Attention Deficit Disorder ADD/ADHD Bibliography
Also see discussion of attention deficit disorder (ADD & ADHD) research

1. Harley JP, Ray RS, Tomasi L, et al. Hyperkinesis and food additives: testing the Feingold hypothesis. Pediatrics 1978;61:818–21.
2. Levy F, Dumbrell S, Hobbes G, et al. Hyperkinesis and diet: a double-blind crossover trial with a tartrazine challenge. Med J Aust 1978;1:61–4.
3. Williams JI, Cram DM. Diet in the management of hyperkinesis: a review of the tests of Feingold’s hypotheses. Can Psychiatr Assoc J 1978;23:241–8 [review].
4. Rowe KS, Rowe KJ. Synthetic food coloring and behavior: a dose response effect in a double-blind, placebo-controlled, repeated-measures study. J Pediatr 1994;125:691–8.
5. Boris M, Mandel FS. Foods and additives are common causes of the attention deficit hyperactive disorder in children. Ann Allergy 1994;72:462–8.
6. Carter CM, Urbanowicz M, Hemsley R, et al. Effects of a few food diet in attention deficit disorder. Arch Dis Child 1993;69:564–8.
7. Egger J, Stolla A, McEwen LM. Controlled trial of hyposensitisation in children with food-induced hyperkinetic syndrome. Lancet 1992;339:1150–3.
8. Prinz RJ, Roberts WA, Hantman E. Dietary correlates of hyperactive behavior in children. J Consult Clin Psychol 1980;48:760–9.
9. Rosen LA, Booth SR, Bender ME, et al. Effects of sugar (sucrose) on children’s behavior. J Consult Clin Psychol 1988;56:583–9.
10. Wolraich ML, Lindgren SD, Stumbo PJ, et al. Effects of diets high in sucrose or aspartame on the behavior and cognitive performance of children. N Engl J Med 1994;330:301–7.
11. Wolraich ML, Wilson DB, White JW. The effect of sugar on behavior or cognition in children. A meta-analysis. JAMA 1995;274:1617–21.
12. Milberger S, Biederman J, Faraone SV, et al. Is maternal smoking during pregnancy a risk factor for attention deficit hyperactivity disorder in children? Am J Psychiatry 1996;153:1138–42.
13. Tuthill RW. Hair lead levels related to children’s classroom attention-deficit behavior. Arch Environ Health 1996;51:214–20.
14. Krigman MR, Bouldin TW, Mushak P. Metal toxicity in the nervous system. Monogr Pathol 1985;(26):58–100.
15. Starobrat-Hermelin B, Kozielec T. The effects of magnesium physiological supplementation on hyperactivity in children with attention deficit hyperactivity disorder (ADHD). Positive response to magnesium oral loading test. Magnes Res 1997;10:149–56.
16. Mitchell EA, Aman MG, Turbott SH, Manku M. Clinical characteristics and serum essential fatty acid levels in hyperactive children. Clin Pediatr 1987;26:406–11.
17. Stevens LJ, Zentall SS, Deck JL, et al. Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder. Am J Clin Nutr 1995;62:761–8.
18. Aman MG, Mitchell EA, Turbott SH. The effects of essential fatty acid supplementation by Efamol in hyperactive children. J Abnorm Child Psychol 1987;15:75–90.
19. Bhagavan HN, Coleman M, Coursin DB. The effect of pyridoxine hydrochloride on blood serotonin and pyridoxal phosphate contents in hyperactive children. Pediatrics 1975;55:437–41.
20. Coleman M, Steinberg G, Tippett J, et al. A preliminary study of the effect of pyridoxine administration in a subgroup of hyperkinetic children: a double-blind crossover comparison with methylphenidate. Biol Psychiatry 1979;14:741–51.
21. Brenner A. The effects of megadoses of selected B complex vitamins on children with hyperkinesis: controlled studies with long term followup. J Learning Dis 1982;15:258–64.
22. Haslam RHA. Is there a role for megavitamin therapy in the treatment of attention deficit hyperactivity disorder? Adv Neurol 1992;58:303–10.

2. Fatty Acids (2007) & ADHD

Learn more about ADD & ADHD.

The researchers noted that a number of learning and behavorial difficulties in children have been tied to deficiencies in polyunsaturated fatty acids (PUFAs) and that these conditions may be helped through supplementation.

They also investigated added micronutrients because it is known that synergestic effects are helpful. The researchers studied 132 children (7-12) with learning/behavioral problems over 15 weeks. They found significant moderate to marked positive results in rating by parents of symptoms, hyperactivity, inattention, impulsivity compared to a placebo group. They also found that the addition of micronutrients made no additional difference.

Then, in a crossover, they tested the placebo group with the supplement and found that they also benefited.

They concluded that these essential fatty acids, which are not synthesized by the body, may be helpful for ADD & ADHD, and improvments may continue to 30 weeks.

Researchers: Sinn N, Bryan J., Commonwealth Scientific and Industrial Reasearch Organization Human Nutrition, Adelaide, South Australia

Published: Effect of supplementation with polyunsaturated fatty acids and micronutrients on learning and behavior problems associated with child ADHD, J Dev Behav Pediatr. 2007 Apr;28(2):82-91.

3. Fish Oil (2002) & ADHD

Learn more about ADHD.

The researchers wanted to determine whether deficiencies in highly unsaturated fats (HUFAs) may contribute to ADHD learning and behavior problems.

Editor's note: HUFAs are polyunsaturated fatty acids with a double bond; omega-3 fatty acids are HUFAs, and cannot be created by the body.

They examined 41 children 8-12 with learning problems (mostly dyslexia) and ADHD symptoms who were given HUFA supplements or placebo for 12 weeks.

The children's behavioral and learning difficulties were evaulated at the beginning and end of the period and after 12 weeks there was marked improvement in standard behavioral test scores on 7 out of 14 scales. For 3 out of 14 scales the change was statistically significant.

They concluded that HUFA supplements appear to lower ADHD symptoms in those with specific learning difficulties and that given the tolerability, safety, and simplicity of the treatment further research be completed.

Researchers: Richardson AJ, Puri BK., University Department of Physiology, Oxford, England, UK

Published: A randomized double-blind, placebo-controlled study of the effects of supplementation with highly unsaturated fatty acids on ADHD-related symptoms in children with specific learning difficulties, Prog Neuropsychopharmacol Biol Psychiatry. 2002 Feb;26(2):233-9


Bladder Infections

1. Urinary Tract Infections - Research Bibliography

Also see discussion of bladder infections (UTI) recommendations and research.

1. Sanchez A, Reeser JL, Lau HS, et al. Role of sugars in human neutrophilic phagocytosis. Am J Clin Nutr 1973;26:1180–4.
2. MacGregor RR. Alcohol and immune defense. JAMA 1986;256:1474.
3. Barone J, Herbert JR, Reddy MM. Dietary fat and natural-killer-cell activity. Am J Clin Nutr 1989;50:861–7.
4. Horesh AJ. Allergy and infection. Proof of infectious etiology. J Asthma Res 1967;4:269–82.
5. Rudolph JA. Allergy as a cause of frequent recurring colds and coughs in children. Dis Chest 1940;6:138.
6. Berman BA. Pseudomononucleosis of allergic origin: a new clinical entity. Ann Allergy 1964;22:403–9.
7. Randolph TG, Hettig RA. The coincidence of allergic disease, unexplained fatigue, and lymphadenopathy; possible diagnostic confusion with infectious mononucleosis. Am J Med Sci 1945;209:306–14.
8. Mori S, Ojima Y, Hirose T, et al. The clinical effect of proteolytic enzyme containing bromelain and trypsin on urinary tract infection evaluated by double blind method. Acta Obstet Gynaecol Jpn 1972;19:147–53.
9. Sirsi M. Antimicrobial action of vitamin C on M. tuberculosis and some other pathogenic organisms. Indian J Med Sci 1952;6:252–5.
10. Axelrod DR. Ascorbic acid and urinary pH. JAMA 1985;254:1310–1.
11. Hussey GD, Klein M. A randomized, controlled trial of vitamin A in children with severe measles. N Engl J Med 1990;323:160–4.
12. Chandra RK. Effect of vitamin and trace-element supplementation on immune responses and infection in elderly subjects. Lancet 1992;340:1124–7.
13. Avorn J, Monane M, Gurwitz JH, et al. Reduction of bacteriuria and pyuria after ingestion of cranberry juice. JAMA 1994;271:751–4.
14. Dignam R, Ahmed M, Denman S, et al. The effect of cranberry juice on UTI rates in a long term care facility. J Am Geriatr Soc 1997;45:S53.
15. Walker EB, Barney DP, Mickelsen JN, et al. Cranberry concentrate: UTI prophylaxis. J Family Pract 1997;45:167–8 [letter].
16. Sobota AE. Inhibition of bacterial adherence by cranberry juice: Potential use for the treatment of urinary tract infections. J Urol 1984;131:1013–6.
17. Schlager TA, Anderson S, Trudell J, Hendley JO. Effect of cranberry juice on bacteriuria in children with neurogenic bladder receiving intermittent catheterization. J Pediatr 1999;135:698–702.
18. Ofek I, Goldhar J, Zafriri D, et al. Anti-Escherichia coli adhesin activity of cranberry and blueberry juices. New Engl J Med 1991;324:1599 [letter].
19. Blumenthal M, Busse WR, Goldberg A, et al. (eds). The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin: American Botanical Council and Boston: Integrative Medicine Communications, 1998, 428.
20. Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs and Cosmetics. New York: John Wiley and Sons, 1996, 104–5.
21. Blumenthal M, Busse WR, Goldberg A, et al. (eds). The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin: American Botanical Council and Boston: Integrative Medicine Communications, 1998, 317.
22. Kienholz VM, Kemkes B. The anti-bacterial action of ethereal oils obtained from horse radish root (Cochlearia armoracia L.). Arzneimittelforschung 1961;10:917–8 [in German].
23. Schindler VE, Zipp H, Marth I. Comparative clinical investigations of an enzyme glycoside mixture obtained from horse radish roots (Cochlearia armoracia L). Arzneimittelforschung 1961;10:919–21 [in German].
24. Sun DX, Abraham SN, Beachey EH. Influence of berberine sulfate on synthesis and expression of pap fimbrial adhesin in uropathogenic Escherichia coli. Antimicrob Agents Chemother 1988;32:1274–7.
25. Doan DD, Nguyen NH, Doan HK, et al. Studies on the individual and combined diuretic effects of four Vietnamese traditional herbal remedies (Zea mays, Imperata cylindrica, Plantago major and Orthosiphon stamineus). J Ethnopharmacol 1992;36:225–31.
26. European Scientific Cooperative for Phytotherapy. Proposal for European Monographs, Vol. 3. Bevrijdingslaan, Netherlands: ESCOP Secretariat, 1992.
27. Blumenthal M, Busse WR, Goldberg A, et al. (eds). The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin: American Botanical Council and Boston: Integrative Medicine Communications, 1998, 224–5.
28. Aune A, Alraek T, LiHua H, Baerheim A. Acupuncture in the prophylaxis of recurrent lower urinary tract infection in adult women. Scand J Prim Health Care 1998;16:37–9.


Cataract (lens problems)

1. Alpha lipoic acid (1995) useful in cataract formation

See more information about cataracts.

Researchers found that alpha Lipoic Acid can prevent development of cataracts. It also is helpful for nerve degeneration and injury from radiation.

Published: Packer, et al. Free Radic Biol Med 1995 Aug;19(2):227-50

2. Antioxidants (1998) antioxidant vitamins and nuclear opacities: the longitudinal study of cataract.

See more about cataracts treatment and information.

Leske MC; Chylack LT Jr; He Q; Wu SY; Schoenfeld E; Friend J; Wolfe J University Medical Center at Stony Brook, New York 11794-8036, USA. Ophthalmology (United States) May 1998, 105 (5) p831-6 OBJECTIVE: The association of antioxidant nutrients and risk of nuclear opacification was evaluated in the Longitudinal Study of Cataract.

DESIGN: Nutritional data were collected at baseline on the 764 participants, which included assessment of dietary intake, use of vitamin supplements, and plasma levels of vitamin E. Ophthalmologic and other data were collected at baseline and at yearly follow-up visits, including lens photographs, which were graded using the Lens Opacities Classification System III protocol.

MAIN OUTCOME MEASURES: Analyses examined whether the nutritional factors at baseline were related to increases in nuclear opacification at follow-up. The MULCOX2 approach, an extension of the Cox regression model, was used. Results are presented as relative risks (RRs) and 95% confidence intervals. INTERVENTION: Intervention was not applicable. RESULTS: The risk of nuclear opacification at follow-up was decreased in regular users of multivitamin supplements (RR = 0.69; 0.48-0.99), vitamin E supplements (RR = 0.43; 0.19-0.99), and in persons with higher plasma levels of vitamin E (RR = 0.58; 0.36-0.94).

CONCLUSIONS: In regular users of multivitamin supplements, the risk of nuclear opacification was reduced by one third; in regular users of vitamin E supplements and persons with higher plasma levels of vitamin E, the risk was reduced by approximately half. These results are similar to those obtained in our earlier case-control study. Because these data are based on observational studies only, the results are suggestive but inconclusive. The possible effect of nutritional supplements on the lens requires confirmation by ongoing clinical trials.

3. Antioxidants (2001) and Cataract Prevention

See more about cataracts treatment and information.

Researcher finds that different antioxidants can help prevent varying types of cataract as follows:

- People with the highest blood concentrations if either beta- or alpha-carotene were 30-50% less likely to develop nuclear cataracts, which are those located in the central part of the lens.

- People with high blood levels of lycopene (found in high concentration in cooked tomatoes) were associated with a 60% lower risk if cortical cataracts, which are those located in the outer layer of the lens.

- People with high lutein concentrations were 50% less likely to develop posterior subcapular cataracts, which are those located toward the bottom rear of the lens.

So in essence the study shows that a diet rich in antioxidants can reduce the risk of cataracts.

References: Gale CR, Hall NF, Phillips DI, et al. "Plasma antioxidant vitamins and carotenoids and age-related cataract." Ophthalmology, 2001;108:1992-1998. Jacques PF, Chylack LT. Jr., Hankinson SE, et al. "Long-term nutrient intake and early age-related nuclear lens opacities," Archives of Ophthalmology, 2001;119:1009-1019.

4. Antioxidants (2001) May Slow Cataract Progression

11/21/01 - NEW ORLEANS — A nutritional diet that includes beta-carotene (18 mg/day), vitamin C (750 mg/day) and vitamin E (600 mg/day) has been shown to modify the progression of cataracts, according to the Roche European-American Cataract Trial results.

Of the 297 patients randomized in the trial, 231 were followed for 2 years, 158 were followed for 3 years and 36 were followed for 4 years. After a 3-month placebo run-in, patients were randomized by clinical center to vitamin or placebo control group and followed every 4 months.

No statistically significant differences existed between treatment groups at baseline. After 2 years of treatment, a small positive effect was noted in the U.S. group; at 3 years, positive effects were noted in both the U.S. and U.K. groups.

See more information about cataracts and lens support with vitamins and supplements.

5. Bilberry extract (1989) and vitamin E - Cataracts

In one study, a combination of bilberry and vitamin E stopped cataract formation in 97 percent of the patients – without side effects. Bravetti, G.O. Preventive medical treatment of senile cataract with vitamin E and Vaccinium myrtillus anthocyanosides. Clinical evaluation. Ann Ottalmol Clinical Ocul. 115 (1989): 109.

See nutritional recommendations for cataracts as well as recommendations for self help and prevention.

6. Carnosine (1999) & Senile Cataract

Learn more about cataracts.

Chinese and Russian researchers completed a preliminary study whose result showed that carnosine gives a pronounced effect on primary senile cataracts, the effective rate being 100%. For mature senile cataracts, the effect rate was 80%.

Wang AM, et al. Use of carnosine as a natural anti-senescence drug for human beings. Department of Biochemistry and Department of Neurobiology, Harbin Medical University, China 1999.

7. Carnosine (2009) combats cataracts

See more about cataracts treatment and information.

In the July 28, 2009 issue of the journal Biochemistry, Italian researchers report that the dipeptide carnosine shows promise not only in preventing cataracts but also in helping to treat the condition. Cataracts, which are characterized by a clouding of the eye's lens, are a major cause of visual impairment among older men and women, and surgery is currently the only effective treatment.

Enrico Rizzarelli of the University of Catania and his colleagues tested the effects of D- and L-carnosine on bovine cultured alpha-crystallin, the major structural protein in the lens of the eye. The cultures were treated with guanidine, a compound that is known to cause cataracts via the formation of alpha-crystallin fibrils. Co-incubation of the cultures with carnosine helped inhibit fibrillation, and the addition of carnosine to pre-existing fibrils was found to almost completely dissolve them.

8. Diet (2011), Cataract Risk & Vegetarianism

Learn more about cataracts.

In this study the researchers looked into the relationship between diet and risk of cataract. The study subjects were 27,670 non-diabetic people aged 40 and more, a large proportion of whom were vegetarians.

The researchers used a testing model known as the Cox proportional hazards regression to evaluate the risk.

They found a strong correlation between the risk of cataract and the type of diet. The subjects who ate the most meat had the highest rate of cataracts, and those who ate fish, but not meat had a lower rate, vegetarians had a lower rate and vegans had the lowest rate of cataract incidence.

Researchers: Paul N Appleby, Naomi E Allen, and Timothy J Key

Published: Diet, vegetarianism, and cataract risk, Am J Clin Nutr May 2011 ajcn.004028

9. Glutathione (2000) Antioxidant for cataracts

Learn more about cataracts treatment and information.

These and other studies demonstrating the effectiveness of glutathoine as a powerful anti-oxidant are also important with respect to macular degeneration and other eye diseases.

Research published in 2000 has demonstrated that glutathione (GSH) is an essential antioxidant which is particularly concentrated in the lens of the eye. It detoxifies oxidants (free-radicals) such as H202 and dehydroascrobic acid. When there are very low levels of GHS in the lens, it has been found that even low levels of oxidants can damage the lens.

Research published: Giblin FJ. Glutathione: a vital lens antioxidant. J Ocul Pharmacol Ther 2000 Apr; 16(2):121-35.

Another study published in 2002 older people had a greater drop in glutathoine blood status than younger people with a corresponding increase in oxidized glutathione by-product over time suggests more oxidation and the higher risk of age-related eye diseases.

References: Brubaker RF, et al. Ascorbic acid content of human corneal epithelium. Invest Ophthalmol Vis Sci 2000 Jun;41(7):1681-3.

Ayalasomayajula SP, et al. Induction of vascular endothelial growth factor by 4-hydroxynonenal and its prevention by glutathione precursors in retinal pigment epithelial cells. Eur J Pharmacol 2002 Aug 9;449(3):213-20.

10. Leafy Green Veggies (2004) Protect Eyes

In the lab, researchers looked at the effects of lutein and zeaxanthin on samples of human eye lens cells. They compared the action of these antioxidants on the cells to that of vitamin E.

They treated the cells with concentrations of the antioxidants and then exposed them to ultraviolet radiation, about the same amount that a person gets with a mild tan.

Adding lutein and zeaxanthin to the cells reduced signs of ultraviolet damage by 50%-60%. Vitamin E reduced the same signs of damage by 25%-32%.

This study provides more evidence that these antioxidants found in plants such as spinach, kale, and collard greens, can help prevent cataracts by protecting the eyes from ultraviolet radiation.

Published: Chitchiumroonchokchai, C. Journal of Nutrition, December 2004; vol 134: pp 3225-3232

Learn more about cataracts.

11. Lipoic acid (1995) Cataracts

Learn more about holistic treament of cataracts.

Scientists have found that lipoic acid treatment on cataracts in rats has measurable benefit and conclude that it may be of therapeutic use in preventing cataracts and their related complications in human eyes, not only for cataracts, but for glaucoma as well.

Published: Kilic F; Handelman GJ; Serbinova E; Packer L; Trevithick JR. Modelling cortical cataractogenesis 17: in vitro effect of a-lipoic acid on glucose-induced lens membrane damage, a model of diabetic cataractogenesis. Biochem Mol Biol Int, 1995 Oct, 37:2, 361-70

12. Long Term Lutein Supplementation Improves Visual Acuity in Age-Related Cataracts
In a 24-month study, visual acuity and glare sensitivity improved in the lutein group, with visual acuity significantly improved over baseline (p>005).

Olmedill B. et al: Lutein, but not alpha tocopherol, supplementation improves visual function in patients with age-related cataracts: A 2 year double-blind, placebo controlled study. Nutrition 19:21-24, 2003

13. Low levels of vitamin E (1993)
Low blood levels of vitamin E were associated with approximately twice the risk of both cortical and nuclear cataracts, compared to median or high levels. Vitale, et al. Epidemiology 1993 May;4(3):195-203

14. Lutein (1995) and Zeaxanthin - Cataracts & Cancer

Learn more about natural treament of cataracts.

Researchers found that xanthophylls lutein and zeaxanthin are the only carotenoids which are found in the lens of the eye. They also found that large levels of antioxidant vitamins, such as carotenoids in the blood plasma and in patients' diets can be connected to a lower risk of developing cataracts.

For example, a diet that includes significant amounts of of spinach, a dark leafy green high in lutein and zeaxanthin was consistently connected with a smaller risk for cataract development. Correspondingly, high lipid antioxidant status is connected to healthier and longer eye lens functioning.

Why? The research suggests that xanthophylls block blue light which is phototoxic.

Likewise, there is a strong inverse connection between between large intakes of of dark leafy green vegetables, rich in lutein and zeaxanthin, and a lower risk for another oxidative stress related disease - cancer.

Lutein and zeaxanthin are the only carotenoids that have been reported to be present in a number of locations within the human eye: the retina, the macula, and the lens.

Published: KJ Yeum etal, "Measurement of Carotenoids, Retinoids, and Tocopherols in Human Lenses," Investigative Ophthalmology and Visual Science, December, 1995, Vol. 36. No. 13, pp. 2756-2761.

15. Lutein (1999) and Cataract Prevention

Learn more about holistic treament of cataracts, lutein, and zeaxanthin.

Researchers found that the carotenoids lutein and zeaxanthin may be particularly effective in cataract prevention. The Harvard Medical School study included almost 80,000 females nurses and over 35,000 male health professionals. The female group completed diet questionnaires in 1980 and 1984, with follow-up until 1992. By 1992, 1471 of them had had cataracts removed. The male group completed questionnaires in 1986 and with follow-up for 8 years. By 1994 they had had 840 cataracts removed.

The researchers found that the 20% of nurses with the most lutein and zeaxanthin in their diet had 22% lower risk of cataract than did women with the least amounts in their diet. Among the men, the 20% with the highest intake had a 19% lower risk of cataracts compared to the 20% with the lowest intake.

There was a significant benefit due to spinach, kale and broccoli in the diet, but no confirmed results from pther carotenoids or vitamin A.

Researchers: Harvard Medical School

Published: Chasan-Taber, Lisa, et al. A prospective study of carotenoid and vitamin A intakes and risk of cataract extraction in US women. American Journal of Clinical Nutrition, Vol. 70, October 1999, pp. 509-16

Brown, Lisa, et al. A prospective study of carotenoid intake and risk of cataract extraction in US men. American Journal of Clinical Nutrition, Vol. 70, October 1999, pp. 517-24

Mares-Perlman, Julie A. Too soon for lutein supplements. American Journal of Clinical Nutrition, Vol. 70, October 1999, pp. 431-2 (editorial)

16. Lutein (1999) diet and cryptoxanthin - Cataracts

Learn more about natural treament of cataracts.

A 1999 study showed that lutein and cryptoxanthin in the diet were connected with a 70% lower risk of cataracts in the eyes in people aged less than 65.

Published: Lyle, et al. Am J Clin Nutr 1999 Feb;69(2):272-7

17. Lutein, Zeaxanthin and Vitamin E (2008) Reduce Risk of Cataracts

Learn more about natural treament of cataracts.

In a long-term 10-year study the use of dietary supplements and presence of cataracts was assessed in more than 35,000 middle-aged U.S. women. The researchers found significant evidence that women who had diets/supplements including more zeaxanthin, lutein and vitamin E were less likely to develop cataracts than women who are lacking intake of these nutrients. The women with the highest levels of these nutrients were 18% less likely to get cataracts.

Published: Archives of Ophthalmology (Arch. Ophthalmol. 2008;126:102-9) from the Women's Health Study.

18. N-acetylcarnosine (2002) & cataracts
PURPOSE: To evaluate the effects of 1% N-acetylcarnosine (NAC) solution on lens clarity over 6 and 24 months in patients with cataracts. TRIAL DESIGN: Randomised, placebo-controlled study. PARTICIPANTS: 49 subjects (76 affected eyes) with an average age of 65.3 +/- 7.0 years with a diagnosis of senile cataract with minimum to advanced opacification in various lens layers. METHODS:

Learn more about supporting lens health. Can-C contains 1% NAC.

In this controlled study 13 patients with lens opacity received 1% NAC eyedrops or a placebo (10 patients). The lens condition was evaluated at start and each two months for six months, or every six months for two years - in two different trials. The cataracts were assessed for vision sharpness and glare and were measured with stereocinamatographic retro-illumination and slit-images.

After six months 90% of the patients who had received NAD showed improvement in vision sharpness, and 89% showed improvement in glare. M.o<

The improvements continued after 24 months' treatment with NAC and none had deterioration of vision - while in the control group there was significant worsening after 24 months compared to both the start measurements and the treated patients.

There were no reports of systemic or ocular side effects and the drops were well tolerated. The researchers concluded that NAC shows promise for treating and preventing cataracts.

Researchers: Babizhayev MA, et al, Innovative Vision Products, Inc., Delaware, USA

Published: Efficacy of N-acetylcarnosine in the treatment of cataracts, Drugs in R&D, 2002;3(2):87-103.

19. N-Acetylcarnosine (2009) & Cataracts

Learn more about support of lens health. Can-C eye drops are formulated with 1% N-Acetylcarnosine.

This study was designed to substantiate and fuller examine the results found in a 2002 study on the effectiveness of 1% N-Acetylcarnosine in improving cataract.

The subjects were 75 patients ranging from 54 to 78 years of age with no history of cataract surgery or other vision conditions except cataracts and with vision of 20/40 or worse as well as 72 controls. The patients had reported symptoms of glare sensitivity and were looking for quick relief.

After nine months the researchers found that most patients' glare scores improved or returned to normal standards.

The researchers emphasized that only the natural form of NAC in L-isomeric form was used and claimed this was important for outcomes. They discussed the mechanisms of cataract improvment to include:

  • prevention of free-radical-induced negative effect on antioxidents in the lens (superoxide dismutase);
  • prevention of oxidation (carbohydrate & metal-catalyzed) on interactions with proteins in the lens;
  • non-enzyme induced bonding capacity of carnosine which in turn protects the lens crystalline struction (proteins) from being adversely changed;
  • free-radical scavenging action of aldehyes, lipid hydroperoxides, and oxygen radicals;
  • interaction btween l-carnosine and proteasome activity; and
  • disaggregation of lens crystallins activity.

Researchers: Babizhayev MA, et al, Innovative Vision Products, Inc., DE

Published: N-Acetylcarnosine sustained drug delivery eye drops to control the signs of ageless vision: glare sensitivity, cataract amelioration and quality of vision currently available treatment for the challenging 50,000-patient population, Clinical Interventions to Aging. 2009;4:31-50.

20. N-Acetyl-Carnosine (NAC) (2001) & Cataracts

See more about cataracts treatment and information. Can-C Eyedrops contain 1% NAC.

A study was designed to document and quantify the changes in lens clarity over 6 and 24 months in 2 groups of 49 volunteers (76 eyes) with an average age of 65.3 +/- 7.0 enrolled at the time of diagnosis of senile cataracts of minimal to advanced opacification.The patients received N-acetylcarnosine, 1% sol (NAC) (26 patients, 41 eyes = Group II), placebo composition (13 patients, 21 eyes) topically (two drops, twice daily) to the conjunctival sac, or were untreated (10 patients, 14 eyes); the placebo and untreated groups were combined into the control (reference) Group I.

Patients were evaluated upon entry, at 2-month (Trial 1) and 6-month (Trial 2)-intervals for best corrected visual acuity (b/c VA), by ophthalmoscopy and the original techniques of glare test (for Trial 1), stereocinematographic slit-image and retro-illumination photography with subsequent scanning of the lens. The computerized interactive digital analysis of obtained images displayed the light scattering/absorbing centers of the lens into 2-D and 3-D scales.

The intra-reader reproducibility of measuring techniques for cataractous changes was good, with the overall average of correlation coefficients for the image analytical data 0.830 and the glare test readings 0.998. Compared with the baseline examination, over 6 months 41.5% of the eyes treated with NAC presented a significant improvement of the gross transmissivity degree of lenses computed from the images, 90.0% of the eyes showed a gradual improvement in b/c VA to 7-100% and 88.9% of the eyes ranged a 27-100% improvement in glare sensitivity.

Topographic studies demonstrated less density and corresponding areas of opacification in posterior subcapsular and cortical morphological regions of the lens consistent with VA up to 0.3. The total study period over 24 months revealed that the beneficial effect of NAC is sustainable. No cases resulted in a worsening of VA and image analytical readings of lenses in the NAC-treated group of patients. In most of the patients drug tolerance was good. Group I of patients demonstrated the variability in the densitometric readings of the lens cloudings, negative advance in glare sensitivity over 6 months and gradual deterioration of VA and gross transmissivity of lenses over 24 months compared with the baseline and 6-month follow-up examinations.

Statistical analysis revealed the significant differences over 6 and 24 months in cumulative positive changes of overall characteristics of cataracts in the NAC-treated Group II from the control Group I.The N-acetylated form of natural dipeptide L-carnosine appears to be suitable and physiologically acceptable for nonsurgical treatment for senile cataracts.

Peptides 2001 Jun;22(6):979-94

21. N-Acetyl-Carnosine and Cataracts discussion ('99-'02)

Carnosine's best-known effect, however, is its ability to prevent the formation of advanced glycated end products (protein crosslinks). Carnosine competes with proteins for the binding sites they would occupy on sugar molecules, making it the best glycation preventative currently recognized in the world of nutrition research.

Can-C Eyedrops contain 1% NAC.

Carnosine has been found to significantly extend the life span of cultured cells and fruit flies, inhibit the toxic effects of the protein that accumulates in the brains of Alzheimer's patients, protect against the toxic effects of copper- zinc in the brain and enhance the state of balance (homeostasis) under which physiological systems work best. And, finally, it has been shown to prevent and/or reverse cataract.14,15

14. Quinn PJ, et al. Carnosine: its properties, functions and potential therapeutic applications. Mol Aspects Med 1992; 13(5):379-444. 15. Specht S, et al. Continuing damage to rat retinal DNA during darkness following light exposure. Photochem Photobiol 2000; 71(5):559-66.

When administered topically to the eye in the form of N-acetyl-L-carnosine-(functionally, a time-release form of carnosine), this dipeptide can move easily into both the water-soluble (aqueous) and lipid-containing parts of the eye. Once there, it helps to prevent DNA strand breaks induced by UV radiation and enhances DNA repair.16 Once it has entered the lipid areas of the eye, N-acetyl-L-carnosine partially breaks down and becomes L-carnosine.

Chinese and Russian researchers have studied cataract-preventive nutrients for nearly a decade. A Chinese study done by A.M. Wang in 1999, used 96 patients aged 60 years or older having senile cataracts of various degrees of maturity with the duration of the disease from 2 to 21 years. Patients instilled one to two drops of the carnosine-containing solution in each eye three to four times each day for a period of treatment ranging from three to six months. The level of eyesight improvement and the change of lens transparency were considered as an evaluation index of the curative effect of carnosine. The result showed that carnosine gives a pronounced effect on primary senile cataracts, the effective rate being 100%. For mature senile cataracts, the effect rate was 80%.17

17. Wang AM, et al. Use of carnosine as a natural anti-senescence drug for human beings. Department of Biochemistry and Department of Neurobiology, Harbin Medical University, China 1999.

The Russians most recent contribution was published in 2002 in the journal Drugs Research and Development.18 In two separate studies, they applied a one percent solution of N-acetyl-carnosine to the affected eyes of cataract patients twice a day. Only patients with mild cataracts-not anticipated to require surgery within the next two years-in one or both eyes were selected to participate. A matched control group received placebo drops, and another small matched group received no drops at all. The first study lasted six months, while the second continued for a total of 24 months. Tests of visual acuity and glare sensitivity were administered every two months in the first study and every six in the second.

After six months, a full 90% of eyes treated with N-acetyl-carnosine showed improvements in visual acuity ranging from 7% to 100%. Glare sensitivity improved 27% to 100% in 88.9% of carnosine recipients, and image analysis (a measurement of visual clarity) improved in 41.5% of treated eyes. Lens examination revealed fewer areas of lens opacity in the posterior subcapsular region. No worsening of vision was found in the eyes treated with N-acetylcarnosine, and all of these benefits were sustained through the 24 months that treatment continued.

These study results are evidence that N-acetyl-carnosine is one of the most important nutrients for cataract prevention. The entire body of research on carnosine reveals its promise as an anti-aging nutrient that works at several levels to protect multiple organ systems.

18. Babizhayev M, et al. Efficacy of N-acetylcarnosine in the treatment of cataracts. Drugs Research & Development 2002; 3(2):87-103.

22. NASA Study of Cataract in Astronauts (NASCA)
Cross-sectional data analysis revealed a small deleterious effect of space radiation for cortical cataracts and possibly for PSC cataracts. These results suggest increased cataract risks at smaller radiation doses than have been reported previously. SOURCE: Chylack LT Jr, Peterson LE, Feiveson AH, et al. NASA study of cataract in astronauts (NASCA). Report 1: Cross-sectional study of the relationship of exposure to space radiation and risk of lens opacity. Radiat Res 2009;172(1):10-20.

23. Nutrition (1993) and Oxidation: Cataracts

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Taylor A., Journal of the American College of Nutrition, 1993 Apr, 12(2):138-46 Pub type: Journal Article; Review; Review, Tutorial. (UI: 93217072)

Abstract:
Opacification of the lens, or cataract, is causally related to the precipitation of proteins or other constituents upon aging. Proteins in the lens are unusually long lived and are subject to extensive damage, including (photo) oxidation. Accumulation of damaged proteins also appears to be due in part to attenuated activity of some proteolytic pathways, which in younger tissue may serve to identify and remove such moieties. The damaged proteins accumulate, aggregate, and precipitate.

Compared with other health problems, surgery to remove cataract and related visits to physicians consume the largest proportion of the Medicare budget, i.e., $3.2 billion annually in the United States. The situation is exacerbated in many parts of the world where there is a dearth of ophthalmologists to perform the required number of procedures. Historically efforts to delay cataract assumed a low profile in ophthalmologic research.

Recent data, however, indicate that consuming elevated levels of antioxidants such as ascorbate, carotenoids, and tocopherol is associated with delayed development of various forms of cataract. The same beneficial relationship to vision pertains to plasma antioxidant status and to fruit and vegetable intake.

Thus, it seems that assuring optimal antioxidant intake can extend lens function. It has been estimated that in the United States over half of the cataract extractions and associated costs would be obviated if cataract could be delayed by 10 years. The data reviewed indicate that optimizing nutrition will help achieve that objective.

24. Riboflavin (1991), vitamins C, E, carotene, niacin, thiamine & cataracts

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Researchers found that increased riboflavin, vitamins C, E, and carotene, niacin, and thiamine in the diet significantly lessened the risk of all cataract types. They also found that when different antioxidant nutrients were combined the beneficial results were the greatest.

Published: Leske, et al. Arch Ophthalmol 1991 Feb;109(2):244-51.

25. Smoking - Cataracts (1993)
Cigarette smoking causes about 20 percent of all cataracts. Men who smoke more than a pack a day increase their risk for cataracts by 205 percent.; for female smokers, risk increases 63 percent. Christan, W.G. et al. Cigarette smoking and the risks of cataract. Investigative Ophthalmology. In ARVO Abstracts, April 1991. Also, Christen, W.G., and Seddon, J.M. Cigarette smoking and cataract. American Journal of Preventive Medicine 9 (1993): 65-66.

26. Study Suggests Lutein and Zeaxanthin Offer Lens Protection
About 20 million Americans have vision-obstructing cataracts, with 500,000 new cases diagnosed annually. The estimated current cost of $3.4 billion annually to surgically extract cataracts is expected to increase along with the growing number of people over the age of 65. Among the risk factors associated with age-related cataracts, UV exposure and oxidative stress appear to be the most relevant. The lens is equipped with antioxidant mechanisms - such as glutathione peroxidase, vitamins C and E and carotenoids - to defend against the harmful effects of UV radiation and reactive oxygen species (ROS). Indeed, some epidemiologic studies suggest a reduced risk of developing various types of cataract with higher intake of vitamin C, E or lutein and zeaxanthin, the only carotenoids present in the lens and macula.

Although considerable efforts are being made to define the potential role of the xanthophylls lutein and zeaxanthin in the macula, information about their uptake and function in the lens is extremely limited. Epithelial cells, the outermost cellular layer of the lens, are exposed to UV irradiation not filtered by the cornea. UV-induced damage is mediated via production of ROS, and characterized by alterations in cell growth, morphology, changes in membrane potential, and oxidation of lipids, proteins and DNA. The present study examined the ability of xanthophylls to protect cultures of immortalized human lens epithelial cells (HLE) against UVB insult.

Results:

Cultured HLE cells accumulated xanthophylls and alpha tocopherol in a dose and time-dependent manner, with uptake of lutein exceeding that of zeaxanthin. Cultures were pretreated with either xanthophylls (2 µmol/L) or alpha tocopherol (10 µmol/L) for 4 hours, then exposed to 300 J/m2 UVB radiation - a dose roughly equivalent to that a person receives when they get a mild tan. Lipid peroxidation was observed to decrease by 47-57% compared with UVB-treated control cells.

The ability of xanthophylls and vitamin E to inhibit UVB-induced stress signaling was also assessed. Pretreatment with xanthophylls and alpha tocopherol inhibited UVB-induced activation of c-JUN NH2 terminal kinase and p38 activation by 50-60% and 25-32%, respectively. The concentration of Vitamin E required to significantly inhibit these stress signaling markers was roughly 10-fold higher than that of the xanthophylls, suggesting that xanthophylls are more potent for protecting HLE cells against UVB insult in this model.

Conclusions

According to the researchers from Ohio State University, their results are the first to provide physical evidence suggesting that lutein and zeaxanthin decrease damage caused by UV radiation. "In addition to protective enzymes and compounds like vitamins C and E, we think that low concentrations of lutein and zeaxanthin in the eye's lens help shield the eye from the harmful effects of UVB radiation", they stated in a post-publication interview.

Reference

  1. Jacques PF. The potential preventive effects of vitamins for cataract and age-related macular degeneration. Int J Vitam Nutr Res 69: 198-205, 1999.
  2. Taylor A et al. Long-term intake of vitamins and carotenoids and odds of early age-related cortical and posterior subcapsular lens opacities. American Journal of Clinical Nutrition 75:540-9, 2002.
  3. Chasen-Taber et al. A prospective study of carotenoid and vitamin A intakes and risk of cataract extraction in US women. American Journal of Clinical Nutrition 70:509-516, 1999.
  4. Alves-Rodrigues A and Shao A. Review. The Science Behind Lutein. Toxicology Letters 150:57-83, 2004
  5. Chitchumroonchokchai C et al. Xanthophylls and alpha tocopherol decrease UVB-induced lipid peroxidation and stress signaling in human lens epithelial cells. Journal of Nutrition 134:3225-32, 2004.

27. Study Suggests Statins Can Cause Cataracts (2011 Study)
Now a study reported in the journal BMJ (Volume 340, page 2197) suggests that statins, the widely used class of cholesterol-lowering drugs, are associated with an increased risk of cataracts. Investigators reviewed information from more than two million people in England and Wales, ages 30 to 84, in the QResearch medical database between 2002 and 2008. Of that group, 225,992 were new users of one of the following statins: simvastatin (Zocor), atorvastatin (Lipitor), pravastatin (Pravachol), rosuvastatin (Crestor), or fluvastatin (Lescol). The investigators found that statin use was associated with an increased risk of cataracts in both men and women. The risk of cataracts rose within one year of starting statin treatment, persisted during treatment, and then returned to normal within a year after discontinuing the statin. Bottom line: This study was not designed to show whether statins could cause cataracts, but it does show an association between the two. These findings conflict with other recent studies that have found that statins may prevent cataract development. More studies are needed to provide a definitive answer. In the meantime, it's important to see your eye doctor regularly to monitor for cataracts and other eye diseases.

28. Sugar can impair the lens (1991)
All types of sugars, not just white sugar, can impair the eye's len’s ability to keep itself clear. Gaby, A.R., and Wright, J.V. Nutritional Factors in Degenerative Eye Disorders: Cataract and Macular Degeneration. Wright/Gaby Nutritional Institute, 1991.

29. Vitamin A - Cataracts (1992)

In the Nurses Health Study, a large cohort of nurses had been following for almost 20 years. In this longitudinal study, increased dietary intake of Vitamin A was associated with a 39% reduction in risk of cataract extraction. Hankinson, S.E. Stampfer, M.J. et al. BMJ Vol.305,1992.

See more information about cataracts.

30. Vitamin A (1944) Cataracts

Learn more about holistic treament of cataracts.

Researchers noted as early as 1944, after reviewing data from the Nutrition and Eye Disease Study, that moderate levels of Vitamin A in patients' diets were connected to a 40% lower risk of opaque lenses, or cataracts. The researchers adjusted the risk for age, sex, smoking, and heavy drinking and found that for those who were smokers, the cataract risk was reduced by 50%.

Published: Mares-Perelman, J.A., Klein, B.E.K., et al. Relationship Between Lens Opacities and Vitamin and Mineral Supplement Use. Ophthalmology 1944;101:315-325.

31. Vitamin C - Cataracts
In studies done since 1935, vitamin C has been shown to prevent and even reverse the negative effects of sugar on the eyes. Blondin, J., Baragi, V.K., Schwartz, E.R., Sadowski, J., and Taylor, A. Prevention of eye lens protein damage by dietary vitamin C. Federal Prodceedings 45 (1986): 478.

32. Vitamin C - cataracts & opacities (1997)
Subjects taking vitamin C supplements for more than 10 years had a 77% lower risk of early lens opacities (cataracts) and 83% lower risk of moderate lens opacities. Jacques, et al. The American Journal of Clinical Nutrition, Oct. 1997

33. Vitamin C - cataracts (1995)
The vitamin C content of the eye is 20 times greater than that in the blood. Results from some studies including the Beaver Dam Eye Study, suggest that people with high levels of vitamin C are at less risk of cataracts than those with low levels of vitamin C. Mares Perlman JA; Brady WE; Klein BE; Klein R; Haus GJ; Palta M; Ritter LL; Shoff SM. Diet and nuclear lens opacities. Am J Epidemiol, 1995 Feb, 141:4, 322-34

34. Vitamin C & Cataracts 2010 Indian Study

A recent study published in the journal "Archives of Ophthalmology" showed an inverse linkbetween vitamin C and cataracts. This Indian study was a population-based cross-sectional analytic study measuring the plasma vitamin C levels in 5638 people 60 years of age or older. These people were checked for cataracts and type of cataracts.

Low levels of lutein, zeaxanthin, retinol and vitamin C all showed to be correlated to cataracts. However, low vitamin C levels had by far the strongest association and were also consistent by type of cataract.

Ref: Ophthalmology. 2011;118(10):1958-1965

35. Vitamin C (1997) Cataracts (NHS)

Learn more about natural treament of cataracts.

The 1997 Nurses Health Study indicates that long-term consumption of vitamin C supplements can reduce the development of cataracts. Researchers considered the connection between development of cataracts and vitamin C supplementation over 10 to 12 years in 247 56 to 71 year old nurses from the Boston area. The researchers did detailed eye exams to determine how much the eyes' lens were clouded and found that those women how had taken vitamin C supplements for over ten years had 77% fewer early lens opacities and 83% fewer moderate lens opacities.

Published: Jacques PF; Taylor A; Hankinson SE; Willett WC; Mahnken B; Lee Y; Vaid K; Lahav M. Long-term vitamin C supplement use and prevalence of early age-related lens opacities. Am J Clin Nutr, 1997 Oct, 66:4, 911-6

Researchers: Jacques PF; Taylor A; Hankinson SE; Willett WC; Mahnken B; Lee Y; Vaid K; Lahav M., US Department of Agriculture and Harvard School of Public Health

36. Vitamin C and Bioflavonoids Help Prevent Cataracts (2006)

Two studies show significant reductions in cataracts for those in the highest percentage of vitamin C intake.

In the first study, Japanese researchers followed 35,000 people. They evaluated the participants for their vitamin C intake and cataract formation. They found that those in the highest 20% of vitamin C intake had a 40% reduced risk of getting cataracts.

The second study followed 177 (116 women, 61 men) participants over the age of 60. In this study, the researchers found that if you are in the top 5% of vitamin C intake, your risk is reduced some 20% compared to the lowest 5%.

But that's not all this study found. If you ingest more than 3,290 mcg daily of lutein, your risk drops 14% compared to ingesting less than 256 mcg daily. Zeaxanthin had a smaller risk reduction, but mostly in men.

Interestingly, the study also found that sunlight exposure is also a major risk factor. If you were out in the sun a lot in your early years, your risk triples compared to being closeted indoors.

Ref: International Journal for Vitamin and Nutrition Research, 2006; 76(6); Nutr, 2007 January 30.

Read more about cataracts.

37. Vitamin C May Also Offer Protection Against Cataracts
The journal Ophthalmic Epidemiology published research regarding their study of age-related cataracts just this past April. The findings showed that higher plasma levels of Vitamin C reduced the prevalence of nuclear and posterior subcapsular cataracts.

1. Ferrigno L, Aldigeri R, Rosmini F, Sperduto RD, Maraini G; The Italian-American Cataract Study Group. Associations between plasma levels of vitamins and cataract in the Italian-American Clinical Trial of Nutritional Supplements and Age-Related Cataract (CTNS): CTNS Report #2. Ophthalmic Epidemiol. 2005 Apr;12(2):71-80.

38. Vitamin C Might Prevent Cataracts in Women
BOSTON, Feb 22, 2002 (United Press International via COMTEX) -- Women who take vitamin C supplements during their younger and middle-age years may reduce their chances of cataracts later in life, according to a new study released Friday. Researchers led by Allan Taylor of Tufts University in Boston came to that conclusion after analyzing data from the Nurses Health Study, an on-going study based on a group of women nurses in the Boston area whose diet, lifestyle and health status have been followed for the past 26 years. They looked at 492 non-diabetic study participants ages 53 to 73 and reviewed their diets, particularly their long-term vitamin supplement intake, extracted from food questionnaires dating from 1980 up to 1995. All of the women underwent eye examinations to screen for a variety of cataracts. Thirty-four percent of the group was found to have cortical opacities, a type of cataract where the fiber cells of the cortex deteriorate. Study results showed that among women age 60 and younger, daily vitamin C intake from both diet and supplements during the previous 13 to 15 years of the woman's life significantly minimized the chances of developing that one type of cataract. Among women younger than 60, consumption of 362 milligrams daily of vitamin C was linked with a 57 percent drop in cortical opacities. Routine use of vitamin C supplements for at least a decade was associated with an overall 60 percent reduction in cataracts when compared to no vitamin supplement use. Researchers also found women who never smoked and had high intakes of the nutrients folate and carotenoids also showed a reduction in cataracts. The findings suggest certain nutrients, when taken consistently and regularly throughout life, could potentially decrease the chances of one of the most common age-related conditions. The study is published in Friday's issue of American Journal of Clinical Nutrition.

39. Vitamin E - Cataracts (1991)
The Lens Opacity Case Control1 and Study and a Canadian study by Robertson, Donner and Trevithic2 each suggested about a 40-45% descreased risk of cataract or opacity with higher vitamin E intake through diet or supplement use.1 Leske MC, Chylack LT Jr, Wu S. The lens opacities case control study: risk factors for cataract. Arch Ophthalmol 1991;109;244-251. 2Robertson JM, Donner AP, Trevithick JR. A possible role for vitamins C and E in cataract prevention. Am J Clin Nutr 1991;53:346S-351S.

40. Vitamin E & Cataracts - Low levels of vitamin E (1991)

Like low levels of beta-carotene, a low level of vitamin E also increases cataract risk and reduces photooxidation. Roberton, J.M. A possible role for vitamin C and E in cataract prevention. American Journal of Clinical Nutrition 53 (1991): 3465-3515

Editor's Note: See our nutritional recommendations for cataracts, including whole food vision formulas and whole food multi-vitamins that include vitamin E.

Also see self help and prevention recommendations for cataracts.

41. Vitamin E and Cataract Prevention 2008 Study
An observational 10-year study of more than 35,000 middle-aged U.S. women observed the women’s use of dietary supplements and occurrence of cataracts. The study found significant evidence that women who got more lutein, zeaxanthin and vitamin E were less likely to develop cataracts than women who are lacking intake of these nutrients. In fact, the women who got the most lutein, zeaxanthin and vitamin E were 18% less likely to get cataracts. These nutrients are hot topics in research right now, including the ongoing AREDS II study. Ref: *Christen, W. Archives of Ophthalmology, January 2008; vol 126: pp 102-109. WebMD Medical News: "Nutrients May Help Save Eyes." National Institutes of Health Office of Dietary Supplements: "Vitamin E." News release, JAMA/Archives.

42. Vitamin E, C, (1997) alpha-lipoic acid and taurine

A 1997 study demonstrated that vitamins E and C, alpha-lipoic acid, and taurine appear to help protect the eye from lens damage which is caused by low level radiation. Bantseev, et al. Biochem Mol Biol Int 1997 Sept;42(6):1189-97.

See more information about cataracts


Celiac Disease

1. Celiac Disease research bibliography
These are earlier studies. Also see discussion of research on celiac disease

1. Srinivassan U, Leonard N, Jones E, et al. Absence of oats toxicity in adult coeliac disease. BMJ 1996;313:1300–1.
2. Jantauinen EK, Pikkarainen PH, Kemppainen TA, et al. A comparison of diets with and without oats in adults with celiac disease. N Engl J Med 1995;333:1033–7.
3. Greenberger JN, Isselbacher KJ. Disorders of absorption. In: Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrison’s Principles of Internal Medicine, 14th ed. New York: McGraw-Hill, 1998, chapter 285.
4. Faulkner-Hogg KB, Selby WS, Loblay RH. Dietary analysis in symptomatic patients with coeliac disease on a gluten-free diet: the role of trace amounts of gluten and non-gluten food intolerances. Scand J Gastroenterol 1999;34:784–9.
5. Holmes GKT, Prior P, Lane MR, et al. Malignancy in coeliac disease—effect of a gluten free diet. Gut 1989;30:333–8.
6. Mora S, Barera G, Ricotti A, et al. Reversal of low bone density with a gluten-free diet in children and adolescents with celiac disease. Am J Clin Nutr 1998;67:477–81.
7. Mora S, Barera G, Beccio S, et al. Bone density and bone metabolism are normal after long-term gluten-free diet in young celiac patients. Am J Gastroenterol 1999;94:398–403.
8. McFarlane XA, Bhalla AK, Robertson DAF. Effect of a gluten free diet on osteopenia in adults with newly diagnosed coeliac disease. Gut 1996;39:180–4.
9. Baker PG, Read AE. Reversible infertility in male coeliac patients. BMJ 1975;2:316–7.
10. Sewell P, Cooke WT, Cox EV, Meynell MJ. Milk intolerance in gastrointestinal disorders. Lancet 1963;2:1132–5.
11. Haeney MR, Goodwin BJF, Barratt MEJ, et al. Soya protein antibodies in man: their occurrence and possible relevance in coeliac disease. J Clin Pathol 1982;35:319–22.
12. Mike N, Haeney M, Asquith P. Soya protein hypersensitivity in coeliac disease: evidence for cell mediated immunity. Gut 1983;24:A990.
13. Ament ME, Rubin CE. Soy protein—another cause of the flat intestinal lesion. Gastroenterology 1972;62:227–34.
14. Auricchio S, Follo D, de Ritis G, et al. Does breast feeding protect against the development of clinical symptoms of celiac disease in children? J Pediatr Gastroenterol Nutr 1983;2:428–33.
15. Udall JN, Colony P, Fritze L, et al. Development of gastrointestinal mucosal barrier. II. The effect of natural versus artificial feeding on intestinal permeability to macromolecules. Pediatr Res 1981;15:245–9.
16. Connon JJ. Celiac disease. In: Shils ME, Olson JA, Shike M, eds. Modern Nutrition in Health and Disease, 8th ed. Philadelphia: Lea & Febiger, 1994, 1062.
17. Crofton RW, Glover SC, Ewen SWB, et al. Zinc absorption in celiac disease and dermatitis herpetiformis: a test of small intestinal function. Am J Clin Nutr 1983;38:706–12.
18. Solomons NW, Rosenberg IH, Sandstead HH. Zinc nutrition in celiac sprue. Am J Clin Nutr 1976;29:371–5.
19. Rude RK, Olerich M. Magnesium deficiency: possible role in osteoporosis associated with gluten-sensitive enteropathy. Osteoporos Int 1996;6:453–61.
20. Russell RM, Smith VC, Multak R, et al. Dark-adaptation testing for diagnosis of subclinical vitamin-A deficiency and evaluation of therapy. Lancet 1973;2:1161–4.
21. Basha B, Rao S, Han ZH, Parfitt, AM. Osteomalacia due to vitamin D depletion: neglected consequence of intestinal malabsorption. Am J Med 2000;108(4):296–300.
22. O’Mahony S, Howdle PD, Losowsky MS. Review article: management of patients with non-responsive coeliac disease. Aliment Pharmacol Ther 1996;10:671–80 [review].
23. Hallert C, Astrom J, Walan A. Reversal of psychopathology in adult celiac disease with the aid of pyridoxine (vitamin B6). Scand J Gastroenterol 1983;18:299–304.
24. Patel RS, Johlin FC Jr, Murray JA. Celiac disease and recurrent pancreatitis. Gastrointest Endosc 1999;50:823–7.
25. Carroccio A, Iacono G, Montalto G, et al. Pancreatic enzyme therapy in childhood celiac disease. A double-blind prospective randomized study. Dig Dis Sci 1995;40:2555–60.


Chronic Fatigue

1. Chronic Fatigue Syndrome bibliography

Also see discussion of chronic fatigue syndrome (CFS) and research

1. De Lorenzo F, Hargreaves J, Kakkar VV. Pathogenesis and management of delayed orthostatic hypotension in patients with chronic fatigue syndrome. Clin Auton Res 1997;7:185–90.
2. Fulcher KY, White PD. Randomised controlled trial of graded exercise in patients with the chronic fatigue syndrome. Br Med J 1997;314:1647–52.
3. McCully KK, Sisto SA, Natelson BH. Use of exercise for treatment of chronic fatigue syndrome. Sports Med 1996;21:35–48 [review].
4. Blackwood SK, MacHale SM, Power MJ, et al. Effects of exercise on cognitive and motor function in chronic fatigue syndrome and depression. J Neurol Neurosurg Psychiatry 1998;65:541–6.
5. LaManca JJ, Sisto SA, DeLuca J, et al. Influence of exhaustive treadmill exercise on cognitive functioning in chronic fatigue syndrome. Am J Med 1998;105:59S–65S.
6. Paul L, Wood L, Behan WM, et al. Demonstration of delayed recovery from fatiguing exercise in chronic fatigue syndrome. Eur J Neurol 1999;6:63–9.
7. Clapp LL, Richardson MT, Smith JF, et al. Acute effects of thirty minutes of light-intensity, intermittent exercise on patients with chronic fatigue syndrome. Phys Ther 1999;79:749–56.
8. Shaw DL, Chesney MA, Tullis IF, Agersborg HPK. Management of fatigue: a physiologic approach. Am J Med Sci 1962;243:758–69.
9. Crescente FJ. Treatment of fatigue in a surgical practice. J Abdom Surg 1962;4:73.
10. Hicks J. Treatment of fatigue in general practice: a double-blind study. Clin Med 1964;Jan:85–90.
11. Formica PE. The housewife syndrome: treatment with the potassium and magnesium salts of aspartic acid. Curr Ther Res 1962;Mar:98–106.
12. Kaufman W. The use of vitamin therapy to reverse certain concomitants of aging. J Am Geriatr Soc 1955;3:927–36.
13. Ellis FR, Nasser S. A pilot study of vitamin B12 in the treatment of tiredness. Br J Nutr 1973;30:277–83.
14. Lawhorne L, Rindgahl D. Cyanocobalamin injections for patients without documented deficiency. JAMA 1989;261:1920–3.
15. Gaby AR. Literature Review & Commentary. Townsend Letter for Doctors & Patients 1997;Feb/Mar:27 [review].
16. Lapp CW, Cheney PR. The rationale for using high-dose cobalamin (vitamin B12). CFIDS Chronicle Physicians’ Forum 1993;Fall:19–20.
17. Heap LC, Peters TJ, Wessely S. Vitamin B status in patients with chronic fatigue syndrome. J R Soc Med 1999;92:183–5.
18. Kuratsune H, Yamaguti K, Takahashi M, et al. Acylcarnitine deficiency in chronic fatigue syndrome. Clin Infect Dis 1994;18(suppl 1):S62–7.
19. Plioplys AV, Plioplys S. Amantadine and L-carnitine treatment of chronic fatigue syndrome. Neuropsycholbiol 1997;35:16–23.
20. Forsyth LM, Preuss HG, MacDowell AL, et al. Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome. Ann Allergy Asthma Immunol 1999;82:185–91.
21. Cox IM, Campbell MJ, Dowson D. Red blood cell magnesium and chronic fatigue syndrome. Lancet 1991;337:757–60.
22. Howard JM, Davies S, Hunnisett A. Magnesium and chronic fatigue syndrome. Lancet 1992;340:426.
23. Clague JE, Edwards RH, Jackson MJ. Intravenous magnesium loading in chronic fatigue syndrome. Lancet 1992;340:124–5.
24. Gantz NM. Magnesium and chronic fatigue. Lancet 1991;338:66 [letter].
25. Hinds G, Bell NP, McMaster D, McCluskey DR. Normal red cell magnesium concentrations and magnesium loading tests in patients with chronic fatigue syndrome. Ann Clin Biochem 1994;31(Pt. 5):459–61.
26. Kuratsune H, Yamaguti K, Sawada M, et al. Dehydroepiandrosterone sulfate deficiency in chronic fatigue syndrome. Int J Mol Med 1998;1:143–6.
27. De Becker P, De Meirleir K, Joos E, et al. Dehydroepiandorsterone (DHEA) response to i.v. ACTH in patients with chronic fatigue syndrome. Horm Metab Res 1999;31:18–21.
28. Bou-Holaigah I, Rowe PC, Kan J, Calkins H. The relationship between neurally mediated hypotension and the chronic fatigue syndrome. JAMA 1995;274:961–7.
29. Whorwood CB, Shepard MC, Stewart PM. Licorice inhibits 11ß-hydroxysteroid dehydrogenase messenger ribonucleic acid levels and potentiates glucocorticoid hormone action. Endocrinology 1993;132:2287–92.v 30. Baschetti R. Chronic fatigue syndrome and liquorice. New Z Med J 1995;108:156–7 [letter].
31. Brown D. Licorice root—potential early intervention for chronic fatigue syndrome. Quart Rev Natural Med 1996;Summer:95–7.
32. Price JR, Couper J. Cognitive behaviour therapy for adults with chronic fatigue syndrome. Cochrane Database Syst Rev 2000;(2):CD001027 [review].


Colds and Flu

1. Garlic (2001) Colds & Flu

Learn more about colds and flu.

Garlic may be helpful in preventing colds and flu due to its anti-bacterial properties. One researcher thinks that taking garlic may reduce chances of catching a cold by half.

In a 2001 study in England, 146 volunteers took either a placebo or capsule of an allicin-containing garlic supplement daily for 90 days during the winter. 24 colds were recorded among those taking the supplement, compared to 65 amongst those taking the placebo.

The study also found that those taking the supplement who did catch a cold were more likely to make a speedier recovery than those taking the placebo and the chances of re-infection following a cold were significantly reduced.

Researcher: Peter Josling, director the Garlic Centre in East Sussex.


Computer Eye Strain

1. AOA (2007) Advises Daily Computer Users of the Risk of Computer Vision Syndrome

Learn more about computer eye strain

Americans who use computers daily should be aware of the risk of computer vision syndrome (CVS), more commonly known as computer eye strain, which gives rise to dry eyes, eye strain, neck and back pain, light sensitivity and fatigue. These symptoms can result from individual visual problems, poor work station configuration or improper work habits.

In responses to the American Optometry Association's (AOA) 2007 Eye-Q survey of 1,005 Americans 18 years and older, it was found that most people (82%) frequently work with a computer or a handheld electronic device and 42% spent three+ hours a day doing so. Most Americans (78%) do not have their computer monitor positioned at the correct height (below eye level).

Pre-existing uncorrected vision problems like hyperopia and astigmatism, inadequate eye focusing or eye coordination abilities and age-related eye issues may contribute to CVS, and the constant refocusing effort required while working at a computer stresses the eye muscles, affecting individuals' comfort and productivity.

After prolonged computer or handheld device use, subjects experienced:

  • 41% - eye strain
  • 45% - neck or back pain

While many of these symptoms are temporary, some may continue experiencing visual problems, such as such as blurred distance vision, even after computer work has stopped. Yet only 11% of respondents said that they currently use special computer glasses or computer screen filters to help reduce glare and discomfort.

2. Astaxanthin (2006) Reduces Eye Strain (Asthenopia)

A number of Japanese research studies show the benefit of supplementing with Astaxanthin in reducing asthenopia (eye fatigue), computer eye strain and related symptoms.

A couple of randomized double blind placebo controlled pilot studies demonstrated the positive effects of astaxanthin supplementation on visual function. For example, a study by Nagaki et al., (2002), demonstrated that subjects (n=13) who received 5 mg astaxanthin per day for one month showed a 54% reduction of eye fatigue complaints.

In a sports vision study led by Sawaki et al., they demonstrated that depth perception and critical flicker fusion had improved by 46% and 5% respectively on a daily dose of 6 mg (n=9). The effect of astaxanthin on visual performance prompted a number of other clinical studies to evaluate the optimum dose and identify the mechanism of action.

A study by Nakamura (2004), demonstrated significant improvements in reducing asthenopia and positive accommodation for the 4 mg (p<0.05) and 12 mg (p<0.01) groups. However, it was not until Nitta et al., (2005), who established the optimum daily dose at 6 mg (n=10) for a period of 4 weeks by comparing eye fatigue using a visual analogue scale (VAS) based questionnaire and accommodation values. Overall, the 6 mg group improved significantly better at week 2 and 4 of the test period.

Furthermore, questionnaire results obtained by Shiratori et al., (2005) and Nagaki et al., (2006), also confirmed the previous findings that astaxanthin supplementation at 6 mg for 4 weeks improved symptoms associated with tiredness, soreness, dryness and blurry vision. Another study by Takahashi & Kajita (2005), also demonstrated that astaxanthin attenuates induced-eye fatigue, as opposed to treating eye fatigue, which suggests prevention rather than treatment.

Astaxanthin treated groups (asthenopia negative) were able to recover quicker than the control group after heavy visual stimulus. Later, Iwasaki & Tawara (2006) also confirmed the same tendencies of subjective eye fatigue complaints in a randomized double-blind placebo controlled double-crossover study.

3. Asthenopia (2002-2006 Studies) Reducing with Astaxanthin

A couple of randomized double blind placebo controlled pilot studies demonstrated the positive effects of astaxanthin supplementation on visual function. For example, a study by Nagaki et al., (2002), demonstrated that subjects (n=13) who received 5 mg astaxanthin per day for one month showed a 54% reduction of eye fatigue complaints. In a sports vision study led by Sawaki et al., they demonstrated that depth perception and critical flicker fusion had improved by 46% and 5% respectively on a daily dose of 6 mg (n=9). The effect of astaxanthin on visual performance prompted a number of other clinical studies to evaluate the optimum dose and identify the mechanism of action.

A study by Nakamura (2004), demonstrated significant improvements in reducing asthenopia and positive accommodation for the 4 mg (p<0.05) and 12 mg (p<0.01) groups. However, it was not until Nitta et al., (2005), who established the optimum daily dose at 6 mg (n=10) for a period of 4 weeks by comparing eye fatigue using a visual analogue scale (VAS) based questionnaire and accommodation values. Overall, the 6 mg group improved significantly better at week 2 and 4 of the test period. Furthermore, questionnaire results obtained by Shiratori et al., (2005) and Nagaki et al., (2006), also confirmed the previous findings that astaxanthin supplementation at 6 mg for 4 weeks improved symptoms associated with tiredness, soreness, dryness and blurry vision. Another study by Takahashi & Kajita (2005), also demonstrated that astaxanthin attenuates induced-eye fatigue, as opposed to treating eye fatigue, which suggests prevention rather than treatment. Astaxanthin treated groups (asthenopia negative) were able to recover quicker than the control group after heavy visual stimulus. Later, Iwasaki & Tawara (2006) also confirmed the same tendencies of subjective eye fatigue complaints in a randomized double-blind placebo controlled double-crossover study.

4. Lutein (2009) and Computer Eye Strain

Learn more about computer eye strain

This study noted improvements, after taking lutein, in seeing contrast on a computer screen in 37 (age 22-30) subjects taking lutein with long-term exposure computer monitors. The subjects were observed following 12 weeks of lutein supplementation. There was a trend towards improved visual acuity and measures of contrast sensitivity in the subjects taking lutein verse the placebo group. The study concluded that a higher intake of lutein may have beneficial effects on the visual performance.

Published: British Journal of Nutrition, 2009

Researchers: Beijing

5. Lutein, blackcurrant extract may reduce visual fatigue (2009)

Visual fatigue such as computer eye strain caused by staring at the computer for long hours, may be eased a daily supplement containing blackcurrant fruit extract (200 mg), lutein (5 mg), and zeaxanthin (1 mg), according to a randomized, double-blind, placebo-controlled cross-over trial.

The subjects were randomly assigned to receive either the lutein supplement, or placebo, for two weeks, followed by two weeks of washout, and a further two weeks with the opposite intervention.

After completing a two hour visual proof reading task, the researchers measured signs of visual fatigue, including so-called eye fixation related potentials (EFRP).

Source: Applied Ergonomics
Volume 40, Issue 6, Pages 1047-1054
“The effect of lutein supplementation on visual fatigue: A psychophysiological analysis”
Authors: A. Yagi, K. Fujimoto, K. Michihiro, B. Goh, D. Tsi, H. Nagai


Crohn's Disease

1. Crohn's Disease Bibliography

Also see discussion of crohns disease and research.

1. Mayberry JF, Rhodes J. Epidemiological aspects of Crohn's disease: a review of the literature. Gut 1984;886–99.
2. Heaton KW, Thornton JR, Emmett PM. Treatment of Crohn's disease with an unrefined-carbohydrate, fibre-rich diet. BMJ 1979;2(6193):764–6.
3. Brandes JW, Lorenz-Meyer H. Sugar free diet: a new perspective in the treatment of Crohn disease? Randomized, control study. Z Gastroneterol 1981;19:1–12.
4. Shoda R, Masueda K, Yamato S, Umeda N. Epidemiologic analysis of Crohn's disease in Japan: increased dietary intake of n-6 polyunsaturated fatty acids and animal protein relates to the increased incidence of Crohn's disease in Japan. Am J Clin Nutr 1996;63:741–5.
5. Riordan AM, Hunter JO, Cowan RE, et al. Treatment of active Crohn's disease by exclusion diet: East Anglian Multicentre Controlled Trial. Lancet 1993;342:1131–4.
6. Alic M. Baker's yeast in Crohn's disease—can it kill you? Am J Gastroenterol 1999;94:1711 [letter/review].
7. Wantke F, Gotz M, Jarisch R. Dietary treatment of Crohn's disease. Lancet 1994;343:113 [letter].
8. O'Morain C, Segal AW, Levi AJ. Elemental diet as primary treatment of acute Crohn's disease: a controlled trial. Br Med J (Clin Res Ed) 1984;288:1859–62.
9. Gorard DA, Hunt JB, Payne-James JJ, et al. Initial response and subsequent course of Crohn's disease treated with elemental diet or prednisolone. Gut 1993;34:1198–202.
10. Teahon K, Pearson M, Levi AJ, Bjarnason I. Practical aspects of enteral nutrition in the management of Crohn's disease. JPEN J Parenter Enteral Nutr 1995;19:365–8.
11. Raouf AH, Hildrey V, Daniel J, et al. Enteral feeding as sole treatment for Crohn's disease: controlled trial of whole protein v amino acid based feed and a case study of dietary challenge. Gut 1991;32:702–7.
12. Rigaud D, Cosnes J, Le Quintrec Y, et al. Controlled trial comparing two types of enteral nutrition in treatment of active Crohn's disease: elemental versus polymeric diet. Gut 1991;32:1492–7.
13. Park RH, Galloway A, Danesh BJ, et al. Double-blind controlled trial comparing elemental and polymeric diets as primary therapy in active Crohn's disease. Eur J Gastroenterol Hepatol 1991;32:1492–7.
14. McDonald PJ, Fazio VW. What can Crohn's patients eat? Eur J Clin Nutr 1988;42:703–8.
15. Gaby AR. Commentary. Nutr Healing 1998;January:1,10–1 [review].
16. Persson PG, Ahlbom A, Hellers G. Diet and inflammatory bowel disease: a case-control study. Epidemiology 1992;3:47–52.
17. Cottone M, Rosselli M, Orlando A, et al. Smoking habits and recurrence in Crohn's disease. Gastroenterol 1994;106:643–8.
18. Leichtmann GA, Bengoa JM, Bolt MJG, Sitrin MD. Intestinal absorption of cholecalciferol and 25-hydrocycholecalciferol in patients with both Crohn's disease and intestinal resection. Am J Clin Nutr 1991;54:548–52.
19. Harris AD, Brown R, Heatley RV, et al. Vitamin D status in Crohn's disease: association with nutrition and disease activity. Gut 1985;26:1197–203.
20. Driscoll RH, Meredith SC, Sitrin M, Rosenberg IH. Vitamin D deficiency and bone disease in patients with Crohn's disease. Gastroenterol 1982;83:1252–8.
21. Vogelsang H, Ferenci P, Resch H, et al. Prevention of bone mineral loss in patients with Crohn's disease by long-term oral vitamin D supplementation. Eur J Gastroenterol Hepatol 1995;7:609–14.
22. Mate J, Castanos R, Garcia-Samaniego J, Pajares JM. Does dietary fish oil maintain the remission of Crohn's disease: a case control study. Gastroenterology 1991;100:A228 [abstract].v 23. Belluzzi A, Brignola C, Campieri M, et al. Effect of an enteric-coated fish-oil preparation on relapses in Crohn's disease. N Engl J Med 1996;334:1557–60.
24. Lorenz R, Weber PC, Szimnau P, et al. Supplementation with n-3 fatty acids from fish oil in chronic inflammatory bowel disease—a randomized, placebo-controlled, double-blind cross-over trial. J Intern Med Suppl 1989;225:225–32.
25. Lorenz-Meyer H, Bauer P Nicolay C, et al. Omega-3 fatty acids and low carbohydrate diet for maintenance of remission in Crohn's disease. A randomized controlled multicenter trial. Study Group Members (German Crohn's Disease Study Group). Scand J Gastroenterol 1996;31:778–85.
26. Belluzzi A, Brignola C, Campieri M, et al. Effects of new fish oil derivative on fatty acid phospholipid-membrane pattern in a group of Crohn's disease patients. Dig Dis Sci 1994;39:2589–94.
27. Plein K, Hotz J. Therapeutic effects of Saccharomyces boulardii on mild residual symptoms in a stable phase of Crohn's disease with special respect to chronic diarrhea—a pilot study. Z Gastroenterol 1993;31:129–34.
28. Bleichner G, Blehaut H, Mentec H, Moyse D. Saccharomyces boulardii prevents diarrhea in critically ill tube-fed patients. A muticenter, randomized, double-blind placebo-controlled trial. Intensive Care Med 1997;23:517–23.
29. Imes S, Plinchbeck BR, Dinwoodie A, et al. Iron, folate, vitamin B-12, zinc, and copper status in out-patients with Crohn's disease: effect of diet counseling. J Am Dietet Assoc 1987;87:928–30.
30. Sandstead HH. Zinc deficiency in Crohn's disease. Nutr Rev 1982;40:109–12.
31. Driscoll RH Jr, Meredith SC, Sitrin M, et al. Vitamin D deficiency and bone disease in patients with Crohn's disease. Gastroenterology 1982;83:1252–8.
32. Dvorak AM. Vitamin A in Crohn's disease. Lancet 1980;i:1303–4.
33. Skogh M, Sundquist T, Tagesson C. Vitamin A in Crohn's disease. Lancet 1980; i:766 [letter].
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Diabetes Mellitus

1. Alpha Lipoic Acid (2006) & Diabetes Mellitus

Learn more about diabetes.

Researchers evaluated whether oral alpha lipoic acid would improve insulin sensitivity in type 2 diabetic patients.

The researchers treated 12 patients over four weeks, and 12 subjects with normal glucose tolerance served as a control group. After four weeks, the insulin sensitivity of the diabetics was significantly improved (M from 3.202+/-1.898 to 5.951+/-2.705 mg/kg/min (mean+/-sD), p<0.01; and IsI from 4.706+/-2.666 to 7.673+/-3.559 mg/kg/min per mIU/l x 100 (mean+/-sD), p<0.05.) The difference was not significantly different between the treated patients and the control group after the end of the period.

Researchers: Kamenova P., Department of Diabetology, University Hospital of Endocrinology, Medical University, Sofia, Bulgaria

Published: Improvement of insulin sensitivity in patients with type 2 diabetes mellitus after oral administration of alpha-lipoic acid, Hormones (Athens). 2006 Oct-Dec;5(4):251-8.

2. Alpha Lipoic Acid (2011) & Diabetes

Learn more about diabetes.

In this study the reseachers evaluated the effectiveness and safety of alpha lipoic acid function in producting against nerve damage in diabetic patients.

The 4-year, double-blind, randomized study assessed 460 diabetic patients with mid to moderate nerve damage as a result of their diabetic condition.

The researchers found that, while ALA did not produce results in one goal of the study (NIS, NIS-LL, and 7 neurophysiologic tests), it did result in a significant improvement of nerve damage impairments and prevented further degredation. In addition it was well tolerated.

Researchers: Ziegler D, Low PA, Litchy WJ, Boulton AJ, Vinik AI, Freeman R, Samigullin R, Tritschler H, Munzel U, Maus J, Schütte K, Dyck PJ., Institute for Clinical Diabetology, German Diabetes Center at the Heinrich Heine University, Germany

Published: Efficacy and safety of antioxidant treatment with α-lipoic acid over 4 years in diabetic polyneuropathy: the NATHAN 1 trial, Diabetes Care. 2011 Sep;34(9):2054-60

3. Diabetes Mellitus Bibliography through 2000
Also see Research discussion for diabetes mellitus

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4. Diabetes Mellitus Research - 2001 & newer

Learn more about diabetes

.
  1. Androne L, Gavan NA, Veresiu IA, Orasan R. In vivo effect of lipoic acid on lipid peroxidation in patients with diabetic neuropathy. In Vivo. 2000;14(2):327-330.
  2. Melhem MF, Craven PA, Derubertis FR. Effects of dietary supplementation of alpha-lipoic acid on early glomerular injury in diabetes mellitus. J Am Soc Nephrol. 2001;12:124-133.
  3. Melhem MF, Craven PA, Liachenko J, et al. Alpha-lipoic acid attenuates hyperglycemia and prevents glomerular mesangial matrix expansion in diabetes. J Am Soc Nephrol. 2002;13:108-116.
  4. <
  5. Packer L, Kraemer K, Rimbach G. Molecular aspects of lipoic acid in the prevention of diabetes complications. Nutrition. 2001;17(10):888-895.
  6. Ziegler D, Ametov A, Barinov A, et al. Oral treatment with alpha-lipoic acid improves symptomatic diabetic polyneuropathy: The SYDNEY 2 trial. Diabetes Care. 2006;29:2365-70.

5. Exercise (2012) & Diabetes

Learn more about Diabetes mellitus

A long term study of 1826 patients examined the effect of exercise on their likelihood of developing diabetes. The study participants did not have either diabetes or cardiovascular problems at the onset of the study.

Over five years of followup, the researchers measured the amount of activity the of the participants by monitoring the number of steps they took during the day. The people with in the lowest 1/4 of the range, with less than 3,500 steps per day, had a much higher likelihood of developing diabetes and 243 new cases of diabetes were identified in that group. When the remainder of the group's activity was measured and compared to the lowest 1/4 - it was determined that the group with the lowest amount of activity had a 75% chance of developing diabetes.

Researchers: Amanda M. Fretts, PHD, Barbara V. Howard, PHD, Barbara McKnight, PHD, Glen E. Duncan, PHD, Shirley A.A. Beresford, PHD, Darren Calhoun, PHD, Andrea M. Kriska, PHD, Kristi L. Storti, PHD and David S. Siscovick, MD

Published: Modest Levels of Physical Activity Are Associated With a Lower Incidence of Diabetes in a Population With a High Rate of Obesity, Diabetes Care August 2012 vol. 35 no. 8 1743-1745

6. Ginseng (1995) & Diabetes

Learn more about diabetes.

Researchers examined the effectiveness of ginseng for non-insulin dependent patients.

This was a double-blind, placebo-controlled study of thirty six patients who had recently been diagnosed as non-insulin dependent were treated for 8 weeks with 100 or 200mg panax gingseng daily. The researchers evaulated the results via psychophysical testing, glucose and fat levels in blood, body weight and aminoterminalpropeptide concentration.

The study found better fasting blood-glucose levels, improved psychophysical performance, and better mood. Better hemoglobin A1C values also result from the 200mg dosage. The placebo reduced body weight and altered the serum fats, but did not change fasting blood glucose.

Editors Note: A 2011 study using Korean red ginger with 15 overweight patients and for only 30 days did not find the same result.

Researchers: Sotaniemi EA, Haapakoski E, Rautio A., Department of Internal Medicine, University of Oulu, Finland.

Published: Ginseng therapy in non-insulin-dependent diabetic patients, Diabetes Care. 1995 Oct;18(10):1373-5.

7. Gymnema Sylvestre (2010) & Diabetes

Learn more about diabetes.

The researchers wanted to evaluate the traditional herb Gymnema sylvestre (GS) as a possible anti-diabetic agent, which has been used in India for centuries.

They used a high molecular weight GS extract with type II diabetic patients, looking at plasma insulin, glucose, and C-peptide, for a 60 day period. They found marked increased in circulating insulin and C-peptide which were tied to reductions in fasting and after-meals blood glucose.

They also did in vitro measurements with human islets of Langerhans which also stimulated insulin secretion from the human beta cells.

They concluded that these in vivo and in vitro examinations indicated that the herb may be an alternative therapy for diabetic hyperglycemia.

Researchers: Al-Romaiyan A, Liu B, Asare-Anane H, Maity CR, Chatterjee SK, Koley N, Biswas T, Chatterji AK, Huang GC, Amiel SA, Persaud SJ, Jones PM., Diabetes Research Group, King's College London, London, SE1 1UL, UK

Published: A novel Gymnema sylvestre extract stimulates insulin secretion from human islets in vivo and in vitro, Phytother Res. 2010 Sep;24(9):1370-6.

8. Tumeric (2012) & Type 2 Diabetes

Learn more about treatment of diabetes mellitus.

A 2012 study examined whether turmeric (curcumin) would be helpful in preventing type 2 diabetes. The double-blind, randomized study utilized curcumin extract and included 240 subjects who were given either curcumin extract or a placebo for 9 months. The patients were prediabetic - they had levels of blood glucose that were determined to be higher than normal, but not high enough to be considered diabetes.

The researchers monitored beta-cell functioning, insulin levels and resistance and other measures. After the 9 month period, 16.5% of the placebo patients had developed type 2 diabetes, but none in the curcumin group developed the condition. In addition other measures in the curcumin group improved including overall functioning of beta cells.

Beta cells are the cells in the pancreas that maintain and release insulin, which in turn, regulates the amount of sugar in the blood. They produce a number of byproducts which contral related processes.

Researchers: Somlak Chuengsamarn, MD, Suthee Rattanamongkolgul, MD, Rataya Luechapudiporn, PHD, Chada Phisalaphong, PHD and Siwanon Jirawatnotai, PHD

Published: Curcumin Extract for Prevention of Type 2 Diabetes, Diabetes Care July 6, 2012


Diabetic Retinopathy

1. Alpha lipoic acid (1997) - Diabetic Retinopathy, Cataracts

See more information about cataracts treatment and information and diabetic retinopathy treatment and information.

Researchers found that alpha lipoic acid has the capacity to lessen formation of diabetic cataracts, as well as diabetic retinopathy, and therefore appears to be an ideal neuroprotective supplement in the treatment of all brain and neural disorders aggrevated or caused by free radical processes.

Published: Packer, L., Ann N y Acad Sci 1994 Nov 17;738:257-64. Packer, L. Free Radic Biol Med 1997;22(1-2):359-78

2. Anthocyanosides (1973), Vascular Permeability and Reduced Hemorrhaging (1981)

See more about diabetic retinopathy treatment and information.

Thirty one patients with various types of retinopathy who were put on anthocyanosides showed a positive influence on both vascular permeability and resistance to hemorrhage. Those with diabetic retinopathy had the largest effect. Long term use of these plant nutrients is helpful in improving vascular permeability. Sharrer A. & Ober M. Klin Monatsbl Augenheilkd 1981 May;178(5):386-9 and Neumann, Munch Med Wochenschr 1973 May 18;115(20):952-4

3. Bilberry extract (1987) - diabetic retinopathy
See more about diabetic retinopathy treatment and information.

79% of 37 patients with visible diabetic retinal abnormalities improved after taking 160 mg of bilberry extract twice daily, compared to 0% of the placebo control group, and 86% of those with abnormalities of angiography findings showed moderate to considerable improvement. Perossini, et al. Ann Ottalmol Clin Ocul 1987.

This is a small study but supports others with similar results.

4. Bilberry (1995, 1997) - diabetic retinopathy

See more about diabetic retinopathy treatment and information.

Researchers found that bilberry extracts could improve vision sharpness and help faster adaption to changing light conditions. European physicians already recommend bilberry extracts for other eye complaints such as retinitis pigmentosa, and diabetic retinopathy.

One study assessed the effectiveness of a bilberry extract (anthocyanosides) in animals finding that vascular permeability is decreased. This means that blood barrier permeability is normalized.

Published" "Topic: Bilberry Fruit," The Lawrence Review of Natural Products, October 1995, Pages 1-2.

Other research found that lipoic acid may be helpful in blood flow to nerve tissue in the eyes, fighting free radicals, and improving functioning of the nerves in patients with diabetic neuropathy. In one study 328 type II diabetes patients with symptoms of peripheral neuropathy were treated with intravenous introduction of lipoic acid or a placebo for three weeks. Improvements in symptoms were noted. In another study, type II diabetic patients also having cardiac autonomic neuropathy received a daily oral dose of 800 mg lipoic acid or a placebo for four months. Again, symptoms were improved in those taking the lipoic acid.

Published: Ziegler D; Gries FA. Alpha-lipoic acid in the treatment of diabetic peripheral and cardiac autonomic neuropathy. Diabetes, 1997 Sep, 46 Suppl 2:, S62-63-61

5. Bioflavonoids (1996) - diabetic retinopathy
See more about diabetic retinopathy treatment and information.

Bioflavonoids were found to normalize blood vessels' permeability in diabetic patients. Valenci, et al. Diabet Med 1996 Oct;13(10):882-8

6. Carotenoids (1999) & glucose tolerance

Learn more about diabetic retinopathy.

Oxidative stress is one result of diabetes is characterized. Consequently there is an impact on vision.

Researchers took a look at data from part of the Third National Health and Nutrition Examination Survey (1988-1991) and assessed alpha- and beta-carotene, cryptoxanthin, lutein/zeaxanthin, and lycopene concentrations in people aged 40-74 with a normal blood sugar levels, high blood sugar levels, recently diagnosed diabetes, and previously diagnosed diabetes. This data was adjusted for age, sex, race, education, serum cotinine, serum cholesterol, body mass index, physical activity, alcohol consumption, vitamin use, and carotene and energy intake.

The researcher's conclusions were that low blood serum carotenoid levels were directly related to increased risk for diabetes and insulin resistance.

Published: Ford, et al. Am J Epidemiol 1999 Jan 15;149(2):168-76

7. Chromium (1995) supplements

See more about diabetic retinopathy treatment and information.

Researchers found that 73% of type I and II diabetics who were given chromium supplements were able to reduce their requirement for insulin or oral hypoglycemic medications. Taking chromium and niacin together reduced fasting blood sugar levels and improved glucose tolerance. Note to readers - never change your medications for diabetes without checking with your doctor first.

Published: J Trace Elem Exp Med 1995: 8:183-90; Urberg M, Zemel MB, Metabolism 1987; 36:896-99

8. Chromium, Vit. E, Magnesium (1997), etc & diabetic retinopathy

Learn more about diabetic retinopathy treatment and information.

Researchers feel that some trace minerals such as chromium and magnesium, high-dose vitamin E, soluble fiber, and possibly taurine may be likely to lessen risk for macrovascular disease (retinopathy) in diabetics.

Published: McCarty, Med Hypothesis 1997 Aug;49(2):143-52

9. Diabetic Retinopathy (2005) Occurs in Prediabetes

Learn more about diabetic retinopathy treatment and information.

The NIH reported in 2005 that diabetic retinopathy has been found in nearly 8 percent of pre-diabetic participants in the Diabetes Prevention Program (DPP), according to a report presented today at the American Diabetes Association's 65th Annual Scientific Sessions.

Pre-diabetes is a condition in which blood glucose levels are higher than normal but not high enough for a diagnosis of diabetes. The condition is sometimes called "impaired fasting glucose (IFG)" or "impaired glucose tolerance (IGT)," depending on the test used to diagnose it. People with pre- diabetes have an increased risk of developing type 2 diabetes, heart disease, and stroke.

10. Essential Fatty Acids (1998) - diabetic retinopathy

Learn more about diabetic retinopathy treatment and information and diabetes mellitus.

Evening primrose, borage and black currant oil are good sources of Omega-6 essential fatty acids including gamma-linolenic acid (GLA). Supplementation with GLA may offer a method to bypass the disturbance in omega-6 essential fatty acid metabolism associated with diabetes and diabetic retinopathy.(5) 5. Petrosian AM, Haroutounian JE, Adv Exp Med Biol 1998;442:407-13.

11. Ginkgo Biloba (1988) and Diabetic Retinopathy

Learn more about diabetic retinopathy treatment and information.

According to a 1988 double blind study in France, gingko biloba can help improve diabetic retinopathy by improving the flow of blood to the brain and extremities.

Reference: Lanthony P, Cosson JP. Evolution of color vision in diabetic retinopathy treated by extract of Ginkgo biloba. Journal For Ophthalmology 1988;11:671–74 [in French].

12. Gymnema Sylvestre (2005) and Diabetes Study

Learn about information on Diabetes and Diabetic Retinopathy.

A small study (India, 2005) examined the effects of an extract of Gymnema sylvestre on high blood sugar. Twenty-two people with type 2 diabetes were given extract for 18 to 20 months as a supplement to their regular medical regimen of oral anti-hyperglycemic agents.

During that period, an some them apparently showed reductions in blood glucose and A1c's. A few were reportedly able to discontinue their conventional anti-hyperglycemic drug and manage their blood glucose levels with the extract alone. Moreover, raised insulin levels were apparently found in the blood of the patients.

The authors, who published related research in 1990 in the same journal, believe that beta cell regeneration is the source of the improvement; however, members of the scientific community have previously questioned both their findings and their conclusions.

Published: 2005, Journal of Ethnopharmacology

13. Lipoic acid (1997) diabetic retinopathy

Learn more about diabetic retinopathy.

Lipoic acid improves distribution and metabolism of glucose in the body. Used as a supplement, lipoic acid may help with glucose absorption into muscle tissue and it may decrease the damaging effects on proteins of high glucose levels. Lipoic acid may also be helpful in improving blood flow in nerve tissue, we reduces stress from oxidation and therefore improve nerve conduction in diabetic neuropathy.

Two different randomized, double-blind, placebo-controlled trials have tested the effects of lipoic acid on diabetic neuropathy over a three week to four month period, resulting in improvement of symptoms in both trials.

Published: Ziegler D; Gries FA. Alpha-lipoic acid in the treatment of diabetic peripheral and cardiac autonomic neuropathy. Diabetes, 1997 Sep, 46 Suppl 2:, S62-63-61

14. Low magnesium levels (1985) diabetic retinopathy

Learn more about diabetic retinopathy.

Researchers have found that, in type I diabetes (insulin-dependent) the metabolism of several trace elements is different, leading researchers to conclude that these nutrients (or lack of them) might have specific functions in the development of the disease.

Magnesium deficiency is the most evident and also may heighten the risk of both ischemic heart disease and severe retinopathy.

Increased urinary loss of zinc is another common result of diabetes. Chromium increases tissue sensitivity to insulin and raises HDL cholesterol and the HDL:LDL ratio.

Selenium is critical to protecting the cell against oxidative damage by peroxides produced from lipid metabolism.

Published: Tuvemo, T. Pediatrician 1983-85;12(4):213-9

15. Magnesium (1978) High serum levels of magnesium

Learn more about diabetic retinopathy treatment and information.

In a 1978 study, the serum magnesium levels (how much magnesium there is in the blood) in 71 insulin-taking diabetic patients who had diabetes for 10 to 20 years were measured. The patients had diabetic retinopathy. They were divided into groups depending on the degree of severity of their diabetic retinopathy.

It was found that the diabetic patients with higher serum magnesium levels had less severe diabetic retinopathy than those with lower levels.

The conclusion was that low serum magenesium levels are a risk factor for diabetic retinopathy.

Published: Diabetes 1978 Nov;27(11):1075-7, P. McNair, et al.

16. Taurine - (1999) diabetic retinopathy

Learn more about diabetic retinopathy.

The condition diabetic retinopathy results because having diabetes increases the demands on the eye for various nutrients. The retina’s need for taurine is one of the nutrients involved. Glucose rapidly and specifically decreases taurine levels in retina cells.

Giving patients taurine supplements not only helps manage diabetic retinopathy, but taurine also appears to lessen the development of “sugar cataracts” because of its anti-oxidant qualities.

Published: Stevens et al, Am J Physiol 1999 Oct;277(4 Pt 1):E760-E771

Reference also: Malone JI, Benford SA, Malone J Jr, Diabetes Complications

17. Vitamin B12 (1958) diabetic retinopathy

Learn more about diabetic retinopathy.

Patients with Type I diabetes, "juvenile diabetes," are often subject to retinal complications such as diabetic retinopathy. In an early study, about 1/2 of 15 patients with type I diabetic retinopathy who received vitamin B12 at the same time as they took their daily insulin shot experienced complete recovery from signs of retinal problems after 12 months.

Published: Kornerup T, Strom L. Acta Paediatr 1958.

18. Vitamin C, E, Beta Carotene, Selenium (1987) - ARMD

Learn more about diabetic retinopathy.

Researchers found in a clinical study of patients with macular degeneration or diabetic retinopathy. In the trial 60% of the people received 500 mg of vitamin C, 400 IU of vitamin E, 15,000 IU of beta carotene and selenium supplements. These people showed slower development of their condition and or a lessening of symptoms.

Published: South Med J; 1987

19. Vitamin E (1993) Diabetic Retinopathy

Learn more about diabetic retinopathy and diabetes.

Researchers found that vitamin E helps support glucose tolerance diabetics who are not insulin-dependent. This should result in fewer complications from diabetes mellitus, such as diabetic retinopathy.

Published: Paolisso, G, et al. Am J Clin Nutr 1993; 57:650-56

20. Yoga (2012) Decreases Inflammation

Learn more about rheumatoid arthrits.

In a randomized, controlled trial, researchers looked at the biological mechanisms responsible for effects such as stress reduction, which have been well documented.

Researchers studied caregivers for dementia patients who did 12 minutes of yoga daily for 8 weeks compared to a control group who listened to relaxing music for the same time period. About 16% of caregivers begin to themselves have health problems after they begin to spend the time, attention and energy to care for someone else.

The scientists found in the yoga participants a change in 68 gene responses including adjustments for caregiver burden, sex, and body mass index. These changes manifested as reduced inflammation - a common symptom/issue for patients with depression, heart disease, diabetes and rheumatoid arthritis.

Editor's Note: This particular study looked at subjects performing Kirtan Kriya yoga, but any form of classic yoga, involving a variety of postures which give movement and enhance energy flow to all parts of the body will yield similar results. With respect to vision, inflammation is a major issue in diabetic retinopathy, optic neuritis (swollen optic nerve), and macular edema.

Researchers: Black, Cole, Irwin, Breen, St. Cyr, Nazarian, Shalsa, Lavretsky, University of California.

Published: Psychoneuroendocrinology, July 14, 2012 (online)


Dry Eyes

1. Dry Eyes (2012) Tied to Migraine Headaches

Learn more about holistic treament of dry eyes.

Researchers have long suspected that there may be a connection between dry eyes and migraine headaches - this study investigates that tie by investigating the relationship between tear capacity and migraine symptoms in patients.

See the summary of the migraines & dry eyes study.

Published: Cornea. 2012 Jun 15, Dry Eyes and Migraines: Is There Really a Correlation?

2. Essential Fatty Acids (1980), Vitamins B6 and C - Dry Eyes

Learn more about dry eye treatment and information.

D.F. Horrobin and colleagues carried out some preliminary studies using the supplemental intake of essential fatty acids, vitamin B6 and vitamin C to treat dry eyes. The rationale for this treatment was based on the biosynthesis of prostaglandin E1 (PGE1), which is necessary for acqueous tear secretion by the lacrimal glands. Patients received 2 x 500 mg capsules of Evening Primrose Oil, 50 mg of vitamin B6 and 1 gram of Vitamin C three times daily.

The results showed that 10 of the 17 patients had substantial improvement of symptoms and Schirmer Test in 2-6 weeks, 3 patients reported improved symptoms though without improved Schirmer testing. The authors' conclusion was that this treatment approach is effective in many cases.

References:
1) Horrobin DF, Campbell A. McEwen CG. Treatment of the Sicca Syndrome and the Sjogren's Syndrome with E.F.A. Pyroxidine and Vitamin C. Prog Lipid Res 8(4). 263-4, 1981.
2)Horrobin DF Campbell A. Srogren's Syndrome and the Sicca Syndrome: The Role of Essential Fatty Acids and Vitamin C. Medical Hypothesis. 6: 225-232 1980.

3. Essential Fatty Acids (1981) - dry eyes

Learn more about dry eye treatment and information.

A controlled study evaluated immune-enhancing effects of Black Current Seed oil (BCSO), a significant source of omega-3 and omega-6 fatty acids.

The study and previous research suggests that the combination of omega-3 and omega-6 fatty acids in black current seed of both results in increased PGE1, which both stimulates acqueous tear secretion and reduces the production of PGE2, which acts as an inflammatory agent.

References:

  • Horrobin DF, Campbell A, McEwan CG. Treatment of the Sicca Syndrome and the Sjogren's Syndrome with E.F.A. Pyridoxine and Vitamin C. Prog Lipid Res 8(4) 253-4 1981
  • Oxholm P. Manthorpe R, Prause JU, Horrobin D. Patients with Sjogren's Syndrome Treated For 2 Months with Evening Primrose Oil. Scand J Rheumotology 1986. 15 103-106.
  • Wu D, Maydani M, Leka L. Effect of dietary supplementation with black current seed oil on immune response of healthy elderly subjects. Amer J Clin Nutr 1999,70 536-543.

4. Evening primrose oil (1980) Omega-6 & dry eyes

In a small pilot study published in 1980, 17 patients with dry eye syndrome were treated with evening primrose oil. They were chosen to be part of the study due to lack of tear secretion, chronic need of eyedrops, the Schirmer Test, and a clinical exam. Patients received 500 mg capsules of evening Primrose oil, 50 mg vitamin B6 and 1 g vitamin C 3x a day.

Result
Ten of the 17 patients showed substantial improvement of both symptoms and Schirmer test in 2-6 weeks. 3 additional patients reported improved symptoms even though the Schirmer Test was unimproved. The authors felt that this treatment is effective in many, but not all cases.

1. Horrobin DF, Campbell A. McEwen CG: Treatment of the Sicca Syndrome with E.F.A., Pyroxidine and Vitamin C. Prog Lipid Res 8(4):253-4, 1981.
2. Horrobin DR Campbell A. Sjogren’s Syndrome and the Sicca Syndrome: the Role of Prostaglandin E1 Deficiency. Treatment with Essential Fatty Acids and Vitamin C. Medical Hypothesis. 6:225-232 1980.

Editor's Note: See more information about our preferred nutritional recommendations dry eyes. Both evening primrose oil and black current seed oil provide omega-6 fatty acids.

5. Eye drops (1988) without preservatives

Eye drops used without preservatives have been shown to enhance corneal healing and improve dry eye problems. Laflamme, M.Y., and Swieca, R. A comparative study of two preservative-free tear substitutes in the management of severe dry eye. Canadian Journal of Ophthalmology 23 (1988): 174-76.

Editor’s Notes: Preservatives in many products can aggravate dry eye symptoms, and even kill corneal cells. Eye drops that promise to “get the red out” will reduce circulation in the eye, decrease production of the tear film, and worse, eventually make your eyes even drier.

The most popular products featuring eye drops without preservatives are the homeopathic eye drops for women and the homeopathic eye drops for men -- both as effective aides for Dry Eyes.

6. Fish Oil (2003) and Dry Eye Syndrome

In a 2003 study, women with a higher dietary intake of omega-3 fatty acids were at decreased risk of developing dry eye syndrome (DES).

The Women's Health Study collected dietary information and whether they suffered from dry eye syndrome from 32,470 female health professionals who were aged between 45 and 84 years.

The researchers found that the greater the dietary intake of omega-3 fatty acids the less the risk of DES, after adjustments for age, other demographic factors, postmenopausal hormone therapy, and total fat intake. Tuna fish consumption also had a protective effect against DES, and results were similar in other models after adjustments for diabetes, hypertension, and connective tissue diseases.

"Although this is the first study that has evaluated this relationship, and confirmation from other studies is needed, the findings are consistent with clinical observations and postulated biological mechanisms," the authors wrote. "Thus, further research on the role of omega-3 fatty acids in the prevention and/or treatment of DES would be of interest."

Advanced Vision Research, Inc., supported this study and has financial arrangements with its authors.

References:
K. A. Trivedi and colleagues from Harvard Medical School in Boston, Massachusetts
ARVO 2003 Annual Meeting: Abstract 811/B786, presented May 4, 2003; abstracts 2111 and 2112, presented May 6, 2003.

7. Hormone Replacement Therapy and Dry Eyes (2001)

Dry-Eye Syndrome: An Overlooked Side Effect of HRT

WESTPORT, CT (Reuters Health) Nov 07 - Women on hormone replacement therapy (HRT), particularly estrogen-only regimens, are at increased risk of keratoconjunctivitis sicca, also known as dry-eye syndrome, researchers report in the November 7th issue of The Journal of the American Medical Association.

"Dry-eye syndrome is a very common condition affecting millions of middle-aged and older women, and physicians should recognize the possibility that HRT may have ocular side effects," Dr. Debra A. Schaumberg, of Brigham and Women's Hospital in Boston, told Reuters Health. Dr. Schaumberg and colleagues used the Women's Health Study cohort, which included 25,665 postmenopausal women, to study the relationship between HRT and dry-eye syndrome. Participants provided information on the use of HRT at baseline, 12 and 36 months, along with data on dry-eye syndrome at 4 years.

The prevalence of dry-eye syndrome was significantly related to HRT use.

Women who used estrogen alone had the highest prevalence at 9.1%, while women who never used HRT had the lowest prevalence at 5.9%. The prevalence of dry-eye syndrome in women who used estrogen plus progesterone/progestin regimens was 6.7%.

In multivariate analyses, the adjusted odds ratio for dry-eye syndrome was 1.69 and 1.29 for estrogen use alone and estrogen plus progesterone/progestin use, respectively, compared with no HRT use. The risk of dry-eye syndrome appears to increase with longer duration of HRT, according to the data. "Each 3-year increase in the duration of HRT use was associated with a significant 15% elevation in risk of clinically diagnosed dry-eye syndrome or severe symptoms," the investigators report in JAMA.

Dry-eye syndrome is an under-recognized side effect of HRT, Dr. Schaumberg said, "with the caveat that, until our study, there were no epidemiological data available to link the two." Dry-eye syndrome can have "a significant impact on quality of life and can increase risk of ocular infection," the researcher added. JAMA 2001;286:2114-2119.

See more information about dry eyes including nutritional recommendations for dry eyes.

8. Omega-6 Fatty Acid Helps Relieve Dry Eyes For Contact Lens Users Study 2008

The purpose of this study was to evaluate the effects of oral treatment with omega-6 fatty acids in the form of evening primrose oil (EPO) on subjective symptoms, ocular surface signs and tear film characteristic in patients with contact lens-associated dry eye.

A total of 76 female soft contact lens wearers were treated for six months either with EPO or placebo (olive oil). Subjects underwent three examinations (baseline, three and six months). At each examination, subjects were given a questionnaire relating to lens comfort and dry eye symptoms, and they underwent a series of tests of tear film characteristics (tear meniscus height, break-up time), meibomian gland function (lipid layer thickness and quality) and ocular surface parameters (hyperemia and staining).

The EPO group showed a significant improvement in the specific symptom of "dryness" at three and six months and also a significant improvement in overall lens comfort at six months. Tear meniscus height was increased in the EPO group at six months relative to baseline, although all other objective signs were unchanged. This study provides evidence for a beneficial effect of particular orally administered omega-6 fatty acids in alleviating dry eye symptoms and improving overall lens comfort in patients suffering from contact lens-associated dry eye.

SOURCE: Kokke KH, Morris JA, Lawrenson JG. Oral omega-6 essential fatty acid treatment in contact lens associated dry eye. Cont Lens Anterior Eye 2008;31(3):141-6.

9. Vitamin A & Cyclosporine A (2008) - Dry Eye Syndrome

Learn more about natural treament of dry eyes.

A 2008 study shows that using eyedrops with Vitamin A Palmitate can improve symptoms of blurred vision and tear film after just 4 weeks of usage. It was a prospective, randomized, controlled, parallel group study whose purpose was to compare the efficacy of vitamin A (retinyl palmitate) and cyclosporine A 0.05% eye drops in treating patients with dry eye disease.

In 3 identical clinical trials, 150 patients with dry eye disease were treated either 2x daily with cyclosporine A 0.05%, or 4x daily with retinyl palmitate 0.05%, or neither. In addition, preservative-free artificial tears were given 4x daily in every group. Corneal dye staining observation, Schirmer tear tests, tear film break-up times, dry eye symptom scores, and impression cytologic analysis results were obtained before treatment and at the first, second, and third months after treatment began.

Results:
Both vitamin A eye drops and topical cyclosporine A 0.05% treatments led to significant improvement in blurred vision, tear film break-up times, Schirmer I score results, and impression cytologic findings in patients with dry eye syndrome (P < .05) compared to the control group treated with preservative-free artificial tears alone.

Conclusions:
Both vitamin A eye drops and topical cyclosporine A 0.05% treatments are effective for the treatment of dry eye disorder.

Department of Ophthalmology and Visual Science, College of Medicine, The Catholic University of Korea, Seoul, Korea

Published: published online 09 October 2008

Researchers: Choun-Ki Joo, Department of Ophthalmology, KangNam St Mary's Hospital, #505 Ban-Po Dong, Seocho-Ku, Seoul 137-040, Korea

Note: two recommended products for dry eyes which contain vitamin A as retinyl palmitate are BioTears and VivaDrops.


Electromagnetic Pollution (EMF)

1. Cell Phone Radiation (2011) Changes Brain Metabolism

Learn more about EMF pollution

.

A 2011 study showed that a 50-minute cell phone radiation exposure was connected to increased brain glucose metabolism in the region closest to the antenna. The researchers have preliminary indication of long-term effects. Glucose metabolism, is an indicator of brain activity and this finding raises concerns that if cell phone radiation is effecting glucose levels, it may also be effecting neurotransmitters and neurochemical activities.

Researchers:Nora D. Volkow et al, Director of the National Institute on Drug Abuse of the National Institutes of Health

Published: "Cell Phone Radiofrequency Radiation Exposure and Brain Glucose Metabolism," JAMA Feb 23, 2011

2. EMF Pollution (2011) & Brain Functioning

Learn more about EMF Pollution.

A 2011 paper1 published confirms that very weak varying electric fields in brain tissue significantly affect neural functioning.

This is the first conclusive evidence that suggests that exposure to EMFs (especially the very high electric fields underneath high voltage overhead powerlines as well as low-frequency magnetic fields from mobile phones) may well cause problems that many have suspected.2

The possibility that low level fields have such an impact has been dismissed by scientists, even though doctors have used very high pulsed magnetic fields known as Transcranial Magnetic Stimulation (TMS) to "reset the brain" for many years.The actual mechanism by which TMS works was not proven, but was thought to depolarize the synapses. The 2011 research suggests that a more subtle electric field effect synchronising mechanism is at work. The fact that synchronisation effects have now been found at very low electric field levels has potentially large implications for general EMF exposure guidelines.

The brain displays continual electrical activity with countless overlapping electric fields, generated by the neural circuits of scores of communicating neurons.

New research suggests that at least low frequency electric fields do much more and may represent an additional important form of neural communication.

  1. Anastassiou CA, Perin R, Markram H, Koch C. Ephaptic coupling of cortical neurons. Nat Neurosci. 2011 Feb;14(2):217-23. Epub 2011 Jan 16
  2. Alasdair and Jean Philips Electromagnetic Fields: A Human EMC Problem? (May 2006)

3. EMF Pollution (2012) Brain Areas Related to Learning, Memory, Alzheimer’s Impacted by EMF Exposure

Learn more about EMF pollution

A 2012 Greek study has measured changes in animal brain proteins after exposure to RF electromagnetic fields, similar to the kind of microwave radiation emitted from cell phones, portable phones, WiFi and wireless computer equipment.

The parts of the brains used for learning and memory were impacted by microwave radiation, including the hippocampus, cerebellum and frontal lobe, at exposures below the ICNIRP (International Commission on Non-Ionizing Radiation Protection) safety guidelines. A total of 143 proteins in the brain were changed over a period of 8 months, providing new evidence for a potential relationship between everyday cell phone use, wireless transmitters and wireless computer equipment and electrosensitivity symptoms, such as headaches, dizziness and sleep disorders, as well as with tumors, Alzheimer’s and even metabolic effects.

The study simulated 3 hours of cell phone exposure over eight months, 8 hours of DECT portable phone exposure over eight months, and included a sham exposure control group.

Several proteins employed in the proper functioning of the neurons and proteins of the brain metabolism were impacted in nearly all of the brain regions studied.

This is important. According to wikipedia.com, "The key to neural function is the synaptic signaling process, which is partly electrical and partly chemical. The electrical aspect depends on properties of the neuron's membrane. Like all animal cells, every neuron is surrounded by a plasma membrane, a bilayer of lipid molecules with many types of protein structures embedded in it. A lipid bilayer is a powerful electrical insulator, but in neurons, many of the protein structures embedded in the membrane are electrically active." (italics ours)

One of the researchers, Adamantia Fragopoulou said, "Our study is important because it shows for the first time protein changes in the mouse brain after EMF exposure and in particular in very crucial regions like hippocampus, cerebellum and frontal lobe, all involved in learning, memory and other complicated functions of the mammalian brain. We have demonstrated that 143 proteins are altered after electromagnetic radiation, including proteins that have been correlated so far with Alzheimer’s, glioblastoma, stress and metabolism. In its perspective, this study is anticipated to throw light in the understanding of such health effects like headaches, dizziness, sleep disorders, memory disorders, brain tumors, all of them related, to the function of the altered brain proteins."

Here's the link to the full abstract.

Researchers: Adamantia Fragopoulou and Lukas Margaritis

Published: "Brain proteome response following whole body exposure of mice to mobile phone or wireless DECT base radiation," Electromagnetic Biology and Medicine, Early Online: 1–25, 2012


Enlarged Prostrate

1. Enlarged Prostate (Benign Prosatic Hyperplasia ) Bibliography

Also see discussion of enlarged prostate (benign prosatic hyperplasia) and research.

  1. Lees AM, Mok HYI, Lee RS, et al. Plant sterols as cholesterol-lowering agents: clinical trials in patients with hypercholesterolemia and studies of sterol balance. Atherosclerosis 1977;28:325–38.
  2. Pelletier X, Belbraouet S, Mirabel D, et al. A diet moderately enriched in phytosterols lowers plasma cholesterol concentrations in normocholesterolemic humans. Ann Nutr Metab 1995;39:291–5.
  3. Jones PJ, Raeini-Sarjaz M, Ntanios FY, et al. Modulation of plasma lipid levels and cholesterol kinetics by phytosterol versus phytostanol esters. J Lipid Res 2000;41:697–705.
  4. Grundy SM, Ahrens EH Jr, Davignon J. The interaction of cholesterol absorption and cholesterol synthesis in man. J Lipid Res 1969;10:304–15 [review].
  5. Berges RR, Windeler J, Trampisch HJ, et al. Randomised, placebo-controlled, double-blind clinical trial of beta-sitosterol in patients with benign prostatic hyperplasia. Lancet 1995;345:1529–32.
  6. Kiriakdis S, Stathi S, Jha HC, et al. Fatty acid esters of sitosterol 3ß-glucoside from soybeans and tempeh (fermented soybeans) as antiproliferative substances. J Clin Biochem Nutr 1997;22:139–47.
  7. Awad AB, Chan KC, Downie AC, Fink CS. Peanuts as a source of ß-sitosterol, a sterol with anticancer properties. Nutr Cancer 2000;36:238–41.
  8. Berges RR, Windeler J, Trampisch HJ, et al. Randomised, placebo-controlled, double-blind clinical trial of beta-sitosterol in patients with benign prostatic hyperplasia. Lancet 1995;345:1529–32.
  9. Klippel KF, Hiltl DM, Schipp B. A multicentric, placebo-controlled, double-blind clinical trial of ß-sitosterol (phytosterol) for the treatment of benign prostatic hyperplasia. Br J Urol 1997;80:427–32.


Fuch's Dystrophy

1. > More information about Fuch's Dystrophy

2. Free radicals (2010) implicated in Fuchs endothelial corneal dystrophy (FECD)

Learn more about Fuch's Dystrophy treatment and information.

A research study published in 2010 indicates that free radical damage is a contributor in the development of Fuchs endothelial corneal dystrophy (FECD), a potentially blinding disease characterized by the programmed cell death of epithelial cells in the eye's cornea (the clear tissue in the front of the eye). This is the most common reason for corneal transplant surgery.

Although genetic factors in FECD have been identified, mechanisms involved in its development were unclear. For their study, the researchers compared corneal epithelial tissue samples from FECD patients who received corneal transplants to samples derived from subjects who did not have the disease. They discovered a reduction in the level of antioxidants in the majority of FECD specimens and increased DNA damage.

They therefore concluded that oxidative stress - stress by free radicals plays a key role in development of Fuchs endothelial corneal dystrophy. The finding is significant for the nearly 4% of the population over 60 who are affected by FECD.

The researchers recommended that patients who are at risk supplement with a multivitamin, consume more leafy green vegetables and wear ultraviolet protection.

References:
Published: The American Journal of Pathology, November, 2010.
Researchers: Ula V. Jurkunas, MD and her colleagues at the Schepens Eye Research Institute in Boston


Glaucoma (optic nerve problems)

1. Alpha lipoic acid (1995) & glaucoma

See more information about glaucoma.

Pretreatment with alpha lipoic acid has been found to reduce neuronal damage from excitotoxic damage from cyanide, glutamate and iron ions, demonstrating a strong neuroprotective effect for neural tissue. J Cereb Blood Flow Metab 1995 Jul;15(4):624-30

2. Alpha lipoic acid (1995) & glaucoma

See more information about glaucoma.

In a study of open angle glaucoma patients who received 150mg of Alpha Lipoic Acid each day, 45-47% of the eyes had enhancement of color visual fields and visual sensitivity when compared to controls using only topical medical therapy. More advanced cases had an even better response compared to their controls. Filina, et al., Vestn Oftalmol 1995 Oct-Dec;111(4):6-8

3. Antioxidants (2008) Protect Trabecular Meshwork in Glaucoma

See more information about glaucoma treatment and information.

An independent study finds that the antioxidants vitamin E and N-acetyl cysteine (NAC) may reduce the progression of glaucoma. Additionally noted is that effectively reducing or even reversing oxidation may facilitate a healing response in the trabecular meshwork or outflow pathway in the eyes of glaucoma patients. A key suspect in the progression of POAG is local oxidative stress. Oxidative free radicals and reactive oxygen species (ROS) are reported to trigger degeneration in the trabecular meshwork, subsequently leading to increases in IOP and glaucoma.

"The finding of a protective effect of vitamin E and N-acetyl cysteine (a key component of glutathione) adds to the growing evidence that antioxidants are beneficial in POAG and are worthy of further investigation.” Dr. Yuan He

Reference: Yuan He, et al. Mitochondrial Complex I defect induces ROS release and degeneration in trabecular meshwork cells of POAG patients: Protection by antioxidants, Invest Ophthalmol Vis Sci 49:1447-58, 2008.

4. Bilberry, pine bark (2008) combo ward off glaucoma

A 2008 Italian study tested thirty-eight subjects with elevated pressures. 20 were treated with bilberry and French maritime pine bark, the rest were given nothing. Visual acuity, IOP, and ocular blood flow were measured after 2, 3 and 6 months. After two months the mean IOP decreased. No side effects were observed and ocular blood flow improved.

An improved ocular blood flow may contribute to the prevention of glaucoma.

The researchers also looked at the arteries of the eyes with color Doppler imaging and saw better flood flow in the subjects receiving the treament. This suggests that fluids in the eye were being restored.

One of the researchers, Steigerwalt, said, "Our study is the first demonstration showing that dietary intervention can help to control IOP and increase ocular blood flow in asymptomatic subjects and if taken in time, may prevent an evolution to higher pressure and symptomatic glaucoma."

Published: Molecular Vision 2008; 14:1288-1292, "Effects of Mirtogenol on ocular blood flow and intraocular hypertension in asymptomatic subjects"

Reference: Authors: Robert Steigerwalt Jr, Belcaro Gianni, Morazzoni Paolo, Ezio Bombardelli,2 Carolina Burki, Frank Schönlau , University of Chieti-Pescara in San Valentino, Italy

5. Bilberry/Pine Bark (2010) & Glaucoma (Mirtogenol )

A study published in a 2010 issue of the journal Clinical Opthamology examined the effects of Mirtogenol in a group of 79 patients living with "asymptomatic ocular hypertension". The participants were separated into three groups:

  • received 80 mg of Mitroselect bilberry extract and 40 mg of Pycnogenol daily
  • applied a medicinal eye drop (Latanoprost)
  • utilized both treatments

The trial lasted a total of 24 weeks and yielded the following results:

  • The Mirtogenol group lowered their intraocular pressure (IOP) from 38.1 to 29 mmHg or 24%.
  • The Latanoprost patients found an IOP reduction from 37.7 to 27.2 mmHg or 28%.
  • The combination group began with an IOP of 38 mmHg and ended with an IOP of 23 mmHg – a 40%
  • Healthy or normal eye pressure should range between about 10 to 21 mmHg.

In conclusion, the authors reported that, "The combination of both was more effective for lowering IOP and the combination yielded better retinal blood flow. No serious side effects occurred during the study, apart from standard side effects in patients related to Latanoprost". According to the National Institutes of Health, Latanoprost may cause the following adverse reactions in some users: dry eyes, eye color changes, irritation and redness of the eyelids.

Learn more about glaucoma, dry eyes, and drugs that harm the eyes.

Researchers: Robert D Steigerwalt, Jr, Gianni Belcaro, Paolo Morazzoni, Ezio Bombardelli, Carolina Burki, and Frank Schönlau

Published: Mirtogenol® potentiates latanoprost in lowering intraocular pressure and improves ocular blood flow in asymptomatic subjects, Clin Ophthalmol. 2010; 4: 471–476

6. Carotenoids (1994) and green leafy vegetables

See more information about holistic glaucoma treatment and information.

Holistic eye doctors know that green leafy vegetables are good for vision health.

In addition to beta carotene, researchers have found that other carotenoids, lutein and zeaxanthin, which found in dark green leafy vegetables are more essential to vision health. Several published studies indicate that lutein and zeaxanthin supplements may slow vision loss due to glaucoma, and in some cases improve eyesight.

Published: Science News, Volume 146, 1994.

7. Coleus forskolin (1984) & Glaucoma

Learn more about glaucoma.

A small double-blind, placebo-controlled study found that .3%, .6% & 1.% effectly lowered the intraocular pressure (IOP) in healthy subjects. The .3% concentration resulted in a 22.8% decrease; the .6% concentration resulted in a 27.8% decrease after 3 hours, and the 1% concentration resulted in a 26.5% decrease after 4 hours.

Further, the researchers found that the higher concentrations were about as effective as the lower concentrations, but lasted longer, with the 1% concentration lasting 7 hours, but the .3% concentration only lasting 4 hours.

The subjects noticed only very short term, minor sensations like itching or burning.

Researchers: Badian M, Dabrowski J, Grigoleit HG, Lieb W, Lindner E, Rupp W.

Published: Effect of forskolin eyedrops on intraocular pressure in healthy males [in German], Klin Monbl Augenheilkd. 1984 Dec;185(6):522-6

8. Coleus forskolin (1987) & Glaucoma

Learn more about glaucoma.

Forskolin is the ingredient from the coleus forskolii plant that has been found to be helpful for glaucoma.

A small placebo-controlled study investigated the effects of forskolin on intra-ocular pressure in 10 healthy subjects. First they received oxybuprocaine eyedrops for local anaesthesia. Some then received 1% forskolin eyedrops and others received placebo and IOP was measured hourly. A marked reduction in IOP was noted in those receiving either test and placebo.

Next a different anaesthetic was used, proxymetacaine - and again the subjects were treated with either test or placebo. In this instance, forskolin resulted in significant reduction compared to placebo, and it was concluded that the first anesthetic used, oxybuprocaine, itself had an effect on IOP.

Researchers: B H Meyer, A A Stulting, F O Müller, H G Luus, M Badian

Published: The effects of forskolin eye drops on intra-ocular pressure, South African medical journal, 06/1987; 71(9):570-1.

9. Computer Use (2004) & Glaucoma

Spending too much time looking at a computer screen may raise your risk of the vision-robbing eye disease glaucoma, particularly if you're nearsighted, according to a new Japanese study.

Glaucoma is a group of eye diseases that ultimately cause damage to the optic nerve. It can lead to blindness if not treated.

Heavy computer users who were farsighted or nearsighted seemed to have a higher risk for visual field abnormalities, say the researchers.

Source: Journal of Epidemiology and Community Health, December 2004; vol 58: pp 1021-1027

10. Depth Perception (2006) Deficits in Glaucoma Suspects

Learn more information about glaucoma treatment and information.

A 2006 study investigated depth perception in glaucoma suspects compared to glaucoma patients and controls. Glaucoma suspects (n=16), patients (n=18), and normal age-matched controls (n=19) aged 40- 65 years were prospectively evaluated for depth perception deficits using the Frisby Test. Stereocuity was measured by stereothreshold in seconds of arc for each group.

Glaucoma suspects showed significantly increased mean stereothreshold compared to age-matched normals (144.1 +/- 35.2 vs. 26.6 +/- 3.7 seconds of arc). The mean stereothreshold in glaucoma patients was also increased compared to age-matched normals (148.1 +/- 33.8 vs. 26.6 +/- 3.7 seconds of arc).

Glaucoma suspects show depth perception deficits. Evidence of impaired stereovision in glaucoma suspects suggests that binocular interactions are disrupted in the absence of visual field defects using standard automated perimetry.

SOURCE: Gupta N, Krishnadev N, Hamstra SJ, Yucel Y. Depth Perception Deficits in Glaucoma Suspects. Br J Ophthalmol. 2006 May 3; [Epub ahead of print].

11. Diet (2008) Glaucoma Risk Reduction through Nutrition

Several studies published in 2008 looked at glaucoma risk and nutrition and found a possible relationship between eating fruits and vegetables and lowered glaucoma risk.

Study I

The first study investigated whether specific nutrients might account for an apparent relationship between glaucoma risk and fruit and vegetable consumption. The researchers also investigated potential links between glaucoma risk and antioxidants, calories, fat, protein, and carbohydrates obtained from natural food sources. The study evaluated data from the Study of Osteoporotic Fractures Research Group1.

Summary I:

  • Glaucoma risk was decreased 69% in women who consumed at least one serving per month of green collards and kale compared with those who consumed fewer than one serving per month.
  • Glaucoma risk was decreased 64% in women who consumed more than two servings per week of carrots compared with those who consumed fewer than one serving per week.
  • Glaucoma risk was decreased 47% in women who consumed at least one serving per week of canned or dried peaches compared with those who consumed fewer than one serving per month.

Researcher: Anne L. Coleman, MD, PhD, professor of ophthalmology in the Jules Stein Eye Institute of the David Geffen School of Medicine at the University of California Los Angeles and professor of epidemiology in the UCLA School of Public Health, study published in the American Journal of Ophthalmology, 2008

Study II

The second study drew data from the same research1.

Summary II:

This study further analyzed the results of the first study above regarding the effects of nutrition on the African-American community who have a higher percentage of glaucoma.

The data included 584 black women of whom 13% had glaucoma in at least one eye.

  • Three or more servings per day of all fruits or fruit juices decreased the odds of glaucoma by 79% compared to consuming less than one serving per day.
  • Eating more than two servings per week of fresh oranges and peaches was associated with less glaucoma risk.
  • Eating more than one serving per week of green collards or kale decreased the odds of glaucoma by 57% compared to 1 serving per month or less.
  • There was a protective trend for glaucoma in those eating more fruit or fruit juices), fresh oranges, fresh peaches, spinach), and green collards or kale.
  • Higher intakes of some nutrients were also associated with decreased risk: vitamin A; folate; a-carotene; ß-carotene; and lutein/zeaxanthin.
  • The researcher notes that it’s dangerous to draw too many conclusions from the nutrition-related data found so far, saying that the studies are exploratory and there are clear associations, but not conclusive proof, that, for example, eating collards prevented glaucoma. There could be environmental differences or differences in how their bodies metabolize nutrients. But the association was worth pursuing.

    Researcher: JoAnn A. Giaconi, MD, assistant clinical professor of ophthalmology at the Jules Stein Eye Institute at UCLA. Published: Giaconi JA, et al. IOVS 2008;49; ARVO E-abstract 5453.

    1. Coleman AL, Stone KL, Kodjebacheva G, Yu F, Pedula KL, Ensrud KE, Cauley JA, Hochberg MC, Topouzis F, Badala F, Mangione C; Study of Osteoporotic Fractures Research Group

    12. East Baltimore Eye Survey (1988)

    Learn more information about glaucoma treatment and information.

    A 3-year survey examined 5,308 individuals in East Baltimore. They found that approximately 40 percent of people with glaucoma have normal, not elevated, internal eye pressure. It is also confirmed that many people with elevated IOP never develop the optic nerve damage consistent with glaucoma (Beaver Dam Study had the same conclusion).

    13. Exercise (2004) & Glaucoma

    Research has shown that glaucoma patients who take a brisk, 40-minute walk five days a week for three months can reduce the pressure in their eyes by approximately 2.5 millimeters – similar to the reduction seen when using beta-blockers.

    Reference: Passo, M.S. et. al. Regular exercise lowers intraocular pressure in glaucoma patients. Investigative Ophthalmology 35. In ARVO Abstracts, March 15, 1994.

    Read more information on prevention strategies for glaucoma.

    14. Ginkgo (2003) and glaucoma

    Learn more information about glaucoma treatment and information.

    There has been little scientific evidence that the oral use of herbs can help glaucoma.

    However, a clinical trial published in 2003 suggests that ginkgo biloba extract has possibilities.

    The research looked at the effect of inkgo biloba extract on pre-existing visual field damage in normal tension glaucoma.

    In normal tension glaucoma damage occurs to the optic nerve and visual field are present despite intraocular pressure measurements being 'normal'. The exact mechanisms behind the damage are unknown, but there are two primary factors:

    • reduced blood flow to the optic nerve
    • versus relatively high intraocular pressure

    The researchers felt that because some patients with normal tension glaucoma can experience narrowing of the peripherial field despite conventional medical treatment, the value of other treatments is worthy of investigation. Since Ginkgo biloba has been shown to improve blood flow at a tissue level, it was an obvious candidate for selection in such investigations.

    In a randomized, double-blind, placebo-controlled, crossover trial, 27 patients with bilateral visual field damage (less peripherial vision) resulting from normal tension glaucoma received Ginkgo biloba extract or a placebo. Visual field tests were performed at the beginning of the trial and at the end of each 4-week period.

    The researchers measured any changes in the visual field and the development of any ocular or systemic complications. After Ginkgo biloba treatment, a significant improvement in visual field indices was recorded, but there were no significant changes found in intraocular pressure, blood pressure or heart rate.

    No ocular or systemic side effects were noted in any patient during the trial. The authors concluded that Ginkgo biloba extract can improve pre-existing visual field damage in some individuals with normal tension glaucoma. However, they observed that the exact explanation is not currently understood.

    Source: Findarticles.com
    Reference: Quaranta L, Bettelli S, Uva MG et al. Effect of Ginkgo biloba extract on preexisting visual field damage in normal tension glaucoma. Ophthalmology 2003; 110: 359-36

    15. Ginkgo Biloba (2003) and Glaucoma

    Learn more information about glaucoma treatment and information.

    Research has identified non- interocular pressure related risk factors for glaucoma. The prevalence of normal-tension glaucoma (NTG) is greater than previously realized, and that progressive damage can occur even with IOP-lowering intervention. Since Ginkgo has been shown to increase ocular blood flow1, the effects of a ginkgo extract on pre-existing visual field damage in normal tension glaucoma was evaluated in a prospective, randomized, double-blind crossover trial2.

    Twenty seven patients with bilateral visual field damage resulting from NTG received ginkgo extract (40 mg, 3x daily) for 4 weeks, followed by a wash-out period of 8 weeks, then 4 weeks of placebo treatment. Other patients underwent the same regimen, but took the placebo first and ginkgo last. Visual field tests, performed at baseline and at the end of each phase of the study, were evaluated for changes in visual field and any ocular or systemic complications.

    After ginkgo treatment, a significant improvement in visual field indices was observed.

    No significant changes were found in intraocular pressure, blood pressure, or heart rate after placebo or ginkgo treatment. The investigators concluded that Ginkgo biloba is a useful therapy for some patients with NTG. An accompanying editorial in Ophthalmology points out that the mechanisms of ginkgo are plausible, and that the beneficial effects were not maintained in this study after discontinuation of ginkgo treatment. Both of these observations lend credence to the findings.

    References:

    1. Chung HS et al. Ginkgo biloba extract increases ocular blood flow velocity. J Ocul Pharmacol Ther 15:233-40, 1999.
    2. Quaranta L et al. Effect of Ginkgo biloba extract on preexisting visual field damage in normal tension glaucoma. Opthalmol 110:359-62 (discussion 362-4), 2003.

    16. Ginkgo biloba (2006) & Steroid-Induced Changes in the Trabecular Meshwork & Intraocular Pressure

    Learn more information about glaucoma treatment and information.

    This study examined the effects of Ginkgo on intraocular pressure in young rabbits with (steroid-induced) glaucoma (ocular hypertension).

    The rabbits received topical TobraDEX and/or 5 µg of Ginkgo biloba extract 4x daily for 2 weeks, and their intraocular pressure was measured periodically.

    When trabecular meshwork (TM), the network of fibers in the eye, were examined and it was found that Ginkgo biloba extract suppressed the intraocular pressure. Not only did the treatment reduce the accumulation of extracellular materials within the layers of the TM but better TM cell health resulted.

    In addition, the researchers examined lab-cultured human TM cells and found that ginkgo substantially reduced cell-death and reduced DEX-induced myocilin (a protein) expression. Ginkgo biloba extract modulated the expression of alphaB-crystallin and heat-shock proteins 70 and 90alpha but not other stress-related genes. Furthermore, changes associated with steroids were found less in GBE-treated or GBE-primed TM cells.

    Ginkgo biloba extract, significantly suppressed steroid-induced IOP elevation in rabbits, and it seems to prevent the adverse effects of steroids on TM cells. The researchers felt that Ginkgo biloba extract could be a therapeutic agent or dietary supplement to prevent steroid-induced glaucoma.

    Published: Jia LY, Sun L, Fan DS, et al. Effect of Topical Ginkgo biloba Extract on Steroid-Induced Changes in the Trabecular Meshwork and Intraocular Pressure. Arch Ophthalmol 2008;126(12):1700-1706.

    17. Glaucoma (2006) Glaucoma & Other Diseases

    Despite intense research, the pathogenesis of primary open-angle glaucoma (POAG) is still not completely understood. There is ample evidence for a pathophysiological role of elevated intraocular pressure; however, several systemic factors may influence onset and progression of the disease.

    Systemic peculiarities found in POAG include alterations of the cardiovascular system, autonomic nervous system and immune system, as well as endocrinological, psychological and sleep disturbances. An association between POAG and other neurodegenerative diseases, such as Alzheimer disease and Parkinson disease, has also been described. Furthermore, the diagnosis of glaucoma can affect the patient's quality of life.

    SOURCE: Pache M, Flammer J. A sick eye in a sick body? systemic findings in patients with primary open-angle glaucoma. Surv Ophthalmol 2006;51(3):179-212.

    Learn more information about glaucoma, including nutritional recommendations and prevention recommendations for glaucoma.

    Heavy computer users are at greater risk for glaucoma. Read this computer use and glaucoma warning.

    18. Green Tea (2010) Green Tea Can Help Combat Glaucoma

    Researchers in China say that green tea may protect against eye diseases such as glaucoma.

    The researchers confirmed that substances found in green tea, which is known for its antioxidant and disease-fighting properties, were absorbed in the lens, retina and other eye tissue. Until this research it was not actually known whether green tea substances actually passed from the gastrointestinal tract into eye tissue.

    The researchers analyzed the eye tissue of laboratory rats that drank green tea and found that several "catechins" in green tea that contain antioxidants -- including vitamin C, vitamin E, lutein and zeaxanthin -- were absorbed by the eye in significant amounts.

    The researchers said green tea catechins reduced harmful oxidative stress in the eye for up to 20 hours, saying, "Our results indicate that green tea consumption could benefit the eye against oxidative stress."

    Reference: Chi Pui Pang of the Chinese University of Hong Kong and Hong Kong Eye Hospital, study published in the April, 2010, Journal of Agricultural and Food Chemistry

    19. Homocysteine (2004) levels in glaucoma

    Learn more information about glaucoma treatment and information.

    "Elevated homocysteine levels in aqueous humor of patients with pseudoexfoliation glaucoma"

    In a study published in 2004, researchers wanted measure homocysteine levels in open-angle pseudoexfoliation glaucoma patients. Pseudoexfoliation, according to wikipedia, is an eye-disease "characterized by the accumulation of microscopic granular amyloid-like protein fibers."

    The researchers looked at total homocysteine levels in the aqueous humor and plasma of 29 patients with pseudoexfoliation glaucoma and 31 control patients with cataract.

    They observed elevated (200%) homocysteine levels in the glaucoma patients. Additionally, the ratio of plasma to aqueous humor was much lower in these patients.

    The researchers concluded that high levels of homocysteine in the aqueous humor may trigger the abnormal fiber accumulation.

    Researchers: Bleich S, Roedl J, Von Ahsen N, Schlotzer-Schrehardt U, Reulbach U, Beck G, Kruse FE, Naumann GO, Kornhuber J, Junemann AG., Dept. of Psychiatry and Psychotherapy, Friedrich-Alexander-University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany. stefan.bleich@psych.imed.uni-erlangen.de

    Published: PMID: 15234308 [PubMed - indexed for MEDLINE]

    20. Hypnosis Can Help Lower Intraocular Pressure
    The research study below shows that hypnosis can lower intraocular pressure for those with open-angle glaucoma.

    For more information, go to Psychosomaticmedicine.org.

    21. Hypnosis on Intraocular Pressure Glaucoma
    Research study show hypnosis can help lower eye pressure (intracular pressure) for those with glaucoma. For full study, go to Psychosomaticmedicine.org.

    22. Increased Homocysteine Levels in Tear Fluid of Glaucoma Patients

    Homocysteine (Hcy) levels in tear fluid and plasma of patients with primary open-angle glaucoma (POAG) were assessed to determined the association between Hcy levels, dry eye syndrome and B vitamin status in glaucoma patients. This prospective case-control study included 36 patients with POAG and 36 controls. Hcy concentrations were measured by high-performance liquid chromatography.

    Patients with POAG had significantly higher mean Hcy levels both in tear fluid (205 +/- 84 nmol/l) and in plasma (13.43 +/- 3.53 micromol/l) than control subjects (130 +/- 53 nmol/l and 10.50 +/- 3.33 micromol/l, respectively). Hcy in tear fluid was significantly correlated with plasma Hcy in POAG patients, but not in controls. POAG patients with dry eye disease had significantly higher Hcy levels both in tear fluid and plasma than POAG patients without dry eye disease. There was no association between Hcy levels and B vitamin status in subjects with POAG.

    The study suggests increased Hcy levels in tear fluid and plasma of patients with POAG. Elevated Hcy levels might be a risk factor for POAG and dry eye syndrome in subjects with glaucoma.

    SOURCE: Roedl JB, Bleich S, Schlotzer-Schrehardt U, et al. Increased homocysteine levels in tear fluid of patients with primary open-angle glaucoma. Ophthalmic Res 2008;40(5):249-56

    23. Lipoic acid (1998) - Glaucoma

    Learn more about holistic treatment of glaucoma.

    Alapha Lipoic Acid and Glaucoma

    This monograph discusses research results using lipoic acid as an aid for glaucoma. Researchers gave 75 patients with open-angle glaucoma 75 mg daily for 2 months or 150 mg daily for one month, compared to 31 control subjects. They found that, both biochemically, and in terms of visual acuity, the group receiving the larger dosage had the best results.

    Note, the same monograph discusses use of alpha lipoic acid in treating cataracts, diabetes, ischemia-reperfusion injury, liver disease from alcohol abuse, and other therapeutic results. This research has been replicated in a number of other studies.

    Published: Monograph, Alpha Lipoic Acid; Altern Med Rev 1998 Aug;3(4):308-11

    24. Lipoic acid / Vitamin B (1991) - Glaucoma

    Learn more about holistic treatment of glaucoma.

    Researchers looked at tyrosine (an amino acid) metabolism with respect to the effects of lipoic acid in patients with primary open-angle glaucoma. There were two control groups, one consisting of glaucoma patients not given lipoic acid and patients with ocular hypertension.

    In the majority of glaucoma patients administration of lipoic acid did not result in improvement of tyrosine metabolism. Tyrosine metabolism normalized in the patients given lipoic acid, and various parameters that were measured improved.

    Both the researchers' findings and the data in published studies further recommend using lipoic acid combined with vitamins B1, B2, B5, B6, and vitamin C for glaucoma treatment.

    Published: Filina, AA & Sporova, NA. Vestn Oftalmol 1991 May-Jun;107(3):19-21

    25. Magnesium (1995) glaucoma

    Learn more about holistic treatment of glaucoma.

    Scientists found that glaucoma patients with either open angle glaucoma or normal-tension glaucoma who received 2x a day supplements of magnesium for 4 weeks experienced improvement of the width of peripherial vision and reduced peripheral vasospasms, which have been tied to glaucoma, stroke and heart attack.

    Published: Gasper, et al; Ophthalmologica 1995;209(1):11-3

    26. Mini-Strokes (2009) May Cause Vision Loss for Those with Normal Tension Glaucoma

    Learn more about glaucoma recommendations.

    The study looked at incidence of glaucoma in people with normal rather than high ocular pressure, known as normal-tension glaucoma. They found that people who experience cerebral infracts (silent mini-strokes) may be more likely to have normal-tension glaucoma.

    When 286 people with normal-tension glaucoma were studied, the researchers found that there was a higher than expected incidence of silent cerebral infarcts among those patients whose loss of vision progressed more rapidly.

    Published: Ophthalmology, July, 2009.

    Researchers: Dr. Dexter Y.L. Leung and others, Glaucoma Service, Hong Kong Eye Hospital

    27. Natural Occurring Growth Factor May Regenerate Retinal Nerve Fiber

    Researchers, building on earlier Glaucoma Foundation research, found that oncomodulin, a naturally occurring growth factor, stimulates the regeneration of injured retinal nerve fibers. The optic nerve doesn’t normally regenerate after injury. However, through unknown mechanisms, macrophage activation in the eye stimulates retinal ganglion cells (RGCs) to regenerate long axons beyond the site of the injury.

    Oncomodulin appears to stimulate this regeneration process, offering future hope for reversing optic-nerve damage due to glaucoma, tumors, or traumatic eye injury.

    Research: 2008: Boston’s Children’s Hospital and Harvard Medical School

    28. Omega-3 (1973) glaucoma

    Learn more about holistic treatment of glaucoma.

    Researchers have found that Eskimos, who have a high level of omega-3 from fish oils correspondingly have less occurences of open angle glaucoma.

    Published: Albrick, P.H., Angle closure surveys in Greenland Eskimos, Canadian Journal of Ophthalmology 8 (1973): 260-64.

    29. Physical Activity (2009) & Glaucoma

    Learn more about glaucoma.

    These researchers looked at data from the National Runners’ Health Study in order to evaluate the relationship between vigorous physical activity, (ie, degree of cardiac fitness) in athletes and glaucoma risk.

    The eye health of nearly 30,000 male runners, who did not have diabetes (a glaucoma risk factor), and who raced and ran regularly, was followed over a period of 7.7 years. The researchers were looking at the dose-response relationship, the pattern of physiological reaction, of their exercise to glaucoma risk.

    In addition, the researchers took into account the runners' age, consumption of fish, meat, alcohol and fruit, and whether they smoked or had high blood pressure.

    Over the 7.7 year followup period, 200 glaucoma cases were reported. The slowest men, who also were the men who ran the least, had the highest % of glaucoma cases, while the men who ran the most and were fastest had the lowest risk, or no cases of glaucoma at all.

    It is particularly interesting that the researchers actually treated running in terms of dosage, with risk decreasing 37% per meter per second in better running speeds, using the slowest men in 10-km races as a baseline:

    • In those who ran 3.6 to 4.0 meters/second there was 29% risk reduction.
    • In those who ran 4.1-4.5 meters/second there was a 54% risk reduction.
    • In those who ran 4.6-5.0 meters/second there was a 51% risk reduction.
    • In 781 men who exceeded 5.0 meters/second, there were no glaucoma cases.

    These relationship held true when adjusted for performance in long races versus shorter daily runs.

    The results suggest that vigorous physical activity may very well reduce glacuoma risk.

    Researcher: Paul T. Williams

    Published: Relationship of incident glaucoma versus physical activity and fitness in male runners. Med Sci Sports Exerc 2009;41(8):1566-1572

    30. Replacing Immune Cells May Impede Onset of Glaucoma
    A study in the Journal of Experimental Medicine (2003;197[10]:1335-1344) found that inflammatory immune response, which is suppressed in the normal eye, might be an early step in the onset of pigment dispersion glaucoma. Pigment dispersion glaucoma occurs when the iris begins to shed melanin into the front part of the eye. This is followed by increasing pressure within the eye, which strangles the optic nerve and kills the retinal cells attached to it.

    The researchers examined the eyes of model mice with pigment dispersion glaucoma before the visible onset of the disease and found that the diseased eyes failed to successfully suppress T-cells--white blood cells that cause the iris to shed pigment. This failure preceded clinical evidence of pigment dispersion. They also found that the eyes contained bone marrow-derived white blood cells that were programmed to cause inflammatory responses. Jun Song Mo, M.D., the study's lead author, told the press, "It is relevant that one of the two genes known to be responsible for pigment dispersion glaucoma in mice is active in these same white blood cells."

    The research team concluded that the eyes of the genetically predisposed mice lost immune privilege before the pigment dispersion began.

    "What this suggested to us," said J. Wayne Streilein, M.D., senior author of the study, "is that maybe the first thing that the genes for pigment dispersion glaucoma do is break down immune privilege and leave the eyes vulnerable to inflammation."

    The researchers tested their theory of inappropriate immune response even further by replacing the bone marrow of mice predetermined to develop pigment dispersion glaucoma with bone marrow from normal mice. Following the procedure, the team found that the immune-privileged status was maintained in the eyes, inflammation never developed and pigment dispersion failed to occur.

    "These results are very exciting and encouraging. We feel that this is a major breakthrough in understanding how this disease is triggered and may be cured," said Streilein. "We are eager to understand more completely the interrelationship between loss of immune privilege and development of glaucoma. Moreover, we are also interested to know whether a similar immune dependency might occur in other blinding eye diseases, such as macular degeneration and retinitis pigmentosa"--AR

    31. Smoking (2009) Additional Risk Factor in Elder Women for Glaucoma

    Learn more about glaucoma recommendations.

    Researchers sampled the fluid in the eye and blood of 120 female glaucoma patients (age 40-90) who were smokers (40), ex-smokers (40) and non-smokers (40). Both inflammation and cell death processes were studied using techniques of enzyme immunoassay and western blot procedures. They looked at the interleukin-6 (a protein that stimulates immune responses in the body) as a marker of inflammation marker and caspase-3 (a protein involved in stages of cell death) and poly (ADP-ribose) polymerase 1 (a protein involved in DNA repair and cell death) as apoptosis (cell death) "markers".

    They found that Inflammation and cell death marker levels increased in samples taken from the women who smoked and concluded that smoking could be an important additional risk factor for glaucoma progression in elderly women.

    Published: Zanon-Moreno V, Garcia-Medina JJ, Zanon-Viguer V, et al. Smoking, an additional risk factor in elder women with primary open-angle glaucoma. Mol Vis 2009;15:2953-2959.

    32. Stress (1977) and Glaucoma

    Learn more about holistic treatment of glaucoma.

    Researchers found that stress may be connected to glaucoma risk. After reviewing incidence of above average stress in patients, researchers have indicated that high stress leads to a 3times higher risk for high eye pressure. High levels of pressure have been connected to glaucoma (although glaucoma can also occur with 'normal' levels of eye pressure.

    Published: Grignolo, F.M. et. al. Variations of intraocular pressure induced by psychological stress. Klinische Monatsblaten Augenheilkd 170 (1977): 562-69.

    33. Studies Show Relationship of Blood Pressure and Glaucoma
    Glaucoma may continue to progress after the reduction of IOP to targeted levels. Research is providing increasing support for the idea that vascular risk factors may be the cause. Several population-based studies have suggested that low diastolic perfusion pressure is associated with an increased incidence of open-angle glaucoma (OAG). Perfusion pressure is defined as the difference between arterial and venous pressure, which, in the eye, by convention equals IOP. Blood pressure and IOP are therefore the principal components of ocular perfusion pressure (perfusion pressure = blood pressure – IOP). • Choi J, Kim KH, Jeong J, et al. Circadian fluctuation of mean ocular perfusion pressure is a consistent risk factor for normal-tension glaucoma. Invest Ophthalmol Vis Sci. 2007;48:104-111. • Tielsch JM, Katz J, Sommer A, et al. Hypertension, perfusion pressure, and primary open-angle glaucoma. A population-based assessment. Arch Ophthalmol. 1995;113:216-221. • Leske MC, Connell AM, Wu SY, et al. Risk factors for open-angle glaucoma. The Barbados Eye Study. Arch Ophthalmol. 1995;113:918-924. • Hulsman CA, Vingerling JR, Hofman A, et al. Blood pressure, arterial stiffness, and open-angle glaucoma: the Rotterdam study. Arch Ophthalmol. 2007;125:805-812. Perfusion pressure can be affected by IOP and blood pressure, but which is really the most important? In a given patient, it could be IOP alone, blood pressure alone, or a combination of the two. For more related studies, go to www.glaucomatoday.com/articles/0409/GT0409_06.php

    34. Study: Glaucoma (2004) linked to Heavy Computer Use
    Spending too much time looking at a computer screen may raise your risk of the vision-robbing eye disease glaucoma, particularly if you're nearsighted, according to a new Japanese study. Glaucoma is a group of eye diseases that ultimately cause damage to the optic nerve. It can lead to blindness if not treated. Heavy computer users who were farsighted or nearsighted seemed to have a higher risk for visual field abnormalities, say the researchers. Source: Journal of Epidemiology and Community Health, December 2004; vol 58: pp 1021-1027

    35. Taurine (2003 Study)

    Taurine, an amino acid concentrated in the eye and found in the optic nerve, may help counter excess levels of nerve-damaging glutamate in the body. An acute dose has been clinically shown to promote blood flow during oxidative stress by restoring vessels' ability to dilate.

    Fennessy FM, et al. Taurine and vitamin C modify monocyte and endothelial dysfunction in young smokers. Circulation 107:410-15, 2003.

    36. Thiamine (1979) & chronic open angle glaucoma

    Learn more about holistic treatment of glaucoma.

    Researchers looked at blood levels of Vitamin C and Thiamine in glaucoma patients. They found that the patients with chroonic open angle glaucoma patients had a far lower thiamine blood level than controls and related poor absorption of that thiamine. However there were not distinct differences between the controls and the vitamin C blood levels.

    Asregadoo, Ann Ophthalmol 1979 Jul;11(7):1095-1100

    37. Thyroid Problems Linked to Glaucoma 2002 Study

    Researchers at the University of Alabama at Birmingham believe that thyroid disorders may increase the risk of glaucoma. Their study, published in the British Journal of Ophthalmology, reviewed data from the 2002 National Health Interview Survey to quantify the association between a self-reported diagnosis of glaucoma and a self-reported history of thyroid problems.

    Of the 12,376 survey participants, 4.6% reported glaucoma, and 11.9% reported a history of thyroid problems. The prevalence of glaucoma among those who reported thyroid problems was 6.5% compared with 4.4% among those who did not report thyroid problems. This association between glaucoma and thyroid problems remained after adjusting for differences in age, gender, race and smoking status.

    The results of this study lend support to the hypothesis that thyroid disorders may increase the risk of glaucoma. Although further research on the topic is expected, study authors suspect that hypothyroidism may diminish outflow in the eye.

    SOURCE: The association between thyroid problems and glaucoma, Cross, et al, British Journal of Ophthalmology 2008;92:1503-1505.

    38. Vascular changes (1993) and glaucoma

    Learn more about holistic treatment of glaucoma.

    Changes in the vascular (blood) system in the eyes, which limit nutrient-bearing blood flow to the nerve tissue in the eyes may be the primary cause of glaucoma.

    Researchers looked at disc haemorrhages and retinal vein occlusions in the eye and concluded that they were all different manifestations of the same cause, restricted flow of blood in the eye.

    Published: Acta Ophthalmol (Copenh) 1993 Aug;71(4):433-44

    39. Vascular obstruction (1993) - glaucoma cause

    Learn more about holistic treatment of glaucoma.

    Data about Open Angle Glaucoma which had been compiled by an eye doctor between 1980 to 1991 was analysed looking especially at disc haemorrhages and retinal vein occlusions. The researcher found a connection between the three, which in all categories, increased with duration.

    It was felt that mixed incidents suggested that the haemorrhages and occlusions were manifestations of the same vascular disease, the only difference being the size of the blood artery or vein.

    The researchers concluded that the various vascular obstructions damaged ability of the tissues to pick up nutrition and therefore might be the primary cause of glaucoma.

    Published: Sonnsjo & Krakau, Acta Ophthalmol (Copenh) 1993 Aug;71(4):433-44

    40. Vitamin B12 (1965) and glaucoma

    Learn more about holistic treatment of glaucoma.

    This early study, later substantiated by a 1992 Vitamin B12 & Glaucoma Study found that glaucoma patients where were treated with vitamin B12 for over a 5 year period had improved visual acuity (sharpness) and better overall management of the condition

    Published: Glacome, 1992; ; Oftalmol Zh. 1965; 20(6); Klin Oczna 1974 Nov;44(11):1183-7

    41. Vitamin B12 (1992) - glaucoma

    Learn more about holistic treatment of glaucoma.

    Research indicates that a statistically significant number of glaucoma patients with long-term supplementation of Vitamin B12 - 1,500 mcg of vitamin B12 over five years - found improvement in or no further deterioration to eyesight due to glaucoma. This was true although eye pressure remained constant.

    Published: Sakai, T. Murata, M., and Amemiya, T. Effect of long-term treatment of glaucoma with vitamin B12. Glaucoma 14 (1992): 167-70.

    42. Vitamin C (1969) and Glaucoma

    Learn more about holistic treatment of glaucoma.

    In several studies, researchers found that Vitamin C, in larger doses, have lowered intraocular eye pressure - this is important for glaucoma. This happened through several body mechanisms, including increased blood osmolarity (a measure of pressure, as in osmosis), lower aqueous production, improved movement of fluids in the eye and collagen support.

    Published: Acta Ophthalmology Scand, 1969.

    43. Vitamin E (2008) Neuroprotection by Vitamin E in Glaucoma

    See other glaucoma vitamins & supplements.

    Learn more information about glaucoma treatment and information.

    Vitamin E is known as a major fat-soluble antioxidant. It intercepts free radicals preventing chain reactions of lipid destruction. However the discovery of complex molecules that control vitamin E metabolism fostered the idea that the vitamin E may be more than an antioxidant.

    Vitamin E is now known to affect the expression and activity of immune and inflammatory cells, and to enhance dilation of blood vessels. It is also known to inhibit the activity of protein kinase C (PKC), a family of enzyme-like proteins enzyme that control other proteins and which plays a role in development of glaucoma. PKC inhibitors have been shown to relax the trabecular meshwork and to affect matrix metalloproteinase and PGF2 alpha, both of which can degrade cell structur).

    Vitamin E and PKC could also have a vaso-regulatory effect in the retina. In different experimental models, retinal vascular dysfunction due to hyperglycemia was reportedly prevented by vitamin E via the diacylglycerol-PKC pathway1,2.

    These findings prompted researchers at Istanbul University to evaluate the clinical potential of vitamin E in glaucoma patients. They reported prevention of visual field loss in this preliminary study, and conclude that vitamin E deserves further attention in preventing glaucomatous damage3.

    Study Design and Methods
    Thirty glaucomatous patients (60 eyes) with controlled IOP, were randomly divided into three groups. Group (A) received no vitamin E, while groups (B) and (C) were given a daily dose of 300 and 600 mg of vitamin E respectively, as d-alpha tocopheryl acetate for 12 months. Blood levels of vitamin E were measured via HPLC.

    Disease progression for each subject was monitored via visual field measurements and color Doppler imaging of ophthalmic and posterior ciliary arteries at baseline, and at 6 and 12 months. Retinal blood flow of ophthalmic and posterior ciliary arteries was evaluated, and resistivity and pulsatility indexes were obtained. Mean deviation values for Fastpac visual fields were recorded at all time points, and the difference in mean deviation values calculated. The change in mean deviations of Groups (B) and (C) were compared with Group (A), and the Mann-Whitney U-test was employed for statistical analysis.

    Results
    There were no significant differences between the groups in mean ages, IOP, best corrected visual acuities of 10/10 ratios and disease etiologies. The average differences between the pulsatility indexes (PI) and resistivity indexes (RI) of both ophthalmic arteries and posterior ciliary arteries of both supplemented groups were significantly lower than those of the non-supplemented groups at 6 months and 1 year. RI decreases observed in posterior ciliary arteries at both time points, and PI decreases observed in ophthalmic arteries at the 6th month were statistically significant.

    Compared with those receiving vitamin E, non-treated subjects showed a statistically significant reduction in visual field (change in mean deviation) at 6 and 12 months).

    1. Kunisaki M et al. Vitamin E prevents diabetes-induced abnormal retinal blood flow via the diacylglycerol-protein kinase C pathway. Am J Physiol 269:239-46, 1995.
    2. Lee IK et al. d-alpha tocopherol prevents hyperglycemia induced activation of the diacylglycerol (DAG)-protein kinase C pathwayin vascular smooth muscle cells by an increase in DAG kinase activity. Diabetes Res Clin Pract 45:183-90, 1999.
    3. Engin KN et al. Clinical evaluation of the neuroprotective effect of alpha tocopherol in glaucomatous damage. Eur J Ophthalmol 17:528-33, 2007.


    Gout

    1. Gout Bibliography

    Also see discussion of gout and research

    1. Ralston SH, Capell HA, Sturrock RD. Alcohol and response to treatment of gout. BMJ 1988;296:1641–2.
    2. Scott JT. Alcohol and gout. BMJ 1989;298:1054.
    3. Emmerson BT. Effect of oral fructose on urate production. Ann Rheum Dis 1974;33:276–80.
    4. Blau LW. Cherry diet control for gout and arthritis. Tex Rep Biol Med 1950;8:309–11.
    5. Loenen H, Eshuis H, Lowik M, et al. Serum uric acid correlates in elderly men and women with special reference to body composition and dietary intake (Dutch Nutrition Surveillance System). J Clin Epidemiol 1990;43:1297–303.
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    Hay Fever

    1. Hay Fever Bibliography

    Also see discussion of hay fever and research. Related condition: allergies and sensitivities.



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    High Cholesterol

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    Also see discussion of high cholesterol and research.

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    2. Olive Oil (2011) Standards updated and beneficial effect

    Learn about information on High Cholesterol.

    The beneficial health effects of olive oil are due to both its high content of monounsaturated fatty acids and its high content of antioxidative substances. Studies have shown that people who consumed about 2 tablespoons of virgin olive oil daily for 1 week showed less oxidation of LDL cholesterol and higher levels of antioxidant compounds, particularly phenols, in the blood.

    The International Olive Oil Council (IOOC) sets standards of quality used by the major olive oil producing countries. The United States is not a member of the IOOC, and the U.S. Department of Agriculture does not legally recognize its classifications. California has set high standards for its olive oil through the California Olive Oil Council (COOC). The COOC has adopted the standards set by the International Olive Oil Council, but went one step further. The international standard for free acidity content is less than 0.8% and the COOC standard for free acidity content is less than 0.5%. If olive oil makers from California meet these standards, they can put the COOC seal of quality on their bottles.

    There is a simple home test for the purity of olive oil, although it is not conclusive: refrigeration. Wikipedia says that when genuine olive oil is refrigerated, it should become thicker if not nearly solid. Blended olive oils and non-olive oils posing as olive oil will not solidify when refrigerated.

    3. Omega-3 fatty acids protect bypass patients (2005)
    A report published in the May 17 2005 issue of the Journal of the American College of Cardiology summarized the findings of Italian researchers that giving omega-3 fatty acids to patients before and after coronary artery bypass graft surgery helps protect them from atrial fibrillation, a type of heart arrhythmia that is often associated with the procedure.

    4. Plant Sterols (2009) & Cholesterol

    Learn more about managing High Cholesterol

    Plant sterols are naturally-occuring steroid compounds found in plants and are frequently used to enrich foods or are available as dietary supplements. Good sources of these compounds (also known as phytosterols) are found in nuts, cereals, vegetables, fruits and berries. Carefully designed vegetarian diets can produce high levels of phytosterols in the diet.

    Phytosterols were first found to help reduce cholesterol as early as 1953, and have been marketed in many forms since then.

    Researchers have found that the greatest benefit is when plant sterols are consumed in smaller amounts more often during the day rather than in one larger amount daily. In this study, the scientists tested giving one group of study participants 1 larger dose each morning and another group, three smaller doses daily.

    The study began with a control phase wherein the subjects were on a precise weight-maintaining diet and no supplementary plant sterols. In the second phase, they were on the same diet but had 1.8 grams of plant sterols added at breakfast. In the third phase, again the same diet, but this time 1.8 grams divided 3 ways for each of three meals.

    It was found that with consumption three times a day LDL cholesterol dropped by 6%.

    Researchers: Lichtenstein, and colleagues at the Cardiovascular Nutrition Laboratory at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University in Boston, MA.

    Published European Journal of Clinical Nutrition, 2009

    5. Tocotrienols (1993) & Cholesterol

    Learn more about high cholesterol.

    Researchers, in vitro, evaluated the role of trocotrienols in regulation of cholesterol production.

    For several cell types they incubated the cells with gamma-tocotrienol and found that it inhibited the incorporation rate of acetate but not mevalonate in cholesteral, noting 50% to 80% inhibition over various time periods.

    Their conclusion was that tocotrienols have an effect on the mevalonate pathway in cells of mammals.

    Researchers: Parker RA, Pearce BC, Clark RW, Gordon DA, Wright JJ, Department of Metabolic Diseases, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey

    Published: Tocotrienols regulate cholesterol production in mammalian cells by post-transcriptional suppression of 3-hydroxy-3-methylglutaryl-coenzyme A reductase., J Biol Chem. 1993 May 25;268(15):11230-8

    6. Tocotrienols (2012) & High Cholesterol

    Learn more about high cholesterol.

    The researchers point out that most studies testing vitamin E as a cholesterol lowering supplement find it unsuccessful. However, tocotrienols, which are compounds of the same molecular formula, but different structure (isomers) as vitamin E have been found to lower LDL levels.

    In this animal study rabbits on a cholesterol diet for 60 days wupplements with several forms (alpha, beta, delta and gamma) of tocotrienols and a control. They found that the functions of the left ventricle (aortic flow and developed pressure) improved marked recovery with the alpha and gamma forms, but not the delta form.

    Their conclusion was that the two tocotrienols isomers, alpha and gamma are helpful.

    Researchers: Das S, Mukherjee S, Lekli I, Gurusamy N, Bardhan J, Raychoudhury U, Chakravarty R, Banerji S, Knowlton AA, Das DK, Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT

    Published: Mol Cell Biochem. 2012 Jan;360(1-2):35-45. Epub 2011 Sep 15


    Hypertension

    1. Coleus forskohlii (2011) & Hypertension

    Learn more about high blood pressure.

    Researchers in India tested 49 patients with high blood pressure, dividing them into two groups, one of whom received one of two forms of coleus forskohlii in tablet form. Eight of the patients did not complete the treatment. The patients were also advised to follow correct diets, avoid stale food, reduce salt intake, avoid spicy foods, and take mild exercise.

    While both forms of the herb were helpful, one was more effective, in which a decoction was made from the herb, filtered, and again heated making it more concentrated. The concentrations ranged from 2.50mg/500mg to 2.31mg/700mg in the two forms.

    The groups had 12.07% and 10.75% improvements in systolic blood pressure and 9.80% and 8.65% in diastolic pressure (sitting posture). The groups had 12.99% and 13.25% improvements in systolic pressure and 10.10% and 10.75% diastolic pressure (lying down).

    Researchers: Madhavi Jagtap, H. M. Chandola, and B. Ravishankar

    Published: Ayu. 2011 Jan-Mar; 32(1): 59–65.

    2. CoQ10 (2001) & Hypertension

    Learn more about high blood pressure.

    This was a 12 week double-blind, random, placebo-controlled study treating 46 men and 37 women with COQ10 for 12 weeks. They all had systolic hypertension.

    The reduction in systolic blood pressure was 17.8 +/- mm Hg. None of the subjects had orthostatic hypotension (in which one feels dizzy upon standing suddenly). The researchers determined that COQ10 was safely used as an alternative treatment option.

    Researchers: Burke BE, Neuenschwander R, Olson RD. Research Service, Department of Veterans Affairs Medical Center, Boise, Idaho 83702, USA.

    Published: South Med J. 2001 Nov;94(11):1112-7.

    3. CoQ10 (2002) & Hypertension

    Learn more about hypertension and diabetes.

    The researchers wanted to look at supplementing with coenzyme Q10 (CoQ10) for subjects with both high blood pressure and type II diabetes.

    They assigned 74 type II diabetes patients and high cholesterol to 4 groups in a random, double-blind, placebo-controlled study. For 12 weeks the groups took 100mg COQ10 (2x daily), or 200mg fenofibrate (1x daily) or both or neither. They evaluated the results by looking at blood pressure, long-term glycemic control and oxidative stress.

    They found that there was a 3x increase in blood levels of CQ10 consuntration and that systolic and diastolic blood pressure were markedly reduced. They found that fenofibrate did not change blood pressure. They also found that the improvements, however, did not result in reduced oxidative stress as measured by F2-isotopes.

    Researchers:Hodgson JM, Watts GF, Playford DA, Burke V, Croft KD, University of Western Australia Department of Medicine and HeartSearch, Royal Perth Hospital, Perth, Western Australia, Australia.

    Published: Eur J Clin Nutr. 2002 Nov;56(11):1137-42

    4. COQ10 (2012) & Hypertension in Metabolic Syndrome Patients

    Learn more about hypertension (high blood pressure).

    The researchers wanted to find out whether coenzyme Q10 would be helpful as an additional, or adjunct, treatment for high blood pressure patients with metabolic syndrome.

    This was a double-blind, randomized, place-controlled study of 30 metabolic syndrome patients who had high blood pressure and who were already using high blood pressure medication.

    While they noted that COQ10 on its own may be helpful, they found that it did not enhance the effects of other high blood pressure medication.

    Researchers: Young JM, Florkowski CM, Molyneux SL, McEwan RG, Frampton CM, Nicholls MG, Scott RS, George PM, Lipid and Diabetes Research Group, Diabetes Research Institute, Christchurch Hospital Campus, New Zealand

    Published: A randomized, double-blind, placebo-controlled crossover study of coenzyme Q10 therapy in hypertensive patients with the metabolic syndrome, Am J Hypertens. 2012 Feb;25(2):261-70. doi: 10.1038/ajh.2011.209

    5. Fish Oil (2010) (Omega-3 Fatty Acid) & High Blood Pressure

    Learn more about hypertension, or high blood pressure.

    Studies of diet have indicated that a daily meal of fish can lower blood pressure; this study looks at salmon, a fatty fish, 3 times a week is helpful.

    324 subjects, 20-40 years old, received one of 4 energy-restricted diets: salmon (with 2.1g omega-3 fatty acids), cod (with .3g omega-3 fatty acids), fish oil capsules (1.3g omega-3 fatty acids), or sunflower seeds (the control). Body weight, diastolic and systolic blood pressure, and DHA was measured at the beginning of the study and after 8 weeks.

    After evaluating the results, the researchers concluded that salmon consumption 3 times a week can lower diastolic blood pressure similar to fish oil, and more than lean fish over 8 weeks in young overweight adults.

    Researchers: Ramel A, Martinez JA, Kiely M, Bandarra NM, Thorsdottir I.

    Published: Moderate consumption of fatty fish reduces diastolic blood pressure in overweight and obese European young adults during energy restriction, Nutrition. 2010 Feb;26(2):168-74. Epub 2009 May 31

    6. Fish Oil (2012) & Hypertension

    Learn more about hypertension.

    The researchers wanted to evaluate the veracity of the belief that fish oil is helpful in reducing blood pressure.

    They evaluated 17 studies involving more than 1500 hypertensive and normotensive subjects. They found, in 8 studies, a statistically significant reduction in systolic and diastolic blood pressure in hypertensive patients. They found, in 9 studies, a non-significant reduction in normal blood pressure subjects.

    Their conclusion was that in high blood pressure patients there is a small but statistically significant benefit, but that it should not be recommended as an alternative to blood pressure lowering medication.

    Researchers: Campbell F, Dickinson HO, Critchley JA, Ford GA, Bradburn M., University of Sheffield, Sheffield, UK.

    Published: A systematic review of fish-oil supplements for the prevention and treatment of hypertension, Eur J Prev Cardiol. 2012 Jan 30

    7. Hypertension Bibliography

    Also see discussion of hypertension and research.

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    42. Whelton PK, He J, Cutler JA, et al. Effects of oral potassium on blood pressure: meta-analysis of randomized controlled clinical trials. JAMA 1997;277:1624–32.
    43. Motoyama T, Sano H, Fukuzaki H, et al. Oral magnesium supplementation in patients with essential hypertension. Hypertension 1989;13:227–32.
    44. Patki PS, Singh J, Gokhale SV, et al. Efficacy of potassium and magnesium in essential hypertension: a double-blind, placebo controlled, crossover study. BMJ 1990;301:521–3.
    45. Dyckner T, Wester PO. Effect of magnesium on blood pressure. BMJ 1983;286:1847–9.
    46. Griffith LE, Guyatt GH, Cook RJ, et al. The influence of dietary and nondietary calcium supplementation on blood pressure. An updated metaanalysis of randomized controlled trials. Am J Hypertens 1999;12:84–92.
    47. Ness AR, Chee D, Elliott P. Vitamin C and blood pressure—an overview. J Human Hypertens 1997;11:343–50.
    48. Fotherby MD, Williams JC, Forster LA, et al. Effect of vitamin C on ambulatory blood pressure and plasma lipids in older persons. J Hypertens 2000;18:411–5.
    49. Kohashi N, Katori R. Decrease of urinary taurine in essential hypertension. Jpn Heart J 1983;24:91–102.
    50. Abe M, Shibata K, Matsuda T, Furukawa T. Inhibition of hypertension and salt intake by oral taurine treatment in hypertensive rats. Hypertension 1987;10:383–9.
    51. Fujita T, Ando K, Noda H, et al. Effects of increased adrenomedullary activity and taurine in young patients with borderline hypertension. Circulation 1987;75:525–32.
    52. Calver A, Collier J, Vallance P. Dilator actions of arginine in human peripheral vasculature. Clin Sci 1991;81:695–700.
    53. Pezza V, Bernardini F, Pezza E, et al. Study of supplemental oral l-arginine in hypertensives treated with enalapril + hydrochlorothiazide. Am J Hypertens 1998;11:1267–70 [letter].
    54. Asgary S, Naderi GH, Sarrafzadegan N, et al. Antihypertensive and antihyperlipidemic effects of Achillea wilhelmsii. Drugs Exp Clin Res 2000;26:89–93.
    55. Silagy C, Neil AW. A meta-analysis of the effect of garlic on blood pressure. J Hypertension 1994;12:463–8.
    56. Louria DB, McAnally JF, Lasser N, et al. Onion extract in treatment of hypertension and hyperlipidemia: A preliminary communication. Curr Ther Res 1985;37:127–31.
    57. Bowman IA. The everlasting mistletoe and the cardiovascular system. Texas Heart Inst J 1990;17(4):310–4 [review].
    58. British Herbal Medicine Association. British Herbal Pharmacopoeia. West Yorks, UK: BHMA, 1983.
    59. Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. American Botanical Council, Austin, TX. Integrative Medical Communications, Boston, MA: 1998, 152–3.
    60. Petkov V, Manolov P. Pharmacological analysis of the iridoid oleuropein. Arzneimittelforschung 1972;22:1476–86.
    61. Weiss RF. Herbal Medicine. Gothenburg, Sweden: AB Arcancum, 1988, 160–1.
    62. Jin H, Zhang G, Cao X, et al. Treatment of hypertension by ling zhi combined with hypotensor and its effects on arterial, arteriolar and capillary pressure and microcirculation. In: Nimmi H, Xiu RJ, Sawada T, Zheng C (eds). Microcirculatory Approach to Asian Traditional Medicine. New York: Elsevier Science, 1996, 131–8.
    63. Schmidt U, Kuhn U, Ploch M, Hübner W-D. Efficacy of the hawthorn (Crataegus) preparation LI 132 in 78 patients with chronic congestive heart failure defined as NYHA functional class II. Phytomed 1994;1(1):17–24.
    64. Kramer W, Thormann J, Kindler M, Schlepper M. Effects of forskolin on left ventricular function in dilated cardiomyopathy. Arzneimittelforschung 1987;37:364–7.
    65. Han KH, Choe SC, Kim HS, et al. Effect of red ginseng on blood pressure in patients with essential hypertension and white coat hypertension. Am J Chin Med 1998;26:199–209.
    66. Haji Faraji M, Haji Tarkhani A. The effect of sour tea (Hibiscus sabdariffa) on essential hypertension. J Ethnopharmacol 1999;65:231–6.
    67. Markovitz JH, Matthews KA, Kannel WB, et al. Psychological predictors of hypertension in the Framingham Study. Is there tension in hypertension? JAMA 1993;270:2439–43.
    68. Schnall PL, Schwartz JE, Landesbergis PA, et al. Relation between job strain, alcohol, and ambulatory blood pressure. Hypertension 1992;19:488–94.
    69. Matthews KA, Cottington EM, Talbott E, et al. Stressful work conditions and diastolic blood pressure among blue collar factory workers. Am J Epidemiol 1987;126:280–91.
    70. Pickering TG. Does psychological stress contribute to the development of hypertension and coronary heart disease? Eur J Clin Pharmacol 1990;39(Suppl 1):S1–S7.
    71. Perini C, Müller FB, Bühler FR. Suppressed aggression accelerates early development of essential hypertension. J Hypertens 1991;9:499–503.
    72. Eisenberg DM, Delbanco TL, Berkey CS, et al. Cognitive behavioral techniques for hypertension: are they effective? Ann Intern Med 1993;118:964–72.
    73. Irvine MJ, Logan AG. Relaxation behavior therapy as sole treatment for mild hypertension. Psychosomatic Med 1991;53:587–97.
    74. Johnston DW, Gold A, Kentish J, et al. Effect of stress management on blood pressure in mild primary hypertension. BMJ 1993;306:963–6.
    75. Patel CH. Yoga and bio-feedback in the management of hypertension. Lancet 1973;2:1973–5.
    76. Schneider RH, Staggers F, Alexander C, et al. A randomized controlled trial of stress reduction for hypertension in older African Americans. Hypertension 1995;26:820–9.
    77. Patel C, Marmot MG, Terry DJ, et al. Trial of relaxation in reducing coronary risk: four year follow up. BMJ 1985;290:1103–6.
    78. Lee HS, Kim JY. Effects of acupuncture on blood pressure and plasma renin activity in two-kidney one clip goldblatt hypertensive rats. Am J Chin Med 1994;22:215–9.
    79. Chiu YJ, Chi A, Reid IA. Cardiovascular and endocrine effects of acupuncture in hypertensive patients. Clin Exper Hypertens 1997;19:1047–63.
    80. Peng L, Feng-yen S, An-zhong Z. The effect of acupuncture on blood pressure: the interrelation of sympathetic activity and endogenous opioid peptides. Acupunct Electrother Res 1983;8:45–56.
    81. Zhou Y, Wang Y, Fang Z, et al. Influence of acupuncture on blood pressure, contents of NE, DA and 5-HT of SHR and the interrelation between blood pressure and whole blood viscosity. Chen Tzu Yen Chiu 1995;20:55–61 [in Chinese].
    82. Radzievsky SA, Lebedeva OD, Fisenko LA, Majskaja SA. Function of myocardial contraction and relaxation in essential hypertension in dynamics of acupuncture therapy. Am J Chin Med 1989;17:111–7.
    83. Williams T, Mueller K, Cornwall MW. Effect of acupuncture-point stimulation on diastolic blood pressure in hypertensive subjects: a preliminary study. Phys Ther 1991;71:523–9.
    84. Weihai Y, Hongxu L. Clinical observation on the immediate hypotensive effect of zanzhu point. J Tradit Chin Med 1996;16:273–4.
    85. Utsunomiya N, Shigematsu Y, Ikeda K, et al. Fall in high blood pressure after applying acupuncture to SHR. Jpn Heart J 1978;19:594.
    86. Yiping Z, Qiong C, Zhengming H, Yinong C. Experimental research on treatment of hypertension with acupuncture. J Tradit Chin Med 1993;13:277–80.
    87. Tam K-C, Yiu H-H. The effect of acupuncture on essential hypertension. Am J Chin Med 1975;3:369–75.
    88. Kraft K, Coulon S. Effect of a standardized acupuncture treatment on complains, blood pressure and serum lipids of hypertensive, postmenopausal women. A randomized, controlled clinical study. Forsch Komplementarmed 1999;6:74–9 [in German].
    89. Rongxing Z, Yanhua Z, Lu Y. Hypotensive effect of ototherapy in relation to symptomatic and dispositional types of patients. J Tradit Chin Med 1992;12:124–8.
    90. Kangmei C, Shulian Z, Ying Z. Clinical application of traditional auriculoacupoint therapy (continued). J Tradit Chin Med 1993;13:152–4.
    91. Rongxing Z, Yanhua Z, Jialiang W, et al. Anti-hypertensive effect of auriculo-acupoint pressing therapy—clinical analysis of 274 cases. J Tradit Chin Med 1991;11:189–92.
    92. Peng Y, Fenglan L, Xin W. Treatment of essential hypertension with auriculopressure. J Tradit Chin Med 1991;1117–21.
    93. Tran T, Kirby J. Effects of upper cervical adjustments upon the normal physiology of the heart. ACA J Chiro 1977;XI:S58–62.
    94. McGuiness J, Vicenzino B, Wright A. The influence of a cervical mobilization technique on respiratory and cardiovascular function. Manual Therapy 1997;(2):216–20.
    95. Vicenzino B, Cartwright T, Collins D. Cardiovascular and respiratory changes produced by lateral glide mobilization of the cervical spine Manual Therapy 1998;3(2):67–71.
    96. Dulgar G, Hill D, Sirucek A, et al. Evidence for possible anti-hypertensive effect of basic technique apex contact adjusting. J Chiro 1980;14:S97–S102.
    97. Nansel D, Jansen R, Cremata E, et al. Effects of cervical adjustments on lateral-flexion passive end-range asymmetry and on blood pressure, heart rate and plasma catecholamine levels. J Manipulative Physiol Ther 1991;14:450–6.
    98. Fichera AP, Celander DR. Effect of osteopathic manipulative therapy on autonomic tone as evidenced by blood pressure change and activity of the fibrinolytic system. J Am Osteopath Assoc 1969;68:1036–8.
    99. McKnight M, DeBoer KD. Preliminary study of blood pressure changes in normotensive patients under chiropractic care. J Manipulative Physiol Ther 1988;11:261–6.
    100. Yates RG, Lamping DL, Nancy LA, Wright C. Effects of chiropractic treatment on blood pressure and anxiety: a randomized, controlled trial. J Manipulative Physiol Ther 1988;11:484–8.
    101. Morgan JP, Dickey JL, Hunt HH, Hudgins PM. A controlled trial of spinal manipulation in the management of hypertension. J Am Osteopath Assoc 1985;85(5):308–12.
    102. Mannino J. The application of neurologic reflexes to the treatment of hypertension. J Am Osteopath Assoc 1979;79:225–31.
    103. Wagnon RJ, Sandefur RM, Ratliff CR. Serum aldosterone changes after specific chiropractic manipulation. Am J Chiropr Med 1988;1(2):66–70.
    104. Goodman R. Hypertension and the atlas subluxation complex. Chiropractic: J Chiropractic Res Clin Invest 1992;8(2)30–2.


    Indigestion

    1. Anti-acids (2012) & Clostridium difficile risk

    Learn more about natural indigestion recommendations

    The Canadian Health Ministry is warning people about the possible risk of potentially dangerous clostridium difficile-related diarrhea from use of prescription anti-acids, known as "protein-pumps". Protein-pumps are used to treat acid reflux, and stomach and small intestine ulcers.

    While there is not yet conclusive evidence, a number of different studies strongly suggest a connection between prescription anti-acids and clostridium difficile problems, especially in vulnerable people: the elderly, those with severe underlying illness, hospitalization, or those taking antibiotics.

    Symptoms include severe watery or bloody diarrhea, fever, loss of appetite, nausea, and abdominal pain or tenderness.

    Here's a list of drugs (sold in Canada):

    • Dexlansoprazole (Dexilant)
    • Esomeprazole (Nexium and its generic equivalent)
    • Omeprazole (Losec and its generic equivalents)
    • Lansoprazole (Prevacid and its generic equivalents)
    • Pantoprazole (Pantoloc and Panto IV, and their generic equivalents)
    • Pantoprazole/magnesium (Tecta)
    • Rabeprazole (Pariet and its generic equivalents)
    • These products may also be found in combination with other drugs, for example: Vimovo contains esomeprazole

    2. Indigestion (2005): Heartburn Remedy Side Effects

    Learn more about natural indigestion recommendations

    Antacid preparations such as (Prilosec, Prevacid, Nexium, Pepcid, and Zantac) inhibit the acids in the stomach helpful to digestion. However, there are other consequences as well. The use of these antiacids leaves users more at risk for serious Clostridium difficile infections as well as diarrhea.

    The Centers for Disease Control reports that more and more cases of Clostridium difficile are being reported by non-hospitalized healthy adults. Some scientists wonder whether this rise in C. difficile infection rates is tied to heavy use of antiacids.

    Published: Journal of the American Medical Association, 2005.

    Editor's Note: Try digestive enzymes during meals.

    3. Indigestion Research Bibliography

    Also see discussion of indigestion (stomach ache, acid stomach) and research.

    1. Suarez F, Levitt MD, Adshead J, Barkin JS. Pancreatic supplements reduce symptomatic response of healthy subjects to a high fat meal. Dig Dis Sci 1999;44:1317–21.
    2. Schulz V, Hänsel R, Tyler VE. Rational Phytotherapy: A Physician’s Guide to Herbal Medicine. 3rd ed, Berlin: Springer, 1998, 168–73.
    3. Ritter R, Schatton WFH, et al. Clinical trial on standardized celandine extract in patients with functional epigastric complaints: Results of placebo-controlled double-blind trial. Comp Ther Med 1993;1:189–93.
    4. Benninger J, Schneider HT, Schuppan D, et al. Acute hepatitis induced by greater celandine (Chelidonium majus). Gastroenterol 1999;117:1234–7.
    5. Kraft K. Artichoke leaf extract--recent findings reflecting effects on lipid metabolism, liver and gastrointestinal tracts. Phytomedicine 1997;4:370–8 [review].
    6. Kirchhoff R, Beckers C, Kirchhoff GM, et al. Increase in choleresis by means of artichoke extract. Phytomedicine 1994;1:107–15.
    7. Westphal J, Hörning M, Leonhardt K. Phytotherapy in functional upper abdominal complaints. Results of a clinical study with a preparation of several plants. Phytomedicine 1996;2:285–91.
    8. Blumenthal M, Busse WR, Goldberg A, et al. (eds). The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin: American Botanical Council and Boston: Integrative Medicine Communications, 1998, 425–6.
    9. Tewari JP, Srivastava MC, Bajpai JL. Pharmacologic studies of Achillea millefolium Linn. Indian J Med Sci 1994;28(8):331–6.
    10. Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs, and Cosmetics, 2d ed. New York: John Wiley and Sons, 1996, 303.
    11. Bradley PR. British Herbal Compendium, vol. 1. Great Britain: British Herbal Medicine Association, 1990, 218–9.
    12. Forster HB, Niklas H, Lutz S. Antispasmodic effects of some medicinal plants. Planta Med 1980;40:303–19.
    13. May B, Kuntz HD, Kieser M, Kohler S. Efficacy of a fixed peppermint/caraway oil combination in non-ulcer dyspepsia. Arzneimittelforschung 1996;46:1149–53.
    14. Westphal J, Hörning M, Leonhardt K. Phytotherapy in functional upper abdominal complaints. Results of a clinical study with a preparation of several plants. Phytomedicine 1996;2:285–91.
    15. Madisch A, Heydenreich CJ, Wieland V, et al. Treatment of functional dyspepsia with a fixed peppermint oil and caraway oil combination as compared to cisapride. Arzneimittelforschung 1999;49;925–32.
    16. Fiegel VG, Hohensee F. Experimental and clinical screening of a dry, water extract of tiliae libri. Arzneimittelforschung 1963;13:222–5 [in German].
    17. Sadek HM. Treatment of hypertonic dyskinesias of Oddi’s sphincter using a wild Tilia suspension. Hospital (Rio J) 1970;77:141–7 [in Portuguese].
    18. Langer M. Clinical observations on an antispastic factor extracted from Tiliae silvestris alburnum. Clin Ter 1963;25:438–44 [in Italian].
    19. Thamlikitkul V, Bunyapraphatsara N, Dechatiwongse T, et al. Randomized double blind study of Curcuma domestica Val for dyspepsia. J Med Assoc Thai 1989;72:613–20.
    20. Mills SY. Out of the Earth: The Essential Book of Herbal Medicine. London: Viking Press, 1991, 448–51.
    21. Weiss RF. Herbal Medicine. Beaconsfield, UK: Beaconsfield Publishers Ltd, 1985.
    22. Blumenthal M, Busse WR, Goldberg A, et al. (eds). The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin: American Botanical Council and Boston: Integrative Medicine Communications, 1998, 425–6.
    23. Weiss RF. Herbal Medicine. Beaconsfield, UK: Beaconsfield Publishers Ltd, 1988, 185–6.
    24. Blumenthal M, Busse WR, Goldberg A, et al. (eds). The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin: American Botanical Council and Boston: Integrative Medicine Communications, 1998, 198.
    25. Micklefield GH, Redeker Y, Meister V, et al. Effects of ginger on gastroduodenal motility. Int J Clin Pharmacol Ther 1999;37:341–6.
    26. Goso Y, Ogata Y, Ishihara K, Hotta K. Effects of traditional herbal medicine on gastric acid. Biochem Physiol 1996;113C:17–21.
    27. Reed PI, Davies WA. Controlled trial of a carbenoxolone/alginate antacid combination in reflux oesophagitis. Curr Med Res Opin 1978;5:637–44.


    Insomnia

    1. Calcium (2009) & Insomnia

    Learn more about insomnia.

    Researchers have found that mild calcium deficiency, often associated with menopause, can contribute to insomnia along with other related conditions such as nerve sensitivity and irritability.

    The authors writethat deficiencies in calcium and magnesium can cause one to awaken after several hours sleep and have difficulty getting back to sleep.

    Sources:
    Insomnia: Studies Confirm Calcium And Magnesium Effective, Medical News Today; 2009
    Bookman Press 1998; 2000-02-08; Vitamins: Calcium.
    Prescription for Nutritional Healing, Phyllis A. & James F. Balch, MD, 2003

    2. Lemon Balm (2004) & Insomnia

    Learn more about insomnia.

    Though the sample size was small, including 18 healthy volunteers, this study was a double-blind, placebo-controlled, randomized, balanced crossover experiment, which is the top level of scientific methodology. 18 healthy volunteers received two doses of M. Officinalis extract (300 mg, 600 mg). They were tested for modulation of moods, stress measurements and cognitive performance both before they took the dose and one hour after. Then there was a 7 day washout period to make sure no traces of the Melissa remained in their physiology and a placebo was administered with the same tests.

    The participants showed significantly lower negative moods effect of the stress test, higher self-ratings of calmness, and increased speed of mathematical processing with no reduction of accuracy after ingestion of the 300mg dose of Melissa.

    Researchers: Kennedy, D. O., Little W, Scholey A. B.

    Published: Attenuation of Laboratory-Induced Stress in Humans after Acute Administration of Melissa Officinalis (Lemon Balm), (2004 Psychosomatic Medicine 66 (4): 607-13.

    3. Lemon Balm (2011) & Insomnia

    Learn more about insomnia.

    Twenty subjects with mild to moderate anxiety disorders and sleep disturbances were involved in a 15 day study of a Melissa Officinalis extract. Using clinician rating criteria, the treatment reduced anxiety by 18%, anxiety-related symptoms by 15% and lowered insomnia by 42%. This is a good preliminary study showing evidence to continue studying Melissa Officinalis as a treatment for stress related symptoms. Further studies which use blind, balanced controls and placebo groups will strengthen the evidence.

    Researchers: Cases J, Ibarra A, Feuillère N, Roller M, Sukkar SG.

    Published: Pilot trial of Melissa Officinalis L. leaf extract in the treatment of volunteers suffering from mild-to-moderate anxiety disorders and sleep disturbances, Med J Nutrition Metab. 2011 Dec;4(3):211-218.

    4. Magnesium (2006) & Insomnia

    Learn more about insomnia.

    Taking a supplement with melatonin, magnesium and zinc improved their sleep and quality of life.

    Research: "Rapid recovery from major depression using magnesium treatment" Eby GA, Et al. A double-blind placebo controlled trial included 57 patients with insomnia in a long-term care facility in Italy. Med Hypotheses. 2006;67(2):362-70. Epub 2006 Mar 20

    5. Melatonin (2009) & Insomnia

    Learn more about insomnia.

    This is a review of existing research on the use of a form of melatonin for insomnia in older patients. The researchers concluded that melatonin does improve both insomnia and quality of life, does not have the addictive and other side effects of prescription sleeping aids, can be used with other medications, and does not have any adverse effects on patients who have or do use other drugs.

    Researchers: Zisapel N. Department of Neurobiology, Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.

    Published: Controlled release melatonin (Circadin) in the treatment of insomnia in older patients: efficacy and safety in patients with history of use and non-use of hypnotic drug, Harefuah, 2009 May;148(5):337-41, 348

    6. Melatonin, Magnesium, Zinc (2011) & Insomnia

    Learn more about insomnia.

    A double- blind controlled trial involved 43 patients with primary insomnia. Patients took a food supplement with melatonin, magnesium and zinc every night one hour before bed. The control group took a placebo. The group taking the supplement had considerable improvement in ease of going to sleep, staying asleep, quality of sleep and daytime functionality.

    Researchers: Rondanelli M, Opizzi A, Monteferrario F, Antoniello N, Manni R, Klersy C., Section of Human Nutrition and Dietetics, Faculty of Medicine, University of Pavia, Pavia, Italy.

    Published: The effect of melatonin, magnesium, and zinc on primary insomnia in long-term care facility residents in Italy: a double-blind, placebo-controlled clinical trial; J Am Geriatr Soc., 2011 Jan;59(1):82-90.

    7. Valerian, Lemon Balm (2006) & Insomnia

    Learn more about insomnia.

    918 children in multiple centers were treated successfully. Dyssomnia is a form of insomnia caused by disruptions in physiological functioning often due to environmental factors. Although this research was conducted by a pharmaceutical company it is worth noting that European pharmaceutical companies and doctors have long accorded the same respect to aromatherapy, herbal and homeopathic treatments as given to allopathic treatment in the U.S. Also this study cannot be considered of primary importance because it was not a blind trial with a control group, but it did included 918 subjects. Similar studies conducted by universities and hospitals rarely have this large a group.

    Researchers: Müller SF, Klement, Et al. Schwabe Pharmaceuticals, Karlsruhe, Germany.

    Published: A combination of valerian and lemon balm is effective in the treatment of restlessness and dyssomnia in children, Phytomedicine. 2006 Jun;13(6):383-7.

    8. Vitamin B12 (1996) & Insomnia

    Learn more about insomnia.

    Researchers evaluated results of treating 106 patients who suffered from various forms of insomnia with a combination of vitamin B12, bright light, chronotherapy and/or hypnotism. 32% of the patients experienced moderate to marked improvement. This study did not evaluate use of B12 alone, and other research has suggested that B12 alone does not bring about statistically significant improvements.

    Nonetheless, since B12 supports the nervous system, it may well be that a B12 deficiency contributes to insomnia as a secondary condition.

    Research: A multicenter study of sleep-wake rhythm disorders: therapeutic effects of vitamin B12, bright light therapy, chronotherapy and hypnotics., Yamadera H., et al.; Psychiatry Clin Neurosci. 1996 Aug;50(4):203-9.


    Iritis

    1. Curcumin, Echinacea (2010, 2006) & Iritis

    Learn more about iritis

    Recent studies on anterior uveitis, also known as iritis, demonstrate that both echnichea and curcumin (tumeric) may be helpful.


    Keratoconus

    1. Magnesium (2005) & Keratoconus

    Learn more about keratoconus.

    Early research into probable causes of keratoconus determined that one likely factor was magnesium deficiency. Reports pointed out that magnesium deficiency could negatively impact how the cornea works.

    A number of white papers were reviewed in 2005 which collectively indicated that the connection is significant - that magnesium deficiencies cause molecular and cellular abnormalities which are similar to the abnormalities in cells comprising the cornea in keratoconus patients. The abnormal contructs occur both within cells and in the spaces outside the cells. The changes include thinning and breaking down of membranes, cell and collagen fiber degeration, mitochondria swelling, and biochemical abnormalities in synthesis of protein.

    Reviewer: A. Thalasselis, Institute of Vision, Mar del Plata, Argentina.

    Published: The possible relationship between keratoconus and magnesium deficiency, Thalasselis A., Ophthalmic & Physiological Optics, Jan. 2005, 25(1), pp 7-12.


    Leber's Hereditary Optic Neuropathy

    1. Antioxidants(2007, 2011) & Leber's

    Learn more about Leber's.

    A number of studies associate antioxidants with improvements in the treatment of eye disease, particular conditions of the optic nerve such as Leber's.

    These provide some potential lines of future research in looking at treatment for Leber's Hereditary Optic Neuropathy (LHON).

    These studies include:

    Providing nerve cell stability and reducing free radical damage due to toxins including environmental toxins, smoking, and alcohol abuse. These anti-oxidants include vitamins and natural plant extracts, such as Vitamins A, C & E, Co- Ginkgo biloba, curcumin (tumeric).1

    A metabolite of vitamin E is Alpha-tocotrienol-quinone which has some reversing-symptoms benefit in trials in early onset vision loss.2

    Other treatments, such as brimonidine, are under consideration in protection of the optic nerve with mixed results.3

    Finally, gene therapy has been used experimentally.

    Footnotes:

    1. Ritch R. 2007. Natural compounds: evidence for a protective role in eye disease. Can J Ophthalmol. 2007 Jun;42(3):425-38

    2. Shrader, W. D.; Amagata, A.; Barnes, A.; Enns, G. M.; Hinman, A.; Jankowski, O.; Kheifets, V.; Komatsuzaki, R. et al. 2011. Alpha-Tocotrienol quinone modulates oxidative stress response and the biochemistry of aging. Bioorganic & Medicinal Chemistry Letters 21 (12): 3693-3698

    3. Newman NJ, Biousse V, David R, Bhatti MT, Hamilton SR, Farris BK, Lesser RL, Newman SA, Turbin RE, Chen K, Keaney RP. 2005. Prophylaxis for second eye involvement in leber hereditary optic neuropathy: an open-labeled, nonrandomized multicenter trial of topical brimonidine purite. Am J Ophthalmol. Sep;140(3):407-15

    2. Gene Therapy (2009) for Leber's Disease

    In a 2009 Phase I clinical trial, researchers injected a benign virus carrying a connected copy of an essential gene into a teenage boy's retina. This patient had lost vision due to a genetic disorder called "Leber's Congenital Amaurosis (LGA).

    The result was improved vision as the gene therapy enabled the body to make new rods and cones (which normally are irreplaceable once lost).

    Other young patients given the same procedure also were able to see better. All the children that underwent this procedure gained enough vision to walk independently.

    Published: The Lancet, 2009, by Albert M Maguire MD and others, University of Pennsylvania School of Medicine

    Learn more about Lebers Hereditary Optic Neuropathy including complementary nutritional and other recommendations.

    3. Smoking (1999) & Lebers Risk Factors

    Learn more about Leber's Hereditary Optic Neuropathy.

    Smoking has long been identified as a factor in higher risk for many diseases and vision conditions. This research identified smoking as a causative factor for Leber's as well.

    Leber's is a hereditary condition, passed through the mother, where mitochondria mutate in the retinal nerves, causing loss of central vision.

    In this study researchers matched family members, analyzing both combined male/female family groups and subgroups of men, where there was an inherited risk of Leber's. They found a significant connection between smoking and incidence of Leber's in all the subgroups, with a higher rate in males. The connection was higher in older aged groups and where smoking rates were higher.

    The researchers concluded that the amount of smoking and number of years which subjects had been smoking were also correlated with higher risk of Leber's symptoms.

    Researchers: K. Tsao, P. Aitken, and D. Johns

    Published: Smoking as an aetiological factor in a pedigree with Leber's hereditary optic neuropathy, British Journal of Ophthalmology, 1999 May; 83(5): 577–581.

    4. Toxins & Nutrition(1998) & Leber's

    Learn more about Leber's.

    Researchers have identified both exposure to toxins and nutritional deficiencies as been connected to incidence of mitochondria-mutated conditions such as Leber's.

    In Cuba, in the 1990's an epidemic affected 50,000 patients with symptoms common to both lazy eye due to alcohol/tobacco toxins and Leber's. There was characteristic damage leading to these conclusions. The patients exhibited both vitamin deficiencies and mitochondrial damage from methanol and cyanide toxins.

    The researchers were particularly interested in determining why impaired production of cellular energy led to this kind of damage, and why, within the nervous system, why the optic nerve's ganglion cells were especially vulnerable.

    The researchers comprehensively evaluated both the patients via neuroophthalmologic exams, as well as blood, cerebrospinal fluid, DNA, and, from deceased patients, the nerves running down the back of the leg and the eye and optic nerve itself. Blood folic acid levels were low, and blood formate levels were high. These were then tested via animal models.

    Finding: These patients' vision conditions improved when their nutritional deficiencies were corrected, and their exposure to toxins ceased.

    The researchers concluded that mitochondria (noting that the mitochondria in cells of the eye are most vulnerable) can be damaged either genetically or by way of nutritional deficiencies or exposure to toxins. There is a threshold, once passed, which results in irreversable damage.

    Researcher: Sudan, A., et. al

    Published: Acquired mitochondrial impairment as a cause of optic nerve disease., Trans Am Ophthalmol Soc. 1998;96:881-923.


    Light Sensitivity

    1. Lutein, Zeaxanthin and Light Sensitivity 2008

    The February 2008 issue of Optometry & Vision Science published a study about lutein and zeaxanthin which found that many visual performance issues (including contrast sensitivity) are compromised under glaring light conditions. The human macular pigments (MPs), lutein and zeaxanthin, were found to be strongly related to improvements in glare disability and photostress recovery of those people with “normal eyesight”.1 This includes dealing with bright sunlight outdoors, light from your computer monitors, bright car headlights, etc.

    The study included forty healthy individuals (mean age of 23.9) who were followed for 6 months measuring their MP. After six months of lutein and zeaxanthin supplementation, average MP improved and had shown to significantly reduce the harmful effects of glare.


    Macular Degeneration

    1. Acetyl-L-carnitine, omega-3 fatty acids, CoQ10 (2005) & Macular Degeneration Drusens

    This study looked at positive changes in patients with early age-related macular degeneration treated with a combination of acetyl-L-carnitine, n-3 fatty acids, and coenzyme Q10.

    This study was double-blind (neither the 106 patients nor the researchers knew the who was receiving which treatment), random and included placebos. The purpose was to determine the effectiveness of a combined acetyl-L-carnitine, N3 fatty acids, and CoQ10 on the visual capacity and changes within the eye (in the fundus) in early age-related macular degeneration). The patients were divided into a test group and a control group.

    "The primary efficacy variable was the change in the visual field mean defect (VFMD) from baseline to 12 months of treatment, with secondary efficacy parameters: visual acuity (Snellen chart and ETDRS chart), foveal sensitivity as measured by perimetry, and fundus alterations as evaluated according to the criteria of the International Classification and Grading System for AMD."

    The treated group had significant improvement by the end of the study. In addition, in the treated group 2% experienced deterioration in VFMD, and 17% of the placebo group showed clinically significant deterioration.

    The researchers also found that the lessening of the drusen-covered area of treated eyes was also statistically significant as compared to placebo patients.

    The results indicated that an appropriate combination of compounds which affect mitochondrial lipid metabolism, may improve and subsequently stabilize visual functions, and it may also improve fundus alterations in patients affected by early AMD.

    Published: Ophthalmologica. 2005 May-Jun;219(3):154-66.

    2. Antioxidant Vitamins, Zinc (2001) & AMD - AREDS Study

    See more about macular degeneration treatment and information.

    This is a summary of the Age-Related Eye Disease Study (AREDs) clinical trials, a nationwide study sponsored by the National Eye Instititue, NIH, 2001

    Antioxidant Vitamins and Zinc Reduce Risk of Vision Loss from Age-Related Macular Degeneration

    The study found that High levels of antioxidants and zinc significantly reduce the risk of advanced age-related macular degeneration (AMD) and its associated vision loss (but not cataract).

    High Risk: Researchers found that people at high risk of advanced macular degeneration lowered their risk by about 25% when treated with a high-dose combination of vitamin C, vitamin E, beta-carotene, and zinc. For those with intermediate AMD, or advanced AMD in one eye only -- the nutrients reduced the risk of by about 19%.

    "This is an exciting discovery because, for people at high risk for developing advanced AMD, these nutrients are the first effective treatment to slow the progression of the disease,"
    -- Paul A. Sieving, M.D., Ph.D., NEI Director

    The three stages of AMD analyzed in this study are:

    • Early AMD. People have, in one or both eyes, either several small drusen or a few medium-sized drusen with no vision loss.
    • Intermediate AMD. Those with intermediate AMD have, in one or both eyes, either many medium-sized drusen or one or more large drusen and little or no vision loss.
    • Advanced AMD. In addition to drusen, people with advanced AMD have, in one or both eyes, either:
      • A breakdown of light-sensitive cells and tissue in the central retinal area (advanced dry form); or
      • Abnormal, fragile blood vessels under the retina that leak fluid or bleed (advanced wet form)

    The formulation used in the AREDs study contained several antioxidant vitamins, which are nutrients that can help maintain healthy cells and tissues. They also contained zinc, which is an important mineral incorporated into many body tissues:

    • 500 milligrams of vitamin C;
    • 400 international units of vitamin E;
    • 15 milligrams of beta-carotene;
    • 80 milligrams of zinc as zinc oxide;
    • 2 milligrams of copper as cupric oxide

    It has been known from earlier studies that people with diets rich in green, leafy vegetables have a lower AMD risk, but it is hard to gain the therapeutic levels needed through diet alone. Therefore the supplements were needed./p>

    The study also showed that people who take a daily multivitamin can lower the risk of vision loss by adding the same high levels of antioxidants and zinc as in the study.

    The study was comprised of 4,757 participants, 55-80 years of age, in 11 clinical centers nationwide. They were given one of four treatments:

    1. zinc alone;
    2. antioxidants alone;
    3. antioxidants and zinc;
    4. a placebo

    The benefits of the nutrients were seen only in people who began the study at high risk for developing advanced AMD, and in that group those taking antioxidants and zinc had the lowest risk of developing advanced stages of AMD.

    Side Effects Reported:

    Zinc About 7.5 percent of participants in the zinc only group had urinary tract problems that required hospitalization. Participants in the two groups that took zinc also reported anemia at a slightly higher rate; however, testing of all patients for this disorder showed no difference among treatment groups.

    Beta-Carotene Yellowing of the skin, a well-known side effect of large doses of beta-carotene, was reported by a few of the participants taking antioxidants.

    Published: October 2001 issue of Archives of Ophthalmology

    Researchers: major nationwide study, by National Institutes of Health, National Eye Institute, in collaboration with Bausch & Lomb who provided the formulations specified by NEI.

    3. Antioxidants (1991) - macular degeneration

    See more about macular degeneration treatment and information.

    After 18 months, subjects with macular degeneration who took antioxidants on a consistent basis were 2.5X more likely to improve on visual acuity testing, and four times less likely to deteriorate in their worst eye, compared to those who took them less consistently. J. Cat Refr Surg, Mar 1991.

    4. Antioxidants (1996) & macular degeneration

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    The ARMD population manifested decreased intake of vitamin E, magnesium, zinc, vitamin B6 and folic acid. Patients with advanced ARMD taking antioxidants twice daily maintained vision in their better functioning eyes significantly better than those taking a placebo. Richer, J Am Optom Assoc 1996 Jan;67(1):12-29 J Am Optom Assoc 1996 Jan;67(1):30-49

    5. Antioxidants (1997) and angiogenic factor associated with age-related macular degeneration (exudative type)

    See more about macular degeneration treatment and information.

    Ishihara N, Yuzawa M, Tamakoshi A Department of Ophthalmology, Nihon University School of Medicine, Tokyo, Japan. Nippon Ganka Gakkai Zasshi 1997 Mar;101(3):248-51

    To confirm the hypothesis that antioxidants and angiogenic factors may be associated with the development of age-related macular degeneration (exudative type), we compared serum levels of vitamins A, C, and E and carotinoid, zinc, selenium and b-FGF (basic-fibroblast growth factor) in 35 patients with age-related macular degeneration (exudative type) with the levels in 66 controls. The average serum zinc level was significantly lower in the patient group than in the control group. Serum vitamin E-alpha levels also tended to be lower. Most serum b-FGF levels were below the standard value in each group. Based on the above results, we conclude that subnormal levels of zinc and vitamin E may be associated with the development of age-related macular degeneration.

    6. Antioxidants (2001) and Zinc - AREDS Study Synopsis

    See more about macular degeneration treatment and information.

    Also see the more detailed description of AREDS

    Clinical Trial Finds Antioxidants and Zinc Beneficial in Reducing Risk of Severe AMD.

    Patients with advanced cases of dry age-related macular degeneration (AMD) can moderately lower the risk of developing the more severe wet form of the disease and preserve vision by taking a daily dose of antioxidant vitamins and zinc. This finding is the result of the Age-Related Eye Disease Study (AREDS), a randomized, placebo-controlled clinical trial funded by the National Eye Institute. AREDS evaluated over 3600 men and women between the ages of 55 and 80 for an average of 6.3 years. Published in the October, 2001 issue of the Archives of Ophthalmology, AREDS also evaluated whether antioxidants and zinc might reduce cataract development but found no beneficial effect.

    Dr. Paul Sieving, Director of the National Eye Institute, stated, "Now that we know antioxidants and zinc are helpful in reducing the risk of severe disease, it is even more important for older-age Americans to have regular eye exams. Intervening in at-risk individuals could help reduce severe disease and vision loss in millions of Americans." Specifically, the AREDS study found that AMD patients with advanced cases of dry AMD or vision loss due to wet AMD in one eye, who took daily supplements containing vitamin C, vitamin E, beta carotene, and zinc, had a 20% chance of developing wet macular degeneration over a five-year period. By comparison, the control group taking a placebo pill lacking any nutrients had a 28% chance of developing wet macular degeneration over a five-year period. This finding is important because delaying the onset of wet AMD and its accompanying vision loss by several years can prolong the independence and mobility of seniors and preserve their quality of life.

    Dosages Used in the Study:

    The daily therapeutic dosages of each of the nutrients used in the AREDS study are as follows: vitamin C, 500 mg; vitamin E, 400 IU; beta carotene, 15 mg; and zinc, 80 mg

    Cancer prevention studies have found that high doses of beta carotene increase the risk of developing lung cancer in cigarette smokers. These studies strongly suggest that cigarette smokers, or those with smoking histories, should avoid taking beta carotene to prevent advanced macular degeneration.

    7. Antioxidants (2002) Lutein, Zeaxanthin and Macular Degeneration Study

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    A study by Dr. Paul Bernstein from the University of Utah indicated that low eye levels of antioxidants, lutein and zeaxanthin, could contribute to Aged-Related Macular Degeneration. The study compaged carotenoid levels in 63 patients with Aged-Related Macular Degeneration to 138 patients with this disease. The study also showed that supplementing with just 4 mg per day of lutein could return lutein levels back to normal.

    Ophthalmology, 2002;109:1780-1878

    8. Antioxidants (2004) Age related macular degeneration and micronutrient antioxidants.

    See more about macular degeneration treatment and information.

    Curr Eye Res. 2004 Dec;29(6):387-401. Hogg R, Chakravarthy U. Ophthalmology & Vision Science, Institute of Clinical Science, The Royal Victoria Hospital, Belfast, Northern Ireland.

    "Age-related macular degeneration is a common clinical entity. The late-stage manifestations of age-related macular degeneration have devastating consequences for vision. Various risk factors have been identified in the development of the condition, which are consistent with the premise that oxidative stress plays an important role in its pathogenesis.

    "Thus, the possibility that antioxidant balance can be manipulated through diet or supplementation has created much interest. Associations between diet and nutrition and the clinical features of macular degeneration have been described. Scrutiny of the literature shows consistency in the report of notable reductions in serum micronutrients in wet Age related macular degeneration, however, the evidence for causation is still circumstantial. In this comprehensive review of the clinical literature, we have assessed the evidence for a link between diet and nutrition as risk factors for the development of macular degeneration. All published case control, population-based, and interventional studies on macular degeneration were examined. Although initial support appeared to be moderate and somewhat contradictory, the evidence that lifetime oxidative stress plays an important role in the development of ARM is now compelling. The positive outcomes in the Age-Related Eye Diseases Study, a major controlled clinical trial, have given hope that modulation of the antioxidant balance through supplementation can help prevent progression to Age related macular degeneration."

    9. Antioxidants (2008) and Macular Degeneration Prevention Study

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    A new study reveals part of the magic behind a diet rich in antioxidants, showing how artichokes, blueberries and pecans can hold at bay the leading cause of age-related blindness in developed countries.

    Researchers at Brigham Young University and Weill Medical College of Cornell University discovered a link between two processes in the retina that, in combination, contribute to a disease called macular degeneration. They found antioxidants disrupt the link and extend the lifetime of irreplaceable photoreceptors and other retinal cells.

    “The implication is that people at risk of macular degeneration could help prevent the disease by consuming antioxidants,” said Heidi Vollmer-Snarr, a BYU chemist who earned a doctorate from Oxford and began work on this disease as a postdoctoral researcher at Columbia.

    The new study finds a destructive synergy between the buildup of a compound called A2E and damage to cellular “power plants” called mitochondria. A2E is a natural byproduct of cellular activity that, unlike other compounds, won’t break down or be disposed by the body.

    A problem occurs when A2E encounters oxidative stress created by light exposure. In these circumstances, A2E disrupts energy production in mitochondria. The resulting energy shortage pulls the plug on daily cleaning and maintenance of photoreceptors and another type of retinal cell.

    The result is more A2E buildup, and the cycle of destruction hastens the death of these vital visual cells, which are not replaced when they die. The experiments performed with visual cells from rats, cows and humans showed that antioxidants could completely counter the damage.

    Again, researches found that antioxidants disrupt the above link and extend the lifetime of irreplaceable photoreceptors and other retinal cells.

    This study will be published in the upcoming issue of the Journal of Biological Chemistry.

    10. Antioxidants (2008), blue light & risk of macular degeneration

    Learn more about macular degeneration recommendations.

    A combination of low levels of antioxidants and exposure to the sun's blue light (as distinquished from ultra violet light) may increase risk of macular degeneration. Blue light alone is not tied to macular degeneration, however researchers have found that there is a consistent and significant connection between with age-related macular degeneration and patients in the lowest quartile nutritional intake of vitamin C, vitamin E, zeaxanthin, and dietary zinc.

    The likelihood for neovascular age-related macular degeneration were even more among those patients with the lowest combined antioxidant levels, particularly the combination of vitamin C, zeaxanthin, and vitamin E. The researchers found similar connections in patients with early age-related macular degeneration.

    Researchers agree that there is a risk to the eyes from sun exposure, but what interesting is that different wavelengths of light inflict damage on different parts of the eye.

    The cornea and lens absorb "invisible" ultraviolet light and are damaged (cataracts) by ultra violet light. The retina absorbs visible light, including blue light, and this study demonstrated that not only can the retina be damaged by blue light, but that blue light exposure combined with low antioxidant levels causes retinal damage, including macular degeneration.

    Source reference: Fletcher AE, et al "Sunlight exposure, antioxidants, and age-related macular degeneration" Arch Ophthalmol 2008; 126: 1396-1403.

    11. Association of Aspirin Use With AMD

    A prospective analysis using a questionnaire to 2,389 baseline participants was conducted with an Australian population-based cohort with four examinations during a 15-year period (1992–1994 to 2007–2009) to determine whether regular aspirin use is associated with a higher risk for developing age-related macular degeneration (AMD).

    The conclusion of the study was that, after adjustment for age, sex, smoking, history of cardiovascular disease, systolic blood pressure and body mass index, persons who were regular aspirin users had a higher risk of developing neovascular AMD (9.3% in users and 3.7% in nonusers).

    Regular aspirin use is associated with increased risk of incident neovascular AMD, independent of a history of cardiovascular disease and smoking.

    SOURCE: Liew G, Mitchell P, Wong TY, et al. The association of aspirin use with age-related macular degeneration. JAMA Intern Med. 2013;173(4):258–64.

    12. Astaxanthin (2008) & Macular Degeneration

    Learn more about macular degeneration recommendations.

    Researchers, noting the large presence of carotenoids in the macula as well as other research which links free radical damage to macular degeneration, studied whether carotenoids in dietary supplements would be helpful.

    In the study 145 patients with age related macular degeneration were randomly assigned to one of two groups. The test group was given lutein (10 mg), zeaxanthin (1 mg), astaxanthin (4 mg) in an antioxidant/vitamin nutritional supplement for two years.

    The results were measured by gauging changes in visual acuity after one year and again after two years. The researchers also looked at perception of visual contrasts. National Eye Institute visual function questionnaire (NEI VFQ-25) scores were reviewed after 1 and 2 years.

    Those people in the group receiving the antioxidant/vitamin supplement showed significant improvement in visual acuity (vision sharpness). In addition, the researchers concluded that people given lutein/zeaxanthin and astaxanthin together with other nutrients were more likely to report significant improvements.

    Researchers: Parisi V, et al.

    Published: Carotenoids and antioxidants in age-related maculopathy, European Journal Ophthalmology. 2012 Mar;22(2):216-225. doi: 10.5301/ejo.5000069.

    13. Bacterium, Gene (2005) Play Roles in Elderly Vision Loss

    See more about macular degeneration treatment and information.

    Researchers at the Massachusetts Eye and Ear Infirmary found C. pneumoniae in the diseased eye tissue of five of nine people with wet AMD but not in the eyes of 20 people without AMD. The findings offer more evidence that AMD may be caused by inflammation, the researchers said.

    The study appears in the November issue of the journal Graefe's Archive for Clinical and Experimental Ophthalmology.

    "We found that C. pneumoniae infection led to increased production of vascular endothelial growth factor (VEGF), the key protein involved in wet AMD. That C. pneumoniae infection of human eye cell types increases VEGF production is therefore significant and could explain in part why VEGF levels are increased in many people with wet AMD," Kalayoglu said.

    "Our hypothesis is that C. pneumoniae may be the key link between CFH and AMD. That is, patients with CFH variations may be particularly susceptible to the damaging effects of chronic infection, and an infectious organism like C. pneumoniae may be particularly effective in accelerating inflammation and driving progression of AMD in these patients," Kalayoglu said.

    14. Bilberry extract (2005) & AMD, and Cataracts

    Learn more about macular degeneration treatment and information and cataracts.

    A 2005 Russian study looked at antioxidants' effect on damaging free radicals for cataracts and macular degeneration.

    Bilberry's flavonoids are known as potent antioxidants, scavenging free radicals. They are effective for many age-related ocular disorders. The scientists looked at senescence-accelerated (accelerated biological aging) OXYS rats who were suffering from early senile cataract and macular degeneration. Young rats were given control diets or those supplemented with 25% bilberry extract or vitamin E. At 3 months testing showed that more then 70% of control OXYS rats had cataract and macular degeneration while the supplementation of BE completely prevented impairments in the lenses and retina.

    The vitamin E had no significant effects but both antioxidants decreased lipid peroxides in the retina and serum of OXYS rats. The results suggest that the OXYS rat strain is the useful model for testing treatment for macular degeneration and cataracts and that long-term supplementation with bilberry extract is effective in prevention of macular degeneration and cataract.

    Researchers: Fursova AZh, Gesarevich OG, Gonchar AM, Trofimova NA, Kolosova NG.

    Published: Dietary supplementation with bilberry extract prevents macular degeneration and cataracts in senesce-accelerated OXYS rats, Adv Gerontol. 2005;16:76-9.

    15. Cardiovascular Risk Factors (2008) and AMD

    See more about macular degeneration treatment and information.

    This 2008 study assessed the association of cardiovascular risk factors and ocular perfusion pressure with early and advanced age-related macular degeneration (AMD) in Latinos. Data were collected from a population-based sample of self-identified adult Latinos using standardized protocols for assessing blood pressure and intraocular pressure (IOP) measurement and stereoscopic macular photography. Hypertension was defined as either a history of hypertension or systolic blood pressure (SBP) higher than 140 mmHg +/- diastolic blood pressure (DBP) 85 mmHg or higher. Ocular perfusion pressure (OPP) was defined as the difference between mean arterial blood pressure and IOP. AMD was diagnosed from photographic grading by masked trained graders.

    Gradable retinal photographs were available in 5,875 participants. After adjusting for age, gender and cigarette smoking, higher DBP and uncontrolled diastolic hypertension were associated with exudative AMD. Higher OPP was associated with a decreased risk of geographic atrophy (GA). Low pulse pressure was associated with a lower risk of exudative AMD. Obesity was associated with increased retinal pigment.

    These data suggest that in Latinos, cardiovascular risk factors may play a role in advanced AMD. Given that Latinos have a high prevalence of cardiovascular risk factors, an intervention aimed at reducing these risk factors may also have a beneficial impact on the risk of having early and advanced AMD.

    SOURCE: Fraser-Bell S, Wu J, Klein R, et al. Cardiovascular risk factors and age-related macular

    16. Carotenoids (1995) antioxidants & AMD

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    Laboratory data shows that carotenoid and antioxidant vitamins help to protect the retina from oxidative damage initiated in part by absorption of light. When the dietary intake of different carotenoids as analyzed, the sum of lutein and zeaxanthin , the retinal carotenoids forming macular pigment, had the strongest protective effects against neovascular AMD.

    Published: DM Snodderly, Am J Clin Nutr 1995 Dec;62(6 Suppl):1448S-1461S

    17. Collard greens (1988) spinach: macular degeneration

    Learn more about macular degeneration treatment and information.

    Eating collard greens and spinach at a frequency of two to four times a week was enough to lower the risk of macular degeneration by 46 percent, and was even greater at five to six times per week. Goldberg, J. et al. Factors associated with age-related macular degeneration: An analysis of data from the First National Health and Nutrition Examination Survey. American Journal of Epidemiology 128 (1988): 700-20.

    Editor’s Note: Lutein and Zeaxanthin are the two carotenoids found in collard greens and spinach. When taken as supplements, they are best taken separately from beta-carotene because they compete for absorption.

    18. CoQ10 (2003) Intake May Improve Retinal Function in Those with Macular Degeneration

    Learn more about macular degeneration.

    Researchers reported that CoQ10 may improve the function of cell tissue in the retinal pigment and those improve function of the retina in those with age-related macular degeneration.

    In this small study, 14 patients who had been diagnosed with early age-related macular degeneration received a formulation with CoQ10, acetyl-L-carnitine, polyunsaturated fatty acids, and vitamin E. A matched control group received vitamin E alone. Followup testing occurred at 3, 6, 9, 12, and 24 months.

    Those receiving the formulation had all retinal and vision functions slightly improved after three months and they remained level throughout the two-year study period, while degeneration and visual function among participants in the control group continued to slowly decline.

    Published: Feher J, Papale A, Mannino G, Gualdi L, Balacco Gabrielli C. Mitotropic compounds for the treatment of age-related macular degeneration. The metabolic approach and a pilot study. Ophthalmol. 2003 Sept- Oct:217(5):351-7

    Researchers: Dr. Janos Feher, and associates, University of Rome, Italy

    19. DHA (2012) & Macular Degeneration

    Learn more about macular degeneration recommendations.

    It is well known that the proper functioning of the retina gets worse with age. A substance, known as A2E, a component of the toxic material lipofuscin, accumulates in retinal pigment cells. Researchers analyzed the effect of giving DHA (docosahexaenoic acid)supplementats to mice who had A2E in the cells of their retinas. This done of periods ranging from 1 to 18 months, and took into account the proportion of DHA versus fatty acids, and diets without DHA.

    The scientists found that A2E accumulations were reduced, and was tied to better retina functioning for mice who already had retina degeneration, and slowed this limitation for mice with more advanced retina problems.

    They concluded that DHA in the diet could have a broad preventative therapeutic effect.

    Researchers: Blake Dornstauder, Miyoung Suh, Sharee Kuny1, Frederic Gaillard1, Ian M. MacDonald, Michael T. Clandinin and Yves Sauve.

    Published: Invest. Ophthalmol. Vis. Sci. April 24, 2012 vol. 53 no. 4 2256-2265

    20. DHEA (2006) Age-related Macular Degeneration and DHEA

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    Study suggests correlation between reduced blood serum levels of DHEA and increased severity of macular degeneration.

    Am J Ophthalmol. 2006 Nov 13;

    Serum Dehydroepiandrosterone Sulphate Level in Age-related Macular Degeneration

    Tamer C, Oksuz H, Sogut S.
    Ophthalmology Department.

    PURPOSE: To evaluate plasma dehydroepiandrosterone sulphate (DHEAS) levels in patients diagnosed with age-related macular degeneration (AMD) and controls. DESIGN: Case-controlled, prospective, comparative noninterventional study. METHODS: This study involved 32 men and 35 women with exudative AMD, 37 men and 38 women with nonexudative AMD, and 32 men and 32 women of an age-matched control group. The Wisconsin Age-Related Maculopathy Grading System was used to asses the severity of AMD lesions. DHEAS levels were measured and compared according to a gender based subdivision. Analysis of variance was used to assess the association between DHEAS and AMD. Linear regression model was used to examine the relation among DHEAS level and AMD severity scale. RESULTS: Mean +/- SD of DHEAS levels in exudative AMD, nonexudative AMD, and controls in men was 2.67 +/- 0.68 mumol/l, 2.89 +/- 0.95 mumol/l, and 4.43 +/- 1.44 mumol/l, respectively (P = .001), and in women was 1.64 +/- 0.72 mumol/l, 1.85 +/- 0.73 mumol/l, and 2.78 +/- 0.91 mumol/l, respectively (P = .001). Post hoc Tukey analyses revealed a significant reduction in serum DHEAS level in both AMD groups, compared with controls for men and women (P = .001), while no difference was found between AMD groups in both men and women (P = .668 and 0.49, respectively). Regression analyses revealed an inverse correlation among serum DHEAS level and AMD severity scale both in men and women (P = .006 and .007, respectively).

    CONCLUSIONS: This study suggests an inverse correlation between serum DHEAS level and AMD severity scale with a considerably reduced DHEAS level in AMD.

    21. Early Age-Related Maculopathy (2006) in Eyes After Cataract Surgery

    Learn more about macular degeneration treatment and information.

    Patients aged 60 years and older who had undergone cataract surgery at Westmead Hospital, Sydney, Australia during 2001 to 2003 were examined for age-related maculopathy (ARM). Interviews using standardized questionnaires and stereo retinal photography were performed. Retinal photographs were graded using the Wisconsin ARM grading system. The proportions with ARM were compared between surgical and non-surgical eyes, and between this surgical cohort and the Blue Mountains Eye Study population.

    Of the 622 eligible patients, 73% were re-examined, after a mean of 2.8 years. Surgical eyes had a higher proportion of early ARM compared to non-surgical eyes and to the early ARM prevalence found in Blue Mountains Eye Study participants of similar age.

    This study found an increased prevalence of early ARM in surgical eyes of patients one to three years after cataract surgery. Whether this increase in early ARM prevalence leads to an increased prevalence of late ARM warrants further investigation.

    SOURCE: Pham TQ, Cugati S, Rochtchina E, et al. Early age-related maculopathy in eyes after cataract surgery. Eye 2006; Jan 27 [Epub ahead of print].

    22. Eggs (2006) for Elder Eyes | Macular Degeneration

    In a 2006 study, published in the Journal of Nutrition, 33 people age 60 or older were divided into two groups. During the first five weeks, one group ate one egg per day while the other group ate no eggs; both groups stopped eating eggs for a period of time and then the groups were reversed for another five weeks.

    In the egg-eating groups, blood levels of lutein and zeaxanthin rose 26% in the first phase of the study and 38% in the second phase. Neither group experienced any significant change in their cholesterol levels.

    One regular egg per day, despite having relatively little lutein and zeaxanthin, was enough to raise these antioxidant levels in seniors without raising their cholesterol levels. This finding suggests that eggs—and possibly eggs from chickens that eat grass and other fresh vegetation in particular ("grass-fed") — could be a part of a healthy diet for older people trying to prevent macular degeneration.

    (J Nutr 2006;136:2519–24)

    23. Essential Fatty Acids (2001) and macular degeneration

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    Fish Protect Against Macular Degeneration

    Eating fish, especially tuna fish, may protect against age-related macular degeneration (AMD), which is a currently untreatable disease that causes fuzziness, shadows or other distortions in the center of vision.

    Over several years, investigators questioned study participants about their diets and calculated the types of fat and total fat they ate.

    Those who ate more fat overall increased their risk of AMD, while those who ate fish reduced their risk of developing the eye disease.

    Diets containing saturated fats from animals and unsaturated fats from vegetables were associated with modest increases in the risk of developing AMD, although long-chain fats from fish, especially tuna fish, actually reduced the risk.

    A specific fish fat, called docosahexaenoic acid (DHA), may help protect and promote healthy retinal function.

    It is also concentrated in the retina of the eye. DHA was modestly inversely related to AMD. The intake of fish, the food source of DHA, was also inversely related.

    Source: American Journal of Clinical Nutrition 2001;73:209-218

    24. Exercise (1990) & Macular Degeneration Prevention

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    Summary of 15 year cumulative study on exercise and macular degeneration

    M D Knudtson, R Klein and B E K Klein
    Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI


    Background: The researchers felt that heart disease and macular degeneration (AMD) appeared to share common risk factors, but there had been little research to support the idea. Because it was known that physical activity improves the cardiovascular risk profile this study intended to investigate the relationship.

    Methods: A 15-year cumulative incidence of AMD was determined through four examination phases at 5-year intervals of a population-based study conducted in Beaver Dam, Wisconsin, USA, initiated in 1988–90 (n = 3874 men and women between ages 43 and 86 years). Early AMD, and the wet and dry forms of AMD were determined by observing stereoscopic colour photographs of the interior of the eye. Measures of physical activity were obtained through a questionnaire completed by the participants.

    Results: After controlling for age, sex, history of arthritis, systolic blood pressure, body mass index, smoking and education, people with an active lifestyle (regular activity 3x week) were less likely to develop wet AMD compared with people without an active lifestyle. After adjusting for multiple variable, the increased categories of number of blocks walked per day decreased the risk of wet AMD. Physical activity was not related to the incidence of early AMD or dry AMD.

    Conclusions: Physical activity is helpful for wet AMD, aside from other variables. Adding physical activity may be protective against developing AMD.

    25. Fat (2009) & Macular Degeneration

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    Two studies indicate that omega-3 fatty acids, fish, nuts and olive oil, help protect against macular degeneration, and trans fatty acids, increase the risk of developing AMD.

    Researchers at the University of Sydney, Australia analyzed data from 2,454 people in the Blue Mountains Eye Study of men and women aged 49 and older. Those who consumed one serving of fish per week were shown to have a 31% lower adjusted risk of developing early AMD compared with those who consumed less.

    Researchers at the Centre for Eye Research Australia analyzed data from 6,734 men and women aged 58 to 69 in the Melbourne Collaborative Cohort Study. Dietary questionnaires completed over 4 years were analyzed for their diet. Follow up exams found 2,872 cases of early age-related macular degeneration and 88 cases of late disease.

    A high intake of trans-unsaturated fats was associated with a significant increase in late macular degeneration, with the top 25% in amount of trans-fats consumption had a 76% greater risk than those whose intake was among the lowest 25%.

    They also found that olive oil was a protection against late disease. Those who consumed at least 100 milliliters (about 3.5 oz) per week olive oil were found to have a 52% lower risk of late AMD than those who consumed less than 1 milliliter per week.

    For early AMD, those whose omega-3 fatty acid intake was among the top 25% had a 15% lower risk compared with those whose intake was among the lowest 25%.

    Trans fatty acids increase cholesterol levels and inflammation, both of which affect the eyes' blood vessels, while omega-3 fatty acids may help protect the retina. Although the main fats contained in olive oil were not connected to macular degeneration risk, the oil contains antioxidants and anti-inflammatory compounds that could be protective. "A diet low in trans-unsaturated fat and rich in omega-3 fatty acids and olive oil may reduce the risk of AMD," the authors concluded.

    Reference: May, 2009 issue of the American Medical Association journal Archives of Ophthalmology
    Source: Lef.org

    26. Fish Consumption (2000), Cholesterol and Incidence of AMD

    See more information about macular degeneration treatment options

    Those consuming fish more than one time week were half as likely to develop macular degeneration than those consuming it less than once per month. Those consuming the highest amount of cholesterol in their diet were 2.7 times more likely to develop advanced macular degeneration.

    Reference: Smith, et al. Arch Ophthalmol 2000, Mar;118(3):401-4

    27. Fish Oil (2000) Essential Fatty Acids

    Learn more about macular degeneration treatment and information.

    According to a 2000 study, researchers found that eating fish as seldom as one to three times a month may cut the risk of developing age-related macular degeneration. Australian researchers have been studying more than 3,600 people aged 49 and older and found that those who ate the most fish cut their risk of late-stage AMD by half compared to people who ate fish less than once a month. However, a fish-rich diet didn't seem to reduce the risk of early-stage AMD. They also found that people eating greater amounts of saturated fat and cholesterol appeared to increase the risk of AMD.

    Researchers speculate that the omega-3 fatty acids found in fish may provide a protective effect. Similar fatty acids exist and are used in the eye's retina.

    Published: March, 2000 Archives of Ophthalmology

    28. Ginkgo Biloba (1986) and macular degeneration

    Learn more about macular degeneration treatment and information.

    An early French double blind study in 1986 found that Ginkgo Biloba could help people with macular degeneration, possibly due to its benefit of improving blood circulation to the brain.

    References: Lebuisson DA, Leroy L, Rigal G. Treatment of senile macular degeneration with Ginkgo biloba extract. A preliminary double-blind, drug versus placebo study. Presse Med 1986;15:1556–58 [in French].

    29. Ginkgo Biloba (2007) and Macular Degeneration

    Learn more about macular degeneration treatment and information.

    Controlled trials have shown that extracts of Ginkgo Biloba can significantly improve visual acuity in ARMD patients within six months of use. And both animal and human studies have revealed that Ginkgo extract can help to prevent retinal detachment, while increasing antioxidant activity in patients' blood, tears and plasma.

    Reference: Fies P, Dienel A. [Ginkgo extract in impaired vision--treatment with special extract EGb 761 of impaired vision due to dry senile macular degeneration] [Article in German]. Wien Med Wochenschr. 2002;152(15-16):423-6. plasma.

    30. Glutathione (1993) - Macular Degeneration

    Learn more about macular degeneration treatment and information.

    A 1993 study investigated whether gultathoine (GSH) had an effect on oxidative injury (by free radicals) to human retinal pigment tissue cells by free radicals in the retina.

    In a lab situation, cultured human eye cells were treated with GSH or its amino acid precursors, and any changes were noted after 30, 60, and 120 minutes.

    The researchers determined that added GSH provided protection and that the amino acid precursors for GSH, glutamate, N-Acetyl-Cysteine, and L-glycine, and selenium also protected against injury at higher concentrations.

    Published: Sternberg, Davidson, Jones, et al. Invest Ophthalmol Vis Sci 1993 Dec;34(13):3661-8

    31. Glutathione (2002) and Macular Degeneration

    Learn more about macular degeneration treatment and information.

    In the early stages of macular degeneration, glutathione has been found to protect retinal pigment epithelial cells from dying. Ayalasomayajula SP, et al. Induction of vascular endothelial growth factor by 4-hydroxynonenal and its prevention by glutathione precursors in retinal pigment epithelial cells.

    Published: Eur J Pharmacol 2002 Aug 9;449(3):213-20.

    32. Glycemic Index (2007) & macular degeneration

    Learn more about macular degeneration treatment and information.

    Age-related macular degeneration (AMD) appears to share several carbohydrate-related mechanisms and risk factors with diabetes-related diseases, including retinopathy and cardiovascular disease (CVD). The objective of a 2007 study was to test the hypothesis that dietary glycemic index (dGI), which has been related to the risk of diabetes and CVD, is associated with the risk and severity of AMD in non-diabetic elderly populations. Dietary information was obtained from 4,099 participants aged 55 to 80 years (56 percent women) who participated in the Age-Related Eye Disease Study (AREDS). A total of 8,125 eligible eyes at baseline were classified into one of five AMD groups according to the size and extent of drusen, the presence of geographic atrophy and neovascular changes.

    Compared with eyes in the first quintile of dGI, eyes in the fourth and fifth quintiles had a significantly or suggestively higher risk of large drusen, geographic atrophy and neovascularization. A significant positive relation between dGI and severity of AMD was noted. There was a 49 percent increase in the risk of advanced AMD (geographic atrophy plus neovascularization) for participants who had a dGI higher than the sex median (women, 77.9 or greater; men, 79.3 or greater). This result indicated that 20 percent of prevalent cases of AMD would have been eliminated if the AREDS participants consumed diets with a dGI below the median.

    The association between dGI and AMD from the AREDS cross-sectional analysis at baseline suggests that a reduction in the dGI, a modifiable risk factor, may provide a means of diminishing the risk of AMD.

    SOURCE: Chiu CJ, Milton RC, Gensler G, Taylor A. Association between dietary glycemic index and age-related macular degeneration in nondiabetic participants in the Age-Related Eye Disease Study. Am J Clin Nutr 2007;86(1):180-8.

    33. Homocysteine (2004) & neovascular age-related macular degeneration

    Learn more about macular degeneration.

    Researchers suggested an association between an elevated blood plasma homocysteine level and wet (neovascular) AMD.

    Researchers evaluated 59 patients in a university outpatient ophthalmology clinic with a mean age of 78 years with wet AMD. They were compared for plasma homocysteine levels with 58 patients who had dry AMD and a mean age of 76.3 years and an aged-matched control group of 56 people.

    After an 8 hour fast, a blood sample was obtained from each participant and levels of plasma homocysteine were measured.

    Results: Homocysteine levels were higher by 27.9% in the wet AMD than in the dry AMD group, and by 21.9% than in the control group. Hyperhomocysteinemia was found in 44.1% of the study group, in 22.4% of the dry AMD group, and in 21.4% of the control group.

    Published: American Journal of Ophthalmology, 2004 Jan;137(1):84-9.

    Researchers: Axer-Siegel R, Bourla D, Ehrlich R, Dotan G, Benjamini Y, Gavendo S, Weinberger D, Sela BA.,Department of Ophthalmology, Rabin Medical Center, Petah Tiqva, Israel

    34. Homocysteine Levels (2004, 2005) & Eye Disease including Macular Degeneration

    In clinical studies elevated homocysteine is associated with the following degenerative eye diseases including: macular degeneration, glaucoma, diabetic retinopathy, and optic neuropathy and ocular complications from behcet disease.

    It is also associated with accelerating the progression of the aging process. - being a major cause or contributing factor to heart disease, abnormal clotting, dementia, depression , multiple sclerosis, Parkinsons Disease, miscarriage and psoriasis.

    Aging, excessive stress, and deficiencies in choline, taurine, n-acetyl-cysteine affect homocysteine levels in the blood.

    References:
    1. Elevated homocysteine levels in aqueous humor of patients with pseudoexfoliation glaucoma. Bleich S, Roedl J, et al. Am J Ophthalmol. 2004 Jul; 138(1):162-4
    2. Plasma homocysteine and total thiol content in patients with exudative age-related macular degeneration. Coral K, Raman R, et al. Eye. 2005 Apr 1

    35. Inflammation and Risk of Developing Age-related Macular Degeneration (2005)
    A recent study published in the June 2005 Archives of Ophthalmology reports a positive association between the systemic inflammatory markers CRP and Il-6 and the rate of progression to advanced AMD. Smoking and obesity were significantly related to elevated levels of both CRP and Il-6. This study also suggests that anti-inflammatory agents may play an important role in preventing AMD.

    36. Intake of carotenoids and reduced risk of macular degeneration
    Study shows: (a) A higher dietary intake of carotenoids was associated with a lower risk for AMD. The specific carotenoids, lutein and zeaxanthin, which are primarily obtained from dark green leafy vegetables, were most strongly associated with a reduced risk for AMD. Individuals consuming the highest levels of carotenoids had a statistically significant 43% lower risk for AMD. A significant trend was seen for a lower risk for AMD with increasing amounts of carotenoids in the diet. The combination of lutein and zeaxanthin was most strongly associated with AMD, (b) The dominant pigments in the macula are lutein and zeaxanthin, which are selectively accumulated in the retina from plasma. Lutein and zeaxanthin can filter out visible blue light ... and might serve to protect the retina from photic damage or other oxidative insults. Seddon, etal. JAMA 1994 Nov 9;272(18):1413-20

    37. Laser therapy (2008) improves vision in patients with Age-related Macular Degeneration

    Learn more about macular degeneration recommendations

    Researchers conducted a clinical trial on 203 patients with age-related macular degeneration (AMD) and measured whether symptoms and distortions improved after low level laser therapy treatment and continuing for a period of between 3 and 36 months.

    They found that the occurrence of metamorphopsia (distorted vision), scotoma (partially diminished vision), and dyschromatopsia (distortion of color vision) was reduced.

    In patients with wet AMD, edema and bleeding improved. The improved vision was maintained for 3-36 months after treatment. Visual acuity in the control group remained unchanged. No adverse effects were observed in those undergoing therapy.

    Researchers: University of Heidelberg, Germany

    Published: Photomed Laser Surg 2008 Jun 26(3) 241-5

    38. Limiting Refined Carbohydrates May Stall Macular Degeneration

    Limiting carbohydrates in the diet may help slow the progression of age-related macular degeneration (AMD), according to a recent study by researchers at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University. The study builds on a recent analysis that found that men and women older than 55 years who consumed diets with higher-than-average dietary glycemic index foods appeared to have an increased risk for early and later stages of AMD. Dietary glycemic index determines how quickly carbohydrates are broken down into glucose: Foods with a high glycemic index are associated with a faster rise and subsequent drop in blood sugar than those with a low glycemic index.

    In the study, investigators analyzed diet questionnaires completed by 4,757 non-diabetic men and women participating in the nationwide Age-Related Eye Disease Study (AREDS), an eight-year study that included participants ages 55 to 80 with varying stages of AMD. They examined the participants' carbohydrate intake over one year and used the data to calculate the participants' dietary glycemic index. Results showed that those who consumed the greatest amount of refined carbohydrates were 17 percent more likely to develop blinding AMD than the group that consumed the least. Based on this data, the investigators believe that limiting dietary refined carbohydrates in at-risk elderly people could reduce the number of advanced AMD cases by 8 percent in five years. The authors note, however, that their findings warrant randomized controlled clinical trials.

    SOURCE: Chiu CJ, Milton RC, Klein R, et al. Dietary carbohydrate and the progression of age-related macular degeneration: A prospective study from the Age-Related Eye Disease Study. Am J Clin Nutr 2007;86(4):1210-8.

    39. Long Chain Fatty Acids and Macular Degeneration (2010 Study)

    Investigators publish new data in the report 'Long-chain and very long-chain polyunsaturated fatty acids in ocular aging and age-related macular degeneration. According to a study from the United States, "Retinal long-chain PUFAs (very long-chain n-3 polyunsaturated fatty acids) play important roles in normal human retinal function and visual development, and some epidemiological studies of LC-PUFA intake suggest a protective role against the incidence of advanced age-related macular degeneration (AMD).

    Liu and colleagues published their study in the Journal of Lipid Research (Long-chain and very long-chain polyunsaturated fatty acids in ocular aging and age-related macular degeneration. Journal of Lipid Research, /p>

    40. Low fat diet and omega-3 oils
    In general, a very low-fat diet (10 percent of calories from fat) that excludes red meat and dairy products has been shown to reduce the risk of macular degeneration. Anderson, R.E., Rapp, L.M., and Wiegard, R.D.. Lipid peroxidation and retinal degeneration. Current Eye Research 3 (1984): 223-27.

    However, the lack of omega-3 fatty acids, in the form of omega-3 oils, is also a risk factor. When treated with omega-3 fatty acids for four weeks, 85 percent of macular degeneration patients over age 70 experienced improved vision. Conner, W.E., Neuringer, M., and Reisbick, S. Essential fatty acids: The importance of n-2 fatty acids in the retina and the brain. Nutrition Reviews 50 (1992): 21-29.
    Editor’s Note: The best sources of omega-3 EFA’s are the flesh of cold water marine fish as well as black currant oil, flaxseed oil and hemp seed.

    41. Low Melatonin Levels (2009) May Increase Risk of Macular Degeneration

    Learn more about macular degeneration recommendations.

    This double-blind study assessed whether melatonin levels were a significant issue in cases of age-related macular degeneration (AMD) patients. The researchers measured 6-sulfatoxymelatonin levels (aMT6s), which is the major metabolite of melatonin in 43 patients' urine, and compared it to 12 gender-matched controls. Variation in the diluteness of urine were taken into account by measuring the urinary creatinine level and aMT6s levels were expressed as aMT6s/creatinine.

    The researchers found that the level of urinary aMT6s/creatinine in AMD patients was significantly lower than that of the controls. In addition, the researchers adjusted the resulting data for other factors such as age, smoking, cancer, and coronary heart disease that have been known to influence the aMT6s level. The researchers also examined the odds-ratio of urinary aMT6s and comparing AMD patients to controls was 0.65), indicating that urinary aMT6s level in AMD patients was lower than in controls even after multivariate adjustment. Urinary aMT6s level in AMD patients was 40% lower than in age-and gender-matched controls.

    The researchers concluded that the significance of the result and the role of melatonin in AMD cases requires further investigation.

    Researchers: Richard Rosen and colleagues from Department of Ophthalmology, New York Eye and Ear Infirmary, New York, NY, and other Ophthalmology institutions.

    Published:(Urinary 6-sulfatoxymelatonin level in age-related macular degeneration patients. Molecular Vision, 2009;15(179-80):1673-1679).

    42. Low selenium levels and smoking (1998)
    There is a borderline association between age-related macular degeneration and both low serum selenium levels and current smoking status. Doc Ophthalmol 1992;81(4):387-400 Mayer, et al. Acta Ophthalmol Scand 1998 Feb;76(1):62-7

    43. Lutein & Zeaxanthin (2006) Macular Degeneration: Ties between Intermediate Age-Related Macular Degeneration, Lutein and Zeaxanthin

    Learn more about macular degeneration

    Researchers evaluated the relationship between lutein plus zeaxanthin in the diet and intermediate age-related macular degeneration (AMD).

    They studied women aged 50-79 in Iowa, Wisconsin, and Oregon with high and low dietary lutein plus zeaxanthin. The range for high was above the 78th percentile, and the low was below the 28th percentiles. Four to 7 years later, these women were recruited to be part of the the Carotenoids in Age-Related Eye Disease Study (CAREDS), when the presence of AMD was determined by inner-eye photographs. They examined the occurrance of AMD in 1787 CAREDS participants, after accounting for variants.

    While, overall, the amount of AMD was not statistically different between the high and low dietary intake groups, when limiting the analyses to women younger than 75 years with stable intake of lutein plus zeaxanthin, and without a history of chronic diseases that are often associated with diet changes, the risk of AMD was substantially lowered. Exploratory analyses of advanced AMD in 34 participants resulted in protective, but statistically nonsignificant, associations in the overall sample and in women younger than 75 years.

    Conclusion Diets rich in lutein plus zeaxanthin may protect against intermediate AMD in healthy women younger than 75 years.

    Researchers: Suzen M. Moeller, PhD; Niyati Parekh, PhD; Lesley Tinker, PhD; Cheryl Ritenbaugh, PhD, MPH; Barbara Blodi, MD; Robert B. Wallace, MD; Julie A. Mares, PhD; for the CAREDS Research Study Group

    Affiliations: Author Departments of Ophthalmology and Visual Sciences (Drs Moeller, Parekh, Blodi, and Mares) and Nutritional Sciences (Drs Moeller and Parekh), University of Wisconsin, Madison; Fred Hutchinson Cancer Research Center, Seattle, Wash (Dr Tinker); Department of Family and Community Medicine, University of Arizona, Tucson (Dr Ritenbaugh); and Department of Epidemiology, University of Iowa, Iowa City (Dr Wallace).

    Published: Arch Ophthalmol. 2006;124:1151-1162.

    44. Lutein (1992) macular degeneration and cataracts

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    Highlights from the Eye Disease Case Control Study Group, 1992

    • Lower risk of neovascular AMD was connected to higher levels of carotenoids in the blood serum samples ... (pg. 1704)
    • Higher risk of neovascular AMD was tied to cigarette smoking, and higher levels of serum cholesterol ... (pg. 1704)
    • Persons with higher carotenoid levels (sum of serum lutein/zeaxanthin, b-carotene, a-carotene, cryptoxanthin, and lycopene levels) had significantly reduced risks of neovascular AMD. This finding is important because of suggestions that AMD occurs after cumulative oxidative insults and that higher levels of micronutrients with antioxidant capability may decrease the risk of AMD.

    Reference: The Eye Disease Case-Control Study Group, "Risk Factors for Neovascular Age-Related Macular Degeneration," Archives of Ophthalmology, December, 1992, Volume 110, Pages 1701-1708.

    45. Lutein (1997) - Dietary increase in macular pigment density

    Learn more about macular degeneration recommendations.

    Researchers found that macular pigment density is positively correlated with lutein and zeaxanthin in the blood. (pg. 1795) This is important because pigment density is, in turn, correlated to risk of macular degeneration. Subjects were given about four times the lutein and two to three times the zeaxanthin as in a normal healthy diet. 77% of the patients experienced increases in macular pigment density. (pp. 1796-7)

    Blue light is harmful to the retina. This includes blue light such as that of surgical light exposures which have been documented for both patients and for surgeons. (pg. 1800)

    Raising macular pigment density in patients reduces the likelihood that the patient's eye condition will advance to neovascular complications since there is substantial evidence that macular pigment protects the retina and retinal pigment epithelium against light damage. (pg. 1800).

    Reference: B. R. Hammond et al, "Dietary Modification of Human Macular Pigment Density," Investigative Ophthalmology & Visual Science, August 1997, Volume 38, No. 9, Pages 1795-1801.

    46. Lutein (1997) & AMD risks

    Learn more about macular degeneration recommendations.

    The macular pigment, lutein, has both an active and a passive protective role in prevention of macular degeneration.

    • Risk factors for macular degeneration (AMD) include light skin color, light iris color, high exposure to ambient light, low levels of dietary xanthophylls, and low level of serum xanthophylls. Low levels of lutein in the eye are correlated with higher risk of development macular degeneration (pg. 538)
    • Cigarette smoking is connected to lesser amounts of macular pigment. (pg. 541)
    • Pigmented layers in the eye are outside the light-sensitive photoreceptor segments, and therefore the macular pigment acts as a color filter through which light must pass before detection. Research in the early 1980s indicated that these pigments consisted of xanthophyll isomers, lutein and zeaxanthin. (pg. 538)
    • These pigments probably behave as a protection against the damage caused by of blue light. It has been known for a long time that carotenoids to protect against photo-oxidation in photosynthetic plants by blue light.
    • Blue light fosters formation of reactive radicals, triplet excited states, superoxide, and singlet oxygen in the retina, and the presence of macular pigments lessens such formation. The xanthophylls comprising macular pigment are effective quenchers of excited triplet states and are reactive toward singlet oxygen and radicals.
    • They actively protect the macula's nerve tissue from the damage.
    • They may also serve passively by shielding those tissues behind the outer layer of the eye from excessive blue light.
    • Increased photo-oxidation accompanies lower macular pigment levels and could contribute to faster development of drusen characteristics on the macula which are associated with AMD. (pg. 552)
    • Long-term lutein supplementation could result in a significant increase in the level of pigmentation within the macula. (pg. 553)
    • Tissues from human donor eyes, both controls and those diagnosed with AMD... (pg. 542) AMD eyes had on average approximately 70% {30% less} of the total carotenoid found in controls... (pg. 547) This difference is not restricted to the macular region as would be expected if atrophy of the macula was the cause .... Lowered levels of macular pigmentation are a causative factor in the development of macular degeneration and not necessarily a result of the degeneration process. (pg. 552)
    • 30mg of lutein per day was taken by subjects and concentration of [serum] lutein increased by about ten times within the first week and remained high thereafter.
    • Macular pigmentation increase appears to-be a slow process--this amounted to a 15%.increase in the pigment level after 72-days of lutein supplementation. (pg. 551) A relationship has- been established between serum levels of lutein and corresponding increases in the concentration of lutein in the macular of the human eye. (pg. 553)

    Published: J T Landrum et al, "The Macular Pigment: A Possible Role in Protection from Age-Related Macular Degeneration," Advances in Pharmacology, 1997, Volume 38, Pages 537-556.

    47. Lutein (1997) AMD blue light

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    A small study with 2 subjects who consumed 30 mg free lutein per day for 140 days resulted in increased Macular Pigmentation in both eyes. This pigmentation protects our eyes from blue light, and may be responsible for protecting us against macular degeneration. The lutein supplementation caused a 10 times increase in blood serum levels of lutein within 10-20 days of treatment.

    Published: Landrum, et al. Exp Eye Res 1997 Jul;65(1):57-62

    48. Lutein (1997) Spinach and Corn in Diet
    Researchers Hammond, Johnson, Russel and colleagues performed a study in which they measured macular pigment in 13 patients who received dietary modifications for a period of up to 15 weeks. Subjects were given daily servings of spinach and corn, which added 11.2 mg lutein and 0.6 mg zeaxanthin. Relative to an average diet, this increased lutein intake 4-fold and Zeaxanthin intake 3-fold. Eight of 10 patients compliant on the spinach/corn supplement diet exhibited an average increase in macular pigment density of 19% (minimum 13%). Hammond, etal. Invest Ophthalvol Vis Sci 1997 Aug;38(9):1795-801

    49. Lutein (1998) Lowers Macular Degeneration Risk

    Learn more about macular degeneration recommendations.

    Vision loss connected with aging may-be prevented or even reversed with better nutrition. Macular pigment protects the retina from loss of acuity, both during the day and at night, and dietary factors enhance macular pigment.

    Macular pigment is composed of the carotenoids lutein and zeaxanthin. Researchers measured macular pigment and visual acuity of 27 healthy 60-84 year-old people, and compared them with 10 younger healthy 24-36 year-old subjects. The amount and quality of macular-pigment clearly determined the degree of visual acuity.

    Subjects over age 60 with high macular pigment density had the same visual acuity as younger subjects. The researchers found that high macular pigment density was connected to retention of visual acuity, suggesting that macular pigment may retard age-related loss of visual function. (pg. 2)

    Risk factors for macular degeneration include smoking, female gender and blue irises; it was found that those people also have lower macular pigment density. (pg. 2). Those with higher macular pigment density are connected with factors of lowered risk, such as high blood serum concentrations of carotenoids, high dietary intake of lutein and zeaxanthin and dark irises. (pg. 3)

    Macular pigment density may be valuable to predict overall eye health, because macular pigment density correlates with preservation of clarity of the lens as well as health of the retina.

    Researchers also felt that by improving retina protection through diet (and attending to other risk factors as well) that retinal or retinal pigment epithelial cells that may be damaged but still viable could recover.

    It appears that patients lose visual acuity before the worst stages of disease but that the worst can be prevented with appropriate diet and lifestyle changes.

    Reference: Schepens Eye Research Institute , An Affiliate of Harvard Medical School, “Improved Nutrition Could Prevent Vision Loss, Schepens Study Finds,” February 1998.

    50. Lutein (1999) Dietary modification with lutein rich food

    Learn about macular degeneration treatment and information.

    Adding lutein-rich foods to your diet can reverse the damaging effects of age-related macular degeneration (ARMD), the leading cause of blindness in people over age 65 in the U.S. Until the late 1990s, research only indicated that diet played an important role in reducing risk.

    Resarchers found that patients showed positive effects in visual sensitivity in one or both eyes by adding lutein-rich foods to their diet. The research supports the hypothesis that lutein is connected to enhancing macular pigment, a key indicator of ARMD risk and pathology.

    The diets of 15 dry macular degeneration patients were supplemented with an additional five ounces of sautéed spinach 4-7 times weekly. Study subjects were tested to establish beginning measurements of contrast sensitivity, low-luminance, low-contrast visual acuity and glare recovery in each eye. Subsequent testing was done at intervals ranging from two months to 12 months after the study began.

    Researchers saw improvements in visual acuity in only three months and striking improvements in vision were often detected in follow-up tests, even though patients did not notice changes. Partial or complete resolution of metamorphopsia (distorted vision) and scotomas (blind spots) was reported in seven of eight applicable cases.

    The conclusion was the treatment of macular degeneration through diet should receive more attention because it is simple, inexpensive and may apply to a broad range of macular degeneration-related problems.

    Many researchers are preoccupied with wet macular degeneration with accompanying commercial and professional interest in high-technology solutions which are more expensive and complicated. These therapies are reasonable for a small percentage of ARMD patients when it is detected early.

    Lutein and zeaxanthin are carotenoids found in leafy green vegetables such as spinach and kale and are concentrated in retinal macular pigment. Concentrations accumulate when those foods are included regularly in the diet. Macular pigment may filter blue light that damages photoreceptors and the retinal pigment epithelium. In addition, carotenoids may act as antioxidants, limiting oxidant stress

    Reference: Dr. Stuart Richer, Atlanta, Feb. 25, 1998, Optometry Section, DVA Medical Center, North Chicago, IL, presented at Southern Council of Optometrists 1999 annual meeting, PRNewswire

    ATLANTA, Feb. 25 /PRNewswire

    51. Lutein (1999) from Spinach and Supplements

    Learn more about treatment options and other research for macular degeneration

    A preliminary study showed the patients consuming lutein from either spinach or supplements demonstrated some improvement of some of the early vision loss from the dry form of macular degeneration.

    Published: Richer, Journal American Optometry Association; January, 1999

    52. Lutein (1999), Zeaxanthin& the Retina - Macular Degeneration (AMD)
    The macular pigment is highly organized within the retina of the human eye. Studies show that the retina contains two carotenoids, lutein and zeaxanthin, with the greatest concentration at the center. Within the central macula, zeaxanthin is the dominant component, up to 75% of the total, whereas in the peripheral retina, lutein predominates, usually being 67% or greater. Typical carotenoid concentrations within other human tissues are much lower. Data show that the macular pigment increases through dietary supplements. Evidence points to a correlation between macular pigment density and a reduction in the risk for age-related macular degeneration (AMD). [“Analysis of Zeaxanthin Distribution within Individual Human Retinas” by John T. Landrum, Richard A. Bone, Linda L. Moore, and Christina M. Gomez, Methods In Enzymology (1999, 299: 457-467).]

    53. Lutein (2004) and AMD

    Learn more about treatment options for macular degeneration

    A small study serves to confirm the effectiveness of lutein for patients with AMD, as reported, for example, in the Chicago Study.

    Singapore Polytechnic researchers tested a group of seven older subjects with early stage AMD, and six subjects of the same age with healthy eyesight. Each subject received 10 mg of lutein supplements daily for 18 to 20 weeks.

    Macular pigment optical density (MPOD low density is considered a risk factor) and blood plasma concentrations of lutein were measured before and after the study. The MPOD average increased significantly in both groups as lutein levels rose. Researchers concluded both a diseased macula may accumulate and synthesize lutein effectively, and people with healthy macula gain benefits from lutein as well.

    Researchers: Singapore Polytechnic

    Published: July, 2004 issue of The Journal Experimental Eye Research

    54. Lutein (2004) and dry AMD

    Learn more about macular degeneration.

    Researchers studied 90 subjects with dry AMD who were divided into three groups and randomly assigned to receive 10 mg of lutein daily, or 10 mg of lutein combined with other nutrients that are known to enhance vision health (such as bilberry, zinc, quercetin, N-acetylcysteine, and others), or a placebo.

    Several measurements were taken over the course of a one year test period. Changes in macular pigment optical density (low density is a risk factor) were recorded; contrast sensitivity was evaluated; and visual perception was assessed with eye chart exams.

    At the end of the trial, the researchers found clear improvements in both the lutein and the lutein-plus-nutrients group, but no noteworthy changes in the placebo group. Even those subjects who had advanced AMD showed improvement with the additional lutein intake. Larger and longer studies are needed to confirm the findings.

    Researchers: Department of Veterans' Affairs, Medical Center Eye Clinic in Chicago

    Published: April 2004 issue of the journal Optometry

    55. Lutein and Prevention of Macular Degeneration
    1994 Study; Dr. Johanna Seddon of Harvard University published a study in the Journal of the American Medical Association that examined the effect of consumption of specific carotenoids on AMD prevention. The results of the study found that the highest correlation of disease prevention was associated with an intake of 6 mg per day of lutein, which led to a 57% decrease in the risk of contracting AMD. Therefore, lutein is the key carotenoid for providing the proper amount of lutein and zeaxanthin.

    Seddon, J.M., U.A. Ajani, et al. (1994). “Dietary carotenoid, vitamins A, C, E, and advanced age-related macular degeneration. Eye Disease Case-Control Study Group Jama 272(18):1413-20

    56. Lutein and Zeaxanthin (2003) & Age-Related Macular Degeneration

    See more on Macular Degeneration

    Catharine R. Gale, Nigel F. Hall, David I. W. Phillips, and Christopher N. Martyn

    From the Medical Research Council Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, United Kingdom.

    PURPOSE. To investigate the relation between lutein and zeaxanthin in blood plasma and age-related macular degeneration in a group of elderly men and women.

    METHODS. The Wisconsin Age-Related Maculopathy Grading System was used to compare early and late macular degeneration in 380 men and women, aged 66 to 75 years, from the UK. Fasting blood samples were taken to measure lutein and zeaxanthin concentrations in the blood plasma.

    RESULTS. The risk of both early or late starting age-related macular degeneration (AMD) was higher in people who had lower plasma concentrations of zeaxanthin. Compared with those in the highest 1/3, people whose plasma concentration was in the lowest 1/3 had 2 times higher odds for risk of age-related macular degeneration.

    CONCLUSIONS. These findings provide support for the view that zeaxanthin may protect against age-related macular degeneration.

    (Investigative Ophthalmology and Visual Science. 2003;44:2461-2465.)© 2003 by The Association for Research in Vision and Ophthalmology, Inc. DOI: 10.1167/iovs.02-0929

    57. Lutein research -1993
    Lutein Research - 1993 - Macular Degeneration Prevention.

    1. AMD, the leading cause of new cases of blindness in persons age 65 years and older... (pg. 104)
    2. Persons with carotenoid levels in the medium and high groups, compared with those in the low group, had markedly reduced risks of neovascular AMD, with levels of risk reduced to one half and one third. (pg. 104) Higher levels of the individual carotenoids (except for lycopene ...) were associated with statistically significant reductions in risk. The two variables found to be significantly associated with risk of AMD [are} carotenoid levels and the antioxidant index. There was a progressive decrease in risk of AMD with increasing levels of carotenoids and increasing level of the antioxidant index. (pg. 107) These results suggest that higher blood levels of micronutrients with antioxidant potential, in particular, carotenoids, may be associated with a decreased risk of the most visually disabling form of AMD. (pg. 104)
    3. Data ... suggest a protective role in AMD for carotenoids, compounds that have potent antioxidant capabilities. Levels of total and individual carotenoids were significantly lower in persons with neovascular AMD than in controls. When we compared the patients with AMD with patients with macular holes, the findings were in the same direction as those in the primary analyses; persons with higher levels of carotenoids were at reduced risk of AMD... Data from the Eye Disease Case-Control Study are consistent with hypotheses suggesting a reduced risk of neovascular AMD in persons with higher levels of circulating micronutrients with antioxidant capabilities, in particular carotenoids. (pg. 108),
    4. The highly significant finding for serum carotenoids is of particular interest because it provides some indirect support for hypotheses suggesting that sunlight exposure is a risk factor for AMD. Singlet oxygen, a potentially damaging chemical species produced when biological systems are exposed to sunlight, has been proposed as the mediator of light damage in the retina. Carotenoids, notably lutein and zeaxanthin, are known to be present in the retina and are known to be highly effective protective agents against singlet oxygen .... Carotenoids may protect the retina from light damage. (pg. 108).
    The Eye Disease Case-Control Study Group, "Antioxidant Status and Neovascular Age-Related Macular Degeneration," published Archives of Ophthalmology, January, 1993, Volume 111, Pages 104-109

    58. Lutein, Omega-3 & Macular Degeneration Study May 2008

    A recent study published in the May 2008 issue of American Journal of Clinical Nutrition, studied the effects of lutein and docosahexaenic acid (DHA – omega-3) on macular degeneration. This four-month study researched 59 women, 60 to 80 years old. The women were randomly assigned a placebo, lutein, DHA, or lutein plus DHA supplement.

    Lutein is found in the healthy macula. DHA is found in the retina. Researchers wanted to study the effects lutein (12 mg/day) and DHA (800 mg/day) had on their serum concentrations and macular pigment optical density (MPOD).

    Both supplements alone helped to increase their concentration levels in the eye, however, both lutein and DHA together had the greatest difference on serum concentrations and MPOD when combined. The study concluded that “lutein and DHA may aid in prevention of age-related macular degeneration.”

    Ref: Elizabeth J Johnson, Hae-Yun Chung, Susan M Caldarella and D Max Snodderly. “The influence of supplemental lutein and docosahexaenoic acid on serum, lipoproteins, and macular pigmentation.” American Journal of Clinical Nutrition. Vol. 87, No. 5, 1521-1529, May 2008.

    59. Lutein, Zeaxanthin and AMD 2007 Study
    Lutein and zeaxanthin has again been linked to lowering the risk of neovascular AMD. Researchers studied 4,519 Age-Related Eye Disease Study (AREDS) participants between 60 and 80 years of age. They found that carotenoids, lutein and zeaxanthin, absorb blue light that could damage the macula, by preventing free radicals from damaging eye cells and by strengthening eye cell membranes.1 This study, published in Archives of Ophthalmology, concluded that a higher intake of Lutein and zeaxanthin may help lower the risk for AMD.

    60. Lutein, Zeaxanthin and AMD 2008

    The Centre for Vision Research at the University of Sydney, Australia, studied the dietary and supplement intakes of antioxidants and the long-term risk of incident age-related macular degeneration (AMD). Over 10 years, 2454 participants were examined and reexamined. Those participants that had higher amounts of lutein and zeaxanthin intake had a reduced risk of incident neovascular AMD and those with above median intake had a reduced risk of soft or reticular drusen. The study concluded that the higher dietary lutein and zeaxanthin intake reduced the risk of long-term incident AMD. It also confirmed finding protective influences from zinc and beta-carotene to help lower the risk of AMD, as did the 10 year study by the US National Institute of Health’s Age-Related Eye Disease Study (AREDS).

    Ref: J.S.L. Tan, J.J. Wang, V. Flood, E. Rochtchina, W. Smith, P. Mitchell. "Dietary Antioxidants and the Long-term Incidence of Age-Related Macular Degeneration: The Blue Mountains Eye Study." Ophthalmology (Elsevier). February 2008, Volume 115, Issue 2, Pages 334-341.

    61. Lutein, Zeaxanthin and Macular Degeneration 2008 Study
    Macular degeneration- In people with the highest level of consumption of lutein and zeaxanthin (from leafy greens), risk of AMD was 35% of the risk in people who ate less greens. Zinc was also protective. This in a study by J.S. Tan, et al. in Opthalmology, February 2008.

    62. Lutein/Zeaxanthin (2008) & Risk Reduction in Age-Related Eye Disease

    Learn more about macular degeneration recommendations

    Lutein and zeaxanthin are the only carotenoids that concentrate in the macula. There is evidence of three mechanisms by which lutein and zeaxanthin may afford protection against AMD: by absorbing blue light, by quenching free radicals and by increasing membrane stability.

    Many previously published studies which have examined the relationship between AMD and these carotenoids have reported an inverse association between the disease and intake of lutein plus zeaxanthin. These carotenoids are commonly obtained from leafy green vegetables, corn, egg yolks, broccoli, peas, squash - as well as from supplements.

    The authors of the Carotenoids in Age-Related Eye Disease Study (CAREDS) now report that a stable intake of these carotenoids over time could reduce the risk of AMD by about 43% in healthy women under 75.

    Design and Methods

    CAREDS is an ancillary study of the Women's Health Initiative (WHI), a prospective cohort study. CAREDS was designed, in part, to evaluate the relationship between lutein/zeaxanthin and the prevalence of intermediate AMD. Over 1780 women aged 50-79 who had high or low intake of lutein plus zeaxanthin at WHI enrollment were recruited into CAREDS 4-7 years later, when the presence of AMD was determined by fundus photographs.

    To maximize extremes in intake of these carotenoids in the study sample, women with intakes of lutein plus zeaxanthin above the 78th (high) and below the 28th (low) percentiles at baseline in the WHI were recruited. Dietary assessments were performed by means of food frequency questionnaires administered at the study's start and over the previous 15 years. Logistic regression analyses examined the prevalence of AMD, after accounting for potential covariates.

    Results

    While an association between dietary intake of these carotenoids and AMD was not observed in the overall study population, secondary analyses disclosed a statistically significant protective effect in women younger than 75 with stable intakes of lutein and zeaxanthin.

    Higher intakes of lutein/zeaxanthin (2, 868 mcg or more daily) compared to lower consumption (792 mcg daily) in women with stable intakes resulted in a substantial 43% lower risk of intermediate AMD (odds ratios [0.57; 95% confidence interval, 0.34-0.95]). The younger women (< 75 years) did not have a history of chronic diseases such as cardiovascular disease and diabetes that are often associated with diet changes and instable intakes of lutein/zeaxanthin rich foods.

    Similar protective associations were observed for large drusen. While not statistically significant, associations in this sub-sample were in the protective direction for the more advanced lesions of pigmentary abnormalities, as well as for the exploratory outcome, advanced AMD.

    The researchers observed the strongest inverse associations between intermediate AMD and high intake of vegetables in general, as well as of green vegetables. Blood levels of the carotenoids were not associated with risk of AMD.

    Comments

    According to lead author Dr. Suzen Moeller of the University of Wisconsin, the findings are consistent with a broad body of evidence from observational and experimental studies suggesting that these carotenoids may protect against AMD. There was evidence that diet instability may have biased the associations and, together with the possibility of selective mortality bias, may explain our inability to detect the hypothesized association in the full study population, wrote Dr Moeller.

    Published: Moeller SM et al. Age-Related Macular Degeneration and Lutein and Zeaxanthin in the Carotenoids in Age-Related Eye Disease Study (CAREDS). Archives of Ophthalmology 124:1151-1162, 2006.

    63. Lycopene (1995) & Macular Degeneration

    Learn more about macular degeneration recommendations.

    Researchers investigated the potential connection between tocopherols and carotenoids level in blood serum and incidence of age-related macular degeneration (ARMD) by viewing and grading photographs of the retina.

    The subjects had retinal pigment abnormalities including soft drusen, late ARMD or neovascular and exudative macular degeneration) and were paired with controls (matched for age, sex, and whether or not they smoked) without evidence of these conditions.

    Average levels of various carotenoids were similar in cases and controls. Average levels of vitamin E were lower in people with exudative macular degeneration. But once the difference was controlled for cholesterol levels, the difference was not significant.

    What was significant was that researchers found that where they found low (lowest 1/4 of subjects) lycopene levels the subjects were twice as likely to have macular degeneration.

    They concluded that low levels of lycopene were related to ARMD.

    Researchers: Julie A. Mares-Perlman, William E. Brady, Ronald Klein, Barbara E. K. Klein, Phyllis Bowen, Maria Stacewicz-Sapuntzakis, and Mari Palta.

    Published: Archives of Ophthalmology 113: 1518-1523 (1995).

    64. Lycopene (1995) and Macular Degeneration

    Learn more about macular degeneration treatment.

    In this study, researchers found that patients with the lowest levels of lycopene,a carotenoid found in tomatoes, were two times more more at risk to develop macular degeneration as compared to patients with the highest levels of lycopene.

    Editor's Note: Consumption of high levels of lutein and lycopene has also been associated with dramatically lower cancer rates for lung and prostate cancer!

    Published: Mares-Perlman, et al. Arch Ophthalmol 1995 Dec;113(12):1518-23

    65. Macular carotenoids: lutein and zeaxanthin.
    Dev Ophthalmol. 2005;38:70-88. The yellow color of the macula lutea is due to the presence of the carotenoid pigments lutein and zeaxanthin. In contrast to human blood and tissues, no other major carotenoids including beta-carotene or lycopene are found in this tissue. The macular carotenoids are suggested to play a role in the protection of the retina against light-induced damage. Epidemiological studies provide some evidence that an increased consumption of lutein and zeaxanthin is associated with a lowered risk for age-related macular degeneration, a disease with increasing incidence in the elderly. Protecting ocular tissue against photooxidative damage carotenoids may act in two ways: first as filters for damaging blue light, and second as antioxidants quenching excited triplet state molecules or singlet molecular oxygen and scavenge further reactive oxygen species like lipid peroxides or the superoxide radical anion.

    66. Macular degeneration (1997) Prevention

    Learn more about macular degeneration recommendations.

    Contrary to the general attitude of opthamologists (in 1997), one doctor felt that there were a variety of treatments that could be helpful for macular degeneration. While some of his methods have not been validated, this review determined that there were a variety of general measures for prevention and remediation of macular degeneration would include a combination of supplementation with trace elements, antioxidants and other vitamins, ozone therapy, increasing physical fitness, improving nutrition (e.g. avoiding hydrogenated oils), abstaining from smoking, and protection from excessive light exposure.

    Published: European Journal Medical Ressearch 1997 Oct 30:2(10):445-54

    67. Macular Degeneration (2005): Heavy Cigarette Smoking Increases Risk

    In addition there was some risk from second-hand smoke, but it was not statistically significant.

    Note: for choroidal neovascularization, the risk was 2.49 times as likely to develop the condition.

    Editor's Note2: Some research suggests that smokers should not supplement with betacarotene as it may increase chances for lung cancer.

    Published: Khan JC et al. Smoking and age related macular degeneration: the number of pack years of cigarette smoking is a major determinant of risk for both geographic atrophy and choroidal neovascularization. British Journal of Ophthalmology 2006;90:75-80.

    Researchers: John R.W. Yates, Ph.D., and associates of the University of Cambridge.

    68. Macular Degeneration (2007) Good Fats and Bad Fats

    In a recent study called the POLANUT study, the results showed a 60% decrease in the occurrence of macular degeneration for those that included fatty fish in their diets more than once a month versus less than one time per month.

    Saturated and monounsaturated fat intake were associated with increased risk for age-related macular degeneration. Total polyunsaturated fatty acid was not significantly associated with age-related macular degeneration. Total and white fish intake was not significantly associated with age-related macular degeneration.

    Eur J Clin Nutr. 2007 Feb 14; Inserm, Research Unit U593 for Epidemiology, Public Health and Development, Bordeaux, France, Universite Victor Segalen Bordeaux 2, Bordeaux, France.

    69. Macular degeneration (AMD) (2001) and Fat Intake
    Dr. Joanna Seddon of the Massachusetts Eye and Ear Infirmary. Harvard Medical School and colleagues have discovered that a diet high in fat may be associated with an increased risk of developing wet macular degeneration (AMD). According to the study published in the August 2001 issue of Archives of Ophthalmology, researchers analyzed the dietary habits and physical condition of over 800 patients with and without wet AMD.

    The results of the study indicated that high intake of vegetable, monounsaturated and polyunsaturated fats were associated with a twofold-increased risk of developing wet AMD. These fats are all commonly found in snack foods such as potato chips, french fries, cakes and commercially prepared pies. HIgh intake of linoleic acid, a fat also found in many snack foods, was associated with the greatest risk of developing wet AMD.

    Conversely, Dr. Seddon and colleagues found that individuals who consumed little food containing linoleic acid and who ate two or more servings of fish per week showed a lower risk of developing AMD. Fish are high in a fat called docosahexanoic acid, or DHA, for short. Heart disease studies have shown a beneficial link between DHA and cardiovascular disease. DHA may also have a healthful effect on blood vessels leading to the retina. Furthermore, DHA is also highly enriched in the retina. Diets rich in DHA may have a positive effect on retinal function and could possibly lesson the risk of developing the disease.

    Previous studies have found that a diet high in fatty foods increases the formation of fatty deposits in blood vessels, a condition called atherosclerosis. These fatty deposits may also affect blood vessels leading to the retina, thereby interfering with the ability to provide the retina with oxygen and nutrients. In AMD, blood vessel growth may be spurred to overcome the adverse affects of atherosclerosis. Unfortunately, the body responds by producing abnormal blood vessels that leak fluid and blood into the macula, thus causing central vision loss.

    Earlier studies have found that cigarette smoking and hypertension increase the risk of developing AMD. This recent finding regarding dietary fat adds another important clue in the development of AMD. Because these same risk factors also increase the risk of cardiovascular disease, it may be that both diseases can result from similar environmental causes. These studies provide valuable information for reducing the environmental risks associated with the disease, especially for people with a family history of AMD.

    Excerpted from “Fighting Blindness News” Fall 2001.

    70. Macular Degeneration 2005 Study Shows Benefits of Nutrients
    This randomized, double-blind, placebo-controlled study enrolled 106 patients with bilateral macular degeneration. The subjects received either a nutrient combination (consisting of 200 mg of acetyl-L-carnitine, 780 mg of omega-3 fatty acids, and 20 mg of coenzyme Q10) or a placebo daily for 12 months, and underwent visual testing every three months. Treatment improved visual field defects in both eyes. Only one of 102 eyes treated deteriorated during the 12-month study, compared to 14 of 110 placebo-treated eyes. Moreover, the area of the eye’s fundus covered by drusen (degenerated retinal pigment cells that are a precursor to macular degeneration) in the treated group decreased by 15% to 23%, while increasing by more than 10% in the placebo group.

    The nutrients were selected based on their biological activities. Specifically, acetyl-L-carnitine facilitates fatty acid oxidation, omega-3 fatty acids regulate neural and sensory development in the retina, and coenzyme Q10 is critical to the generation of energy in the mitochondria. The results suggest that supporting mitochondrial health may be useful in preventing and managing macular degeneration.

    Reference

    * Feher J, Kovasc B, Kovacs I, Schvoller M, Papale A, Balacco Gabrieli C. Improvement of visual functions and fundus alterations in early age-related macular degeneration treated with a combination of acetyl-L-carnitine, n-3 fatty acids, and coenzyme Q10. Ophthalmologica. 2005 May-Jun;219(3):154-66.

    71. Macular Degeneration and the Oils We Eat
    Regular high consumption of vegetable fat more than doubles the risk of macular degeneration as compared to those with a low vegetable fat diet. Higher intake of omega-3 fatty acids tended to reduce the risk of age-related macular degeneration. There was no association found between aged-related macular degeneration and cholesterol.

    Arch. Ophthalmol., August 2001;119:1191-1199

    Editor's Note: The high consumption of vegetable oils and grains, along with meats and eggs eaten from animals fed grains has dramatically thrown our omega-3 to omega-6 ratio out of balance, resulting too much omega-6 fatty acids which tend to be inflammatory. We believe it will eventually be proven that the high levels of omega-6 fatty acids in our diet with high levels of refined carbohydrates eaten are the main causes besides genetics of heart disease, stroke and autoimmune diseases.

    72. Macular Degeneration and Vitamin E and Zinc Deficiency
    Subnormal zinc and vitamin E serum levels may be associated with the development of age-related macular degeneration. Ishihara, et al. Nippon Ganka Gakkai Zasshi 1997 Mar;101(3):248-51

    In a study of adults over 60 there was found to be a significant link between risk of macular degeneration and low blood levels of vitamin E as well as increased sun exposure. Belda, et al Mech Ageing Dev 1999 Mar 1;107(2):159-64

    Subnormal zinc and vitamin E serum levels may be associated with the development of age-related macular degeneration. Ishihara, et al. Nippon Ganka Gakkai Zasshi 1997 Mar;101(3):248-51

    In a study of adults over 60 there was found to be a significant link between risk of macular degeneration and low blood levels of vitamin E as well as increased sun exposure. Belda, et al Mech Ageing Dev 1999 Mar 1;107(2):159-64

    73. Melatonin (2005) and Macular Degeneration

    Learn more about macular degeneration treatment and information.

    In this study, 100 patients with either wet or dry macular degeneration were given 3 mg of Melatonin Zn Se (also contains zinc and selenium in addition to melatonin) orally each night at bedtime for a minimum of 3 months, with 55 patients continuing on for more than 6 months and some onto 12 and 24 months. The patients were then evaluated at regular periods to measure the extent of their ARMD.

    The study reported that at 2-3 months of treatment the visual acuity had been kept stable (vision loss was halted). For the patients who continued onward past 6 months and onto 12-months of nightly use of 3mg Melatonin Zn Se, the health of the fundus (the back portion of the interior of the eyeball) in many patients improved dramatically.

    At the end of the study, the vast majority had dramatically reduced pathologic macular changes.

    Reference: Changxian Yi, Xiaoyan Pan, Hong Yan, Mengxiang Guo, Pierpaoli, W. Effects of Melatonin in Age-Related Macular Degeneration. Ann N.Y. Acad Sci, 2005;1057:384-392.

    74. Meso-Zeaxanthin (2007) & Macular Pigment Density

    Learn more about macular degeneration recommendations.

    A short, 120 day, study assessed supplementation of meso-zeaxanthin, plus lutein and zeaxanthin in 10 subjects. The subjects received 20mg/day of the formulation. Nine more subjects received a placebo. Before and during the 120 days, blood serum samples were analyzed for carotenoid content. Likewise, macular pigment optical density was measured.

    During supplementation with the carotenoids, blood samples revealed the presence of all three carotenoids. Macular pigment optical density, measured at 460 nm, rose at an average rate of 0.59 ± 0.79 milli-absorbance unit/day in the 10 supplemented subjects. This was significantly different from the placebo group (9 subjects) for whom the average rate was -0.17 ± 0.42 milli-absorbance units/day.

    The research suggested that meso-zeaxanthin is absorbed into the serum following ingestion. The data indicate that a supplement containing predominantly meso-zeaxanthin is generally effective at raising macular pigment density, and may turn out to be a useful addition to the defenses against AMD.

    Published: Nutrition & Metabolism 2007, 4:12doi:10.1186/1743-7075-4-12

    75. Meso-Zeaxanthin Aids Eyes 2007 Study

    A supplement of meso-zeaxanthin may bolster macular pigment optical density (MPOD), according to researchers from Florida International University (Nutr Metab. 2007;4:12) (DOI:10.1186/1743-7075-4-12). Lutein and zeaxanthin have been the primary focus of research trials exploring how the xanthophyll carotenoids can support macular pigment and possibly prevent onset of age-related macular degeneration (AMD). Meso-zeaxanthin is the third major carotenoid found in macular pigment.

    In this 120-day supplementation study, 10 subjects received gelcaps containing 20 mg/d of predominantly meso-zeaxanthin, with smaller amounts of lutein and zeaxanthin; 9 additional subjects formed a control group taking a placebo. Supplementation increased blood serum levels of all three carotenoids during the supplementation period. In addition, MPOD, measured at 460 nm, rose at an average rate of 0.59 ± 0.79 milli-absorbance unit/day in the 10 supplemented subjects; no such change was seen in the placebo group. These trial results showed meso-zeaxanthin was absorbed into the serum following supplementation and was effective at raising MPOD.

    76. Meso-Zeaxanthin Deficiency Confirmed in Macular Degeneration 2003 Study

    An autopsy study on donated eyes was done to measure levels of lutein, zeaxanthin, and meso-zeaxanthin in the retina of those with and without macular degeneration.

    This postmortem study helped confirm other studies indicating the importance of all three carotenoids (lutein, zeaxanthin, and meso-zeaxanthin) in maintaining the structural integrity of the macula. Michaelides M, Hunt D et al. The genetics of inherited macular dystrophies. J Med Genet. 2003;40(9):641-50. Meyers SM, Grene T et al. A twin study of age-related macular degeneration. Am J Ophthalmol. 1995; 120: 757-66

    The macular pigment is made up of the following three carotenoids:
    - Lutein 50%
    - Zeaxanthin 25%
    - Meso-zeaxanthin 25%

    Unlike lutein and zeaxanthin, meso-zeaxanthin is not found in the diet, but is converted in the retina from ingested lutein. Yanoff M, Duker JS. Ophthalmology 2nd ed. St. Louis: Mosby; 2004: 925-33. If taken as a supplement, meso-zeaxanthin is absorbed into the blood stream and effectively increases macular pigment levels. Vrabec T, Tantri A et al. Autosomal dominant Stargardt-like macular dystrophy: identification of a new family with a mutation in the ELOVL4 gene. Am J Ophthalmol. 2003;136(3):542-5

    Patients with macular degeneration have been shown to have 30% less meso-zeaxanthin in their macula compared to healthy eyes. Vrabec T, Tantri A et al. Autosomal dominant Stargardt-like macular dystrophy: identification of a new family with a mutation in the ELOVL4 gene. Am J Ophthalmol. 2003;136(3):542-5

    One reason for this deficiency of meso-zeaxanthin is lack of ingested lutein. Another explanation for the missing meso-zeaxanthin observed in macular degeneration may be the inability to adequately convert lutein to meso-zeaxanthin in the retina.

    77. Microcurrent Stimulation (2009) & Macular Degeneration

    Learn more about macular degeneration, retinitis pigmentosa and diabetic retinopathy.

    Microcurrent stimulation is an application of electrotherapy used in this study of patients with macular degeneration. The researchers were looking into appropriate design models for the electrotherapeutic device and the treatment protocol. The factors include the skin interface, reliability, contraints, protocal, and safety.

    In FDA guided and supervised clinical studies on patients dry macular degeneration, 61% of a 400 patients treated with electrotherapy (MSC) had improvments in vision sharpness of 2 or more lines on the Snellen chart. The average intensities of electric current of 60 to 125 muA range were used for this level of result. It is expected that with additional improvments in waveforms, frequency choices, protocols and device applications, these sorts of improvements can be expected in patients with early stages of diabetic retinopathy, retinitis pigmentosa, and dry macular degeneration.

    Editor's Note: The current and frequencies used in our MCS 100ile unit is consistent with the 5 research studies done summarized on our website, and as the most research behind it regarding macular degeneration.

    Researchers: O'Clock GD, Jarding JB.

    Published: Electrotherapeutic device/protocol design considerations for visual disease applications, Engineering in Medicine and Biology Society, 2009. EMBC 2009. Annual International Conference of the IEEE. 2009:2133-6.

    78. Omega 3 Fatty Acids (2005) & Macular Degeneration

    The Lewin Group was commissioned in early 2005 by the Dietary Supplement Education Alliance (DSEA) to critically review the research literature concerning Omega-3 fatty acids, lutein and zeaxanthin. Visual impairment is one of the top four reasons for loss of independence. Age-related diseases of the eye are common and costly (35% of individuals aged 75 and older have AMD).

    For example, eighteen percent of all hip fractures among seniors are attributed to age-related vision loss (hip fracture patients have a substantially increased risk of death for at least 6 years post-fracture). The Lewin Report addresses several hundred studies on the benefits of Omega-3 fatty acids dating back nearly thirty years, including several comprehensive reviews.

    In addition, in 2004, the FDA issued a qualified health claim for reduced risk of coronary heart disease (CHD) associated with foods containing Omega-3 fatty acids. Earlier, in 2000 the FDA announced a similar qualified health claim for reduced risk of CHD for dietary supplements containing EPA and DHA Omega-3 fatty acids.

    Key findings of the Lewin report support the supplementation of omega-3 fatty acids, lutein, and zeaxanthin in helping preserve vision and supporting people to be able to maintain independent living.

    For full article, go to http://www.nowfoods.com/?action=itemdetail&item_id=41654

    79. Omega 3 Fatty Acids (2014) & Macular Degeneration

    Learn more about macular degeneration and treatment options.

    Scientists have found that omega 3 fatty acids have the capacity to actually regulate formation of blood vessels - an important factor in development of macular degeneration. This occurs because of the nutrient's ability to encourage immune cell movement toward the site of extra formations of blood vessels that distort vision in the condition. The results indicate very promising potential for omega 3 as a nutritional therapy - not only for AMD, but for other conditions involving inflammation and creation of additional blood vessels.

    Researchers: from Massachusetts Eye and Ear/Schepens Eye Research Institute, Harvard Medical School and other institutions.

    Published: Cytochrome P450-generated metabolites derived from omega-3 fatty acids attenuate neovascularization, Ryoji Yanai, et al, Proceedings of the National Academy of Sciences, June 2014.

    80. Omega-3 & Macular Degeneration New 2008 Study

    Last month Archives of Ophthalmology published a meta analysis on omega-3 fatty acid and fish intake and its effect on the prevention of age-related macular degeneration (AMD).

    This study identified 274 abstracts, 3 prospective cohort, 3 case-control, and 3 cross-sectional studies.

    Using quantitative methods, a high dietary intake of omega-3 fatty acids was associated with a 38% reduction in the risk of late AMD. Fish intake (2x per week) was associated with reduced risk of early and late AMD.

    More omega-3 and AMD specific studies need to be conducted to further investigate omega-3¹s effect on AMD.

    Ref: Arch Ophthalmol. 2008;126(6):826-833.

    81. Omega-3 (2009) Higher Intake Reduces Risk of Developing Macular Degeneration

    Learn more about macular degeneration treatment and information.

    A longitudinal study published in 2009 investigated whether higher omega-3 intake is associated with a lower risk of developing macular degeneration. The study investigated the progression of the condition in 1837 people over 12 years. The researchers started with "before" data based on a diet questionnaire.

    The researchers found that patients who reported the greatest omega-3 consumption were 20% less likely than their peers to develop AMD over the 12 year period.

    Researchers: John Paul SanGiovanni, Elvira Agrón, A Dhananjayan Meleth, George F Reed, Robert D Sperduto, Traci E Clemons, and Emily Y Chew, Published 2009, American Journal of Clinical Nutrition.

    82. Omega-3 and vitamin D (2007) 40% lower risk of macular degeneration
    Omega-3 & vitamin D tied to lower risk of macular degeneration

    This study reviewed the relationship between consumption of omega-3 fatty acids and omega-3 rich fish and the risk of developing age-related macular degeneration. The researchers concluded that the risk could be lowered by 40%.

    The study further supports other research finding that increasing the proportion of omega-3 to omega-6 fatty acids in the diet is important. A high proportion of omega-6 fatty acids (arachidonic acid AA) is associated with an increased risk of AMD.

    Published: Association Between Vitamin D and Age-Related Macular Degeneration in the Third National Health and Nutrition Examination Survey, 1988 Through 1994, Archives of Ophthalmology, May 125, 2007 Volume 125, Pages 671-679

    Authors: N. Parekh, R.J. Chappell, A.E. Millen, D.M. Albert, J.A. Mares

    83. Omega-3 Fatty Acid Intake Reduces Risk of Macular Degeneration 2008 Studies

    According to a meta-analysis(1) published in the June issue of Archives of Ophthalmology, a higher intake of the omega-3 fatty acids EPA and DHA reduced the risk of age-related macular degeneration (AMD). In analyzing 9 studies that included roughly 88,900 participants, the Australian authors report that higher intakes of EPA and DHA cut the risk of early AMD substantially and yielded a 38% risk reduction for advanced AMD.

    Most recently, a study published in the August issue of the American Journal of Clinical Nutrition is the first in Europeans to show a beneficial association between neovascular AMD and the consumption of oily fish (e.g. mackerel, tuna, salmon, sardines, and herring)(2). The study, funded in part by the European Commission and the Macular Disease Society UK, is consistent with results from studies in the US and Australia.

    Study Design and Methods
    The EUREYE study is a cross-sectional population-based study in persons aged 65 years or older in 7 centers located from north to south Europe. Participants in the cross-sectional population-based EUREYE study underwent fundus photography and were interviewed by using a food-frequency questionnaire. Fundus images were graded by the International Classification System for Age Related Maculopathy.

    Questionnaire data were converted to nutrient intakes with the use of food-composition tables. Survey logistic regression was used to calculate odds ratios (ORs) and 95% CIs of energy-adjusted quartiles of EPA or DHA with neovascular AMD, taking into account potential confounders.

    Results
    Dietary intake data and fundus images were available for 105 cases with neovascular AMD and for 2170 controls without any features of early or late AMD.

    Eating oily fish at least once per week compared with less than once per week was associated with a halving of the odds of neovascular AMD (OR = 0.47; 95% CI: 0.33, 0.68; P = 0.002). Compared with the lowest quartile, there was a significant trend for decreased odds with increasing quartiles of either DHA or EPA. Odds ratios in the highest quartiles were 0.32 (95% CI: 0.12, 0.87; P = 0.03) for DHA and 0.29 (95% CI: 0.11, 0.73; P = 0.02) for EPA.

    In short, habitual consumption of oily fish at least once a week was linked to a 50% reduction in the risk of developing wet AMD. Further, people who consumed at least 300 mg per day of DHA and EPA were 69% less likely to have wet AMD then those consuming less.

    84. Omega-3 Fatty Acids (2003) in Diet May Reduce Risk of Age-Related Macular Degeneration

    Learn more about macular degeneration treatment and information and dry eye syndrome information.

    Two presentations at the Association for Research in Vision and Opthalmology in 2003 suggested that omega-3 fatty acids (but not beta-carotene supplementation) is associated with less risk of age-related macular degeneration (AMD), A third presentation suggested that omega-3 fatty acids may also reduce the risk of dry eye syndrome in women.

    "Higher intake of omega n-3 long-chain polyunsaturated fatty acid (LCPUFA) and fish was associated with decreased risk of having neovascular AMD after adjusting for nutrient- and nonnutrient-based predictors and correlates of AMD," write J. P. SanGiovanni, from the National Eye Institute in Bethesda, Maryland, and colleagues.

    The Age-Related Eye Disease Study (AREDS) was a case-control study of 4,513 participants aged 60 to 80 years at enrollment. Best-corrected visual acuity was 20/32 or better in at least one eye in all subjects.

    Compared with the lowest quintile of total n-3 LCPUFA intake, the risk for neovascular AMD was significantly decreased for the highest quintile (odds ratio [OR], 0.60; 95% confidence interval [CI], 0.40 - 0.88), after statistical adjustment for all nutrient- and nonnutrient-based variables. Docosahexaenoic acid, an n-3 LCPUFA that is selectively accreted and retained in the photoreceptor outer segments, also had a protective effect (OR for highest vs. lowest quintile, 0.53; 95% CI, 0.35 - 0.79).

    Total fish consumption of more than two servings per week was associated with a decreased risk for neovascular AMD compared with no fish in the diet (OR, 0.49; 95% CI, 0.28 - 0.84). Having more than one four-ounce weekly serving of broiled or baked fish (OR, 0.64; 95% CI, 0.44 - 0.94) or tuna (OR, 0.66; 95% CI, 0.45 - 0.98) also protected against neovascular AMD.

    Bausch & Lomb, Inc. helped support this study.

    85. Omega-3 fatty acids (2007) protect against macular degeneration

    Having a greater intake of omega-3 fatty acids and fish was found to be associated with a reduced risk of advanced age-related macular degeneration (AMD) in a report published in the the Age-related macular degeneration occurs when the macula at the back of the eyes' retina deteriorates, which can lead to central vision loss.

    In a study conducted by The Age-Related Eye Disease Study Research Group, 4,519 individuals aged 60 to 80 upon enrollment completed questionnaires concerning the previous year's dietary intake and underwent retinal photography to assess the presence and stage of macular degeneration.

    While 1,115 participants were free of AMD symptoms, 2,746 were classified in intermediate stages, and 658 were found to have advanced (neovascular) age-related macular degeneration. The research team determined that a greater intake of omega-3 fatty acids, as well as fish, which is a source of the omega-3s, was associated with a reduced risk of advanced disease. When fish intake was examined, consuming more than two servings per week provided the greatest protection.

    "Dietary total omega-3 long-chain polyunsaturated fatty acid intake was inversely associated with neovascular AMD, as was docosahexaenoic acid," the authors write. "Higher fish consumption, both total and broiled/baked, was also inversely associated with neovascular AMD."

    Omega-3 fatty acids docosahexaenoic acid and eicosapentaenoic acid may protect the retina by influencing gene expression, retinal cell differentiation, and survival. Other properties of the fatty acids may also be involved, including their ability to reduce inflammation.

    Published: May, 2007 issue of the American Medical Association journal Archives of Ophthalmology.

    The authors conclude, "These results and those from other observational analytic investigations suggest that modifying diet to include more foods rich in omega-3 long-chain polyunsaturated fatty acids could result in a reduction in the risk of having neovascular age-related macular degeneration."

    86. Omega-3 Fatty Acids (2011) & Lower Risk of Macular Degeneration

    Learn more about macular degeneration recommendations.

    This long term (ten years) study reviewed the diet of nearly 40,000 women, health professionals, with an average age of 54.6 years. More than 38,000 of the participants were free of AMD, measured by incident AMD and a reduction of 20/30 or worse. 235 cases of AMD were confirmed in the ten years of follow-up. Comparing the women with the highest and lowest 30% of docosahexaenoic acid intake (an omega-3 fatty acid) the relative risk was .66 (2/3rds) lower. Women who ate 1 or more servings of fish a week, compared to those with less than one serving per month, had a risk of .58. Consumption of other omega-3 fatty acids had similar results.

    Their conclusion substantiated earlier findings that a diet that regularly including omega-3 fatty acids significantly lowered risk of age related macular degeneration in women.

    Researchers: William G. Christen, ScD; Debra A., et al.

    Published: Dietary omega-3 fatty acid and fish intake and incident age-related macular degeneration in women. Arch Ophthalmol. 2011;129(7):921-929

    87. Omega-3 Fatty Acids and Macular Degeneration (2010 study)

    New research indicates that diets rich in omega-3 fatty acids from fish and shellfish may be good for the eyes of older Americans, offering protection against age-related macular degeneration, a common cause of blindness in theU.S.

    The findings are published in the December issue of Ophthalmology, the journal of the American Academy of Ophthalmology.

    Researchers at the Wilmer Eye Institute at Johns Hopkins School of Medicine report that they’ve found that high concentrations of omega-3s in the eye’s retina may be essential for eye health.

    In another study, researcher states “Our study corroborates earlier findings that eating omega-3 rich fish and shellfish may protect against [advanced age-related macular degeneration],” researcher Sheila K. West, PhD, part of the Salisbury Eye Evaluation study, says in a news release.

    While participants in study groups averaged at least one serving of fish or shellfish a week, those who had advanced macular degeneration “were significantly less likely to consume high omega-3 fish and seafood,” she says.

    Information on the eating of fish and shellfish was examined in the study over a one-year period for 2,391 people 65 to 84 who lived along Maryland’s eastern shore.

    88. Omega-3 Fatty Acids and Macular Degeneration Prevention 2009 Study

    A group of researchers led by Dr. Chi-Chao Chan at the National Eye Institute examined the direct effect of omega-3 fatty acids on a mouse model of age-related macular degeneration. A diet with high levels of omega-3 fatty acids resulted in slower lesion progression, with improvement in some lesions. These mice had lower levels of inflammatory molecules and higher levels of anti-inflammatory molecules, which may explain this protective effect.

    The researchers suggest that “a diet enriched in EPA and DHA can reduce the progression of retinal lesions in their mouse model of age-related macular degeneration” and that “the results in these mice are in line with the epidemiological studies of age-related macular degeneration risk reduction by long chain n-3 fatty acids.” The results “further provide the scientific basis for the application of omega-3 fatty acids and their biologically active derivatives in the prevention and treatment of age-related macular degeneration.”

    Journal Reference: Tuo et al. A High Omega-3 Fatty Acid Diet Reduces Retinal Lesions in a Murine Model of Macular Degeneration. American Journal Of Pathology, 2009; DOI

    89. Omega-3 linked with Protection from Macular Degeneration
    Author: Steve Austin, N.D.

    Design:
    A. Observational prospective study -- mean follow of 5 years
    B. Observational retrospective study

    Participants:
    A. 2895 adults > 49 years of age at baseline for whom baseline food frequency questionnaire (FFQ) data were available.
    B. 681 elderly male twins of whom 222 had age-related macular degeneration (AMD) and 459 did not

    Main Outcome Measures:
    A. FFQ data were analyzed, looking for variables associated with the risk of AMD.
    B. Subjects were grouped by smoking status and by quantity and quality of dietary fat intake.

    Key Findings:
    A. Subjects in the highest quintile of omega-3 fatty acid intake had a 59% lower risk for AMD compared with those in the lowest quintile of intake (95% CI, 0.22-0.75). Those eating fish ? once per week had a 42% reduction in risk compared with those with a minimal fish intake (95% CI, 0.37-0.90). Those consuming fish > three times per week had a 75% reduced risk (95% CI, 0.06-1.00).
    B. After multivariate analysis, those consuming fish > twice per week had a statistically significant 37% reduction in risk compared with those consuming less than one serving per week. Those with a median intake of 350 mg of omega-3 oil (the top quartile of intake) had an adjusted 45% lower risk of AMD compared with those consuming only 60 mg/day (the lowest quintile of intake, p=0.02). The protection associated with EPA/DHA intake occurred primarily in those consuming relatively low levels of linoleic acid (adjusted odds ratio of 0.23, p<0.001). Current smokers had almost twice the risk for AMD compared with those who never smoked (p=0.06).

    Practice Implications:
    Allopathic treatment for AMD is relatively ineffective for most patients. Until now, most of the emphasis in prevention and treatment in the realm of natural medicine has focused on the use of lutein and zinc, though a small body of evidence suggested fish consumption might reduce the risk of AMD (Arch Ophthalmol 2000;118:401-4). Both new studies confirm a strong and consistent inverse correlation between EPA, DHA, and fish consumption and AMD.

    The study by Chua and colleagues also tracked alpha-linolenic acid (ALA) intake -- the vegetarian omega-3 oil that partially bioconverts to EPA. In terms of 5-year risk for early AMD, ALA showed the same protective effect, as did EPA/DHA. However, though this difference was not statistically significant, for late AMD, those in the lowest quintile of ALA intake had a lower risk than those consuming more ALA. Until more is known, therefore, there is little reason to assume ALA has the same protective effect that EPA and DHA appear to have.

    Chua's findings regarding associations between total fat, monounsaturated fatty acids, trans fatty acids, polyunsaturated fatty acids [PUFA], and saturated fatty acids, and AMD risk conflict with previously published research (Arch Ophthalmol 2003;12:1728-37). Therefore, we don't know enough about the possible effects of these variables to alter clinical practice.

    Findings from the study by Seddon and colleagues, suggest that cessation from smoking combined with a modest increase in fish or omega-3 fatty acid intake would literally cut the risk for AMD in half. Implementing appropriate changes could save vision in many elderly people. But what sense do these findings make?

    Experimental reports show that DHA protects against retinal oxidative damage. Also, an inflammatory component to AMD has been reported, and EPA and DHA have known antiinflammatory actions. That said, for the most part we still do not understand how EPA and DHA protect against AMD.

    Despite a lack of understanding, encouraging patients to increase intake of fatty fish makes sense. After considering the favorable risk-to-benefit ratio, an argument can also be made for discussing supplementation of EPA/DHA with AMD patients. Optimal dosing remains unclear, but even a few hundred milligrams per day of EPA plus DHA would reach well into the dietary intake reported by those experiencing a protective effect.

    References:
    A. Chua B, Flood V, Rochtchina E, et al. Dietary fatty acids and the 5-year incidence of age-related maculopathy. Arch Ophthalmol 2006;124:981-6.
    B. Seddon JM, George S, Rosner B. Cigarette smoking, fish consumption, omega-3 fatty acid intake, and associations with age-related macular degeneration. Arch Ophthalmol 2006;124:995-1001.

    90. Oral DHA in the Prevention of Exudative AMD: The Nutritional AMD Treatment 2 Study

    This randomize, double-blind study valuated the efficacy of docosahexaenoic acid (DHA)-enriched oral supplementation in preventing exudative age-related macular degeneration (AMD). The study participants were between the ages of 55 – 85 years of age with early lesions of age-related maculopathy and neovasularization. The patients received 840mg/day of DHA and 270 mg/day of EPA (eicosapentaenoic acid), or the placebo from olive oil capsules for 3 years.

    The study results showed that choroidal neovascularization (CNV_ incidence was significantly reduced in DHA-supplemented patients showing a steadily high EPA plus DHA index over three years.

    SOURCE: Souied EH, Delcourt C, Querques G, et al. Oral docosahexaenoic acid in the prevention of exudative age-related macular degeneration: The Nutritional AMD Treatment 2 Study. Ophthalmology. 2013; Feb 7.

    91. Plasma homocysteine [2005] and total thiol content in patients with exudative age-related macular degeneration.

    Learn more about macular degeneration

    The study's purpose was to look at the role of plasma Hcys and thiol content (tSH) as a risk factor for the development of exudative ARMD.

    Sixteen patients with exudative ARMD and 20 age-matched controls had their plasma Hcys levels analysed using a liquid chromotography method. Glutathione (GSH) content was determined using a fluorimeter. Plasma tSH levels were determined spectrophotometrically.

    Plasma Hcys levels in exudative ARMD were 3 times higher compared to healthy patients and the patients with AMD had half the GSH and tSH.

    Researchers: Coral K, Raman R, Rathi S, Rajesh M, Sulochana KN, Angayarkanni N, Paul PG, Ramakrishnan S., 1Biochemistry Research Department, Vision Research Foundation, Sankara Nethralaya, Chennai, India.

    Published: 1 April 2005; doi:10.1038/sj.eye.6701853

    92. Polyunstaturated Fats (2009) High in Diet Increase Risk of Macular Degeneration

    Learn more about macular degeneration treatment and information.

    Less polyunsaturated fat in one's diet may help protect against age-related macular degeneration (AMD), according to results of the Carotenoids in Age-Related Eye Disease Study.

    The investigators tracked nearly 2,000 women aged 50-79 as part of the larger Women's Health Initiative Observational Study. Via questionnaires and retinal photography, they concluded that women who consumed the highest levels of dietary polyunsaturated fats were about two times as likely to develop AMD compared to those women who consumed the least. Mono-unsatured fatty acids were associated with a lower risk of AMD.

    Reference: Arch Ophthalmol. 2009 Nov;127(11):1483-93.

    Editor's Note: The types of fats in one's diet play a major role in eye and overall body health. Avoid polyunsaturated oils such as vegetables oils (do not cook with these oils). Use high quality olive oil in your diet on your salads and food such as adding it to your steamed vegetables (with a little basalmic vinegar or lemon - delicious).

    93. Poor Circulation and Aged Related Macular Degeneration Study 2009
    A large study found strong evidence that older people who have age-related macular degeneration (AMD) are at increased risk for coronary heart disease (CHD), although not for stroke. This result adds to mounting evidence that AMD and cardiovascular disease may share some risk factors–smoking, High Blood Pressure, inflammatory indicators such as C-reactive protein, genetic variants such as complement factor H–and disease mechanisms. The Cardiovascular Health Study (CHS) followed 1,786 white or African American participants, who were free of CHD or stroke at the study’s outset, for about seven years. The CHS received funding from the National Heart, Lung and Blood Institute, a division of the National Institutes of Health. The incidence of CHD was 25.76 percent in patients with AMD, compared with 18.9 percent in those without AMD. The association between AMD and CHD was somewhat stronger in people age 69 to 78 than age 79 and up. Data were adjusted to counter potentially confounding factors like hypertension, diabetes, and smoking.

    94. Pro-vitamin A and E
    There was an inverse relationship between dietary pro-vitamin A carotenoid and vitamin E consumption and the incidence of large macular drusen, and between zinc and the incidence of pigmentary abnormalities. Am J Epidemiol 1998 Jul 15;148(2):204-14

    95. Refined Carbohydrates Diet (2006), Cataracts and Macular Degeneration

    Learn more about macular degeneration treatment and information and cataracts information.

    Since the mid 1990s Research have been indicating that diets high in the complete vitamins, minerals and antioxidant nutrients lower the risk of degenerative eye diseases. Studies additionally suggest an association between consumption of high glycemic carbohydrate foods, cataracts and macular degeneration.

    April 2006 Journal of Clinical Nutrition Study

    526 participants without a previous macular degeneration diagnosis were included. Long-term dietary information was based on data from an average of 4 food-frequency questionnaires collected over a 10-year period before the assessment of ARMD. Dietary glycemic index (GI), a measure of carbohydrate intake quality, was related to ARMD (specifically to retinal pigmentary abnormalities), whereas total carbohydrate intake was not.

    May 2006 Journal of Clinical Nutrition Study

    A food-frequency questionnaire was used to obtain dietary information from 3377 participants in the Age-Related Eye Disease Study (AREDS) focusing on glycemic index and the presence of cortical or nuclear opacities (symptomatic of cataracts). It was found that the patients with the highest dietary intake of high glycemic foods had the highest prevalence opacities. This study was one of a few studies reporting this association in non-diabetic persons and it was the first study that has indicated a solid relationship between dietary GI and the risk of cataracts.

    Published:

    • Dietary glycemic index and carbohydrate in relation to early age-related macular degeneration. Chiu J, Hubbard L, Armstrong J, et al. American Journal of Clinical Nutrition. 2006 Apr;83(4):880-6
    • Dietary carbohydrate intake and glycemic index in relation to cortical and nuclear lens opacities in the Age-Related Eye Disease Study Chiu J, Milton R, et al. American Journal of Clinical Nutrition. 2006 May;83(5):1177-84.

    96. Resveratrol (2005) reduces oxidation and proliferation of human retinal pigment epithelial cells via extracellular signal-regulated kinase inhibition.

    Learn more about macular degeneration recommendations

    Researchers have found that moderate wine drinking and antioxidant-rich diets may decrease risk of age-related macular degeneration. Development of this and other retinal conditions, such as proliferative vitreoretinopathy (PVR), is associated with oxidative stress in the retinal pigment epithelium (RPE), where the health of the retina is maintained by providing structural and nutritional support.

    The researchers indicate that resveratrol, a red wine polyphenol, may be responsible, in part, for these health benefits. To test this hypothesis, the antioxidant and antiproliferative effects of resveratrol were examined in a human RPE cell line (designated ARPE-19). The results suggest that resveratrol can reduce oxidative stress and hyperproliferation of the RPE.

    Published:Chem Biol Interact. 2005 Jan 15;151(2):143-9. King RE, Kent KD, Bomser JA.

    Researchers: Department of Food Science and Technology, Ohio State University, Columbus, OH

    97. Smoking (1994) and carotenoids

    Learn more about macular degeneration risk factors and recommendations

    Smokers with early macular degeneration who consumed the lowest amounts of carotenoids were nearly 6 times as likely to develop advanced macular degeneration than those consuming the highest amounts.

    Published: Seddon, et al. J. Amer Med Assoc; 1994

    98. Statin Drugs and Macular Degeneration (2006)

    Contrary to the expectations of some scientists, cholesterol-lowering 'statin' drugs (such as Lipitor or Zocor) do not appear to stave off age-related macular degeneration (AMD) in the eye. In fact, a review of data from the Cardiovascular Health Study suggests that taking a statin may slightly increase the risk of age-related macular degeneration.

    SOURCE: Archives of Ophthalmology, January 2006.

    Learn more about macular degeneration recommendations and about other drugs that harm the eyes.

    99. Statins May Increase Chances of Getting Macular Degeneration
    January 13th 2006

    Recent recommendations for the aggressive use of medications to lower low-density lipoprotein (LDL) cholesterol levels has contributed to a rising trend in the use of statin drugs. A study published in the January 2006 Archives of Ophthalmology evaluates the use of these drugs, specifically with regard to the risk of age-related macular degeneration (AMD).

    The investigators collected data from the Cardiovascular Health Study, a population-based prospective study, to address the relationship between the use of statins and other cholesterol-lowering medications and AMD. Fundus photographs were taken in 1997 and 1998 on 4249 statin users and non-statin users in the study. 2755 of these participants were available to be classified as cases (AMD) or controls (no AMD).

    The results of this study suggests no association exists between cholesterol-lowering medications and AMD progression. However, there was a suggestion that statin use might increase the risk of developing AMD. These findings are corroborated in several similar studies, including the first National Health Examination and Nutrition Survey. This evidence may seem a bit contrary to some and more than disappointing to the pharmaceutical companies who are now using the popular atherosclerotic-like theory of AMD to justify detailing statin drugs as AMD medications in ophthalmic offices.

    The Doctors Klein (Beaver Dam Study) recently proposed the idea that high LDL levels and low HDL levels may actually offer protection from AMD by down-regulating LDL receptors in the Retinal Pigment Epithelium (RPE), thereby reducing the contribution of cholesterol to drusen. This line of reasoning implies that by lowering serum cholesterol levels with statins; an increased amount of cholesterol may be taken up by the RPE cells with a subsequent increased deposition in drusen and an increased risk of AMD.

    References:

    3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitors and the Presence of Age-Related Macular Degeneration in the Cardiovascular Health Study. McGwin G, Kayvon M, et al. Arch Ophthalmol. January 2006;124(1):33-37 [abstract not yet catalogued in the National Library of Medicine]

    A case control study of age related macular degeneration and use of statins. Smeeth L, Cook C, et al. Br J Ophthalmol. 2005 Sep;89(9):1171-5 [abstract]

    The association of cardiovascular disease with the long-term incidence of age-related maculopathy: the Beaver Dam eye study. Kelin R, Klein BE, et al. Ophthalmology. 2003 Apr;110(4):636-43 [abstract]

    The Use of Cholesterol-lowering medications and Age-related macular degeneration McGwin Jr G, Xie A, et al. Ophthalmology 2005;112:488-494 [abstract]

    Cholesterol lowering drugs and risk of age related maculopathy: prospective cohort study with cumulative exposure measurement. van Leeuwen R, Vingerling JR, Hofman A, et al. BMJ 2003;326:255-256 [abstract]

    Relation of statin use to the 5-year incidence and progression of age-related maculopathy. Klein R, Klein BE, et al. Arch Ophthalmol. 2003 Aug;121(8):1151-5 [abstract]

    100. Stem Cell Transplants Show Some Success in Restoring Vision
    Could an out-patient surgical procedure for cure of age-related macular degeneration (AMD) with stem cells transfer become commonplace in the next decade?

    During a recent visit to discuss the possibility of conducting human trials of retinal stem cell transplants in India, Professor Pete Coffey, from University College London (UCL) Institute of Ophthalmology, London, United Kingdom; reportedly told the Times of India:

    "… some cases, the transplants were so successful that the patients were able to read, cycle and use a computer. By 2011, we will make it a 45-minute out patient operation."

    Professor Pete Coffey and his colleagues at the UCL Institute of Ophthalmology in London, UK, have previously written:

    • "Retinal pigment epithelial (RPE) transplantation aims to restore the subretinal anatomy and re-establish the critical interaction between the RPE and the photoreceptor, which is fundamental to sight."1
    • "Diseases that have been treated with RPE transplantation demonstrating partial reversal of vision loss include primary RPE dystrophies … photoreceptor dystrophies as well as complex retinal diseases such as atrophic and neovascular age-related macular degeneration (AMD).
    • "Unfortunately, in the human trials the visual recovery has been limited at best and full visual recovery has not been demonstrated."
    • "Autologous full-thickness transplants have been used most commonly and effectively in human disease but the search for a cell source to replace autologous RPE such as embryonic stem cells, marrow-derived stem cells, umbilical cord-derived cells as well as immortalised cell lines continues."

    Reference: da Cruz L, Chen FK, Ahmado A, Greenwood J, Coffey P. : RPE transplantation and its role in retinal disease. Prog Retin Eye Res. 2007 Nov;26(6):598-635.

    101. Sternberg P. Treating Age-Related Macular Degeneration (1988)
    Macular degeneration patients have 58 percent less glutathione than people without the disease. Sternberg, P. Treating Age-Related Macular Degeneration . Presented at Science Writers Seminar in Ophthalmology: Research to Prevent Blindness. 1988.
    Editor’s Note: Glutathione protects retinal cells from light damage caused by ultraviolet and blue light sunlight.

    102. Supplements (2003) AMD Outcomes - Lifestyle, Supplement May Improve Outcomes in AMD
    Research indicates changes in lifestyle, including having a lower body mass index, exercising and taking a dietary supplement, may reduce the risk and/or the severity of age-related macular degeneration (AMD), which affects 30% of people 75 years or older. A study of 261 patients age 60 or older with signs of non-advanced AMD, published in the Archives of Ophthalmology (2003;121[6]:785-792).

    Patients were followed for an average of 4.6 years, and their height, weight and blood pressure were measured annually. The data indicated that study participants with a high body mass index (BMI >25) were more than twice as likely to have their AMD worsen than were those with lower weight. Patients who exercised vigorously at least three times a week had a 25% reduction in the risk that the severity of the disease would increase.

    103. Supplements (2007) Improve Visual Acuity in Subjects with Dry Macular 2007

    Learn more about macular degeneration treatment and information.

    Combined Supplements Improve Visual Acuity in Subjects with Dry Macular Degeneration

    This was a controlled, double blind (though not randomized) intervention trial. The subjects included 37 adults with age-related macular degeneration (AMD). The control was similar patients from a previous report matched for inclusion and exclusion conditions.

    Study Medication and Dosage: The patients received retinol (10,000 IU/d), beta-carotene (28,640 IU/d), vitamin C (452 mg/d), vitamin E (200 IU/d), zinc (56 mg/d), copper (1.6 mg/d), taurine (400 mg), EPA (180 mg/d), DHA (120 mg/d), lutein (8 mg/d), and zeaxanthin 400 mcg/d). The control subjects had also received vitamin C (400 mg/d), vitamin E (200 IU), zinc (40 mg), and beta-carotene (300 IU/d), but none of the other supplements.

    Changes from the start of the study period in visual function were measured using a variety of standard research tools (e.g., Best-Corrected Visual Acuity (BCVA) via the Early Treatment Diabetic Retinopathy Study (ETDRS) chart, contrast sensitivity, and retinal imaging).

    77% of the subjects receiving the full complement of supplements demonstrated stabilization or improvement at 6-months. These same subjects saw small improvements in visual acuity that achieved statistical significance (p<0.05). As expected, mean visual acuity declined in the control group.

    Conventional medicine has little to offer many patients with this common eye condition. Progressive deterioration is the norm, though the rate of deterioration can vary significantly. Dry AMD is the most common form. Previous research has suggested the possibility that a wide variety of nutritional supplements help patients with AMD, such as lutein, fish oil, zinc, antioxidants, or some combination thereof. This trial combines most of these supplements at easily attainable dose levels. The outcome--a halting of progression and the beginnings of a reversal--give healthcare practitioners a potential treatment plan from which to get started.

    Interestingly, a standard control group was not part of the trial design not due to the cost, but rather because the independent review board determined that evidence supporting nutritional supplementation is now so strong that the standard of care demands some nutritional supplementation.

    Published: Cangemi FE. TOZAL study: an open case control study of an oral antioxidant and omega-3 supplement for dry AMD. BMC Ophthalmol 2007;7:3-12.

    Author: Steve Austin, N.D.

    104. Taurine - As it affects Rhodopsin Regeneration and the Protection of the Macular Pigment Epithelium
    Taurine is a sulfur-containing amino acid found naturally in egg whites, meat, fish and milk. High concentrations are found in the heart muscle, white blood cells, skeletal muscle and central nervous system.

    In the retina there are two binding proteins specific to taurine. And, intracellular concentrations are higher in the retina than in any other region derived from the central nervous system (1, 2, 3, 4).

    Taurine plays a role in the process of rhodopsin regeneration necessary for night vision. (5) It is essential to the retinal pigment epithelium and the photoreceptors ( cells that we see with) (6) where it is found at levels ten times higher than other free amino acids (7)! Taurine helps protect cell membranes from oxidative attack. It helps transport nutrients across cell membranes, acts as a catalyst to retinal cells that remove cellular debris (8) and assists in the elimination of potentially toxic substances. Taurine in combination with retinol protects lipids twice as much as retinol alone. Taurine protects rod outer segment lipids during exposure to cyclic light. (9) 1. Kennedy AJ et al, Journal of Neurochemistry 1974; 23:1093. 2. Orr HT et al, Journal of Neurochemistry 1976; 26:606. 3. Lopez-Colome AM et al, Journal of Neurochemistry 1980; 34:1047. 4. Lombardi JB, Society for Neuroscience 1981; 7:321. 5. Petrosian AM, Haroutounian JE, Adv Exp Med Biol 1998;442:407-13. 6. Hayes KC et al, Science 1975; 188:949. 7. Wright CE et al, Annual Review of Biochemistry 1986; 55:427. 8. American Biologics, Research Institute, Mexico; Tijuana, B.C. Mexico, 1991. 9. Keys SA, Zimmerman AWF, Exp Eye Res, 1999 Jun;68(6):693-702. Tallan HH et al, Life Sciences 1983; 33:1853.

    105. Taurine (1998) Deficiency

    Learn more about macular degeneration treatment and information.

    Deficiency of taurine, an amino acid, has been shown to lead to retinal degeneration and supplementing it has been used with some success to prevent, treat and stabilize retinal changes. Altern Med Rev 1998 Apr;3(2):128-36. Oftalmol Zh 1989;(8):463-5 Brain Res Brain Res Rev 1991 May-Aug;16(2):151-69 J Neurosci Res 1987;18(4):602-14 .

    106. Vitamin B Trio Effective Against AMD
    Women's Antioxidant & Folic Acid Study

    Results from the vision component of the Women's Antioxidant and Folic Acid Cardiovascular Study, also known as WACS, were presented at the ARVO 2007 Annual Meeting. Researchers from the Brigham and Women's Hospital and the National Eye Institute concluded that the data from this randomized trial indicate that supplementation with folic acid, vitamins B6 and B12 reduced the risk of AMD in women with cardiovascular disease (CVD) (1).

    These three B-vitamins, particularly folic acid, have been shown to reduce high levels of the naturally occurring compound, homocysteine. Research has implicated elevated plasma levels of homocysteine in the development of vascular diseases including choroidal neovascularization in exudative AMD.

    Christen WG, et al. Folic acid plus B-vitamins and age-related macular degeneration in a randomized trial in women. Invest Ophthalmol Vis Sci 48:E-abstract 1152, ARVO, 2007.

    107. Vitamin B, folic acid (2009) - lower risk of eye disease

    Learn more about macular degeneration recommendations

    In the first rigorous trial to show a benefit against macular degeneration from the supplements folic acid and 2 B-vitamins. Researchers found that women who took the combination for several years had a significantly lower chance of developing the condition.

    Women who took a combination of folic acid and vitamins B6 and B12 had a 35 percent to 40 percent lower risk of developing age-related macular degeneration compared to a matched control group of women who took a placebo.

    Researchers: William G. Christen, ScD; Robert J. Glynn, ScD; Emily Y. Chew, MD; Christine M. Albert, MD; JoAnn E. Manson, MD., Brigham and Women's Hospital and Harvard Medical School

    Published: Archives of Internal Medicine. 2009;169(4):335-341.

    108. Vitamin B6 deficiency (1991)
    Patients with confluent soft drusen, or "pre-wet" ARMD, were found to have evidence of vitamin B6 deficiency. B. Lane, Ann Mtg Amer Coll of Nutrition, 1991.

    109. Vitamin D and Reduced Risk of Macular Degeneration: 2011 Study

    Consuming vitamin D from foods or supplements might reduce the risk of developing age-related macular degeneration (AMD) in women younger than 75, according to a study published this week by the Archives of Ophthalmology.

    A team led by researchers at the University at Buffalo, N.Y., examined data on blood levels of vitamin D among 1,313 women 50 to 79 enrolled in the ongoing Women's Health Initiative study. In women younger than 75, vitamin D from foods and supplements (but not from time spent in direct sunlight) was linked with decreased risk of developing early age-related macular degeneration. Those who consumed the most vitamin D had a 59 percent decreased risk of developing it compared with women who consumed the least.

    Ref: Vitamin D and Macular Degeneration Arch Ophthalmol. Amy E. Millen, PhD; Rick Voland, PhD; Sherie A. Sondel, MS; Niyati Parekh, PhD; Ronald L. Horst, PhD; Robert B. Wallace, MD; Gregory S. Hageman, PhD; Rick Chappell, PhD; Barbara A. Blodi, MD; Michael L. Klein, MD; Karen M. Gehrs, MD; Gloria E. Sarto.

    110. Vitamin D3 (2007) low levels tied to macular degeneration

    Learn more about macular degeneration recommendations.

    Researchers have found that low levels of vitamin D3 in the body are connected to an increase in the presence of macular degeneration. The researchers assessed consumption of milk, fish, and vitamin D supplements. Patients who consumed less milk had more risk of early macular degeneration. Patient who consumed less fish had more risk of advanced macular degeneration. Patients who did not drink milk but who took vitamin D supplements had less risk of early macular degeneration.

    The researchers concluded that vitamin D likely helps prevent against macular degeneration but that more investigation is needed to verify these results.

    Researchers: Parekh N, Chappell RJ, Millen AE, Albert DM, Mares JA.

    Published: Association Between Vitamin D and Age-Related Macular Degeneration in the Third National Health and Nutrition Examination Survey, 1988 Through 1994. Arch Ophthalmol. May 2007;125: 661-669.

    111. Vitamins A, C, and E (1994) -Macular Degeneration

    Learn more about macular degeneration treatment and information. Also see information on food sources for dietary nutrients.

    Rsearchers found that the carotenoids found in diet: vitamins A, C, and E had a positive impact on advanced age-related macular degeneration.

    A study on the normal diet habits on patients with age-related macular degeneration (AMD) found that those who ate foods with the highest amounts of carotenoids, (ie, lutein and zeaxanthin), had a 43% lower risk of age-related macular degeneration than those who took the least amounts.

    Researchers: Johanna M. Seddon, Umed A. Ajani, Robert D. Sperduto, Rita Hiller, Norman Blair, Thomas C. Burton, Marilyn D. Farber, Evangelos S. Gragoudas, Julia Haller, Dayton T. Miller, Lawrence A. Yannuzzi, Walter Willet: for the Eye Disease Case-Control Study Group.

    Published: JAMA (The Journal of the American Medical Association) 272: 1413-1420 (1994).

    112. Zeaxanthin & Lutein (2003) Can Significantly Reduce the Chances of Getting AMD (2003)

    Learn more about macular degeneration.

    Researchers reported a 50% reduced risk of developing macular degeneration in subjects with high levels of zeaxanthin in blood plasma zeaxanthin compared with subjects with low levels (<0.03ì). The results were even more profound for the highest 1/5th of the study group, which had much higher levels of the nutrients due to their Mediterranean population customary diet. These results were true after adjustment for age and various other risk factors.

    Published: Invest Ophtalmol Vis Sci 2003;44:2461-2465, C. Gale, Nigel F. Hall, David Phillips and C. Martins. From the Medical Research Council Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, UK.

    113. Zeaxanthin (2010) Helps Visual Acuity in Macular Degeneration

    Learn more about macular degeneration recommendations.

    Study shows supplementing with zeaxanthin (a carotenoid in the lutein family) can raises macula pigment optical density (MP) and has unique visual benefits for patients with atrophic early AMD having visual symptoms.

    Reference: The Zeaxanthin and Visual Function Study in Atrophic Age Related Macular Degeneration (ZVF-FDA IND #78,973) - MP and Foveal Shape Discrimination: S.P. Richer1, W. Stiles1, M. Lavin, K. Graham1, C. Thomas1, D. Park3. J. Nyland1, J Wrobel

    Presented at the Association for Research in Vision and Ophthalmology (ARVO) Annual Meeting, May 2-6, 2010 (Ft. Lauderdale, FL)

    114. Zeaxanthin (2011) and macular degeneration

    Learn more about macular degeneration treatment and information and about food sources for zeaxanthin.

    .

    A 2011 study confirms that vision is improved in the elderly with early macular degeneration by adding Zeaxanthin as a nutritional supplement. Zeaxanthin is a a carotenoid.

    The Zeaxanthin and Visual Function Study (ZVF), demonstrates that dietary Zeaxanthin improved vision, including improvement in night blindness and seeing fine detail.

    The one year study involved elderly veterans who were given 8mg of Zeaxanthin daily. The researcher found improvement in the ability to drive at night, and an average improvement of 1.5 lines or 8.5 letters on an eye chart, and the disappearance of blind spots.

    Some of the people were additionally given 9 mg of lutein daily.

    Zeaxanthin and lutein are two carotenoids (part of a family of antioxidants that give fruits and vegetables their color) found in the retina and macula of the eye. Zeaxanthin protects the cones, or photoreceptors responsible for central vision, color perception, and fine detail.

    Since the average daily diet in the U.S. does not include enough fresh fruits and vegetables, it is difficult, particularly for the elderly, to maintain healthy macular pigment levels to protect their vision.

    Published: November 2011 Journal of Optometry, by researcher Stuart Richer, PhD, OD at the Veterans Administration Hospital in Chicago.

    115. Zeaxanthin Can Reduce Chances of AMD 79% (2006 study)
    A recent study conducted by the Ocular Pathologies Associated with Age group (POLA in French) was reported in an article published in the Investigative Ophthalmology and Visual Science June 2006 issue reports finding a particularly strong inverse association between plasma zeaxanthin and AMD: Subjects with high levels of plasma zeaxanthin had a 93% reduced risk of AMD. Globally, subjects with high total plasma lutein and zeaxanthin had a 79% reduced risks of AMD compared with subjects with low total plasma lutein and zeaxanthin.

    IOVS, June 2006, Vol. 47, No. 6
    Plasma Lutein and Zeaxanthin and Other Carotenoids as Modifiable Risk factors for Age Related Maculopathy and Cataract: the POLA study Cecile Delcourt, Isabelle Carriere, Martine Delage, Pascale Barberger-Gateau, Wolfgang Schalch and the POLA Study Group

    Epidemiological data on the association of xanthophylls and the risk of Age Related Macular Degeneration (AMD) and cataract remain scarce, and are partly inconsistent. Also, until recently, most studies assessed the association of AMD or cataract with the combined plasma concentration of lutein and zeaxanthin, thereby limiting the chances of finding specific associations of lutein or zeaxanthin with these diseases. This study separately assessed these associations in a Mediterranean population study.

    The researchers found that plasma lutein and zeaxanthin showed a strong inverse association with AMD, and that the association with plasma zeaxanthin was particularly strong. Compared with subjects that had low levels of zeaxanthin (<0.04 ìM), subjects with high levels of plasma zeaxanthin (>0.9ìM) had a 93% reduced risk of AMD. Globally, subjects with high total plasma lutein and zeaxanthin (>0.56ìM) had a 79% reduced risks of AMD compared with subjects with low total plasma lutein and zeaxanthin (<0.25ìM).

    With respect to cataract, after adjustment for age and gender, only plasma zeaxanthin showed a strong inverse association with nuclear cataract. Compared with subjects with low plasma zeaxanthin (<0.04ì), those with high plasma zeaxanthin (>0.9ìM) had a 75% decrease risk of nuclear cataract. The other types of cataract did not show any significant association with plasma zeaxanthin. Similarly, subjects with high plasma dehydro-lutein had a significant (66%) reduced risk of nuclear cataract. By contrast plasma lutein was not significantly associated with any type of cataract.

    The results of this study are consistent with those of a recent cross sectional study performed in the United Kingdom. The authors reported a significant (50%) reduced risk of early or late AMD in subjects with high plasma zeaxanthin (>0.05ìM), compared with subjects with low levels (<0.03ì). The associations in this study were even stronger, perhaps because of the higher values in the highest quintile of zeaxanthin and lutein in this Mediterranean population, probably associated with higher dietary intakes of these xanthophylls.

    Previous studies may have obscured the association with cataract, if only zeaxanthin is associated with cataract, by given results for pooled lutein and zeaxanthin.

    The hypothesis of a more important role of zeaxanthin in retina and lens health is supported by several lines of evidence. First, the ratio of zeaxanthin to lutein is much higher in the central retina (1:1 in the macula, 2:1 in the fovea) and in the lens (1:1) than it is in the plasma (~1-5) suggesting that the eye preferentially accumulates zeaxanthin. Moreover, although both lutein and zeaxanthin protect liposomal membranes from light inductive oxidative stress, zeaxanthin appears to be a better photoprotector during prolonged UV exposure, perhaps because there is a different orientation of lutein and zeaxanthin in the biological membranes. Zeaxanthin is also particularly effective in protecting lipid membranes against oxidation by peroxyl radicals.

    116. Zinc deficiency (1996)
    Zinc deficiency can lead to loss of eye function as several zinc-dependent enzymes play important roles in eye function. Levels of these enzymes decline with age. Zinc deficiency may contribute to macular degeneration of the central part of the retina. Results from the Beaver Dam Eye Study, published in 1996, suggest a link between low zinc intakes and risk of macular degeneration. Mares Perlman JA; Klein R; Klein BE; Greger JL; Brady WE; Palta M; Ritter LL. Association of zinc and antioxidant nutrients with age-related maculopathy. Arch Ophthalmol, 1996 Aug, 114:8, 991-7

    117. Zinc supplements (1988)
    Zinc supplements have been used to treat age-related macular degeneration, the leading cause of lack of vision in people aged over 55.In one double-blind study, researchers at Louisiana State University found that patients receiving zinc supplements had significantly less vision-loss than those not taking zinc. Newsome D A et al. Oral zinc in macular degeneration. Arch Opthalmol. 1988;106:192-198

    118. Zinc, Vitamin E (1997) and Macular Degeneration

    Learn more about macular degeneration recommendations.

    Low levels of zinc and vitamin E in blood serum levels may be connected with the development of age-related macular degeneration.

    Published: Ishihara, et al. Nippon Ganka Gakkai Zasshi 1997 Mar;101(3):248-51


    Male Infertility

    1. Male Infertility Research Bibliography

    See the discussion of recommendations for male infertility. The bibliography below are the sources for that discussion.

    1. Goverde HJM, Dekker HS, Janssen HJG, et al. Semen quality and frequency of smoking and alcohol consumption - an explorative study. Int J Fertil 1995;40:135–8.
    2. Abell A, Ernst E, Bonde JP. High sperm density among members of organic farmers’ association. Lancet 1994;343:1498.
    3. Hruska KS, Furth PA, Seifer DB, et al. Environmental factors in infertility. Clin Obstet Gynecol 2000;43:821–9.
    4. Wang SL, Wang XR, Chia SE, et al. A study on occupational exposure to petrochemicals and smoking on seminal quality. J Androl 2001;22:73–8.
    5. Zhang JP, Meng QY, Wang Q, et al. Effect of smoking on semen quality of infertile men in Shandong, China. Asian J Androl 2000;2:143–6.
    6. Fraga CG, Motchnik PA, Shigenaga MK, et al. Ascorbic acid protects against endogenous oxidative DNA damage in human sperm. Proc Natl Acad Sci 1991;88:11003–6.
    7. Dawson EB, Harris WA, Teter MC, Powell LC. Effect of ascorbic acid supplementation on the sperm quality of smokers. Fertil Steril 1992;58:1034–9.
    8. Dawson EB, Harris WA, McGanity WJ. Effect of ascorbic acid on sperm fertility. Fed Proc 1983;42:531 [abstr 31403].
    9. Dawson EB, Harris WA, Powell LC. Relationship between ascorbic acid and male fertility. In: Aspects of Some Vitamins, Minerals and Enzymes in Health and Disease, ed. GH Bourne. World Rev Nutr Diet 1990;62:1–26 [review].
    10. Dawson EB, Harris WA, Rankin WE, et al. Effect of ascorbic acid on male fertility. Ann N Y Acad Sci 1987;498:312–23.
    11. Rolf C, Cooper TG, Yeung CH, Nieschlag E. Antioxidant treatment of patients with asthenozoospermia or moderate oligoasthenozoospermia with high-dose vitamin C and vitamin E: a randomized, placebo-controlled, double-blind study. Hum Reprod 1999;14:1028–33.
    12. Prasad AS, Cossack ZT. Zinc supplementation and growth in sickle cell disease. Ann Intern Med 1984;100:367–71.
    13. Kvist U, Kjellberg S, Bjorndahl L, et al. Seminal fluid from men with agenesis of the Wolffian ducts: zinc-binding properties and effects on sperm chromatin stability. Int J Androl 1990;13:245–52.
    14. Saaranen M, Suistomaa U, Kantola M, et al. Lead, magnesium, selenium and zinc in human seminal fluid: comparison with semen parameters and fertility. Hum Reprod 1987;2:475–9.
    15. Danscher G, Hammen R, Fjerdingstad E, Rebbe H. Zinc content of human ejaculate and motility of sperm cells. Int J Androl 1978;1:576–81.
    16. Carpino A, Siciliano L, Petroni MF, et al. Low seminal zinc bound to high molecular weight proteins in asthenozoospermic patients: evidence of increased sperm zinc content in oligoasthenozoospermic patients. Hum Reprod 1998;13:111–4.
    17. Stankovic H, Mikac-Devic D. Zinc and copper in human semen. Clin Chim Acta 1976;70:123–6.
    18. Hartoma TR, Nahoul K, Netter A. Zinc, plasma androgens and male sterility. Lancet 1977;2:1125–6.
    19. Stankovic H, Mikac-Devic D. Zinc and copper in human semen. Clin Chim Acta 1976;70:123–6.
    20. Kynaston HG, Lewis-Jones DI, Lynch RV, Desmond AD. Changes in seminal quality following oral zinc therapy. Andrologia 1988;20:21–2.
    21. Tikkiwal M, Ajmera RL, Mathur NK. Effect of zinc administration on seminal zinc and fertility of oligospermic males. Indian J Physiol Pharmacol 1987;31:30–4.
    22. Marmar JL, Katz S, Praiss DE, DeBenedictis TJ. Semen zinc levels in infertile and postvasectomy patients and patients with prostatitis. Fertil Steril 1975:26:1057–63.
    23. Omu AE, Dashti H, Al-Othman S. Treatment of asthenozoospermia with zinc sulphate: andrological, immunological and obstetric outcome. Eur J Obstet Gynecol Reprod Biol 1998;79:179–84.
    24. De Aloysio D, Mantuano R, Mauloni M, Nicoletti G. The clinical use of arginine aspartate in male infertility. Acta Eur Fertil 1982;13:133–67.
    25. Tanimura J. Studies on arginine in human semen. Part II. The effects of medication with L-arginine-HCl on male infertility. Bull Osaka Med School 1967;13:84–9.
    26. Scibona M, Meschini P, Capparelli S, et al. L-arginine and male infertility. Minerva Urol Nefrol 1994;46:251–3.
    27. Schacter A, Goldman JA, Zukerman Z. Treatment of oligospermia with the amino acid arginine. J Urol 1973;110:311–3.
    28. Schacter A, Friedman S, Goldman JA, Eckerling B. Treatment of oligospermia with the amino acid arginine. Int J Gynaecol Obstet 1973;11:206–9.
    29. Mroueh A. Effect of arginine on oligospermia. Fertil Steril 1970:21:217–9.
    30. Pryor JP, Blandy JP, Evans P, et al. Controlled clinical trial of arginine for infertile men with oligozoospermia. Br J Urol 1978;50:47–50.
    31. Aydin S, Inci O, Alagol B. The role of arginine, indomethacin and kallikrein in the treatment of oligoasthenospermia. Int Urol Nephrol 1995;27:199–202.
    32. Scott R , MacPherson A, Yates RWS, et al. The effect of oral selenium supplementation on human sperm motility. Br J Urol 1998;82:76–80.


    Migraine Headaches

    1. Butterbur (2012) & Migraine Headache

    Learn more about treatment for migraine headaches.

    Researchers used random, double-blind controlled reviews of a number of drug treatments for migraine headaches, and graded them according to US preventive agency standards. They also reviewed other published studies and got expert opinions for those drugs for which there were no controlled trials.

    They found a number of products which can be effective, depending on the particular needs of any given patient. They looked at effectiveness, side effects, and other disorders that the patient might have. Based on their review, they gave strong recommendations to 4 herbal extracts, nutrients or supplements (butterbur, riboflavin, coenzyme Q10, and magnesium citrate) and 7 drugs (topiramate, propranolol, nadolol, metoprolol, amitriptyline, gabapentin, candesartan) which are used for other conditions such as angina, depression, epilepsy, and high blood pressure.

    Published: Can J Neurol Sci. 2012 Mar;39(2 Suppl 2):S1-59, Canadian Headache Society guideline for migraine prophylaxis. Pringsheim T, Davenport W, Mackie G, Worthington I, Aubé M, Christie SN, Gladstone J, Becker WJ; Canadian Headache Society Prophylactic Guidelines Development Group.

    Researchers: from University of Calgary and the Hotchkiss Brain Institute, Calgary, AB, Canada.

    2. CoQ10 (2005) & Migraines

    Learn more about migraine headaches.

    Researchers have known that riboflavin behaves in a similar manner to coenenzyme Q10 (CoQ10) and that it helps with migraines. In a double-blind, random, controlled study, researcher compared use of a placebo and CoQ10 in 42 migraine sufferers, and found that CoQ10 was effective. It helped with frequency of migraines, number of days that patients felt headaches and/or nausea. No problems were noted. The placebo helpd 14.4% of patients, and CoQ10 helped 47.6% of patients.

    Researchers: Sandor and associates, Headache and Pain Unit, Neurology Department, University Hospital Zurich, Frauenklinikstrasse 26, 8091 Zurich, Switzerland.

    Published: Neurology. 2005 Feb 22;64(4):713-5. Efficacy of coenzyme Q10 in migraine prophylaxis: a randomized controlled trial. Sandor PS, Di Clemente L, Coppola G, Saenger U, Fumal A, Magis D, Seidel L, Agosti RM, Schoenen J.

    3. Migraine Headaches (2012) & Dry Eye Connection

    Learn more about holistic treament of migraine headaches and dry eyes.

    Researchers have long suspected that there may be a connection between dry eyes and migraine headaches - this study investigates that tie by investigating the relationship between tear capacity and migraine symptoms in patients.

    This study had the object of observing and comparing the symptoms of 33 patients who had migraines and 33 controls who had no migraines and no eye conditions. All of the patients were given a complete eye exam including a variety of test to validate or exclude dry eye conditions. Patients who had been experiencing migraines were identified as to whether or not they experienced migraine auras and the intensity of the pain they experienced based on a standard assessment test.

    The researchers determined that 51% of the migraine patients had migraines with aura, 33% had no auras, and 15% had basilar migraine (a variation of migraine, mostly experienced by young people and sometimes including dizziness, ringing in the years, speech slurring, and severe headache).

    There were distinct differences in the dry eye assessments and the researchers concluded that dry eye disease was significantly more likely to be seen in patients who also suffered from migraines. They thought that it is possible that some migraine headaches might be worsened by dry eye syndrome.

    Published: Cornea. 2012 Jun 15, Dry Eyes and Migraines: Is There Really a Correlation? Koktekir BE, Celik G, Karalezli A, Kal A.

    Researchers: Department of Ophthalmology, Faculty of Medicine, Selcuk University, Konya, Turkey Departments of Neurology Ophthalmology, School of Medicine, Baskent University, Ankara, Turkey.

    4. Vitamin B2 (2004) and Migraine Heachaches

    Learn more about migraine headaches

    These researchers wanted to evaluate the usefulness and effectiveness of vitamin B2 (also known as riboflavin) as a migraine headache preventative. The study they conducted was an open-label trial (ie, not blind or double-blind) in a clinic for outpatients. A baseline was established for patients with a history of migraine headaches, noting how often they'd been having attacks, how long they lasted, how strong they were, and what drugs had been used to counter the migraine attacks. The patients were given 400mg vitamin B2 daily and their reports of headaches were monitored at three and six months after the treatment began.

    After both three months and again after six months, the frequency was lowered by 1/2 from about 4 days/monthly to 2 days/monthly. The use of other drugs (that had not worked well) was reduced from 7 a month to 4.5 a month.

    However, the duration and strength of the headaches did not change very much.

    Researchers: Boehnke C, Reuter U, Flach U, Schuh-Hofer S, Einhäupl KM, Arnold G.

    Published: Eur J Neurol. 2004 Jul;11(7):475-7. High-dose riboflavin treatment is efficacious in migraine prophylaxis: an open study in a tertiary care centre.


    Myopia (nearsightedness)

    1. AOA (2011) Eye Q Survey Results

    According to the most recent AOA Eye-Q survey there are still many misconceptions regarding eye health, which consumers take as truth.

    In addition, the rising use of computers and electronic devices is a rising concern for parents - both in the classroom and outside of the classroom. However, still only 29% of parents had this concern. 62% of parents estimate their child spends 1-4 hours daily on a computer or hand-held electronic device.

    The AOA restated that prolonged use of electronic devices can cause eye strain, headaches, fatigue, burning or tired eyes, loss of focus, blurred vision, double vision or head and neck pain, computer vision syndrome (CVS) (or computer eye strain syndrome.

    The increased use of 3D imagery in the classroom may unmask other unlying vision problems that children may have such as lazy eye, convergence insufficiency, poor focusing skills and other visual problems. 53% of parents were concerned that 3-D viewing might be harmful to their children's eyes.

    Eye care and beauty aids

    The 2001 survey also found that many women don't replace old eye makeup for new frequently, and younger women often share eye makeup. Most people use skin care products but fail to protect the delicate skin around the eyes.

    Diet and vision health

    Nearly half (49%) think that carrots are the best food for eye health, and don't know that foods such as spinach, broccoli and apples were the best foods for vision health.

    2. Myopia (2012) Increasing in Asian Children

    Learn more about recommendations for myopia (nearsightedness).

    The children of East Asian countries and cities are now under higher and higher pressure to do well in their education. As an consequence health issues related to a life dedicated to close-up work for vision are increasing. Myopia is now a major health concern now, to 80—90% of school graduates. The risk of glaucoma and other conditions that threaten sight is greater in patients with high myopia (10-20% of secondary school graduates).

    This is a trend seen on other parts of the world as well. Increasing time spent indoors is associated with the higher incidence of myopia in educated populations.

    Researchers: Prof Ian G Morgan PhD a b , Prof Kyoko Ohno-Matsui MD c, Prof Seang-Mei Saw PhD d e

    Published: The Lancet, Volume 379, Issue 9827, 5/5/12.

    3. Prevalence rate of nearsightedness in schoolchildren in rural Mongolia

    Learn more about recommendations for myopia (nearsightedness)

    The amount of myopia, or nearsightedness, among some young Asian populations is reportedly increasing to near epidemic proportions. But rural populations, such as rural Mongolia are emerging economies with limited eye care resources.

    The purpose of this study was to define a level of nearsightedness for school-aged children in rural Mongolia. The total prevalence of nearsightedness (more than -0.5 D spherical equivalent) was 5.8%. Female students exhibited a significantly higher prevalence of nearsightedness in comparison to male students: 8% compared with 3%, respectively. The prevalence rate of nearsightedness in Mongolia is, so far, low in comparison to other Far Eastern countries.

    Published: Optom Vis Sci. 2006 Jan;83(1):53-6.

    4. Refractive status of indigenous people in the Amazon region of Brazil

    This interesting study investigated the vision of the illiterate indigenous people of the upper Rio Negro region of the Amazon rain forest in northwestern Brazil.

    Researchers studied the vision of 486 people, 259 of whom were indigenous people, between 12 and 59 years of age. The subjects were considered to be indigenous if there were at least three generations of indigenous ancestry with no folkloric suggestion of other ancestors.

    Nearsightedness was rare among, only 2.7% of the indigenous subjects, had nearsightedness of -1.00 D or more and 1.6% (four people) had bilateral nearsightedness of -1.00 D or more.

    Those 2.7% and 1.6% of the subjects with myopia were the only educated indigenous people examined. The other Brazilians included ih the study had higher rates of nearsightedness (6.4% of eyes and 5.1% of subjects bilaterally). Of these, the older less-educated adults had a very low prevalence of nearsightedness (3.2% of eyes and 2.0% of subjects), whereas the younger, slightly educated Brazilians had a higher prevalence of Nearsightedness (11.3% of eyes and 9.7% of subjects).

    The low amount of myopia in the illiterate indigenous people is consistent with other studies and suggests that myopia is related to literacy and all that comes with literacy. The generational change among the local mixed race Brazilians further supports this conclusion.

    Published: Optom Vis Sci. 2005 Apr;82(4):267-72

    Researchers: Thorn F, Cruz AA, Machado AJ, Carvalho RA.
    New England College of Optometry, Boston, Massachusetts

    5. Sunlight can help children avoid myopia: Aussie researchers 2009

    Children should spend two to three hours a day outside to prevent them becoming short-sighted, says a study by the Australian Research Council Centre of Excellence in Vision Science.

    A comparison of children of Chinese origin in Australia and Singapore, which has the highest rate of myopia in the world, found the only significant difference was the time spent outdoors.

    Ian Morgan from the ARC Vision Centre yesterday said exposure to daylight appeared to play a critical role in limiting the growth of the eyeball, which is responsible for myopia or short-sightedness.

    Professor Morgan said it had been apparent for a couple of hundred years that more educated people were short-sighted, but the research suggested spending some hours a day outdoors could counteract the myopic effects of study.

    "Video games are as ineffective as reading on vision," he said. "Computers are pretty neutral, watching television doesn't seem to affect vision. The only difference we could find is the amount of time spent outdoors.

    The research says about 30 per cent of six-year-olds in Singapore are short-sighted enough to need glasses, compared with only 3 per cent of Chinese-Australians.

    Both groups spend the same amount of time studying, playing video games, watching television and reading books. But Singapore children spend an average 30 minutes a day outdoors compared with two hours in Australia.

    Professor Morgan said similar trends were seen in India, with 5 per cent of rural-dwelling Indians being short-sighted compared with 10 per cent of their urban cousins and 65 per cent of those living in Singapore.

    Myopia is increasing in urban areas around the world, and is described as an epidemic in parts of east Asia, with Singapore the world capital.

    Australia has a level of myopia more commonly found in the Third World, with only 0.8 per cent of six-year-olds of European origin being short-sighted.

    They spend on average three hours a day outdoors.


    Night Blindness

    1. Bilberry (2005) and Night Blindness

    Learn more about night blindness

    Researchers validated earlier studies that supplementation with bilberry fruit extract (Vaccinium myrtillus) can be helpful for night vision in people who are nearsighted. It should be noted that some studies do not find this result.

    The intent of the study was find out whether earlier reports that bilberry had this benefical effect were validated, and to measure the effect specifically on nearsightedness people. They 60 patient with either moderate or mild myopia were given either 100 mg of a bilberry extract (including 85% anthocyanosides) twice daily or a placebo over a 4 week period

    The group receiving bilberry supplementation did in fact show much better improvement in eye symptoms than those receiving the placebo. It was found that those receiving bilberry also were increasingly sensitive to contract, an important component of good night vision. No night vision improvement was found in those receiving the placebo.

    No side effects were found from taking the bilberry supplement.

    Published: Purified high-dose anthocyanoside oligomer administration improves nocturnal vision and clinical symptoms in myopia subjects, British Journal of Nutrition (2005;93:895–9)

    2. Vitamin A (2000) and Night Blindness

    Learn more about night blindness.

    Researchers examined the effectiveness of treating Napali women with vitamin A and beta-carotene supplements to counter the effects of night blindness, known to researchers as "dark-adaptation threshold."

    298 pregnant women aged 15-45 who experienced varying degrees of night blindness were tested in a placebo-controlled study examining the benefits of supplementation with vitamin A and beta-carotene. Almost half of them were also tested three months after they gave birth. The results were compared to 100 similarly aged American women who were not pregnant. The degree of night blindness was evaluated by looking at the amount of light needed for the pupils of the eyes to constrict after suddenly being exposed to light. The effectiveness was also evaluated by measuring blood retinol concentrations.

    The researchers found that the women who were give vitamin A performed better than those receiving a placebo. The American women had better natural night vision than did the Nepali women.

    The researchers concluded that successful adaption to changes in light were closely tied to serum (blood) retinol levels and markedly improved with vitamin A supplementation.

    Researchers: Congdon NG, Dreyfuss ML, Christian P, Navitsky RC, Sanchez AM, Wu LS, Khatry SK, Thapa MD, Humphrey J, Hazelwood D, West KP Jr. Source Center for Human Nutrition, Department of International Health, The Johns Hopkins School of Hygiene and Public Health, Baltimore, MD, USA.

    Published: Responsiveness of dark-adaptation threshold to vitamin A and beta-carotene supplementation in pregnant and lactating women in Nepal, Am J Clin Nutr. 2000 Oct;72(4):1004-9.

    3. Vitamin A (2005) & Night Blindness

    Learn more about night blindness.

    Previous research has demonstrated that vitamin A supplementation can reverse the effects of night blindness. In this study researchers wanted to evaluted whether a diet contained small amounts of vitamin A would also have a beneficial effect.

    The researchers compared supplementing with vitamin A in food sources versus supplementing with vitamin A, measuring the results by evaluating both dark adaption and plasma (blood) retinol levels in Napali women who suffered from night blindness.

    The women were divided into six groups, receiving various forms of vitamin A in vitamin A–fortified rice, retinyl palmitate, amaranth leaves, goat liver, or carrots. They were evaluated weekly via degree of pupil dilation and blood reinol levels. The groups were also compared to women who were not experiencing night blindness.

    The researchers found that night blindness diminished most in the group receiving goat liver compared to the vitamin A–fortified rice group. The blood retinol level change was greater in those receiving retinyl palmitate and liver groups than in the vegetable groups, and greater in the group receiving goat liver than in the group receiving vitamin A–fortified rice.

    The researchers concluded that all of the methods decreased night blindness, and those methods with better results were not significantly so. Both dietary vitamin A and vitamin A supplementation were effective.

    Researchers: Marjorie J Haskell, Pooja Pandey, Joanne M Graham, Janet M Peerson, Ram K Shrestha, and Kenneth H Brown

    Published: Am J Clin Nutr February 2005 vol. 81 no. 2 461-471


    Osteoarthritis

    1. Boswellia serrata (2011) & Osteoarthritis

    Learn more about osteoarthritis.

    The researchers treated 56 diagnosed with osteoarthritis who were divided into 2 groups. There was no placebo control group.

    One group received boswellia in a capsule form, 6g daily, and the other received both the capsule form and also a cream containing bowellia.

    After 2 months improvement in symptoms were observed in both groups, however the details are unknown.

    Researchers: Gupta PK, Samarakoon SM, Chandola HM, Ravishankar B., Senior Medical Officer, Dehradun, Uttarakhand, India.

    Published: Ayu. 2011 Oct;32(4):478-82.

    Editor's Note: There is another study,Efficacy and tolerability of Boswellia serrata extract in treatment of osteoarthritis of knee--a randomized double blind placebo controlled trial. Phytomedicine. 2003 Jan;10(1):3-7, but we have not been able to locate an abstract. Third hand, it is reported that this was a randomized, controlled cross-over, double-blind study on 30 patients over 8 weeks with beneficial results including reduced pain, better range of motion, reduced knee swelling, and the ability to walk greater distances.

    2. Glucosamine sulfate, Chondroitin Sulfate (2009) & Osteoarthritis

    Learn more about osteoarthritis.

    The trial is known as the Glucosamine/chondroitin Arthritis Intervention Trial (GAIT, sponsored by NIH and was developed because controversy remains as to of the efficacy of glucosamine sulfate in the treatment of knee and hip osteoarthritis. this meta-study evaluated a number of studies on the effect of glucosamine and chondroitin sulfate formulations on development of the condition.

    This trial compared a number of agents: a combination of glucosamine and chondroitin sulfates, and celecoxib; placebo; glucosamine hydrochloride; and chrondrotin sulfate. The study was a double-blind 6 month study of patients with osteoarthritis in the knee. It found that glucosamine hydrochloride and chondroitin alone or in combination did not effectively reduce pain in knee osteoarthritis patients.

    However the study did suggest that the combination of glucosamine hydrochloride and chrondrotin sulfate may be helpful for those with moderate to severe osteoarthritis of the knee.

    Editor's Note: glucosamine hydrochloride and glucosamine sulfate are both salts, but not the same.

    The researchers pointed out that while in the past research had been based mostly on symptoms, newer research examines the capacity of glucosamine sulfate and chondroitin sulfate to change structure, possibly slightly offsetting the narrowing of joint space which gives rise to pain. They concluded that glucosamine sulfate, but not glucosamine hydrochloride, may have small to moderate effect on symptoms (debated by other researchers) but that there is compelling evidence that glucosamine sulfate and chondroitin sulfate may slow the progression of osteoarthritis.

    Reseachers: Bruyere O, Reginster JY, WHO Collaborating Center for Public Health Aspect of Osteoarticular Disorders, University of Liège, Liege, Belgium

    Published: Glucosamine and chondroitin sulfate as therapeutic agents for knee and hip osteoarthritis, Drugs Aging. 2007;24(7):573-80.

    3. MSM (2012) & Osteoarthritis

    Learn more about osteoarthritis.

    Because MSM (methylsulonylmethane) is commonly believed to relieve inflammation the researchers wanted to examine the effectiveness and safety of the ingredient.

    In this animal model study, appropriately modeling human osteoarthritis, they looked at cartilage formation and break-down. For cartilege formation, rats and mice were give a control or one of several MSM containing diets. Consumption of the MSM ingredient did not affect cartilage growth and the weights of body, liver and spleen were markedly lower in one of the groups receiving MSM.

    They did find that the MSM ingredient did significantly decrease cartilage deterioration - doing so more markedly the higher the dose.

    They concluded that MSM did protect cartilage, but that intake of large amounts of MSM brought about atrophy of several organs.

    Researchers: Ezaki J, Hashimoto M, Hosokawa Y, Ishimi Y., Department of Food Function and Labeling, National Institute of Health and Nutrition, 1-23-1 Toyama, Shinjuku-ku, Tokyo, 162-8636, Japan.

    Published: Assessment of safety and efficacy of methylsulfonylmethane on bone and knee joints in osteoarthritis animal model, J Bone Miner Metab. 2012 Aug 10.

    4. Niacinamide (1996) & Osteoarthritis

    Learn more about osteoarthritis.

    This NIH study examined the effects of niacinamide (Vitamin B3) on osteoarthritis in a placebo-controlled, double-blind study.

    The researchers looked at 72 OA patients who were given either niacinamide or placebo for 12 weeks. They assessed the results by measuring impact and pain, range of motion and flexibility of joints, sed rate, blood count, liver functioning, uric acide, cholesterol and fasting blood sugar.

    Overall impact showed an improvement by 29% in the patients on niacinamide and got worse by 10% for those on the placebo. While pain levels did not change, the niacinamide patients were able to reduce their inflammation-lowering medications by 13%. Erythrocyte sed rate decreased by 22% and joint mobility improved by 4.5 degrees compared to the placebo group. There were some mild side effects in 40% of the niacimide group.

    The researchers concluded that niacimide may have a role in treating OA and that further evaluation is warranted.

    Jonas WB, Rapoza CP, Blair WF, Office of Alternative Medicine, National Institute of Health, Bethesda, MD 20892, USA.

    The effect of niacinamide on osteoarthritis: a pilot study, Inflamm Res. 1996 Jul;45(7):330-4.

    5. Osteoarthritis (2005): Glucosamine Sulfate and Ginger

    Learn more about osteoarthritis recommendations

    Studies show that for some people suffering from osteoarthritis, certain supplements can bring effective pain relief.

    Osteoarthritis (OA) is a form of arthritis that causes painful inflammation of the joints and loss of cartilage, and can be particularly troublesome in relation to larger joints that support our body such as the knees and hips.

    A 2005 study compared Celebrex to glucosamine and chondroitin sulfate supplements. These essential cartilage components, in supplement form, have been shown to slow and even reverse the degenerative effects of osteoarthritis. The researchers found that for cases of moderate to severe pain, the combination of glucosamine and chondroitin sulfate was comparable to the effectiveness of Celebrex.

    A 2001 study showed that supplementing with ginger extract may effectively relieve some types of arthritis pain. Researchers tested 250 volunteers with osteoarthritis by giving them a ginger dietary supplement or a placebo. Two thirds of those given the ginger pills reported relief from pain significantly more than those taking the placebo.

    Studies:

    • 2005, presented at annual scientific meeting of the American College of Rheumatology (ACR), which was funded by the National Institutes of Health.
    • 2001, published in the journal Osteoarthritis, Professor Altman of the University of Miami School of Medicine presented his findings to the British Medical Association in London.

    6. Osteoarthritis Research Bibliography

    Also see osteoarthritis discussion

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    Osteoporosis

    1. Osteoporosis Research Bibliography

    Also see osteoporosis discussion.

    1. Feskanich D, Willett WC, Stampfer MJ, Colditz GA. Protein consumption and bone fractures in women. Am J Epidemiol 1996;143:472–9.
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    3. Moriguti JC, Ferriolli E, Marchini JS. Urinary calcium loss in elderly men on a vegetable / animal (1:1) high-protein diet. Gerontology 1999;45:274–8.
    4. Munger RG, Cerhan JR, Chiu BC. Prospective study of dietary protein intake and risk of hip fracture in postmenopausal women. Am J Clin Nutr 1999;69:147–52.
    5. Mannan MT, Tucker K, Dawson-Hughes B, et al. Effect of dietary protein on bone loss in elderly men and women: the Framingham Osteoporosis Study. J Bone Mineral Res 2000;15:2504–12.
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    8. Marsh AG, Sanchez TV, Chaffee FL, et al. Bone mineral mass in adult lacto-ovo-vegetarian and omnivorous males. Am J Clin Nutr 1983;37:453–6.
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    12. Tylavsky FA, Anderson JJ. Dietary factors in bone health of elderly lactoovovegetarian and omnivorous women. Am J Clin Nutr 1988;48(3 Suppl):842–9.
    13. Lau EMC, Kwok T, Woo J, Ho SC. Bone mineral density in Chinese elderly female vegetarians, vegans, lacto-vegetarians and omnivores. Eur J Clin Nutr 1998;52:60–4.
    14. Tkatch L, Rapin CH, Rizzoli R, et al. Benefits of oral protein supplementation in elderly patients with fracture of the proximal femur. J Am Coll Nutr 1992;11:519–25.
    15. Schürch MA, Rizzoli R, Slosman D, et al. Protein supplements increase serum insulin-like growth factor-I levels and attenuate proximal femur bone loss in patients with recent hip fracture. A randomized, double blind, placebo-controlled trial. Ann Intern Med 1998;128:801–9.
    16. Espauella J, Guyer H, Diaz-Escriu F, et al. Nutritional supplementation of elderly hip fracture patients. A randomized, double-blind placebo-controlled trial. Age Aging 2000;29:425–31.
    17. Heaney RP. Nutrient interactions and the calcium requirement. J Lab Clin Med 1994;124:15–6 [editorial/review].
    18. Kerstetter JE, Allen LH. Dietary protein increases urinary calcium. J Nutr 1990;120:134–6.
    19. Kerstetter JE, Looker AC, Insogna KL. Low dietary protein and low bone density. Calcif Tissue Int 2000;66:313.
    20. Zarkadas M, Geougeon-Reyburn R, Marliss EB, et al. Sodium chloride supplementation and urinary calcium excretion in postmenopausal women. Am J Clin Nutr 1989;50:1088–94.
    21. Evans CE, Chughtai AY, Blumsohn A, et al. The effect of dietary sodium on calcium metabolism in premenopausal and postmenopausal women. Eur J Clin Nutr 1997;51:394–9.
    22. McParland BE, Boulding A, Campbell AJ. Dietary salt affects biochemical markers of resorption and formation of bone in elderly women. Br Med J 1989;299:834–5.
    23. Devine A, Criddle RA, Dick IM, et al. A longitudinal study of the effect of sodium and calcium intakes on regional bone density in postmenopausal women. Am J Clin Nutr 1995;62:740–5.
    24. Kynast-Gales SA, Massey LK. Effect of caffeine on circadian excretion of urinary calcium and magnesium. J Am Coll Nutr 1994;13:467–72.
    25. Hernandez-Avila M, Colditz GA, Stampfer MJ, et al. Caffeine, moderate alcohol intake, and risk of fractures of the hip and forearm in middle-aged women. Am J Clin Nutr 1991;54:157–63.
    26. Harris SS, Dawson-Hughes B. Caffeine and bone loss in healthy postmenopausal women. Am J Clin Nutr 1994;60:573–8.
    27. Kanis J, Johnell O, Gullberg B, et al. Risk factors for hip fracture in men from southern Europe: the MEDOS study. Mediterranean Osteoporosis Study. Osteoporos Int 1999;9:45–54.
    28. Hegarty VM, May HM, Khaw KT. Tea drinking and bone mineral density in older women. Am J Clin Nutr 2000;71:1003–7.
    29. Kao PC, P’eng FK. How to reduce the risk factors of osteoporosis in Asia. Chung Hua I Hsueh Tsa Chih (Taipei) 1995;55:209–13 [review].
    30. Wyshak G, Frisch RE. Carbonated beverages, dietary calcium, the dietary calcium/phosphorus ratio, and bone fractures in girls and boys. J Adolescent Health 1994;15:210–5.
    31. Smith S, Swain J, Brown EM, et al. A preliminary report of the short-term effect of carbonated beverage consumption on calcium metabolism in normal women. Arch Intern Med 1989;149:2517–9.
    32. Mazariegos-Ramos E, Guerrero-Romero F, Rodríquez-Morán F, et al. Consumption of soft drinks with phosphoric acid as a risk factor for the development of hypocalcemia in children: a case-control study. J Pediatr 1995;126:940–2.
    33. Kim SH, Morton DJ, Barrett-Connor EL. Carbonated beverage consumption and bone mineral density among older women: the Rancho Bernardo Study. Am J Public Health 1997;87:276–9.
    34. Anderson JJ, Ambrose WW, Garner SC. Biphasic effects of genistein on bone tissue in the ovariectomized, lactating rat model (44243). Proc Soc Exp Biol Med 1998;217:345–50.
    35. Potter SM, Baum JA, Teng H, et al. Soy protein and isoflavones: their effects on blood lipids and bone density in postmenopausal women. Am J Clin Nutr 1998;68(Suppl):1375–9S.
    36. Weinsier RL, Krumdieck CL. Dairy foods and bone health: examination of the evidence. Am J Clin Nutr 2000;72:681–9 [review].
    37. Hopper JL, Seeman E. The bone density of female twins discordant for tobacco use. N Engl J Med 1994;330:387–92.
    38. Chow R, Harrison JE, Notarius C. Effect of two randomised exercise programmes on bone mass of healthy postmenopausal women. Br Med J 1987;295:1441–4.
    39. Lloyd T, Triantafyllou SJ, Baker ER, et al. Women athletes with menstrual irregularity have increased musculoskeletal injuries. Med Sci Sports Exercise 1986;18(4):374–9.
    40. Salamone LM, Cauley JA, Black DM, et al. Effect of a lifestyle intervention on bone mineral density in premenopausal women: a randomized trial. Am J Clin Nutr 1999;70:97–103.
    41. Reid IR, Ames RW, Evans MC, et al. Long-term effects of calcium supplementation on bone loss and fractures in postmenopausal women: a randomized controlled trial. Am J Med 1995;98:331–5.
    42. Hosking DJ, Ross PD, Thompson DE, et al. Evidence that increased calcium intake does not prevent early postmenopausal bone loss. Clin Ther 1998;20:933–44.
    43. Owusu W, Willett WC, Feskanich D, et al. Calcium intake and the incidence of forearm and hip fractures among men. J Nutr 1997;127:1782–7.
    44. Rulm LA, Sakhaee K, Peterson R, et al. The effect of calcium citrate on bone density in the early and mid-postmenopausal period: a randomized, placebo-controlled study. Am J Ther 1999;6:303–11.
    45. Nieves JW, Komar L, Cosman F, Lindsay R. Calcium potentiates the effect of estrogen and calcitonin on bone mass: review and analysis. Am J Clin Nutr 1998;67:18–24.
    46. Bonjour JP, Carrie AL, Ferrari S, et al. Calcium-enriched foods and bone mass growth in prepubertal girls: a randomized, double-blind, placebo-controlled trial. J Clin Invest 1997;99:1287–94.
    47. Welten DC, Kemper HC, Post GB, et al. A meta-analysis of the effect of calcium intake on bone mass in young and middle aged females and males. J Nutr 1995;125:2802–13.
    48. Agnusdei D, Bufalino L. Efficacy of ipriflavone in established osteoporosis and long-term safety. Calcif Tissue Int 1997:61:S23–7 [includes review].
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    51. Adami S, Bufalino L, Cervetti R, et al. Ipriflavone prevents radial bone loss in postmenopausal women with low bone mass over 2 years. Osteoporos Int 1997;7:119–25.
    52. Nozaki M, Hashimoto K, Inoue Y, et al. Treatment of bone loss in oophorectomized women with a combination of ipriflavone and conjugated equine estrogen. Int J Gynaecol Obstet 1998;62(1):69–75.
    53. Gennari C, Adami S, Agnusdei D, et al. Effect of chronic treatment with ipriflavone in postmenopausal women with low bone bass. Calcif Tissue Int 1997;61(Suppl 1):S19–22.
    54. Gennari C, Agnusdei D, Crepaldi G, et al. Effect of ipriflavone—a synthetic derivative of natural isoflavones—on bone mass loss in the early years after menopause. Menopause 1998;5(1):9–15.
    55. Ohta H, Komukai S, Makita K, et al. Effects of 1-year ipriflavone treatment on lumbar bone mineral density and bone metabolic markers in postmenopausal women with low bone mass. Horm Res 1999;51:178–83.
    56. Melis GB, Paoletti AM, Bartolini R, et al. Ipriflavone and low doses of estrogens in the prevention of bone mineral loss in climacterium. Bone Miner 1992;19 (Suppl 1):S49–56.
    57. Gambacciani M, Ciaponi M, Cappagli B, et al. Effects of combined low dose of the isoflavone derivative ipriflavone and estrogen replacement on bone mineral density and metabolism in postmenopausal women. Maturitas 1997;28:75–81.
    58. Hanabayashi T, Imai A, Tamaya T. Effects of ipriflavone and estriol on postmenopausal osteoporotic changes. Int J Gynaecol Obstet 1995;51:63–4 [letter].
    59. Alexandersen P, Toussaint A, Christiansen C, et al. Ipriflavone in the treatment of postmenopausal osteoporosis: a randomized controlled trial. JAMA 2001;285:1482–88.
    60. Brot C, Jorgensen N, Madsen OR, et al. Relationships between bone mineral density, serum vitamin D metabolites and calcium: phosphorus intake in healthy perimenopausal women. J Intern Med 1999;245:509–16.
    61. Sahota O. Osteoporosis and the role of vitamin D and calcium-vitamin D deficiency, vitamin D insufficiency and vitamin D sufficiency. Age Ageing 2000;29:301–4.
    62. Dawson-Hughes B, Dallal GE, Krall EA, et al. Effect of vitamin D supplementation on wintertime and overall bone loss in healthy postmenopausal women. Ann Intern Med 1991;115:505–12.
    63. Adams JS, Kantorovich V, Wu C, et al. Resolution of vitamin D insufficiency in osteopenic patients results in rapid recovery of bone mineral density. J Clin Endocrinol Metab 1999;84:2729–30.
    64. Nordin BEC, Baker MR, Horsman A, Peacock M. A prospective trial of the effect of vitamin D supplementation on metacarpal bone loss in elderly women. Am J Clin Nutr 1985;42(3):470–4.
    65. Lips P, Graafmans WC, Ooms ME, et al. Vitamin D supplementation and fracture incidence in elderly persons. Ann Intern Med 1996;124:400–6.
    66. Komulainen M, Tupperainen MT, Kröger H, et al. Vitamin D and HRT: no benefit additional to that of HRT alone in prevention of bone loss in early postmenopausal women. A 2.5-year randomized placebo-controlled study. Osteoporos Int 1997;7:126–32.
    67. Droisy R, Collette J, Chevallier T, et al. Effects of two 1-year calcium and vitamin D3 treatments on bone remodeling markers and femoral bone density in elderly women. Curr Ther Res 1998;59:850–62.
    68. Chapuy MC, Arlot ME, Duboeuf F, et al. Vitamin D3 and calcium to prevent hip fractures in elderly women. N Engl J Med 1992;327:1637–42.
    69. Maki BE, Holliday PJ, Topper AK. A prospective study of postural balance and risk of falling in an ambulatory and independent elderly population. J Gerontol 1994;49:M72–84.
    70. Pfeifer M, Begerow B, Minne HW, et al. Effects of a short-term vitamin D and calcium supplementation on body sway and secondary hyperparathyroidism in elderly women. J Bone Mineral Res 2000;15:1113–8.
    71. Van Papendorp DH, Coetzer H, Kruger MC. Biochemical profile of osteoporotic patients on essential fatty acid supplementation. Nutr Res 1995;15:325–34.
    72. Kruger MC, Coetzer H, de Winter R, et al. Calcium, gamma-linolenic acid and eicosapentaenoic acid supplementation in senile osteoporosis. Aging 1998;10:385–94.
    73. Hart JP. Circulating vitamin K1 levels in fractured neck of femur. Lancet 1984;ii:283 [letter].
    74. Tamatani M, Morimoto S, Nakajima M, et al. Decreased circulating levels of vitamin K and 25-hydroxyvitamin D in osteopenic elderly men. Metabolism 1998;47:195–9.
    75. Feskanich D, Weber P, Willett WC, et al. Vitamin K intake and hip fractures in women: a prospective study. Am J Clin Nutr 1999;69:74–9.
    76. Booth SL, Tucker KL, Chen H, et al. Dietary vitamin K intakes are associated with hip fracture but not with bone mineral density in elderly men and women. Am J Clin Nutr 2000;71:1201–8.
    77. Knapen MH, Hamulyak K, Vermeer C. The effect of vitamin K supplementation on circulating osteocalcin (Bone Gla protein) and urinary calcium excretion. Ann Intern Med 1989;111:1001–5.
    78. Orimo H, Shiraki M, Fujita T, et al. Clinical evaluation of Menatetrenone in the treatment of involutional osteoporosis—a double-blind multicenter comparative study with 1–alpha-hydroxyvitamin D3. J Bone Mineral Res 1992;7(Suppl 1):S122.
    79. Iwamoto I, Kosha S, Noguchi S, et al. A longitudinal study of the effect of vitamin K2 on bone mineral density in postmenopausal women a comparative study with vitamin D3 and estrogen–progestin therapy. Maturitas 1999;31:161–64.
    80. Shiraki M, Shiraki Y, Aoki C, Miura M. Vitamin K2 (menatetrenone) effectively prevents fractures and sustains lumbar bone mineral density in osteoporosis. J Bone Miner Res 2000;15:515–21.
    81. Craciun AM, Wolf J, Knapen MH, et al. Improved bone metabolism in female elite athletes after vitamin K supplementation. Int J Sports Med 1998;19:479–84.
    82. Feskanich D, Weber P, Willett WC, et al. Vitamin K intake and hip fractures in women: a prospective study. Am J Clin Nutr 1999;69:74–9.
    83. Cohen L, Laor A, Kitzes R. Magnesium malabsorption in postmenopausal osteoporosis. Magnesium 1983;2:139–43.
    84. Cohen L, Kitzes R. Infrared spectroscopy and magnesium content of bone mineral in osteoporotic women. Isr J Med Sci 1981;17:1123–5.
    85. Geinster JY, Strauss L, Deroisy R, et al. Preliminary report of decreased serum magnesium in postmenopausal osteoporosis. Magnesium 1989;8:106–9.
    86. Dimai HP, Porta S, Wirnsberger G, et al. Daily oral magnesium supplementation suppresses bone turnover in young adult males. J Clin Endocrinol Metab 1998;83:2742–8.
    87. Stendig-Lindberg G, Tepper R, Leichter I. Trabecular bone density in a two year controlled trial of peroral magnesium in osteoporosis. Magnesium Res 1993;6:155–63.
    88. Abraham GE, Grewal H. A total dietary program emphasizing magnesium instead of calcium. J Reprod Med 1990;35:503–7.
    89. Sahap AO. Zinc and senile osteoporosis. J Am Geriatr Soc 1983;31:790–1.
    90. Relea P, Revilla M, Ripoll E, et al. Zinc, biochemical markers of nutrition, and type I osteoporosis. Age Ageing 1995; 24:303–7.
    91. Elmståhl S, Gullberg B, Janzon L, et al. Increased incidence of fractures in middle-aged and elderly men with low intakes of phosphorus and zinc. Osteoporos Int 1998;8:333–40.
    92. Strause L, Saltman P, Smith KT, et al. Spinal bone loss in postmenopausal women supplemented with calcium and trace minerals. J Nutr 1994;124:1060–4.
    93. Eaton-Evans J, McIlrath EM, Jackson WE, et al. Copper supplementation and bone-mineral density in middle-aged women. Proc Nutr Soc 1995;54:191A.v 94. Baker A, Turley E, Bonham MP, et al. No effect of copper supplementation on biochemical markers of bone metabolism in healthy adults. Br J Nutr 1999;82:283–90.
    95. Nielson FH, Hunt CD, Mullen LM, Hunt JR. Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women. FASEB J 1987;1:394–7.
    96. Meacham SL, Taper LJ, Volpe SL. Effect of boron supplementation on blood and urinary calcium, magnesium, and phosphorus, and urinary boron in athletic and sedentary women. Am J Clin Nutr 1995;61:341–5.
    97. Hunt CD, Herbel JL, Nielsen FH. Metabolic responses of postmenopausal women to supplemental dietary boron and aluminum during usual and low magnesium intake: boron, calcium, and magnesium absorption and retention and blood mineral concentrations. Am J Clin Nutr 1997;65:803–13.
    98. Nielson FH, Hunt CD, Mullen LM, Hunt JR. Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women. FASEB J 1987;1:394–7.
    99. Gold M. Basketball bones. Science 1980;80:101–2.
    100. Raloff J. Reasons for boning up on manganese. Science News 1986;Sep 27:199 [review].
    101. Strause L, Saltman P, Smith KT, et al. Spinal bone loss in postmenopausal women supplemented with calcium and trace minerals. J Nutr 1994;124:1060–4.
    102. Carlisle EM. Silicon localization and calcification in developing bone. Fed Proc 1969;28:374.
    103. Hott M, de Pollak C, Modrowski D, Marie PJ. Short-term effects of organic silicon on trabecular bone in mature ovariectomized rats. Calcif Tissue Int 1993;53:174–9.
    104. Eisinger J, Clairet D. Effects of silicon, fluoride, etidronate and magnesium on bone mineral density: a retrospective study. Magnes Res 1993;6:247–9.
    105. Ferrari S, Zolezzi C, Savarino L, et al. The oral strontium load test in the assessment of intestinal calcium absorption. Minerva Med 1993;84:527–31.
    106. McCaslin FE, Janes JM. The effect of strontium lactate in the treatment of osteoporosis. Proc Staff Meetings Mayo Clinic 1959;34(13):329–34.
    107. Skoryna SC. Effects of oral supplementation with stable strontium. Can Med Assoc J 1981;125:703–12.
    108. Gaby AR. Preventing and Reversing Osteoporosis. Rocklin, CA: Prima Publishing, 1994, 88–9 [review].
    109. Gaby AR. Preventing and Reversing Osteoporosis. Rocklin, CA: Prima Publishing, 1994, 88–9 [review].
    110. Prior JC. Progesterone as a bone-trophic hormone. Endocr Rev 1990;11:386–98.
    111. Lee JR. Osteoporosis reversal: the role of progesterone. Int Clin Nutr Rev 1990;10:384–91.
    112. Riis BJ, Thomsen K, Strom V, Christiansen C. The effect of percutaneous estradiol and natural progesterone on postmenopausal bone loss. Am J Obstet Gynecol 1987;156:61–5.
    113. Leonetti HB, Longo S, Anasti JM. Transdermal progesterone cream for vasomotor symptoms and postmenopausal bone loss. Obstet Gynecol 1999;94:225–8.
    114. Villareal DT, Holloszy JO, Kohrt WM. Effects of DHEA replacement on bone mineral density and body composition in elderly women and men. Clin Endocrinol (Oxf) 2000;53:561–8.
    115. Kadota S, Li JX, Li HY, et al. Effects of cimicifugae rhizome on serum calcium and phosphate levels in low calcium dietary rats and on bone mineral density in ovariectomized rats. Phytomed 1996/97;3(4):379–85.


    Peptic Ulcers

    1. Stomach Ulcers List of Research
    Also see the discussion of ulcers.

    1. Katchinski BD, Logan RFA, Edmond M, Langman MJS. Duodenal ulcer and refined carbohydrate intake: a case-control study assessing dietary fiber and refined sugar intake. Gut 1990;31:993–6.
    2. Suadicani P, Hein HO, Gyntelberg F. Genetic and life-style determinants of peptic ulcer. A study of 3387 men aged 54 to 74 years: The Copenhagen Male Study. Scand J Gastroenterol 1999;34:12–7.
    3. Yudkin J. Eating and ulcers. BMJ 1980;Feb 16:483 [letter].
    4. Sonnenberg A. Dietary salt and gastric ulcer. Gut 1986;27:1138–42.
    5. Cheney G. Rapid healing of peptic ulcers in patients receiving fresh cabbage juice. Cal Med 1949;70:10.
    6. Doll R, Pygott F. Clinical trial of Robaden and of cabbage juice in the treatment of gastric ulcer. Lancet 1954;2:1200.
    7. Thaly H. A new therapy of peptic ulcer: The anti-ulcer factor of cabbage. Gaz Med Fr 1965;72:1992–3.
    8. Dunaevskii GA, Migonova DK, Rozka IM, Chibisova SM. Value of preserved juice of white cabbage in the complex therapy of peptic ulcer. Vopr Pitan 1970;29:29–33.
    9. Noess K. Ulcer-fiber-cabbage and vitamin U. Tidsskr Nor Laegeforen 1986;106:693–4.
    10. Grimes DS, Goddard J. Gastric emptying of wholemeal and white bread. Gut 1977;18:725–9.
    11. Rydning A, Berstad A, Aadland E, Odegaard B. Prophylactic effect of dietary fiber in duodenal ulcer disease. Lancet 1982;2(8301):736–9.
    12. Ryndning A, Berstad A. Fiber diet and antacids in the short-term treatment of duodenal ulcer. Scand J Gastroenterol 1985;20:1078–82.
    13. Kern RA, Stewart G. Allergy in duodenal ulcer: incidence and significance of food hypersensitivities as observed in 32 patients. J Allergy 1931;3:51.
    14. Reimann HJ, Lewin J. Gastric mucosal reactions in patients with food allergy. Am J Gastroenterol 1988;83:1212–9.
    15. Allison MC, Howatson AG, Caroline MG, et al. Gastrointestinal damage associated with the use of nonsteroidal antiinflammatory drugs. N Engl J Med 1992;327:749–54.
    16. Lenz HJ, Ferrari-Taylor J, Isenberg JI. Wine and five percent ethanol are potent stimulants of gastric acid secretion in humans. Gastroenterology 1983;85:1082–7.
    17. Cohen S, Booth GH Jr. Gastric acid secretion and lower-esophageal-sphincter pressure in response to coffee and caffeine. N Engl J Med 1975;293:897–9.
    18. Feldman EJ, Isenberg JI, Grossman MI. Gastric acid and gastrin response to decaffeinated coffee and a peptone meal. JAMA 1981;246:248–50.
    19. Dubey P, Sundram KR, Nundy S. Effect of tea on gastric acid secretion. Dig Dis Sci 1984;29:202–6.
    20. Korman MG, Hansky J, Eaves ER, Schmidt GT. Influence of cigarette smoking on healing and relapse in duodenal ulcer disease. Gastroenterology 1983;85:871–4.
    21. Patty I, Benedek S, Deak G, et al. Controlled trial of vitamin A therapy in gastric ulcer. Lancet 1982;2(8303):876 [letter].
    22. Patty I, Tarnok F, Simon L, et al. A comparative dynamic study of the effectiveness of gastric cytoprotection by vitamin A, De-Nol, sucralfate and ulcer healing by pirenzepine in patients with chronic gastric ulcer (a multiclinical and randomized study). Acta Physiol Hung 1984;64:379–84.
    23. Pfeiffer CJ, Cho CH, Cheema A, Saltman D. Reserpine-induced gastric ulcers: protection by lysosomal stabilization due to zinc. Eur J Pharmacol 1980;61:347–53.
    24. Jimenez E, Bosch F, Galmes JL, Banos JE. Meta-analysis of efficacy of zinc acexamate in peptic ulcer. Digestion 1992;51:18–26.
    25. Frommer DJ. The healing of gastric ulcers by zinc sulphate. Med J Aust 1975;2:793–6.
    26. Nishiwaki H, Kato S, Sugamoto S, et al. Ulcerogenic and healing impairing actions of monochloramine in rat stomachs: effects of zinc L-carnosine, polaprezinc. J Physiol Pharmacol 1999;50:183–95.
    27. Arakawa T, Satoh H, Nakamura A, et al. Effects of zinc L-carnosine on gastric mucosal and cell damage caused by ethanol in rats. Correlation with endogenous prostaglandin E2. Dig Dis Sci 1990;35:559–66.
    28. Cho CH, Ogle CW. A correlative study of the antiulcer effects of zinc sulphate in stressed rats. Eur J Pharmacol 1978;48:97–105.
    29. Frommer DJ. The healing of gastric ulcers by zinc sulphate. Med J Aust 1975;2:793–6.
    30. Kashimura H, Suzuki K, Hassan M, et al. Polaprezinc, a mucosal protective agent, in combination with lansoprazole, amoxicillin, and clarithromycin increases the cure rate of Helicobacter pylori infection. Aliment Pharmacol Ther 1999;13(4):483–7.
    31. Shive W, Snider RN, DuBilier B, et al. Glutamine in treatment of peptic ulcer. Texas State J Med 1957;Nov:840.
    32. Yan R, Sun Y, Sun R. Early enteral feeding and supplement of glutamine prevent occurrence of stress ulcer following severe thermal injury. Chung Hwa Cheng Hsing Shao Shang Wai Ko Tsa Chih 1995;11:189–92.
    33. Salim AS. The relationship between Helicobacter pylori and oxygen-derived free radicals in the mechanism of duodenal ulceration. Internal Med 1993;32:359–64.
    34. Salim AS. Allopurinol and dimethyl sulfoxide improve treatment outcomes in smokers with peptic ulcer disease. J Lab Clin Med 1992;119:702–9.
    35. Goso Y, Ogata Y, Ishihara K, Hotta K. Effects of traditional herbal medicine on gastric mucin against ethanol-induced gastric injury in rats. Comp Biochem Physiol 1996;113C:17–21.
    36. Beil W, Birkholz W, Sewing KF. Effects of flavonoids on parietal cell acid secretion, gastric mucosal prostaglandin production and Helicobacter pylori growth. Arzneimittelforschung 1995;45:697–700.
    37. Brogden RN, Speight TM, Avery GS. Deglycyrrhizinated licorice: A report of its pharmacological properties and therapeutic efficacy. Drugs 1974;8:330–9.
    38. D’imperio N, Piccari GG, Sarti F, et al. Double blind trial in duodenal and gastric ulcers. Cimetidine and deglycyrrhizinized liquorice. Acta Gastro-Enterologica Belgica 1978;41:427–34.
    39. Morgan AG, Pacsoo C, McAdam WAF. Maintenance therapy: a two year comparison between Caved-S and cimetidine treatment in the prevention of symptomatic gastric ulcer recurrence. Gut 1985;26:599–602.
    40. Bardhan KD, Cumberland DC, Dixon RA, Holdsworth CD. Clinical trial of deglycyrrhizinised liquorice in gastric ulcer. Gut 1978;19:779–82.
    41. Gaby AR. Deglycyrrhizinated licorice treatment of peptic ulcer. Townsend Letter for Doctors 1988;July:306 [editorial/review].
    42. Al-Said MS, Ageel AM, Parmar NS, Tariq M. Evaluation of mastic, a crude drug obtained from Pistacia lentiscus for gastric and duodenal anti-ulcer activity. J Ethnopharmacol 1986;15:271–8.
    43. Huwez FU, Al-Habbal MJ. Mastic in treatment of benign gastric ulcers. Gastroenterol Japon 1986;21:273–4.
    44. Huwez FU, Thirlwell D, Cockayne A, Ala’Aldeen DA. Mastic gum kills Helicobacter pylori. New Engl J Med 1998;339:1946 [letter].
    45. Hills BA, Kirwood CA. Surfactant approach to the gastric mucosal barrier: Protection of rats by banana even when acidified. Gastroenterology 1989;97:294–303.
    46. Sikka KK, Singhai CM, Vajpcyi GN. Efficacy of dried raw banana powder in the healing of peptic ulcer. J Assoc Phys India 1988;36(1):65 [abstract].
    47. Beil W, Birkholz C, Sewing KF. Effects of flavonoids on parietal cell acid secretion, gastric mucosal prostaglandin production and Helicobacter pylori growth. Arzneimittelforschung 1995;45:697–700.
    48. Sivam GP, Lampe JW, Ulness B, et al. Helicobacter pylori--in vitro susceptibility to garlic (Allium sativum) extract. Nutr Cancer 1997;27:118–21.
    49. Chung JG, Chen GW, Wu LT, et al. Effects of garlic compounds diallyl sulfide and diallyl disulfide on arylamine N-acetyltransferase activity in strains of Helicobacter pylori from peptic ulcer patients. Am J Chin Med 1998;26:353–64.
    50. Ernst E. Is garlic an effective treatment for Helicobacter pylori infection? Arch Intern Med 1999;159:2484–5 [letter].
    51. Graham DY, Anderson SY, Lang T. Garlic or jalapeno peppers for treatment of Helicobacter pylori infection. Am J Gastroenterol 1999;94:1200–2.
    52. Chang HM, But PPH. Pharmacology and Applications of Chinese Materia Medica vol 1. Singapore: World Scientific Inc., 1986, 521.
    53. Mills SY. Out of the Earth: The Essential Book of Herbal Medicine. New York: Viking Arkana, 1991, 544–7.
    54. Weiss RF. Herbal Medicine. Gothenburg, Sweden: Ab Arcanum and Beaconsfield, UK: Beaconsfield Publishers Ltd, 1988, 334–5.
    55. Bresnick WH, Rask-Madsen C, Hogan DL, et al. The effect of acute emotional stress on gastric acid secretion in normal subjects and duodenal ulcer patients. J Clin Gastroenterol 1993;17:117–22.
    56. Lam SK, Hui WM, Shiu LP, Ng MM. Society stress and peptic ulcer performation. J Gastroenterol Hepatol 1995;10:570–6.
    57. Piper DW, Tennant C. Stress and personality in patients with chronic peptic ulcer. J Clin Gastroenterol 1993;16:211–4.
    58. Stewart DN, de R. Winser DM. Incidence of perforated peptic ulcer. Effect of heavy air raids. Lancet 1942;2:259–61.
    59. Spicer CC, Stewart DN, de R. Winser DM. Perforated peptic ulcer during the period of heavy air raids. Lancet 1944;1:14.
    60. Aoyama N, Kinoshita Y, Fujimoto S, et al. Peptic ulcers after the Hanshin-Awaji earthquake: Increased incidence of bleeding gastric ulcers. Am J Gastroenterol 1998;93:311–6.


    Retinal Detachment

    1. Ginkgo Biloba (2004) and Retinal Detachment

    Learn more about retinal detachment information and treatment.

    Both animal and human studies, published in 1994 and substantiated in 2004 have revealed that Ginkgo extract can help to prevent retinal detachment, while increasing antioxidant activity in patients' blood, tears and plasma.

    References:

    1. Karazhaeva MI, Saksonova EO, Klebanov GI, Liubitskii OB, Gur'eva NV. [The use of flavonoid antioxidants in the complex treatment of patients with peripheral vitreo-chorioretinal dystrophies and dystrophic retinal detachment] [Article in Russian]. Vestn Oftalmol. 2004 Jul-Aug;120(4):14-8.
    2. Baudouin C, Ettaiche M, Imbert F, Droy-Lefaix MT, Gastaud P, Lapalus P. Inhibition of preretinal proliferation by free radical scavengers in an experimental model of tractional retinal detachment. Experimental Eye Research. 1994 Dec;59(6):697-706.


    Retinitis Pigmentosa

    1. Antioxidants (2006) Protect Cones in Animal Model

    Why the negative affect of high dose vitamin E on RP function? It is possible that high dose vitamin E might have inhibited the absorption or transport of vitamin A, since patients receiving high doses had slight but significant decreases in serum A levels compared with those receiving lower doses in the 1993 Harvard study.

    However, further exploratory studies of combined antioxidants in RP patients may be warranted. A recent study in an animal model of RP found that high dose antioxidants (vitamins E, C, alpha lipoic acid others) significantly reduced oxidative damage in cones, increased cone cell density and preserved cone function. These results, according to the Johns Hopkins authors, suggest that the gradual cone death that occurs after rod cells die is due to oxidative damage, and that antioxidants could provide benefit.

    Komeima K, et al. Antioxidants reduce cone cell death in a model of retinitis pigmentosa. PNAS 103:1130-35, 2006.

    Learn more about retinitis pigmentosa.

    2. Artificial Retina (2011) Project

    Learn about retinitis-pigmentosa treatment and information.

    Scientists through the US Department of Energy are testing artificial retinas that they hope can restore partial sight to people who've lost their vision to the most common causes of blindness.

    The Sylmar, Calif., company produced the devices for the U.S. Energy Department's Artificial Retina Project. The department has been engaged in biological research since the atomic bomb tests of the 1950s raised fears of radiation poisoning.

    The current version is being tested on 17 blind people in the U.S. and Europe, and more patients are being enrolled. At a retina conference in October, patients reported improvements in orientation and mobility. They were able to find a door from 20 feet away and to follow a line on the floor for 20 feet, Mech reported.

    Meanwhile, researchers in the Energy Department's National Laboratories are creating a third-generation artificial retina. Much smaller than its predecessors, the device will contain 200 or more electrodes on a thin, flexible film that curves to fit the shape of the retina. Human tests are scheduled to begin in 2011.

    For more information, go to http://artificialretina.energy.gov/index.shtml

    According to WHO estimates, the five most common causes of blindness around the world in 2002 were: cataracts (47.9%), glaucoma (12.3%), age-related macular degeneration (8.7%), corneal opacity (5.1%), and diabetic retinopathy (4.8%).

    3. Essential Fatty Acids (1988-92) - retinitis pigmentosa

    Learn more about retinitis-pigmentosa treatment and information.

    Studies on Omega-3 and Omega-6 fatty acids

    Both Omega-3 and -6 Fatty Acids are essential nutrients for normal development in mammals. Omega-6 Fatty Acids are necessary primarily for growth, reproduction and the maintenance of skin integrity. Omega-3 Fatty Acids are involved in the development and function of the retina and cerebral cortex and other organs such as the testes. (1)

    Docosahexanoic acid (DHA) and eicosapentaenoic acid (EPA) are essential Omega-3 Fatty Acids found in abundance in cold water fish and their oils. DHA is an essential nutrient for achieving optimal brain and eye function. (2) It comprises about 60% of the rod outer segments in the photoreceptor cells that we see with. (3) Brain tissue is about 60% fat, 25% of which is DHA. DHA levels correlate with visual and mental performance and several neurological and visual disorders, including retinitis pigmentosa.

    Cells in the retina, brain and other parts of the nervous system have connecting arms that transport electrical currents, sending visual information from the retina to the brain and messages from the brain through out the body. DHA supplementation ensures the optimal composition of cell membranes necessary for the most effective transmission of these signals.

    A 1990 study demonstrated that DHA with EPA given in the form of fish oil exerts a beneficial dose-dependent effect on coronary circulation with reduced triglycerides, total cholesterol, and blood pressure while causing no significant increase in bleeding time.(4 )

    Editor's note: We believe DHA' use in wet macular degeneration is unparalleled since its main work in the body is to heal and support blood vessel walls.

    Research:
    1. Connor WE; Neuringer M.; Prog Clin Biol Res; 1988: 282; 275-94.
    2. Neuringer M, Anderson G. J., Connor WE, "The essentiality of n-3 fatty acids for the development and function of the retina and brain," Ann Rev Nutr., 1988; 8: pp/17-41.
    3. Salem et al, 1996; P Martinez et al, 1992).
    4. Haglund etal, "Effects of a new fish oil concentrate on triglycerides, cholesterol, fibrinogen and blood pressure" Nutritional Research 1990; 227:347-53.

    4. Fish Oil (2004) Retinitis Pigmentosa Treatment with fish oils &r DHA

    Learn more about retinitis pigmentosa recommendations

    Researchers wanted to find out whether DHA (docosahexaenoic acid) will slow the course of retinal degeneration in patients with retinitis pigmentosa who are receiving vitamin A.

    208 patients with retinitis pigmentosa, 18 to 55 years old, were randomly assigned to DHA plus vitamin A given as retinyl palmitate (DHA + A group) or control fatty acid plus 15 000 IU/d of vitamin A (control + A group) and followed up over 4 years. Seventy percent of the patients in each group were taking vitamin A, 15 000 IU/d, prior to entry. We compared rates of decline in ocular function in the DHA + A vs control + A groups among the subgroups defined by use or nonuse of vitamin A prior to entry. We also determined whether decline in ocular function was related to red blood cell phosphatidylethanolamine docosahexaenoic acid level, dietary omega-3 fatty acid intake, or duration of vitamin A use. Main outcome measures were Humphrey Field Analyzer visual field sensitivity, 30-Hz electroretinogram amplitude, and visual acuity. RESULTS: Among patients not taking vitamin A prior to entry, those in the DHA + A group had a slower decline in field sensitivity and electroretinogram amplitude than those in the control + A group over the first 2 years (P =.01 and P =.03, respectively); these differences were not observed in years 3 and 4 of follow-up or among patients taking vitamin A prior to entry. In the entire cohort, red blood cell phosphatidylethanolamine docosahexaenoic acid level was inversely related to rate of decline in total field sensitivity over 4 years (test for trend, P =.05). This was particularly evident over the first 2 years among those not on vitamin A prior to entry (test for trend, P =.003). In the entire control + A group, dietary omega-3 fatty acid intake was inversely related to loss of total field sensitivity over 4 years (intake, <0.20 vs > or =0.20 g/d; P =.02). The duration of vitamin A supplementation prior to entry was inversely related to rate of decline in electroretinogram amplitude (P =.008).

    CONCLUSIONS: For patients with retinitis pigmentosa beginning vitamin A therapy, addition of docosahexaenoic acid, 1200 mg/d, slowed the course of disease for 2 years. Among patients on vitamin A for at least 2 years, a diet rich in omega-3 fatty acids slowed the decline in visual field sensitivity.

    Published: Further evaluation of docosahexaenoic acid in patients with retinitis pigmentosa receiving vitamin A treatment: subgroup analyses. Arch Ophthalmol. 2004 Sep;122(9):1306-14.

    Researchers: Berson EL, Rosner B, Sandberg MA, Weigel-DiFranco C, Moser A, Brockhurst RJ, Hayes KC, Johnson CA, Anderson EJ, Gaudio AR, Willett WC, Schaefer EJ. Berman-Gund Laboratory for the Study of Retinal Degenerations, Harvard Medical School, 243 Charles Street, Boston, MA

    5. Lutein (2003) and Increased Visual Acuity

    Learn more about retinitis pigmentosa recommendations.

    In an informal study, a researcher analyzed information from a small online email questionnaire and determined that lutein, which is in dark green leafy vegetables and egg yolks may help people with retinitis pigmentosa (RP) and other degenerative eye conditions.

    Three quarters of the 16 study participants with retinal degenerative conditions reported that taking daily supplements lutein, over a six-month period significantly helped their vision. Lutein is an antioxidant needed by the retina to resist damaging effects of blue light and free radicals.

    Study participants were recruited after a member of an international retinal degeneration patient e-mail list noted that some of her contacts said their vision improved with lutein supplementation.

    The participants took lutein supplements with breakfast daily for 6 months, 40 mg/day for 9 weeks and then 20 mg/day for the remainder. Onehalf of the participants also took 500 mg/day of DHA, vitamin B complex and digestive enzymes. Ten of the participants who already were taking vitamin A and/or beta carotene continued those supplements. They tested their vision on eye charts sent as e-mail attachments and on wall charts they were instructed to create, and returned data via weekly e-mails to the study coordinators.

    Most patients saw improvment in vision sharpness and visual field size. The blue-eyed patients, more at risk, had larger gains in vision than the dark-eyed participants. Also, those who took vitamin A and/or beta carotene supplements prior to the study appeared to benefit more than those who did not. The long-term effects of lutein supplements on the progression of RP should be studied,

    Researchers: Johns Hopkins University, Gislin Dagnelie, Ph.D., and others, Hopkins' Wilmer Eye Institute

    Published in the March issue of Optometry:Journal of the American Optometric Association.

    6. Lutein and Retinitis Pigmentosa (2006)
    Nutrient Supplementation for RP

    Retinitis pigmentosa (RP) refers to a group of inherited progressive retinal dystrophies characterized by photoreceptor degeneration. The rods are affected initially, followed by gradual death of the cones. It's estimated that 1 in 4,000-5,000 people have RP worldwide. Since no generally accepted medical or surgical treatment can stop the course of the disease, researchers have undertaken studies with various nutritional supplements in hopes of improving visual function or slowing disease progression. Along with vitamin A, DHA and an omega-3 rich diet, lutein has recently been reported to be of potential benefit in RP.

    Lutein May Benefit Visual Field and Acuity Spurred by previous studies suggesting lutein as a potential treatment with positive effects on macular pigment density, researchers from the Wilmer Eye Institute conducted a double-blind, randomized placebo-controlled trial with a cross-over design (1). Thirty four adult RP patients were randomized to 2 groups and followed for 48 weeks. One group received lutein supplements (10 mg/day for 12 weeks followed by 30 mg/day) for the first 24 weeks, then placebo for the following 24 weeks. The second group received placebo prior to lutein. Both groups were given a multi-vitamin and mineral supplement.

    Lutein supplementation had a significant effect on central visual field. Visual acuity also improved slightly, though no effect on contrast sensitivity was observed. Comparing the development of vision measures against the natural loss expected to occur over 48 weeks, most measures showed reduced decline. These reductions were significant for normal illumination visual acuity and contrast sensitivity. The results, according to the authors, suggest that lutein supplementation improves visual field and may also modestly improve visual acuity.

    H, et al. Lutein supplementation in retinitis pigmentosa: PC-based vision assessment in a randomized double-masked placebo-controlled clinical trial. BMC Ophthalmology 6:23, 2006.

    7. Lutein plus vitamin A (2010) may slow vision loss due to Retinitis Pigmentosa

    Learn more about retinitis pigmentosa recommendations.

    In a randomized, controlled, double-blind study, researchers found that supplementing with lutein and vitamin A may slow development of retinitis pigmentosa.

    They found that use of a daily supplement of 12 milligrams of lutein formulated with with 15,000 IU of vitamin A was linked to protection of mid-peripheral vision.

    This new data suggests that 40 year olds with retinis pigmentosa who take vitamin A plus lutein would have their mid-peripheral field for an extra 21 years when compared to people not taking the combination. Previous studies have found vitamin A slows the decline in retinal function and vision loss, and this study indicates that combining vitamin A with lutein is better.

    Since there has been some concern with regard to smokers and lutein supplementation, this study looked only at non-smokers.

    Published: Archives of Ophthalmology, 2010, Vol. 128, Issue 4, Pages 403-411 "Clinical Trial of Lutein in Patients With Retinitis Pigmentosa Receiving Vitamin A"

    Researchers: E.L. Berson, B. Rosner, M.A. Sandberg, C. Weigel-DiFranco, R.J. Brockhurst, et al.

    8. Omega-3 Fatty Acids and Retinitis Pigmentosa (2004)

    While a 4 year long study published in 2004 reported that 1,200 mg of supplemental DHA along with high dose vitamin A did not slow the course of RP overall, further subgroup analysis showed benefit for those starting vitamin A supplementation for the first time (5-6). In addition, those study participants taking vitamin A (but not DHA) who also had a higher dietary omega-3 intake experienced substantial benefit. The rate of visual field decline was retarded by 40-50% yearly in those whose omega-3 intakes were equivalent to 1-2 servings of fatty fish weekly.

    Berson EL, et al. Further evaluation of docosahexaenoic acid in patients with retinitis pigmentosa. 12:1306-14, 2004.

    9. Vitamin A (2004), DHA, Omega-3 Fatty Acid and Retinitis Pigmentosa

    Learn more about retinitis-pigmentosa treatment and information.

    A 4 year long study published in 2004 reported that 1,200 mg of supplemental DHA along with high doses of vitamin A did not slow the progress of retinitis pigmentosa overall. However further subgroup analysis showed benefit for those who were taking vitamin A supplementation for the first time. In addition, those study participants taking vitamin A (but not DHA) who also had a higher dietary omega-3 fatty acid intake experienced substantial benefit. The rate of visual field decline was retarded by 40-50% yearly in those whose omega-3 intakes were equivalent to 1-2 servings of fatty fish weekly.

    Berson EL, et al. Clinical trial of docosahexaenoic acid in patients with retinitis pigmentosa receiving vitamin A treatment. Arch Ophthalmol 122:1297-305, 2004.

    10. Vitamins A / E (1993) & Retinitis Pigmentosa

    Learn more about retinitis pigmentosa recommendations.

    Researchers found significant benefit in providing vitamin A supplements and a potential adverse effect of vitamin E on 600 patients with retinitus pigmentosa. Large doses of vitamin A did not result in greater benefit.

    They speculated that among patients with specific rod-specific gene defects vitamin A supplementation may provide benefit. No toxicity was seen for vitamin A or E. High dose vitamin A is not recommended for pregnant women or women planning to become pregnant due to the possibility of birth defects

    Researchers: Berson, Rosner, Sandberg, Hayes, Nicholson, Weigel-DiFranco, and Willette, 1993.

    Published: Archives of Ophthalmology (June 1993), volume 111(6), pages 761-772.

    11. Vitamins E, C, alpha lipoic acid and Retinitis Pigmentosa (2006)

    A 2006 study in an animal model of RP found that high dose antioxidants (vitamins E, C, alpha lipoic acid others) significantly reduced oxidative damage in cones, increased cone cell density and preserved cone function. These results, according to the Johns Hopkins authors, suggest that the gradual cone death that occurs after rod cells die is due to oxidative damage, and that antioxidants could provide benefit.

    Komeima K, et al. Antioxidants reduce cone cell death in a model of retinitis pigmentosa. PNAS 103:1130-35, 2006.

    Learn more about retinitis-pigmentosa.


    Rheumatoid Arthritis

    1. Fish Oil (2003) & Rheumatoid Arthritis

    Learn more about rheumatoid arthritis.

    These researchers noted that fish oils are an excellent source for omega-3 fatty acids, and that they have a beneficial effect of reducing inflammation. Fish oils have shown this beneficial result in double-blind, random, trials with placebo controls, for rheumatoid arthritis, but have not received the marketing that pharmeceutical drugs have and so remain unknown to many health professionals.

    Researchers: Cleland LG, James MJ, Proudman SM.

    Published: The role of fish oils in the treatment of rheumatoid arthritis, Drugs. 2003;63(9):845-53.

    2. Rheumatoid Arthritis Bibliography

    Also see discussion of rheumatoid arthritis and recommendations

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    90. Chopra A, Lavin P, Patwardhan B, Chitre D. Randomized double blind trial of an Ayurvedic plant derived formulation for treatment of rheumatoid arthritis. J Rheumatol 2000;27:1365–72.
    91. Sander O, Herborn G, Rau R. [Is H15 (resin extract of Boswellia serrata, “incense”) a useful supplement to established drug therapy of chronic polyarthritis? Results of a double-blind pilot study. Z Rheumatol 1998 ;57:11–6 [in German].
    92. Deal CL, Schnitzer TJ, Lipstein E, et al. Treatment of arthritis with topical capsaicin: A double-blind trial. Clin Ther 1991;13:383–95.
    93. Bone K. The story of devil’s claw: Is it an herbal antirheumatic? Nutrition and Healing 1998;October:3,4,8 [review].
    94. Kulkarni RR, Patki PS, Jog VP, et al. Treatment of osteoarthritis with a herbomineral formulation: A double-blind, placebo-controlled, cross-over study. J Ethnopharmacol 1991;33:91–5.
    95. Deodhar SD, Sethi R, Srimal RC. Preliminary studies on antirheumatic activity of curcumin (diferuloyl methane). Ind J Med Res 1980;71:632–4.
    96. Srivastava KC, Mustafa T. Ginger (Zingiber officinale) in rheumatism and musculoskeletal disorders. Med Hypoth 1992;39:342–8.
    97. Chopra A, Lavin P, Patwardhan B, Chitre D. Randomized double blind trial of an Ayurvedic plant derived formulation for treatment of rheumatoid arthritis. J Rheumatol 2000;27:1365–72.
    98. Randall C, Meethan K, Randall H, Dobbs F. Nettle sting of Urtica dioica for joint pain—an exploratory study of this complementary therapy. Compl Ther Med 1999;7:126–31.
    99. Mills SY, Jacoby RK, Chacksfield M, Willoughby M. Effect of a proprietary herbal medicine on the relief of chronic arthritic pain: A double-blind study. Br J Rheum 1996;35:874–8.
    100. Upton R, Petrone C, eds. Willow bark (Salix spp.) monograph. Santa Cruz, CA: American Herbal Pharmacopoeia, 1999.
    101. Blumenthal M, Busse WR, Goldberg A, et al., eds. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin: American Botanical Council and Boston: Integrative Medicine Communications, 1998, 430–1.
    102. Langer JG, Gupta OP, Atal CK. Clinical trials on Picrorhiza kurroa. Ind J Pharmacol 1981;13:98–103 [review].
    103. Zeylstra H. Filipendila ulmaria. Br J Phytotherapy 1998;5:8–12.
    104. Dhondt W, Willaeys T, Verbruggen LA, et al. Pain threshold in patients with rheumatoid arthritis and effect on manual oscillations. Scand J Rheumatol 1999;28:88–93.

    3. Vitamin D (2004) & Rheumatoid Arthritis

    Learn more about rheumatoid arthritis.

    Researchers, noting that vitamind D regulates calcium balance and perhaps the immune system, wanted to determine the relationship between consumption of vitamin D and rheumatoid arthritis.

    They evaluated data from a study of 29,368 women, aged 55-69, who were rheumatoid arthritis patients (RA), using a food frequency form the patients had filled out, which included vitamin D supplementation.

    152 cases were tracked over the following 11 years and found that the greater the vitamin D intake, the lower the risk of RA.

    Researchers: Merlino LA, Curtis J, Mikuls TR, Cerhan JR, Criswell LA, Saag KG; Iowa Women's Health Study.

    Published: Vitamin D intake is inversely associated with rheumatoid arthritis: results from the Iowa Women's Health Study, Arthritis Rheum. 2004 Jan;50(1):72-7.

    4. Vitamin D (2007) & Rheumatoid Arthritis

    Learn more about treatment of rheumatoid arthritis

    Researchers discovered that vitamin D receptors were contained in a variety of cells comprising the immune system (dendritic cells) and that they could produce this component. This gave rise to the suggestion that vitamin D plays a role in the regulation of the immune system.

    Vitamin D is developed in the body by exposure to sunlight. Low levels of vitamin D in the blood may be due, not only to limited sunlight exposure, but genetic factors and nutrition.

    Following these conclusions, researchers looked for correlations in rheumatoid arthritis patients and found that they have low blood levels of vitamin D, and that their condition is more severe in the winter when light levels are lower.

    Researchers have also found that consuming greater amounts of vitamin D was correlated with marked improvement, not only in RA symptoms, but in the health of the immune system.

    Researchers: Cutolo M, Otsa K, Uprus M, Paolino S, Seriolo B.

    Published: Vitamin D in rheumatoid arthritis, Autoimmun Rev. 2007 Nov;7(1):59-64. Epub 2007 Aug 14.

    5. Vitamin D (2008) & Rheumatoid Arthritis

    Learn more about treatment of rheumatoid arthritis

    Noting that vitamin D increasingly is being recognized as having many benefit effects, these researchers determined that noting vitamin D deficiency in rheumatoid arthritis patients is important and frequently exists. There's no agreement that vitamin D deficiency alone causes RA, but it is a factor and symptoms are relieved with increased vitamin D intake.

    They further noted that the difficulty is in determining just how to correct the deficiency, concluding that high-dose vitamin D given orally, weekly, can quickly correct the deficiency and then it should be followed by lower doses to keep an adequate level in the system.

    Researchers: Leventis P, Patel S.

    Published: Clinical aspects of vitamin D in the management of rheumatoid arthritis, Rheumatology (Oxford). 2008 Nov;47(11):1617-21


    Sjogren's Syndrome

    1. Essential Fatty Acids (1986) and Sjogren's Syndrome

    Learn more about Sjogrens treatment and information.

    In a 1986 study, 28 patients with primary Sjogren’s Syndrome were studied in a "cross-over" clinical study, and given essential fatty acids (EFA), either Efamol (73% cis-linoleic acid, 9% gammalinolenic acid) or placebo for 8 weeks.

    The result was that 68% if the patients had increased ocular score after treatment (decreased dry eye symptoms).

    Source: Oxholm P, Manthorpe R, Prause JU, Horrobin D:Patients with Primary Sjogrn’s Syndrome Treated for 2 Months With Evening Primrose Oil. Scand J Rheumatology 1986; 15:103-108.

    2. Green tea (2007) may protect against Sjögren’s syndrome

    Learn more about Sjogrens treatment and information.

    Researchers say that that a green tea extract could help prevent the development of Sjögren’s syndrome.

    In Sjogren's the salivary and tear glands are invaded by a type of white blood cell, rendering them less effective. Researchers discovered that a green tea component, polyphenol epigallocatechin-3-gallate (EGCG,) this invasion or infiltration in human cell cultures, strengthening normal human salivary acinar cells. They studied the effect of the compound in mice and found that those that received an oral green tea extract experienced significantly less damage to their salivary glands, with reduced lymphocyte infiltration, as well as lower serum total autoantibody levels, compared to those that did not receive the compound.

    The researchers suspect that EGCG activates our defense system against a protein produced by the white blood cells during inflammation, and which causes cell-death. "The salivary gland cells treated with EGCG had much fewer signs of cell death caused by TNF-alpha," Dr. Hsu observed. "We don’t yet know exactly how EGCG makes that happen. That will require further study. In some ways, this study gives us more questions than answers."

    Research published: March, 2007, Autoimmunity, Medical College of Georgia researchers Stephen Hsu, et al.


    Stargardt's Disease

    1. DHA supplementation for late onset Stargardt disease: NAT-3 (2010 Study)

    2010 study showed some improvement in vision for those with Stargardt's Disease who supplemented with 840 mg per day of DHA (omega-3 fatty acids) for 6 months or more. DHA is the acronym for decosahexanoic acid, an essential omega-3 fatty acid.

    Ref: Authors: Giuseppe Querques, Pascale Benlian, Bernard Chanu, et al Published Date June 2010 Volume 2010:4 Pages 575 - 580 DOI: http://dx.doi.org/10.2147/OPTH.S1004


    Uveitis

    1. Bilberry (2010) and Uveitis

    Learn more about uveitis

    Researchers have found that mice with uveitis who were treated with bilberry extract had increased antioxidant levels in blood and improvements in blood levels of vitamin C and antioxidant enzymes such as glutathione peroxidase and superoxide dismutase (SOD). This uvetis in mice was induced by toxins, and represented a useful animal model of human eye inflammation.

    The bilberry extract, given orally, reduced elevated nitric oxide and malonidaldehyde levels (both toxins in the blood), and increased the ability of the blood to absorb oxegen as well as increasing glutathione, vitamin C, and SOD levels in the blood, as well as other beneficial changes in blood chemistry.

    Researchers: N. Yao, F. Lan, R.-R. He, H. Kurihara; Institute of Traditional Chinese Medicine and Natural Products, Jinan University, Guangzhou 510632, China.

    Published: Journal of Agricultural and Food Chemistry, March 2010. Protective Effects of Bilberry (Vaccinium myrtillus L.) Extract against Endotoxin-Induced Uveitis in Mice.

    2. Curcumin (2010) and Uveitis

    Learn more about uveitis

    Researchers have known for some time that tumeric (curcumin) is helpful for inflammatory conditions. A one year study evaluated the effectiveness of tumeric supplements in preventing relapses of uveitis.

    The researchers looked at 3 groups of uveitis patients: those with autoimmune uveitis, those with herpetic uvetis, and other forms of uveitis. They evaluated frequency and severity of relapses and overall quality of life.

    They found that the specific product which contained curcumin had the capacity to reduce symptoms after a few weeks in more than 80% of the 122 patients.

    Their study also demonstrated promising results for other vision inflammtory-related conditions such as dry eye, diabetic retinopathy, glaucoma, and pathological conditions of the macula such as macular degeneration, choroidal neovascularization, cellophane maculopathy, and retinitis pigmentosa.

    This study substantiates the findings of a small 1999 study: (Efficacy of curcumin in the management of chronic anterior uveitis. Phytother Res. 1999. Department of Ophthalmology, K.G. Medical College, Lucknow, India.

    Researchers: Pia Allegri, Antonio Mastromarino, and Piergiorgio Neri

    Published: Clin Ophthalmol. 2010; 4: 1201–1206.

    3. Echinachea (2006) and Uveitis

    Learn more about uveitis

    A small pilot study examined the value and safety of echinachea in mild forms of uveitis.

    The researchers evaluated the results of treating 51 patients with steriod-dependent, low-grade, autoimmune, anterior or intermediate uveitis. The patients had been taking oral prednisone. 31 of the patients received 150mg echinachea two times a day, and 20 continued with the conventional steriod treament. After 9 months, follow up demonstrated that almost 90% of the patients receiving echinachea showed improvement and vision acuity and reduction of symptoms.

    Researchers: Neri PG, Stagni E, Filippello M, Camillieri G, Giovannini A, Leggio GM, Drago F., Department of Neurosciences - Ophthalmology Section, Polytechnic University of Marche, Ancona, Italy.

    Published: J Ocul Pharmacol Ther. 2006 Dec;22(6):431-6., Oral Echinacea purpurea extract in low-grade, steroid-dependent, autoimmune idiopathic uveitis: a pilot study.