1. Allergies and sensitivies research summaries
Also see discussion of research.

1. Breneman JC. Basics of Food Allergy. Springfield, IL: Charles C Thomas, 1978, 45–53.
2. Darlington LG, Ramsey NW, Mansfield JR. Placebocontrolled, 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].
109. Hartman DE. Missed diagnoses and misdiagnoses of environmental toxicant exposure. The psychiatry of toxic exposure and multiple chemical sensitivity. Psychiatr Clin North Am 1998;21:659–70, vii [review].
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].
123. Pelto L, Isolauri E, Lilius EM, et al. Probiotic bacteria down-regulate the milk-induced inflammatory response in milk-hypersensitive subjects but have an immunostimulatory effect in healthy subjects. Clin Exp Allergy 1998;28:1474–9.
124. Salminen S, Isolauri E, Salminen E. Clinical uses of probiotics for stabilizing the gut mucosal barrier: successful strains and future challenges. Antonie Van Leeuwenhoek 1996;70:347–58 [review].
125. Majamaa H, Isolauri E. Probiotics: a novel approach in the management of food allergy. J Allergy Clin Immunol 1997;99:179–85.
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.
144. Wolkenstein E, Horak F. [Protective effect of acupuncture on allergen provoked rhinitis]. Wien Med Wochenschr 1998;148:450–3 [in German].
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.
165. Wraith DG. Recognition of food-allergic patients and their allergens by the RAST technique and clinical investigation. Clin Allergy 1979:25–36.
166. Lieberman P, et al. Controlled study of the cytotoxic food test. JAMA 1975:728–30.
167. Miller JB. A double-blind study of food extract injection therapy: a preliminary report. Ann Allerg 1977:185–91.
168. Hosen H. Provocative testing for food allergy diagnosis. J Asthma Res 1976:45–51.
169. Morris DL. Use of sublingual antigen in diagnosis and treatment of food allergy. Ann Allergy 1969;27:289–94.
170. Lehman CW. A double-blind study of sublingual provocative food testing: a study of its efficacy. Ann Allergy 1980;45:144–9.
171. Mandell M. Dr. Mandell’s 5-Day Allergy Relief System. Pocket Books, New York, 1979.
172. Tsuei JJ, Lehman CW, Lam FMK, et al. A food allergy study using the EAV acupuncture technique. Am J Acupuncture 1984;12:105–16.
173. Krop J, Swierczek J, Wood A. Comparison of ecological testing with the Vega test method in identifying sensitivities to chemicals, foods and inhalents. Am J Acupuncture 1985;13:253–9.

Alzheimer's Disease

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

1. Munoz DG. Is exposure to aluminum a risk factor for the development of Alzheimer disease?—No. Arch Neurol 1998;55:737–9.
2. Forbes WF, Hill GB. Is exposure to aluminum a risk factor for the development of Alzheimer disease?—Yes. Arch Neurol 1998;55:740–1.
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.
6. Kalmijn S, Lauher LJ, Ott A, et al. Dietary fat intake and the risk of incident dementia in the Rotterdam study. Ann Neurol 1997;42:776–82.
7. Friedland R. American Academy of Neurology’s 52nd Annual Meeting in San Diego, CA, April 29–May 6, 2000.
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.
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2. Memory (2005): DHEA Hormone Deficiency Impairs Memory

The brain requires youthful levels of certain hormones to facilitate cell energy metabolism, maintain proper levels of acetylcholine, and protect brain cell membrane function. As a result, aging persons often require some hormone replacement to achieve the requisite levels.

DHEA (dehydroepiandrosterone) improves brain cell activity and enhances memory. The daily production of DHEA drops from 30 mg at age 20 to less than 6 mg at age 80. DHEA is naturally synthesized in abundance in young people from pregnenolone in the brain and the adrenal glands.

Current findings suggest that DHEA enhances memory by facilitating the induction of neural plasticity, a condition that permits the neurons (nerve cells of the brain) to change in order to record new memories. Studies have shown that DHEA not only improves memory deficits, but also relieves depression in older people and increases their perceived physical and psychological well-being. DHEA has been shown to help preserve youthful neurological function. DHEA also helps to maintain the ability of brain cells to store and retrieve information involved in short-term memory.

(Note: Some persons should not take supplemental DHEA. Men with prostrate issues should consult with their doctors before going taking DHEA. For more information on precautions, go to http://www.lef.org/dhea/side_effects_of_taking_dhea.html

For women, the benefits of estrogen to the brain have long been known. However, the increased risk of breast cancer, heart attack, and other diseases associated with using estrogen drugs is motivating some women to change to DHEA (which converts to estrogen in the body) and, when necessary, to safer forms of estrogen such as estriol.

Editor's Note: If you are considering supplementing with DHEA, we recommend working with a nutritional consultant before adding DHEA to your regimen.

Anemia

1. Anemia (iron-deficiency) research summaries
Also see discussion of anemia research

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Atherosclerosis

1. Atheroscherosis research summaries
Also see discussion of research

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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.

Attention Deficit Disorder (ADD)

1. Attention Deficit Disorder ADD/ADHD Reseach Summaries
Also see discussion of 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.

Bladder Infection (UTI)

1. Urinary Tract Infections
Also see discussion.

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.

Cataracts

1. Alpha lipoic acid (1995) useful in cataract formation
Alpha Lipoic Acid can prevent cataract formation as well as nerve degeneration and radiation injury. 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.
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) 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. The results were discussed at the American Academy of Ophthalmology meeting held in November, 2001.

4. Antioxidants and Cataract Prevention
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.

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.

6. Cataract: Relationship Between Nutrition and Oxidation
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.

7. Cataracts & N-Acetyl-Carnosine (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

8. Glutathione - Antioxidant (2000)
Glutathione, which is particularly concentrated in the lens, has been shown to have a hydroxyl radical-scavenging function in lens epithelial cells. Giblin FJ. Glutathione: a vital lens antioxidant. J Ocul Pharmacol Ther 2000 Apr; 16(2):121-35.

An age-dependent drop in glutathione blood status and a significantly lower level of glutathione has been found in older individuals compared to younger ones. Moreover, an increase of oxidized glutathione by-product over time suggests more oxidation and the incumbent higher risk of age-related eye diseases. Brubaker RF, et al. Ascorbic acid content of human corneal epithelium.

Invest Ophthalmol Vis Sci 2000 Jun;41(7):1681-3.

9. Glutathione Lens Transparency: Cataracts
The reducing compound glutathione (GSH) exists in an unusually high concentration in the lens where it functions as an essential antioxidant vital for maintenance of the tissue's transparency - and a protection against cataracts. In conjunction with an active glutathione redox cycle located in the lens epithelium and superficial cortex, GSH detoxifies potentially damaging oxidants such as H2O2 and dehydroascorbic acid.

Recent studies have indicated an important hydroxyl radical-scavenging function for GSH in lens epithelial cells, independent of the cells' ability to detoxify H2O2. Depletion of GSH or inhibition of the redox cycle allows low levels of oxidant to damage lens epithelial targets such as Na/K-ATPase, certain cytoskeletal proteins and proteins associated with normal membrane permeability. The level of GSH in the nucleus of the lens is relatively low, particularly in the aging lens, and exactly how the compound travels from the epithelium to the central region of the organ is not known.

Recently, a cortical/nuclear barrier to GSH migration in older human lenses was demonstrated by Sweeney et al. The relatively low ratio of GSH to protein -SH in the nucleus of the lens, combined with low activity of the glutathione redox cycle in this region, makes the nucleus especially vulnerable to oxidative stress, as has been demonstrated with use of in vivo experimental animal models such as hyperbaric oxygen, UVA light and the glutathione peroxidase knockout mouse. Effects observed in these models, which are currently being utilized to investigate the mechanism of formation of human senile nuclear cataract, include an increase in lens nuclear disulfide, damage to nuclear membranes and an increase in nuclear light scattering. A need exists for development of therapeutic agents to slow age-related loss of antioxidant activity in the nucleus of the human lens to delay the onset of cataracts.

J Ocul Pharmacol Ther 2000 Apr;16(2):121-35

10. Leafy Green Veggies Protect Eyes
In a recent study published in the December issue of the Journal of Nutrition, researchers examined the effects of lutein and zeaxanthin on samples of human eye lens cells in the laboratory. They also compared the effects of these antioxidants on the cells to the effects of another antioxidant thought to improve eye health, vitamin E. Researchers treated the cells with various concentrations of the antioxidants and then exposed them to ultraviolet radiation. "The dose of UVB radiation we used on the cells is about the same amount a person receives when they get a mild tan," says Bomser. 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%. "Lutein and zeaxanthin accumulate in the retina and in the lens of the eye, but we're not sure how they reach the eye in the first place," says Bomser. "They travel through the bloodstream, but the lens doesn't have a blood supply." This study provides new evidence that these antioxidants, which are found in plants such as spinach, kale, and collard greens, can indeed help prevent cataracts by protecting the eyes from the damaging effects of ultraviolet sunlight. Source: Chitchiumroonchokchai, C. Journal of Nutrition, December 2004; vol 134: pp 3225-3232

11. Lipoic acid - Cataracts
Studies have shown beneficial effects of lipoic acid treatment on cataracts in rats. It may be of therapeutic use in preventing human cataracts and their associated complications. Lipoic acid has also been used to treat glaucoma. 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
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. Low levels of vitamin E - Cataracts
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

15. Lutein (1995) and Zeaxanthin - Cataracts & Cancer
(a) Xanthophylls Lutein and zeaxanthin) are the only carotenoids detected inhuman lens. Elevated plasma or nutrient intake levels of antioxidant vitamins, such as carotenoids, ... are associated with diminished risk for cataract... Elevated intake of spinach, which is high in lutein and zeaxanthin ..... was most consistently associated with a lower risk for cataract extraction. Elevations in lipid antioxidant status is associated with prolonged lens function.
(b) Xanthophylls are likely to eliminate the phototoxic blue light selectively. (c) There is a strong inverse association between elevated consumption of dark green vegetables, which are rich in lutein and zeaxanthin, and a decreased risk for oxidative stress related diseases such as cataract and cancer.
(d) Lutein and zeaxanthin are the only carotenoids that have been reported to be present in several sites of the human eye, such as the retina and the macula. Lutein and zeaxanthin are also the only carotenoids present inhuman lens. Consumption of spinach, which is rich in lutein and zeaxanthin showed a consistent inverse relationship with risk of cataract. Carotenoid intake is related to the risk for cataract. 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.

16. lutein (1999) (dietary) and cryptoxanthin - Cataracts
Dietary lutein and cryptoxanthin were associated with 70% lower risk of nuclear cataracts in those under age 65. Lyle, et al. Am J Clin Nutr 1999 Feb;69(2):272-7

17. Lutein (1999) and Cataract Prevention
Harvard Study Shows Relationship Between Higher Intake of Lutein and Lower Incidence of Cataracts

Researchers at the Harvard Medical School now report that the carotenoids lutein and zeaxanthin may be particularly effective in preventing cataracts. Their studies involved almost 80,000 females nurses and over 35,000 male health professionals who were enrolled in 1980 and 1986 respectively. The female study group completed diet questionnaires in 1980 and 1984 and were then followed up until 1992 at which time 1471 cataract extractions had been performed. The male group completed diet questionnaires in 1986 and were followed up until 1994 at which time 840 cataract extractions had been performed.

The researchers found that nurses with a high intake of lutein and zeaxanthin had a 22 per cent lower risk of cataract extraction than did women with the lowest intake. Among the men, the 20 per cent with the highest intake had a 19 per cent lower risk when compared with the 20 per cent with the lowest intake. The researchers found a significant protective effect of spinach, kale and broccoli, but found no significant effects of other carotenoids and could not confirm a previously reported protective effect of vitamin A. They conclude that lutein and zeaxanthin may reduce the risk of cataract formation and recommend daily consumption of fruits and vegetables high in carotenoids. 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)

18. N-Acetyl-Carnosine and Cataracts
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.

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.