Research Bibliography for Eye Conditions and Other Diseases
Note, to see the newer, better organized research section click here.Allergies & Sensitivities1. Allergies and Sensitivities Bibliography
Alzheimer's Disease1. Alzheimer's Disease Bilbiography
2. 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
3. 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 (Iron Deficiency)1. Anemia (iron-deficiency) Bibliography
Also see more information about anemia and nutritional recommendations. Asthenopia (eye fatigue)1. 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.
2. Study: 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 Atherosclerosis1. Atheroscherosis research bibliography
Attention Deficit Disorder (ADD)1. Attention Deficit Disorder ADD/ADHD Bibliography
Bladder Infections1. 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. Cataracts1. Alpha lipoic acid (1995) useful in cataract formation
See more information about cataracts. 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.
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:
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 including our nutritional recommendations and prevention and self help recommendations for cataracts.
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 (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.
7. Glutathione - Antioxidant (2000)
8. Glutathione Lens Transparency (2000): 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. Also see information about antioxidants and Glutathoine.
9. Leafy Green Veggies Protect Eyes (2004)
In a 2004 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 Learn more about cataracts.
10. Lipoic acid - Cataracts (1995)
11. Long Term Lutein Supplementation Improves Visual Acuity in Age-Related Cataracts
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
12. Low levels of vitamin E (1993)
13. Lutein (1995) and Zeaxanthin - Cataracts & Cancer
14. lutein (1999) (dietary) and cryptoxanthin - Cataracts
15. Lutein (1999) and Cataract Prevention
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)
16. Lutein, Zeaxanthin and Vitamin E Reduce Risk of Cataracts Jan. 2008 Study
17. N-Acetyl-Carnosine (NAC) (2001) & Cataracts
See more about cataracts treatment and information. 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.
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.
19. NASA Study of Cataract in Astronauts (NASCA)
20. Nutrition (1993) and Oxidation: Cataracts
See more about cataracts treatment and information. Taylor A.,
Journal of the American College of Nutrition, 1993 Apr, 12(2):138-46
Pub type: Journal Article; Review; Review, Tutorial. (UI: 93217072)
21. Riboflavin (1991), vitamins C, E, carotene, niacin, thiamine & cataracts
See more about cataracts treatment and information. Dietary intake of riboflavin, vitamins C, E, and carotene, niacin, and thiamine significantly decreased the risk of all cataract types. Combining the different antioxidant nutrients produced the greatest effect. Leske, et al. Arch Ophthalmol 1991 Feb;109(2):244-51.
22. Smoking - Cataracts (1993)
23. Study Suggests Lutein and Zeaxanthin Offer Lens Protection
24. Study Suggests Statins Can Cause Cataracts (2011 Study)
25. Sugar can impair the lens (1991)
26. Vitamin A - Cataracts
27. 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 including nutritional recommendations and prevention recommendations for cataracts.
28. Vitamin C - Cataracts
29. Vitamin C - cataracts & opacities (1997)
30. Vitamin C - cataracts (1995)
31. Vitamin C - Cataracts (NHS) (1997)
32. 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
33. 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. Read more about cataracts and other nutritional recommendations.
34. Vitamin C May Also Offer Protection Against Cataracts
35. Vitamin C Might Prevent Cataracts in Women
36. Vitamin E - Cataracts (1991)
37. 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.
38. Vitamin E and Cataract Prevention 2008 Study
39. Vitamin E, C, alpha-lipoic acid and taurine (1997)
Vitamin E, vitamin C, alpha-lipoic acid, and taurine appear to offer protection against lens damage caused by low level radiation. Bantseev, et al. Biochem Mol Biol Int 1997 Sept;42(6):1189-97. See more information about cataracts, including nutritional recommendations and prevention and self help recommendations for cataracts. Celiac Disease1. Celiac Disease research bibliography
Chronic Fatigue1. 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]. Computer Eye Strain1. AOA (2007) Advises Daily Computer Users of the Risk of Computer Vision Syndrome
The American Optometric Association advises Americans who use computers daily that they should be aware of computer vision syndrome (CVS), which can give rise to problems such as 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. According to the AOA's American 2007 Eye-Q survey of 1,005 Americans 18 years and older, 82 percent of respondents frequently work with a computer or a handheld electronic device and 42 percent spent three or more hours a day in front of a computer or handheld device. Additionally, 78 percent of Americans 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. Forty-one percent of survey respondents have experienced eye strain; 45 percent have had neck or back pain after prolonged computer or handheld device use. Although 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 percent of respondents said that they currently use special computer glasses or computer screen filters to help reduce glare and discomfort. The AOA's guidelines for preventing or reducing computer vision syndrome include having vision checked regularly, limiting the amount of continuous time before the computer, checking the arrangement and height of the monitor, checking the screen for glare, reducing the amount of lighting in the room to match the screen and reminding oneself to blink frequently.
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
A 2009 study from Beijing-based researchers, published in the British Journal of Nutrition, has noted improvements in the sensitivity to contrast on a computer screen in subjects taking lutein! Thirty-seven healthy subjects between the ages of 22 and 30 with long-term computer display light exposure were studied. 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. See the abstract at Journals.cambridge.org. Editor's Note: Lutein is now added to the Astaxanthin as two nutrients that can help reduce computer eye strain.
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 Crohn's Disease1. 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]. 34. Dvorak AM. Vitamin A in Crohn’s Disease. Lancet 1980;i:1303–4 [letter]. 35. Wright JP, Mee AS, Parfitt A, et al. Vitamin A therapy inpatients with Crohn’s disease. Gastroenterology 1985;88:512–4. 36. Hegnhoj J, Hansen CP, Rannem T, et al. Pancreatic function in Crohn’s disease. Gut 1990;31:1076–9. 37. Pizzorno JE, Murray MT. Textbook of Natural Medicine. London: Churchill Livingstone, 1999, 1335–49. 38. Plein K, Burkard G, Hotz J. Treatment of chronic diarrhea in Crohn disease. A pilot Diabetes Mellitus1. Diabetes Mellitus Bibliography
Diabetic Retinopathy1. Alpha lipoic acid (1997) - Diabetic Retinopathy, Cataracts
See more information about cataracts treatment and information and diabetic retinopathy treatment and information. Alpha Lipoic Acid can significantly reduce diabetic cataract formation, as well as neuropathy, and would seem to be an ideal neuroprotective substance in the treatment of all oxidative brain and neural disorders involving free radical processes. 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
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 extracts (1995, 1997) - diabetic retinopathy
See more about diabetic retinopathy treatment and information. Studies confirmed the folk beliefs that bilberry extracts could improve visual acuity and lead to faster visual adjustments between light (eg, glare and darkness, ref 2). European physicians recommend bilberry extracts for other eye complaints (eg, retinitis pigmentosa, diabetic retinopathy). (pg. 1), (b) An experiment using a preparation of anthocyanosides from bilberry ... indicated vaso-protective and anti-edema effects in ... animals. (ref. 3) When vascular permeability is increased in rabbits .. A treatment of anthocyanosides from bilberry decreases vascular permeability. This is achieved when the drug interacts with collagen to increase its cross-links., c) Administration of anthocyanosides ... maintains normal blood barrier permeability and limits the increase in vascular permeability. "Topic: Bilberry Fruit," The Lawrence Review of Natural Products, October 1995, Pages 1-2.
Lipoic acid may be beneficial in improving nerve blood flow, reducing oxidative stress, and improving nerve conduction in diabetic neuropathy.3 The effects of lipoic acid on diabetic neuropathy have been studied in two German randomized, double-blind, placebo-controlled trials. In the first of these, 328 patients with Type II diabetes and symptoms of peripheral neuropathy were treated with either intravenous infusion of lipoic acid or placebo for three weeks. The results showed improvements in symptoms. In another study, patients with Type II diabetes and cardiac autonomic neuropathy were treated with a daily oral dose of 800 mg lipoic acid or placebo for four months. Two out of four symptoms test measurements were significantly improved in those taking the lipoic acid compared with placebo. 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
Bioflavonoids were found to normalize blood vessels' permeability in diabetic patients. Valenci, et al. Diabet Med 1996 Oct;13(10):882-8
6. Chromium (1995) supplements
See more about diabetic retinopathy treatment and information. 73% of type I and II diabetics who took chromium supplements reduced their requirement for insulin or oral hypoglycemic agents. Taking chromium and niacin together reduced fasting blood sugar levels and improved glucose tolerance. J Trace Elem Exp Med 1995: 8:183-90; Urberg M, Zemel MB, Metabolism 1987; 36:896-99
7. Chromium (1997) vitamin E, magnesium, soluble fiber, taurine & diabetic retinopathy
Learn more about diabetic retinopathy treatment and information. Chromium, high-dose vitamin E, magnesium, soluble fiber, and possibly taurine appear likely to lessen risk for macrovascular disease (retinopathy) in diabetics. McCarty, Med Hypothesis 1997 Aug;49(2):143-52
8. 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.
9. 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.
10. 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].
11. Gymnema Sylvestre and Diabetes Study
The Journal of Ethnopharmacology recently published a small study out of India that examined the effects of an extract of the leaves of Gymnema sylvestre on high blood sugar. Twenty-two people with type 2 diabetes were given 400 milligrams of the extract for 18 to 20 months as a supplement to their regular medical regimen of oral anti-hyperglycemic agents. During that period, an unspecified number of the patients apparently showed significant reductions in blood glucose and A1c's. Five of them 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. Sources: Journal of Ethnopharmacology
12. High serum levels of magnesium
13. Lipoic acid - diabetic retinopathy
14. Low magnesium levels - diabetic retinopathy
15. Low serum carotenoid levels
16. Taurine - diabetic retinopathy
Taurine also appears to protect the lens against the development of “sugar cataracts” by an antioxidant effect. (12) 10. Stevens et al, Am J Physiol 1999 Oct;277(4 Pt 1):E760-E771. 12. Malone JI, Benford SA, Malone J Jr, Diabetes Complications
17. Vitamin B12 - diabetic retinopathy
18. Vitamin C, E, Beta Carotene and Selenium
19. Vitamin E - Diabetic Retinopathy
Dry Eyes1. 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:
2. 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:
3. 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 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. 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.
4. 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.
5. 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:
6. 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.
7. 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.
8. Vitamin A and Cyclosporine A (2008) Dry Eye Syndrome: Comparison of Vitamin A and Cyclosporine A
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:
Conclusions: Department of Ophthalmology and Visual Science, College of Medicine, The Catholic University of Korea, Seoul, Korea Accepted 11 August 2008. published online 09 October 2008. Inquiries to 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. Enlarged Prostrate1. Enlarged Prostate (Benign Prosatic Hyperplasia ) Bibliography
Also see discussion of enlarged prostate (benign prosatic hyperplasia) and research.
Also see more information about enlarged prostate, including nutritional recommendations and prevention recommendations for benign prostatic hyperplasia. Fuch's Dystrophy1. 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: Glaucoma1. 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. Carotenoids (1994) and green leafy vegetables
See more information about glaucoma treatment and information. Besides beta carotene, other carotenoids found in dark green leafy vegetables appear to be much more essential to the health of the eye. Several studies have shown that lutein and zeaxanthin supplements may slow vision loss in glaucoma, and in some cases improve eyesight.Science News, Volume 146, 1994.
5. 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].
6. 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).
7. 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:
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
8. 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:
9. Ginkgo biloba (2006) & Steroid-Induced Changes in the Trabecular Meshwork & Intraocular Pressure
Learn more information about glaucoma treatment and information. In this study, published in 2006, young rabbits received topical TobraDEX and/or 5 µg of Ginkgo biloba extract 4x daily for 2 weeks, and their intraocular pressure (was recorded every 3 days. The purpose was to study the effects of Ginkgo on ocular hypertension. The eye was then examined and the network of fibers in the eye were assessed and it was found that Ginkgo biloba extract suppressed steroid-induced IOP elevation in rabbits. Ginkgo treatment reduced the accumulation of extracellular materials within the layers of the trabecular meshwork (TM) and achieved better TM cell health. In cultured human TM cells, 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. Clinical Relevance Ginkgo biloba extract could be a therapeutic agent or dietary supplement to prevent steroid-induced ocular hypertension. SOURCE: 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.
10. Glaucoma & Exercise (2004)
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. 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.
11. 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
12. Glaucoma (2008) Neuroprotection by Vitamin E in Glaucoma
Vitamin E: More Than an Antioxidant Vitamin E is best known as the body's major fat-soluble antioxidant. Its main function is to intercept free radicals and prevent chain reactions of lipid destruction. However the discovery of complex molecules that control vitamin E metabolism such as tocopherol transfer protein, alpha tocopherol membrane receptors, and intracellular transfer proteins, triggered the idea that the activity of vitamin E extends beyond its antioxidant capacity. Vitamin E is now known to affect the expression and activity of immune and inflammatory cells, to enhance vasodilation, and to inhibit the activity of the important cell signaling molecule protein kinase C (PKC). Modulating the PKC pathway may be relevant in glaucoma. For instance, PKC inhibitors have been shown to relax the trabecular meshwork, and to affect matrix metalloproteinase and PGF2 alpha. 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 pathway (1,2). These findings prompted researchers at Istanbul University to evaluate the clinical potential of vitamin E in glaucoma patients. They report prevention of visual field loss in this preliminary study, and conclude that vitamin E deserves further attention in preventing glaucomatous damage (3).
Study Design and Methods 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 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 (Tables, below). 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. 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. Engin KN et al. Clinical evaluation of the neuroprotective effect of alpha tocopherol in glaucomatous damage. Eur J Ophthalmol 17:528-33, 2007.
13. Glaucoma (2008) Risk Reduction through Nutrition
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, was lead author of one study that was recently published in the American Journal of Ophthalmology. The object of her study was to see whether specific nutrients might account for an apparent association between glaucoma risk and fruit and vegetable consumption, and to investigate potential links between glaucoma risk and antioxidants, calories, fat, protein, and carbohydrates obtained from natural food sources. Study 1 Summary (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):
A second nutrition-related study that also drew data from the Study of Osteoporotic Fractures was conducted by JoAnn A. Giaconi, MD, assistant clinical professor of ophthalmology at the Jules Stein Eye Institute at UCLA. Study 2 Summary: 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. Dr. Giaconi’s data included 584 black women; 13 percent (77 women) had glaucoma in at least one eye. [Giaconi JA, et al. IOVS 2008;49; ARVO E-abstract 5453]. Dr. Giaconi who headed this study notes that it’s dangerous to draw too many conclusions from the nutrition-related data that has been found so far. “My study was an exploratory study,” she says. “The data clearly show associations, but we can’t say for sure that the difference in diet caused the difference in glaucoma risk. Did eating more collard greens reduce the likelihood of developing glaucoma, or is there something else about the individuals who eat more collard greens that makes them less likely to develop glaucoma? Maybe those individuals exercise more. Maybe they grew up in a different environment. Maybe they metabolize nutrients differently. We can’t claim that the association is causal, but I believe the association is worth pursuing." For more details, go to http://www.revophth.com/index.asp?page=1_14082.htm
14. Glaucoma (2010): Green Tea Can Help Combat Glaucoma
Researchers in China say studies in rats indicate substances in green tea may protect against eye diseases such as glaucoma. Scientists led by Chi Pui Pang of the Chinese University of Hong Kong and Hong Kong Eye Hospital confirmed green tea substances -- known for antioxidant and disease-fighting properties -- were absorbed in the lens, retina and other eye tissue. The study, published in the Journal of Agricultural and Food Chemistry, suggested until now it was not known if 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 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. "Our results indicate that green tea consumption could benefit the eye against oxidative stress," the study researchers said in a statement. Reported in April, 2010 ACS' bi-weekly Journal of Agricultural and Food Chemistry. Learn more about glaucoma including nutritional recommendations and prevention and self help recommendations. Also see the article, How Heavy Computer Use Contributes to Glaucoma.
15. Glaucoma 2006: A Sick Eye in a Sick Body
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.
16. Glaucoma: Bilberry and pine bark (2008) combo wards off glaucoma: study
In a study performed by researchers from the University of Chieti-Pescara in San Valentino, Italy, thirty-eight subjects with IOP were either given bilberry and French maritime pine bark (20 subjects) or were not treated (18 subjects)1. The visual acuity, IOP, and ocular blood flow were measured at two, three, and six months. After two months of supplementation 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 results of this study indicate that bilberry and pine bark may represent a safe preventative intervention for lowering the risk for developing symptomatic glaucoma by controlling IOP and improving ocular blood flow. This helps to support research for other preventative nutritional approaches to major eye health, such as cataract, age-related macular degeneration, and retinopathy. IOP was also seen to be lowered in 19 of the 20 intervention patients, from an average of 25.2mmHg to 22.0mmHG. Only one of the control patients saw a drop in IOP. The researchers also looked at the eyes' arteries using color Doppler imaging. They saw better flood flow in the intervention group, which was taken as an indication that fluids in the eye were being restored. "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," wrote Steigerwalt. 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
17. Green Tea Could Help Combat Diseases of the Eye
Researchers in China say studies in rats indicate substances in green tea may protect against eye diseases such as glaucoma. Scientists led by Chi Pui Pang of the Chinese University of Hong Kong and Hong Kong Eye Hospital confirmed green tea substances -- known for antioxidant and disease-fighting properties -- were absorbed in the lens, retina and other eye tissue. The study, published in the Journal of Agricultural and Food Chemistry, suggested until now it was not known if 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 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. "Our results indicate that green tea consumption could benefit the eye against oxidative stress," the study researchers said in a statement. Reported in April, 2010 ACS' bi-weekly Journal of Agricultural and Food Chemistry. Editor's Note: Catechins such as those found in green tea are among a number of antioxidants, including vitamin C, vitamin E, lutein, and zeaxanthin, thought to help protect the delicate tissues of the eye from glaucoma and other eye ailments.
18. homocysteine (2004) elevated levels in aqueous humor of patients with pseudoexfoliation glaucoma.
Learn more information about glaucoma treatment and information. Elevated homocysteine levels in aqueous humor of patients with pseudoexfoliation glaucoma. 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 PURPOSE: To determine total homocysteine levels in aqueous humor of pseudoexfoliation open-angle glaucoma patients. DESIGN: Case-control study. METHODS: Total homocysteine levels were measured by enzyme-linked immunosorbent assay in aqueous humor and plasma of 29 patients with pseudoexfoliation glaucoma and 31 control patients with cataract. Patients with factors affecting homocysteine levels were excluded. RESULTS: We observed significantly elevated (twofold) homocysteine levels in the aqueous humor of the glaucoma patients (Z = -5.11, P <.0001). Additionally, the calculated ratio (plasma:aqueous humor) was significantly lower in these patients (Z = -3.57, P <.001), and aqueous homocysteine was significantly correlated with their respective elevated plasma levels (r =.42, P =.02). CONCLUSIONS: Because homocysteine induces vascular injury and alterations of extracellular matrix, high aqueous homocysteine may trigger the abnormal matrix accumulation characteristic. It may reflect the proposed impairment of the blood-aqueous barrier of pseudoexfoliation open-angle glaucoma and be involved in its pathogenesis. PMID: 15234308 [PubMed - indexed for MEDLINE]
19. Hypnosis Can Help Lower Intraocular Pressure
20. Hypnosis on Intraocular Pressure Glaucoma
21. 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
22. Lipoic acid - Glaucoma
23. Lipoic acid - Glaucoma
24. Magnesium - glaucoma
25. Mini-Strokes May Cause Vision Loss for Those with Normal Tension Glaucoma
26. Mirtogenol (2010) and Glaucoma, Lowers Eye Pressure
A study published in a 2010 issue of the journal Clinical Opthamology examined the effects of Mitrogenol in a group of 79 patients living with "asymptomatic ocular hypertension". The participants were separated into three groups:
The trial lasted a total of 24 weeks and yielded the following results:
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.
27. Natural Occurring Growth Factor May Regenerate Retinal Nerve Fiber
Investigators in this animal study identified a calcium-binding protein called oncomodulin as a powerful macrophage-derived growth factor for RGCs and other neurons. In vivo, the oncomodulin promoted regeneration in the mature rat optic nerve; it also stimulated outgrowth from peripheral sensory neurons. The authors of the study believe that oncomodulin could some day prove useful in reversing optic nerve damage caused by glaucoma, tumors, or traumatic injury to the eye.
28. Omega-3 - glaucoma
29. Physical Activity and Glaucoma Incidence Reduction
This study assessed the dose-response relationship of vigorous physical activity (running distance, km x d[-1]) or cardiorespiratory fitness (meters-per-second pace during a 10-km footrace) to the risk for incident glaucoma. Participant-reported, physician-diagnosed incident glaucoma was compared with distance run per week and 10-km footrace performance in a cohort of 29,854 male runners without diabetes followed prospectively for 7.7 years. The survival analyses were adjusted for age, hypertension, current and past cigarette use and intakes of meat, fish, fruit and alcohol. Two hundred incident glaucoma cases were reported during follow up. The risk for reported glaucoma decreased 37% per meter per second increment in a 10-km race performance. Relative to the least fit men (i.e., slowest, < or = 3.5 m x s[-1]), the risk for incident-reported glaucoma declined 29% in those who ran 3.6-4.0 m x s(-1), 54% for those who ran 4.1-4.5 m x s(-1), 51% for those who ran 4.6-5.0 m x s(-1), and glaucoma was nonexistent among the 781 men who exceeded 5.0 m x s(-1). The risk for incident, reported glaucoma decreased 5% per kilometer per day run at baseline, which remained significant when adjusted for the 10-km race performance (5% reduction per kilometer per day), and both body mass index and race performance. Baseline hypertension was unrelated to the incident glaucoma. These data provide preliminary evidence that vigorous physical activity may reduce glaucoma risk, which, in the absence of medical record validation, could represent ocular hypertension in addition to frank glaucoma. Additional follow up with validation is needed to identify the type of glaucoma affected. SOURCE: Williams PT. 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
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, an Additional Risk Factor in Elder Women with Primary Open-Angle Glaucoma 2009 Study
Inflammation and apoptosis (cell death) marker levels increase with smoking in the aqueous humor and plasma samples of women with primary open angle glaucoma. Smoking could be an important additional risk factor for glaucoma progression in elderly women. SOURCE: 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
33. Studies Show Relationship of Blood Pressure and Glaucoma
34. Study: Glaucoma (2004) linked to Heavy Computer Use
35. Thiamine blood level and chronic open angle glaucoma
36. 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.
37. Vascular changes
38. Vascular obstruction (1993)
39. Vitamin B12 - glaucoma
40. Vitamin B12 - glaucoma
41. Vitamin C - Glaucoma
Gout1. 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. 6. Oster KA. Xanthine oxidase and folic acid. Ann Intern Med 1977;87:252–3. 7. Boss GR, Ragsdale RA, Zettner A, Seegmiller JE. Failure of folic acid (pteroylglutamic acid) to affect hyperuricemia. J Lab Clin Med 1980;96:783–9. 8. Stein HB, Hasan A, Fox IH. Ascorbic acid-induced uricosuria: a consequence of megavitamin therapy. Ann Intern Med 1976;84:385–8. 9. Bindoli A, Valente M, Cavallini L. Inhibitory action of quercetin on xanthine oxidase and xanthine dehydrogenase activity. Pharmacol Res Commun 1985;17:831–9. 10. Busse W, Kopp D, Middleton E. Flavonoid modulation of human neutrophil function. J Allergy Clin Immunol 1984;73:801–9. Hay Fever1. Hay Fever Bibliography
Also see discussion of hay fever and research. Related condition: allergies and sensitivities. 1. Speer F. Multiple food allergy. Ann Allerg 1975;34:71–6. 2. Buczylko K, Kowalczyk J, Zeman K, et al. Allergy to food in children with pollinosis. Rocz Akad Med Bialymst 1995;40:568–72. 3. Ogle KA, Bullock JD. Children with allergic rhinitis and/or bronchial asthma treated with elimination diet. Ann Allergy 1977;39:8–11. 4. Holmes HM, Alexander W. Hay fever and vitamin C. Science 1942;96:497. 5. Ruskin SL. High dose vitamin C in allergy. Am J Dig Dis 1945;12:281. 6. Fortner BR Jr, Danziger RE, Rabinowitz PS, Nelson HS. The effect of ascorbic acid on cutaneous and nasal response to histamine and allergen. J Allergy Clin Immunol 1982;69:484–8. 7. Balabolkin II, Gordeeva GF, Fuseva ED, et al. Use of vitamins in allergic illnesses in children. Vopr Med Khim 1992;38:36–40. 8. Cazzola P, Mazzanti P, Bossi G. In vivo modulating effect of a calf thymus acid lysate on human T lymphocyte subsets and CD4+/CD8+ ratio in the course of different diseases. Curr Ther Res 1987;42:1011–7. 9. Kouttab NM, Prada M, Cazzola P. Thymomodulin: Biological properties and clinical applications. Med Oncol Tumor Pharmacother 1989;6:5–9 [review]. 10. Marzari R, Mazzanti P, Cazzola P, Pirodda E. Perennial allergic rhinitis: prevention of the acute episodes with Thymomodulin. Minerva Med 1987;78:1675–81. 11. Gopalakrishnan C, Shankaranarayan D, Nazimudeen SK, et al. Effect of tylophorine, a major alkaloid of Tylophora indica, on immumopathological and inflammatory reactions. Ind J Med Res 1980;71:940–8. 12. Mittman P. Randomized double-blind study of freeze-dried Urtica diocia in the treatment of allergic rhinitis. Planta Med 1990;56:44–7. 13. Weiss RF. Herbal Medicine. Gothenburg, Sweden: Ab Arcanum and Beaconsfield, UK: Beaconsfield Publishers Ltd, 1988, 219 [review]. 14. Weiss RF. Herbal Medicine. Gothenburg, Sweden: Ab Arcanum and Beaconsfield, UK: Beaconsfield Publishers Ltd, 1988, 219 [review]. 15. Baba S, Takasaka T. Double-blind clinical trial of sho-seiryu-to (TJ-19) for perennial nasal allergy. Clin Otolaryngol 1995;88:389–405. High Cholesterol1. High Cholesterol (2005): Beneficial Effects of Olive Oil
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 25 milliliters (mL) -- 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. For more information go to http://www.mercola.com/forms/oil_vinegar.htm
2. High Cholesterol Bibliography
Also see discussion of high cholesterol and research. 1. Kromhout D, Menotti A, Bloemberg B, et al. Dietary saturated and trans fatty acids and cholesterol and 25-year mortality from coronary heart disease: the Seven Countries Study. Prev Med 1995;24:308–15.2. Tell GS, Evans GW, Folsom AR, et al. Dietary fat intake and carotid artery wall thickness: the Atherosclerosis Risk in Communities (ARIC) study. Am J Epidemiol 1994;139:979–89. 3. Ornish D, Brown SE, Scherwitz LW, et al. Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial. Lancet 1990;336:129–33. 4. Denke MA, Grundy SM. Comparison of effects of lauric acid and palmitic acid on plasma lipids and lipoproteins. Am J Clin Nutr 1992;56:895–8. 5. Zock PL, de Vries JHM, Katan MB. Impact of myristic acid versus palmitic acid on serum lipid and lipoprotein levels in healthy women and men. Arterioscler Thromb 1994;14:567–75. 6. Kumar PD. The role of coconut and coconut oil in coronary heart disease in Kerala, south India. Trop Doct 1997;27:215–7. 7. Denke MA, Grundy SM. Comparison of effects lof auric acid and palmitic acid on plasma lipids and lipoproteins. Am J Clin Nutr 1992;56:895–8. 8. Mendis S, Kumarasunderam R. The effect of daily consumption of coconut fat and soya-bean fat on plasma lipids and lipoproteins of young normolipidaemic men. Br J Nutr 1990;63:547–52. 9. Dreon DM, Fernstrom HA, Williams PT, Krauss RM. A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins. Am J Clin Nutr 1999;69:411–8. 10. Hepner G, Fried R, St Jeor S, et al. Hypocholesterolemic effect of yogurt and milk. Am J Clin Nutr 1979;19–24. 11. Agerholm-Larsen L, Raben A, Haulrik N, et al. Effect of 8 week intake of probiotic milk products on risk factors for cardiovascular diseases. Eur J Clin Nutr 2000;54:288–97. 12. Bertolami MC, Faludi AA, Batlouni M. Evaluation of the effects of a new fermented milk product (Gaio) on primary hypercholesterolemia. Eur J Clin Nutr 1999;53:97–101. 13. Anderson JW, Gilliland SE. Effect of fermented milk (yogurt) containing Lactobacillus acidophilus L1 on serum cholesterol in hypercholesterolemic humans. J Am Coll Nutr 1999;18:43–50. 14. Schaafsma G, Meuling WJ, van Dokkum W, Bouley C. Effects of a milk product, fermented by Lactobacillus acidophilus and with fructo-oligosaccharides added, on blood lipids in male volunteers. Eur J Clin Nutr 1998;52:436–40. 15. Agerbaek M, Gerdes LU, Richelsen B. Hypocholesterolaemic effect of a new fermented milk product in healthy middle-aged men. Eur J Clin Nutr 1995;49:346–52. 16. Richelsen B, Kristensen K, Pedersen SB. Long-term (6 months) effect of a new fermented milk product on the level of plasma lipoproteins—a placebo-controlled and double blind study. Eur J Clin Nutr 1996;50:811–5. 17. De Roos NM, Schouten G, Katan MB. Yoghurt enriched with Lactobacillus acidophilus does not lower blood lipids in healthy men and women with normal to borderline high serum cholesterol levels. Eur J Clin Nutr 1999;53:277–80. 18. Thompson LU, Jenkins DJ, Amer MA, et al. The effect of fermented and unfermented milks on serum cholesterol. Am J Clin Nutr 1982;36:1106–11. 19. Rossouw JE, Burger EM, Van der Vyver P, Ferreira JJ. The effect of skim milk, yoghurt, and full cream milk on human serum lipids. Am J Clin Nutr 1981;34:351–6. 20. Santos MJ, Lopez-Jurado M, Llopis J, et al. Influence of dietary supplementation with fish on plasma total cholesterol and lipoprotein cholesterol fractions in patients with coronary heart disease. J Nutr Med 1992;3:107–15. 21. Kromhout D, Bosschieter EB, Coulander CD. The inverse relation between fish consumption and 20-year mortality from coronary heart disease. N Engl J Med 1985;312:1205–9. 22. Ascherio A, Rimm EG, Stampfer MJ, et al. Dietary intake of marine n-3 fatty acids, fish intake, and the risk of coronary disease among men. N Engl J Med 1995;332:977–82. 23. Albert CM, Manson JE, O’Donnell C, et al. Fish consumption and the risk of sudden death in the Physicians’ Health Study. Circulation 1996;94(Suppl 1):I–578 [abstract #3382]. 24. Thorogood M, Carter R, Benfield L, et al. Plasma lipids and lipoprotein cholesterol concentrations in people with different diets in Britain. Br Med J (Clin Res Ed) 1987;295:351–3. 25. Burr ML, Sweetnam PM. Vegetarianism, dietary fiber and mortality. Am J Clin Nutr 1982;36:873–7. 26. Resnicow K, Barone J, Engle A, et al. Diet and serum lipids in vegan vegetarians: a model for risk reduction. J Am Dietet Assoc 1991;91:447–53. 27. Ornish D, Brown SE, Scherwitz LW, et al. Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial. Lancet 1990;336:129–33. 28. Ornish D, Scherwitz LW, Billings JH, et al. Intensive lifestyle changes for reversal of coronary heart disease. JAMA 1998;280:2001–7. 29. Connor SL, Connor WE. The importance of dietary cholesterol in coronary heart disease. Prev Med 1983;12:115–23 [review]. 30. Edington JD, Geekie M, Carter R, et al. Serum lipid response to dietary cholesterol in subjects fed a low-fat, high-fiber diet. Am J Clin Nutr 1989;50:58–62. 31. Raloff J. Oxidized lipids: a key to heart disease? Sci News 1985;127:278. 32. Levy Y, Maor I, Presser D, Aviram M. Consumption of eggs with meals increases the susceptibility of human plasma and low-density lipoprotein to lipid peroxidation. Ann Nutr Metabol 1996;40:243–51. 33. Shekelle RB, Stamler J. Dietary cholesterol and ischaemic heart disease. Lancet 1989;i:1177–9. 34. Hu FB, Stampfer MJ, Rimm EB, et al. A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 1999;281:1387–94. 35. Anderson JW, Chen WJL. Legumes and their soluble fiber: effect on cholesterol-rich lipoproteins. In: Furda I, ed. Unconventional Sources of Dietary Fiber. Washington, DC: American Chemical Society, 1983. 36. Ripsin CM, Keenan JM, Jacobs DR, et al. Oat products and lipid lowering—a meta-analysis. JAMA 1992;267:3317–25. 37. Anderson JW, Allgood LD, Lawrence A, et al. Cholesterol-lowering effects of psyllium intake adjunctive to diet therapy in men and women with hypercholesterolemia: meta-analysis of 8 controlled trials. Am J Clin Nutr 2000;71:472–9. 38. Miettinen TA, Tarpila S. Effect of pectin on serum cholesterol, fecal bile acids and biliary lipids in normolipidemic and hyperlipidemic individuals. Clin Chim Acta 1977;79:471–7. 39. Glore SR, Van Treeck D, Knehans AW, Guild M. Soluble fiber and serum lipids: a literature review. J Am Dietet Assoc 1994;94:425–36. 40. Romero AL, Romero JE, Galaviz S, Fernandez ML. Cookies enriched with psyllium or oat bran lower plasma LDL cholesterol in normal and hypercholesterolemic men from Northern Mexico. J Am Coll Nutr 1998;17:601–8. 41. Rimm EB, Ascherio A, Giovannucci E, et al. Vegetable, fruit, and cereal fiber intake and risk of coronary heart disease among men. JAMA 1996;275:447–51. 42. Knopp RH, Superko HR, Davidson M, et al. Long-term blood cholesterol-lowering effects of a dietary fiber supplement. Am J Prev Med 1999;17:18–23. 43. Lovegrove JA, Clohessy A, Milon H, Williams CM. Modest doses of beta-glucan do not reduce concentrations of potentially atherogenic lipoproteins. Am J Clin Nutr 2000;72:49–55. 44. Uusitupa MI, Ruuskanen E, Makinen E, et al. A controlled study on the effect of beta-glucan-rich oat bran on serum lipids in hypercholesterolemic subjects: relation to apolipoprotein E phenotype. J Am Coll Nutr 1992;11:651–9. 45. Braaten JT, Wood PJ, Scott FW, et al. Oat beta-glucan reduces blood cholesterol concentration in hypercholesterolemic subjects. Eur J Clin Nutr 1994;48:465–74. 46. Davidson MH, Dugan LD, Burns JH, et al. The hypocholesterolemic effects of beta-glucan in oatmeal and oat bran. A dose-controlled study. JAMA 1991;265:1833–9. 47. Onning G, Wallmark A, Persson M, et al. Consumption of oat milk for 5 weeks lowers serum cholesterol and LDL cholesterol in free-living men with moderate hypercholesterolemia. Ann Nutr Metab 1999;43:301–9. 48. Beer MU, Arrigoni E, Amado R. Effects of oat gum on blood cholesterol levels in healthy young men. Eur J Clin Nutr 1995;49:517–22. 49. Bierenbaum ML, Reichstein R, Watkins TR. Reducing atherogenic risk in hyperlipemic humans with flaxseed supplementation: a preliminary report. J Am Coll Nutr 1993;12:501–4. 50. Cunnane SC, Ganguli S, Menard C, et al. High alpha-linolenic acid flaxseed (Linum usitatissimum): some nutritional properties in humans. Br J Nutr 1993;69:443–53. 51. Arjmandi BH, Khan DA, Juma S, et al. Whole flaxseed consumption lowers serum LDL-cholesterol and lipoprotein(a) concentrations in postmenopausal women. Nutr Res 1998;18:1203–14. 52. Jenkins DJA, Kendall CWC, Vidgen E, et al. Health aspects of partially defatted flaxseed, including effects on serum lipids, oxidative measures, and ex vivo androgen and progestin activity: a controlled crossover trial. Am J Clin Nutr 1999;69:395–402. 53. Kelley DS, Nelson GJ, Love JE, et al. Dietary alpha-linolenic acid alters tissue fatty acid composition, but not blood lipids, lipoproteins or coagulation status in humans. Lipids 1993;28:533–7. 54. Chan JK, Bruce VM, McDonald BE. Dietary a-linolenic acid is as effective as oleic acid and linoleic acid in lowering blood cholesterol in normolipidemic men. Am J Clin Nutr 1991;53:1230–4. 55. Pang D, Allman-Farinelli MA, Wong T, et al. Replacement of linoleic acid with alpha-linolenic acid does not alter blood lipids in normolipidaemic men. Br J Nutr 1998;80:163–7. 56. Mantzioris E, James MJ, Bibson RA, Cleland LG. Dietary substitution with an alpha-linolenic acid-rich vegetable oil increases eicosapentaenoic acid concentrations in tissues. Am J Clin Nutr 1994;59:1304–9. 57. Layne KS, Goh YK, Jumpsen JA, et al. Normal subjects consuming physiological levels of 18:3(n-3) and 20:5(n-3) from flaxseed or fish oils have characteristic differences in plasma lipid and lipoprotein fatty acid levels. J Nutr 1996;126:2130–40. 58. Nestel PJ, Pomeroy SE, Sasahara T, et al. Arterial compliance in obese subjects is improved with dietary plant n-3 fatty acid from flaxseed oil despite increased LDL oxidizability. Arterioscler Thromb Vasc Biol 1997;17:1163–70. 59. 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. 60. 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 Diety Heart Study. Circulation 1999;99:779–85. 61. Rice RD. Mediterranean diet. Lancet 1994;344:893–4 [letter]. 62. Anderson JW, Johnstone BM, Cook-Newell ME. Meta-analysis of the effects of soy protein intake on serum lipids. N Engl J Med 1995;3333:276–82. 63. Sirtori CR, Pazzucconi F, Colombo L, et al. Double-blind study of the addition of high-protein soya milk v. cows’ milk to the diet of patients with severe hypercholesterolaemia and resistance to or intolerance of statins. Br J Nutr 1999;82:91–6. 64. Teixeira SR, Potter SM, Weigel R, et al. Effects of feeding 4 levels of soy protein for 3 and 6 wk on blood lipids and apolipoproteins in moderately hypercholesterolemic men. Am J Clin Nutr 2000;71:1077–84. 65. Baum JA, Teng H, Erdman JW Jr, et al. Long-term intake of soy protein improves blood lipid profiles and increases mononuclear cell low-density-lipoprotein receptor messenger RNA in hypercholesterolemic, postmenopausal women. Am J Clin Nutr 1998;68:545–51. 66. Crouse JR 3rd, Morgan T, Terry JG, et al. A randomized trial comparing the effect of casein with that of soy protein containing varying amounts of isoflavones on plasma concentrations of lipids and lipoproteins. Arch Intern Med 1999;159:2070–6. 67. Teixeira SR, Potter SM, Weigel R, et al. Effects of feeding 4 levels of soy protein for 3 and 6 wk on blood lipids and apolipoproteins in moderately hypercholesterolemic men. Am J Clin Nutr 2000;71:1077–84. 68. 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;68:1375–79S. 69. Crouse JR 3rd, Morgan T, Terry JG, et al. A randomized trial comparing the effect of casein with that of soy protein containing varying amounts of isoflavones on plasma concentrations of lipids and lipoproteins. Arch Intern Med 1999;159:2070–6. 70. Greaves KA, Parks JS, Williams JK, Wagner JD. Intact dietary soy protein, but not adding an isoflavone-rich soy extract to casein, improves plasma lipids in ovariectomized cynomolgus monkeys. J Nutr 1999;129:1585–92. 71. Greaves KA, Wilson MD, Rudel LL, et al. Consumption of soy protein reduces cholesterol absorption compared to casein protein alone or supplemented with an isoflavone extract or conjugated equine estrogen in ovariectomized cynomolgus monkeys. J Nutr 2000;130:820–6. 72. Yudkin J, Kang SS, Bruckdorfer KR. Effects of high dietary sugar. Br Med J 1980;281:1396. 73. Reiser S. Effect of dietary sugars on metabolic risk factors associated with heart disease. Nutr Health 1985;3:203–16. 74. Liu K, Stamler J, Trevisan M, Moss D. Dietary lipids, sugar, fiber, and mortality from coronary heart disease. Bivariate analysis of international data. Arteriosclerosis 1982;2:221–7. 75. Urgert R, Schulz AG, Katan MB. Effects of cafestol and kahweol from coffee grounds on serum lipids and serum liver enzymes in humans. Am J Clin Nutr 1995;61:149–54. 76. Superko HR, Bortz WM, Albers JJ, Wood PJ. Lipoprotein and apolipoprotein changes during a controlled trial of caffeinated and decaffeinated coffee drinking in men. Circulation 1989;80:II–86. 77. Nygärd O, Refsum H, Velanb PM, et al. Coffee consumption and plasma total homocysteine: the Hordaland Homocysteine Study. Am J Clin Nutr 1997;65:136–43. 78. Gross G, Jaccaud E, Huggett AC. Analysis of the content of the diterpenes cafestol and kahweol in coffee brews. Food Chem Toxicol 1997;35:547–54. 79. D’Amicis A, Scaccini C, Tomassi G, et al. Italian style brewed coffee: effect on serum cholesterol in young men. Int J Epidemiol 1996;25:513–20. 80. D’Avanzo B, Santoro L, Nobill A, La Vecchia C. Coffee consumption and serum cholesterol. GISSI-EFRIM Study Group. Prev Med 1993;22:219–24. 81. Regular or decaf? Coffee consumption and serum lipoproteins. Nutr Rev 1992;50:175–8 [review]. 82. Dai WS, Laporte RE, Hom DL, et al. Alcohol consumption and high density lipoprotein cholesterol concentration among alcoholics. Am J Epidemiol 1985;122:620–7. 83. Marques-Vidal P, Ducimetiere P, Evans A, et al. Alcohol consumption and myocardial infarction: a case-control study in France and northern Ireland. Am J Epidemiol 1996;143:1089–93. 84. Rimm EB, Klatsky A, Grobbee D, Stampfer MJ. Review of moderate alcohol consumption and reduced risk of coronary heart disease: is the effect due to beer, wine, or spirits? BMJ 1996;312:731–6 [review]. 85. Hendriks HF, Veenstra J, Velthuis-te Wierik EJ, et al. Effect of moderate dose of alcohol with evening meal on fibrinolytic factors. BMJ 1994;304:1003–6. 86. Doll R, Peto AR, Hall E, et al. Mortality in relation to consumption of alcohol: 13 years’ observations on male British doctors. BMJ 1994;309:911–8. 87. Hein HO, Suadicani P, Gyntelberg F. Alcohol consumption, serum low density lipoprotein cholesterol concentration, and risk of ischaemic heart disease: six year follow up in the Copenhagen male study. BMJ 1996;736–41. 88. Baggio G, Pagnan A, Muraca M, et al. Olive-oil-enriched diet: effect on serum lipoprotein levels and biliary cholesterol saturation. Am J Clin Nutr 1988;47:960–4. 89. Kris-Etherton PM, Pearson TA, Wan Y, et al. High-monounsaturated fatty acid diets lower both plasma cholesterol and triacylglycerol concentrations. Am J Clin Nutr 1999;70:1009–15. 90. Grundy SM. Monounsaturated fatty acids and cholesterol metabolism: implications for dietary recommendations. J Nutr 1989;119:529–33 [review]. 91. Keys A, ed. Coronary heart disease in seven countries. Circulation 1970;41(Suppl Q):I1–211. 92. Kris-Etherton PM, Pearson TA, Wan Y, et al. High-monounsaturated fatty acid diets lower both plasma cholesterol and triacylglycerol concentrations. Am J Clin Nutr 1999;70:1009–15. 93. Lichtenstein AH, Ausman LM, Jalbert SM, Schaefer EJ. Effects of different forms of dietary hydrogenated fats on serum lipoprotein cholesterol levels. N Engl J Med 1999;340:1933–40. 94. Willett WC, Stampfer MJ, Manson JE, et al. Intake of trans fatty acids and risk of coronary heart disease among women. Lancet 1993;341:581–5. 95. Normén L, Dutta P, Lia Å, Andersson H. Soy sterol esters and beta-sitostanol ester as inhibitors of cholesterol absorption in human small bowel. Am J Clin Nutr 2000;71:908–13. 96. Gylling H, Miettinen TA. Cholesterol reduction by different plant stanol mixtures and with variable fat intake. Metabolism 1999;48:575–80. 97. Blair SN, Capuzzi DM, Gottlieb SO, et al. Incremental reduction of serum total cholesterol and low-density lipoprotein cholesterol with the addition of plant stanol ester-containing spread to statin therapy. Am J Cardiol 2000;86:46–52. 98. 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. 99. Hallikainen MA, Sarkkinen ES, Uusitupa MI. Plant stanol esters affect serum cholesterol concentrations of hypercholesterolemic men and women in a dose-dependent manner. J Nutr 2000;130:767–76. 100. Vuorio AF, Gylling H, Turtola H, et al. Stanol ester margarine alone and with simvastatin lowers serum cholesterol in families with familial hypercholesterolemia caused by the FH-North Karelia mutation. Arterioscler Thromb Vasc Biol 2000;20:500–6. 101. Nguyen TT, Dale LC, von Bergmann K, Croghan IT. Cholesterol-lowering effect of stanol ester in a US population of mildly hypercholesterolemic men and women: a randomized controlled trial. Mayo Clin Proc 1999;74:1198–206. 102. Moghadasian MH, Frohlich JJ. Effects of dietary phytosterols on cholesterol metabolism and atherosclerosis: clinical and experimental evidence. Am J Med 1999;107:588–94 [review]. 103. Warshafsky S, Kamer RS, Sivak SL. Effect of garlic on total serum cholesterol—a meta-analysis. Ann Intern Med 1993;119:599–605. 104. McCrindle BW, Helden E, Conner WT. Garlic extract therapy in children with hypercholesterolemia. Arch Pediatr Adolesc Med 1998;152:1089–94. 105. Isaacsohn JL, Moser M, Stein EA, et al. Garlic powder and plasma lipids and lipoproteins. Arch Intern Med 1998;158:1189–94. 106. Berthold HK, Sudhop T, von Bergmann K. Effect of a garlic oil preparation on serum lipoproteins and cholesterol metabolism. JAMA 1998;279:1900–2. 107. Lawson L. Garlic oil for hypercholesterolemia—negative results. Quart Rev Natural Med Fall 1998;185–6. 108. Lawson LD. Garlic powder for hyperlipidemia—analysis of recent negative results. Quart Rev Natural Med 1998;Fall:187–9. 109. Lawson LD, Ransom DK, Hughes BG. Inhibition of whole blood platelet-aggregation by compounds in garlic clove extracts and commercial garlic products. Thrombosis Res 1992;65:141–56. 110. Mansell P, Reckless JP. Garlic—effects on serum lipids, blood pressure, coagulation, platelet aggregation, and vasodilatation. BMJ 1991;303:379–80 [editorial]. 111. Hu FB, Stampfer MJ, Manson JE, et al. Frequent nut consumption and risk of coronary heart disease in women: prospective cohort study. BMJ 1998;317:1341–5. 112. Fraser GE, Sabaté J, Beeson WL, Strahan TM. A possible protective effect of nut consumption on risk of coronary heart disease. Arch Intern Med 1992;152:1416–24. 113. Abbey M, Noakes M, Belling GB, Nestel PJ. Partial replacement of saturated fatty acids with almonds or walnuts lowers total plasma cholesterol and low-density-lipoprotein cholesterol. Am J Clin Nutr 1994;59:995–9. 114. Hu FB, Stampfer MJ. Nut consumption and risk of coronary heart disease: a review of epidemiologic evidence. Curr Atheroscler Rep 1999;1:204–9. 115. Spiller GA, Jenkins DA, Bosello O, et al. Nuts and plasma lipids: an almond-based diet lowers LDL-C while preserving HDL-C. J Am Coll Nutr 1998;17:285–90. 116. Spiller GA, Jenkins DJ, Cragen LN, et al. Effect of a diet high in monounsaturated fat from almonds on plasma cholesterol and lipoproteins. J Am Coll Nutr 1992;11:126–30. 117. Sabaté J, Fraser GE, Burke K, et al. Effects of walnuts on serum lipid levels and blood pressure in normal men. N Engl J Med 1993;328:603–7. 118. Zambon D, Campero B, Perez-Heras A, et al. Effects of walnuts on the serum lipid profile of hypercholesterolemic subjects: the Barcelona Walnut Trial. FASEB J 1998;12:A506 [abstract]. 119. Zambon D, Sabate J, Munoz S, et al. Substituting walnuts for monounsaturated fat improves the serum lipid profile of hypercholesterolemic men and women. A randomized crossover trial. Ann Intern Med 2000;132:538–46. 120. Colquhoun D, Moores D, Humphries J, Somerset S. Comparison of a high monounsaturated fatty acid diet (enriched with macadamia nut) and a high carbohydrate diet on blood lipids [abstract]. Proceedings of the 59th European Atherosclerosis Congress. Nice, France: May 1992, 17–21. 121. Curb JD, Wergowski G, Abbott RD, et al. High mono-unsaturated fat macadamia nut diets: effects on serum lipids and lipoproteins. FASEB J 1998;12:A506 [abstract]. 122. Fraser GE. Nut consumption, lipids, and risk of a coronary event. Clin Cardiol 1999;22(7 Suppl):III11–5 [review]. 123. Curb JD, Wergowske G, Dobbs JC, et al. Serum lipid effects of a high-monounsaturated fat diet based on macadamia nuts. Arch Intern Med 2000;160:1154–8. 124. Durak I, Köksal I, Kaçmaz M, et al. Hazelnut supplementation enhances plasma antioxidant potential and lowers plasma cholesterol levels. Clin Chim Actia 1999;284:113–5 [letter]. 125. Edwards K, Kwaw I, Matud J, Kurtz I. Effect of pistachio nuts on serum lipid levels in patients with moderate hypercholesterolemia. J Am Coll Nutr 1999;18:229–32. 126. Mirkin G. Walnuts and serum lipids. N Engl J Med 1993;329:358 [letter]. 127. Mann GV. Walnuts and serum lipids. N Engl J Med 1993;329:358 [letter]. 128. Fraser GE, Jaceldo K, Sabaté J, et al. Changes in body weight with a daily supplement of 340 calories from almonds for six months. FASEB J 1999;13:A539 [abstract]. 129. Fraser GE. Nut consumption, lipids, and risk of a coronary event. Clin Cardiol 1999;22(7 Suppl):III11–5 [review]. 130. Durak I, Köksal I, Kaçmaz M, et al. Hazelnut supplementation enhances plasma antioxidant potential and lowers plasma cholesterol levels. Clin Chim Actia 1999;284:113–5 [letter]. 131. Jenkins DJA, Khan A, Jenkins AL, et al. Effect of nibbling versus gorging on cardiovascular risk factors: serum uric acid and blood lipids. Metabolism 1995;44:549–55. 132. Edelstein SL, Barrett-Connor EL, Wingard DL, Cohn BA. Increased meal frequency associated with decreased cholesterol concentrations; Rancho Bernardo, CA, 1984–1987. Am J Clin Nutr 1992;55:664–9. 133. Reaven PD, McPhillips JB, Barrett-Connor EL, Criqui MH. Leisure time exercise and lipid and lipoprotein levels in an older population. J Am Geriatr Soc 1990;38:847–54. 134. Duncan JJ, Gordon NF, Scott CB. Women walking for health and fitness—how much is enough? JAMA 1991;266:3295–9. 135. Tran ZV, Weltman A. Differential effects of exercise on serum lipid and lipoprotein levels seen with changes in body weight: a meta-analysis. JAMA 1985;254:919–24. 136. Pekkanen J, Marti B, Nissinen A, Tuomilehto J. Reduction of premature mortality by high physical activity: a 20-year follow-up of middle-aged Finnish men. Lancet 1987;1:1473–7. 137. Willich SN, Lewis M, Lowel H, et al. Physical exertion as a trigger of acute myocardial infarction. N Engl J Med 1993;329:1684–90. 138. Hubert HB, Feinleib M, McNamara PM, Castelli WP. Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up of participants in the Framingham Heart Study. Circulation 1983;67:968–77. 139. Glueck CJ, Taylor HL, Jacobs D, et al. Plasma high-density lipoprotein cholesterol: association with measurements of body mass: the Lipid Research Clinics Program Prevalence Study. Circulation 1980;62(Suppl IV):IV62–9. 140. Di Buono M, Hannah JS, Katzel LI, Jones PJH. Weight loss due to energy restriction suppresses cholesterol bioshynthesis in overweight, mildly hypercholesterolemic men. J Nutr 1999;129:1545–8. 141. Wood PD, Stefanick ML, Dreon DM, et al. Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise. N Engl J Med 1988;319:1173–9. 142. Dwyer JH, Rieger-Ndakorerwa GE, Semmer NK, et al. Low-level cigarette smoking and longitudinal change in serum cholesterol among adolescents. JAMA 1988;2857–62. 143. Khosla S, Laddu A, Ehrenpreis S, Somberg JC. Cardiovascular effects of nicotine: relation to deleterious effects of cigarette smoking. Am Heart J 1994;127:1669–71 [editorial/review]. 144. Nyboe J, Jensen G, Appleyard M, Schnohr P. Smoking and the risk of first acute myocardial infarction. Am Heart J 1991;122:438. 145. Kawachi I, Sparrow D, Spiro A, et al. A prospective study of anger and coronary heart disease. Circulation 1996;94:2090–5. 146. Jiang W, Babyak M, Krantz DS, et al. Mental stress-induced myocardial ischemia and cardiac events. JAMA 1996;275:1651–6. 147. Bower B. Women take un-type A behavior to heart. Sci News 1993;144:244. 148. Dimsdale, JE. A perspective on type A behavior and coronary disease. N Engl J Med 1988;318:110–2 [editorial/review]. 149. McCann BS, Warnick R, Knopp RH. Changes in plasma lipids and dietary intake accompanying shifts in perceived workload and stress. Psychosomatic Med 1990;52:97–108. 150. Lundberg U, Hedman M, Melin B, Frankenhaeuser M. Type A Behavior in healthy males and females as related to physiological reactivity and blood lipids. Psychosomatic Med 1989;51:113–22. 151. Friedman M, Theresen CE, Gill JJ, et al. Alteration of type A behavior and reduction in cardiac recurrences in postmyocardial infarction patients. Am Heart J 1984;108:237–48. 152. Vuksan V, Jenkins DJ, Spadafora P, et al. Konjac-mannan (glucomannan) improves glycemia and other associated risk factors for coronary heart disease in type 2 diabetes. A randomized controlled metabolic trial. Diabetes Care 1999;22:913–9. 153. Zhang MY, Huang CY, Wang X, et al. The effect of foods containing refined Konjac meal on human lipid metabolism. Biomed Environ Sci 1990;3:99–105. 154. Arvill A, Bodin L. Effect of short-term ingestion of konjac glucomannan on serum cholesterol in healthy men. Am J Clin Nutr 1995;61:585–9. 155. Walsh DE, Yaghoubian V, Behforooz A. Effect of glucomannan on obese patients: a clinical study. Int J Obes 1984;8:289–93. 156. Nissen S, Sharp RL, Panton L, et al. ß-hydroxy-ß-methylbutyrate (HMB) supplementation in humans is safe and may decrease cardiovascular risk factors. J Nutr 2000;130:1937–45. 157. Frei B. Ascorbic acid protects lipids in human plasma and low-density lipoprotein against oxidative damage. Am J Clin Nutr 1991;54:1113–8S. 158. Simon JA. Vitamin C and cardiovascular disease: a review. J Am Coll Nutr 1992;11:107–27. 159. Gatto LM, Hallen GK, Brown AJ, Samman S. Ascorbic acid induces a favorable lipoprotein profile in women. J Am Coll Nutr 1996;15;154–8. 160. Balz F. Antioxidant Vitamins and Heart Disease. Presented at the 60th Annual Biology Colloquium, Oregon State University, February 25, 1999. 161. Galeone F, Scalabrino A, Giuntoli F, et al. The lipid-lowering effect of pantethine in hyperlipidemic patients: a clinical investigation. Curr Ther Res 1983;34:383–90. 162. Miccoli R, Marchetti P, Sampietro T, et al. Effects of pantethine on lipids and apolipoproteins in hypercholesterolemic diabetic and non diabetic patients. Curr Ther Res 1984;36:545–9. 163. Avogaro P, Bon B, Fusello M. Effect of pantethine on lipids, lipoproteins and apolipoproteins in man. Curr Ther Res 1983;33;488–93. 164. Coronel F, Tornero F, Torrente J, et al. Treatment of hyperlipemia in diabetic patients on dialysis with a physiological substance. Am J Nephrol 1991;11:32–6. 165. Arsenio L, Bodria P, Magnati G, et al. Effectiveness of long-term treatment with pantethine in patients with dyslipidemia. Clin Ther 1986;8:537–45. 166. Prisco D, Rogasi PG, Matucci M, et al. Effect of oral treatment with pantethine on platelet and plasma phospholipids in IIa hyperlipoproteinemia. Angiology 1987;38:241–7. 167. Gaddi A, Descovich GC, Noseda G, et al. Controlled evaluation of pantethine, a natural hypolipidemic compound, in patients with different forms of hyperlipoproteinemia. Atherosclerosis 1984;50:73–83. 168. Da Col PG, et al. Pantethine in the treatment of hyper-cholesterolemia: a randomized double-blind trial versus tiadenol. Curr Ther Res 1984;36:314. 169. Anderson RA, Cheng N, Bryden NA, et al. Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. Diabetes 1997;46:1786–91. 170. Offenbacher EG, Pi-Sunyer FX. Beneficial effect of chromium-rich yeast on glucose tolerance and blood lipids in elderly subjects. Diabetes 1980;29:919–25. 171. Press RI, Geller J, Evans GW. The effect of chromium picolinate on serum cholesterol and apolipoprotein fractions in human subjects. West J Med 1990;152:41–5. 172. Hermann J, Chung H, Arquitt A, et al. Effects of chromium or copper supplementation on plasma lipids, plasma glucose and serum insulin in adults over age fifty. J Nutr Elderly 1998;18:27–45. 173. Riales R, Albrink MJ. Effect of chromium chloride supplementation on glucose tolerance and serum lipids including high-density lipoprotein of adult men. Am J Clin Nutr 1981;34:2670–8. 174. Roeback JR, Hla KM, Chambless LE, Fletcher RH. Effects of chromium supplementation on serum high-density lipoprotein cholesterol levels in men taking beta-blockers. Ann Intern Med 1991;115:917–24. 175. Uusitupa MI, Kumpulainen JT, Voutilainen E, et al. Effect of inorganic chromium supplementation on glucose tolerance, insulin response, and serum lipids in noninsulin-dependent diabetics. Am J Clin Nutr 1983;38:404–10. 176. Uusitupa MI, Mykkanen L, Siitonen O, et al. Chromium supplementation in impaired glucose tolerance of elderly: effects on blood glucose, plasma insulin, C-peptide and lipid levels. Br J Nutr 1992;68:209–16. 177. Boyd SG, Boone BE, Smith AR, et al. Combined dietary chromium picolinate supplementation and an exercise program leads to a reduction of serum cholesterol and insulin in college-aged subjects. J Nutr Biochem 1998;9:471–5. 178. Wang MM, Fox EA, Stoecker BJ, et al. Serum cholesterol of adults supplemented with brewer’s yeast or chromium chloride. Nutr Res 1989;9:989–98. 179. Newman HA, Leighton RF, Lanese RR, Freedland NA. Serum chromium and angiographically determined coronary artery disease. Clin Chem 1978;541–4. 180. Brown WV. Niacin for lipid disorders. Postgrad Med 1995;98:185–93 [review]. 181. Guyton JR, Blazing MA, Hagar J, et al. Extended-release niacin vs gemfibrozil for the treatment of low levels of high-density lipoprotein cholesterol. Niaspan-Gemfibrozil Study Group. Arch Intern Med 2000;160:1177–84. 182. McKenney JM, Proctor JD, Harris S, Chinchili VM. A comparison of the efficacy and toxic effects of sustained- vs immediate-release niacin in hypercholesterolemic patients. JAMA 1994;271:672–7. 183. Knopp RH, Ginsberg J, Albers JJ, et al. Contrasting effects of unmodified and time-release forms of niacin on lipoproteins in hyperlipidemic subjects: clues to mechanism of action of niacin. Metabolism 1985;34:642–50. 184. Gray DR, Morgan T, Chretien SD, Kashyap ML. Efficacy and safety of controlled-release niacin in dyslipoproteinemic veterans. Ann Intern Med 1994;121:252–8. 185. Rader JI, Calvert RJ, Hathcock JN. Hepatic toxicity of unmodified and time-release preparations of niacin. Am J Med 1992;92:77–81 [review]. 186. Knopp RH. Niacin and hepatic failure. Ann Intern Med 1989;111:769 [letter]. 187. Goldberg A, Alagona P Jr, Capuzzi DM, et al. Multiple-dose efficacy and safety of an extended-release form of niacin in the management of hyperlipidemia. Am J Cardiol 2000;85:1100–5. 188. Head KA. Inositol hexaniacinate: a safer alternative to niacin. Alt Med Rev 1996;1:176–84 [review]. 189. Murray M. Lipid-lowering drugs vs. Inositol hexaniacinate. Am J Natural Med 1995;2:9–12 [review]. 190. Dorner Von G, Fisher FW. Zur Beinflussung der Serumlipide und-lipoproteine durch den Hexanicotinsaureester des m-Inositol. Arzneimittel Forschung 1961;11:110–3. 191. Carrol KK, Kurowska EM. Soy consumption and cholesterol reduction: review of animal and human studies. J Nutr 1995;125:594–7S. 192. Crouse JR 3rd, Morgan T, Terry JG, et al. A randomized trial comparing the effect of casein with that of soy protein containing varying amounts of isoflavones on plasma concentrations of lipids and lipoproteins. Arch Intern Med 1999;159:2070–6. 193. Nestel PJ, Yamashita T, Sasahara T, et al. Soy isoflavones improve systemic arterial compliance but not plasma lipids in menopausal and perimenopausal women. Arterioscler Thromb Vasc Biol 1997;17:3392–8. 194. Samman S, Lyons, Wall PM, et al. The effect of supplementation with isoflavones on plasma lipids and oxidisability of low density lipoprotein in premenopausal women. Atherosclerosis 1999;147:277–83. 195. Lees AM, Mok HY, Lees RS, et al. Plant sterols as cholesterol-lowering agents: Clinical trials in patients with hypercholesterolemia and studies of sterol balance. Atheroscler 1977;28:325–38. 196. 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. 197. 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]. 198. Hendriks HF, Weststrate JA, van Vliet T, Meijer GW. Spreads enriched with three different levels of vegetable oil sterols and the degree of cholesterol lowering in normocholesterolaemic and mildly hypercholesterolaemic subjects. Eur J Clin Nutr 1999;53:319–27. 199. Jones PJ, Ntanios FY, Raeini-Sarjaz M, Vanstone CA. Cholesterol-lowering efficacy of a sitostanol-containing phytosterol mixture with a prudent diet in hyperlipidemic men. Am J Clin Nutr 1999;69:1144–50. 200. Blair SN, Capuzzi DM, Gottlieb SO, et al. Incremental reduction of serum total cholesterol and low-density lipoprotein cholesterol with the addition of plant stanol ester-containing spread to statin therapy. Am J Cardiol 2000;86:46–52. 201. 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. 202. Hallikainen MA, Sarkkinen ES, Uusitupa MI. Plant stanol esters affect serum cholesterol concentrations of hypercholesterolemic men and women in a dose-dependent manner. J Nutr 2000;130:767–76. 203. Vuorio AF, Gylling H, Turtola H, et al. Stanol ester margarine alone and with simvastatin lowers serum cholesterol in families with familial hypercholesterolemia caused by the FH-North Karelia mutation. Arterioscler Thromb Vasc Biol 2000;20:500–6. 204. Nguyen TT, Dale LC, von Bergmann K, Croghan IT. Cholesterol-lowering effect of stanol ester in a US population of mildly hypercholesterolemic men and women: a randomized controlled trial. Mayo Clin Proc 1999;74:1198–206. 205. Law M. Plant sterol and stanol margarines and health. BMJ 2000;320:861–4. 206. Parker RA, Pearce BC, Clark RW, et al. Tocotrienols regulate cholesterol production in mammalian cells by post-transcriptional suppression of 3-hydroxy-3-methylglutaryl-coenzyme A reductase. J Biol Chem 1993;268(15):11230–8. 207. Pearce BC, Parker RA, Deason ME, et al. Hypocholesterolemic activity of synthetic and natural tocotrienols. J Med Chem 1992;35:3595–606. 208. Qureshi AA, Bradlow BA, Brace L, et al. Response of hypercholesterolemic subjects to administration of tocotrienols. Lipids 1995;30:1171–7. 209. Qureshi AA, Qureshi N, Wright JJ, et al. Lowering serum cholesterol in hypercholesterolemic humans by tocotrienols (palmvitee). Am J Clin Nutr 1991;53:1021–6S. 210. Wahlqvist ML, Krivokuca-Bogetic A, Lo CS, et al. Differential serum response of tocopherols and tocotrienols during vitamin supplementation in hypercholesterolemic individuals without change in coronary risk factors. Nutr Res 1992;12:S181–201. 211. Mensink RP, van Houwelingen AC, Kromhout D, Hornstra G. A vitamin E concentrate rich in tocotrienols had no effect on serum lipids, lipoproteins, or platelet function in men with mildly elevated serum lipid concentrations. Am J Clin Nutr 1999;69:213–9. 212. Davis GK, Mertz W. Copper. In: Mertz W, ed. Trace elements in human and animal nutrition, vol. 1. 5th ed. San Diego: Academic Press, 1987, 301–64 [review]. 213. Klevay LM. Dietary copper: a powerful determinant of cholesterolemia. Med Hypotheses 1987;24:111–9 [review]. 214. Hermann J, Chung H, Arquitt A, et al. Effects of chromium or copper supplementation on plasma lipids, plasma glucose and serum insulin in adults over age fifty. J Nutr Elderly 1998;18:27–45. 215. Bell S, Goldman VM, Bistrian BR, et al. Effect of beta-glucan from oats and yeast on serum lipids. Crit Rev Food Sci Nutr 1999;39:189–202 [review]. 216. Behall KM, Scholfield DJ, Hallfrisch J. Effect of beta-glucan level in oat fiber extracts on blood lipids in men and women. J Am Coll Nutr 1997;16:46–51. 217. Braaten JT, Wood PJ, Scott FW, et al. Oat beta-glucan reduces blood cholesterol concentration in hypercholesterolemic subjects. Eur J Clin Nutr 1994;48:465–74. 218. Davidson MH, Dugan LD, Burns JH, et al. The hypocholesterolemic effects of beta-glucan in oatmeal and oat bran. A dose-controlled study. JAMA 1991;265:1833–9. 219. Wood PJ. Physicochemical properties and physiological effects of the (1----3)(1----4)-beta-D-glucan from oats. Adv Exp Med Biol 1990;270:119–27. 220. Uusitupa MI, Miettinen TA, Sarkkinen ES, et al. Lathosterol and other non-cholesterol sterols during treatment of hypercholesterolaemia with beta-glucan-rich oat bran. Eur J Clin Nutr 1997;51:607–11. 221. Lia A, Hallmans G, Sandberg AS, et al. Oat beta-glucan increases bile acid excretion and a fiber-rich barley fraction increases cholesterol excretion in ileostomy subjects. Am J Clin Nutr 1995;62:1245–51. 222. Bell S, Goldman VM, Bistrian BR, et al. Effect of beta-glucan from oats and yeast on serum lipids. Crit Rev Food Sci Nutr 1999;39:189–202 [review]. 223. Nicolosi R, Bell SJ, Bistrian BR, et al. Plasma lipid changes after supplementation with beta-glucan fiber from yeast. Am J Clin Nutr 1999;70:208–12. 224. Behall KM, Scholfield DJ, Hallfrisch J. Effect of beta-glucan level in oat fiber extracts on blood lipids in men and women. J Am Coll Nutr 1997;16:46–51. 225. Braaten JT, Wood PJ, Scott FW, et al. Oat beta-glucan reduces blood cholesterol concentration in hypercholesterolemic subjects. Eur J Clin Nutr 1994;48:465–74. 226. Uusitupa MI, Ruuskanen E, Makinen E, et al. A controlled study on the effect of beta-glucan-rich oat bran on serum lipids in hypercholesterolemic subjects: relation to apolipoprotein E phenotype. J Am Coll Nutr 1992;11:651–9. 227. Yacowitz H, Fleischman AI, Bierenbaum ML. Effects of oral calcium upon serum lipids in man. Br Med J 1965;1:1352–4. 228. Bell L, Halstenson CE, Halstenson CJ, et al. Cholesterol-lowering effects of calcium carbonate in patients with mild to moderate hypercholesterolemia. Arch Intern Med 1992;152:2441–4. 229. Karanja N, Morris CD, Illingworth DR, Plasma lipids and hypertension: response to calcium supplementation. Am J Clin Nutr 1987;45:60–5. 230. Denke MA, Fox MM, Schulte MC. Short-term dietary calcium fortification increases fecal saturated fat content and reduces serum lipids in men. J Nutr 1993;123:1047–53. 231. Bostick RM, Fosdick L, Grandits GA, et al. Effect of calcium supplementation on serum cholesterol and blood pressure. Arch Fam Med 2000;9:31–9. 232. Cloarec MJ, Perdriset GM, Lamberdiere FA, et al., Alpha-tocopherol: effect on plasma lipoproteins in hypercholesterolemic patients. Isr J Med Sci 1987;23:869–72. 233. Kesaniemi YA, Grundy SM. Lack of effect of tocopherol on plasma lipids and lipoproteins in man. Am J Clin Nutr 1982;36:224–8. 234. Kalbfleisch JH, Barboriak JJ, Else BA, et al. alpha-Tocopherol supplements and high-density-lipoprotein-cholesterol levels. Br J Nutr 1986;55:71–7. 235. Stampfer MJ, Willett W, Castelli WP, et al. Effect of vitamin E on lipids. Am J Clin Pathol 1983;79:714–6. 236. 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. 237. Traber MG. Does vitamin E decrease heart attack risk? summary and implications with respect to dietary recommendations. J Nutr 2001;131:395S–7S. [review]. 238. Pola P, Savi L, Grilli M, et al. Carnitine in the therapy of dyslipidemic patients. Curr Ther Res 1980;27:208–16. 239. Stefanutti C, Vivenzio A, Lucani G, et al. Effect of L-carnitine on plasma lipoprotein fatty acids pattern in patients with primary hyperlipoproteinemia. Clin Ter 1998;149:115–9. 240. Maebashi M, Kawamura N, Sato M, et al. Lipid-lowering effect of carnitine in patients with type-IV hyperlipoproteinaemia. Lancet 1978;ii:805–7. 241. Rossi CS, Siliprandi N. Effect of carnitine on serum HDL-cholesterol: report of two cases. Johns Hopkins Med J 1982;150:51–4. 242. Pola P, Savi L, Grilli M, et al. Carnitine in the therapy of dyslipidemic patients. Curr Ther Res 1980;27:208–16. 243. Davini P, Bigalli A, Lamanna F, Boehm A. Controlled study on L-carnitine therapeutic efficacy in post-infarction. Drugs Exptl Clin Res 1992;18:355–65. 244. Davis WH, Leary WP, Reyes AJ, Olhaberry JV. Monotherapy with magnesium increases abnormally low high density lipoprotein cholesterol: a clinical assay. Curr Ther Res 1984;36:341–6. 245. Nozue T, Kobayashi A, Uemasu F, et al. Magnesium status, serum HDL cholesterol, and apolipoprotein A-1 levels. J Pediatr Gastroenterol Nutr 1995;20:316–8. 246. Baxter GF, Sumeray MS, Walker JM. Infarct size and magnesium: insights into LIMIT-2 and ISIS-4 from experimental studies. Lancet 1996;348:1424–6. 247. Galloe A, Rasmussen HS, Jorgensen LN, et al. Influence of oral magnesium supplementation on cardiac events among survivors of an acute myocardial infarction. BMJ 1993;307:585–7. 248. Izuka K, Murata K, Nakazawa K, et al. Effects of chondroitin sulfates on serum lipids and hexosamines in atherosclerotic patients: With special reference to thrombus formation time. Jpn Heart J 1968;9:453–60. 249. Nakazawa K, Murata K. Comparative study of the effects of chondroitin sulfate isomers on atherosclerotic subjects. ZFA 1979;34:153–9. 250. Morrison LM, Enrick NL. Coronary heart disease: reduction of death rate by chondroitin sulfate A. Angiology 1973;24:269–87. 251. Childs MT, Bowlin JA, Ogilvie JT, et al. The contrasting effects of a dietary soya lecithin product and corn oil on lipoprotein lipids in normolipidemic and familial hypercholesterolemic subjects. Atherosclerosis 1981;38:217–28. 252. Knuiman JT, Beynen AC, Katan MB. Lecithin intake and serum cholesterol. Am J Clin Nutr 1989;49:266–8. 253. Wilson TA, Meservey CM, Nicolosi RJ. Soy lecithin reduces plasma lipoprotein cholesterol and early atherogenesis in hypercholesterolemic monkeys and hamsters: beyond linoleate. Atherosclerosis 1998;140:147–53. 254. Oosthuizen W, Vorster HH, Vermaak WJ, et al. Lecithin has no effect on serum lipoprotein, plasma fibrinogen and macro molecular protein complex levels in hyperlipidaemic men in a double-blind controlled study. Eur J Clin Nutr 1998;52:419–24. 255. Koide SS. Chitin-chitosan: properties, benefits and risks. Nutr Res 1998;18:1091–101 [review]. 256. Maezaki Y, Tsuji K, Nakagawa Y, et al. Hypocholesterolemic effect of chitosan in adult males. Biosci Biotech Biochem 1993;57:1439–44. 257. Wuolijoki E, Hirvela T, Ylitalo P. Decrease in serum LDL cholesterol with microcrystalline chitosan. Methods Find Exp Clin Pharmacol 1999;21:357–61. 258. Abou-Hozaifa BM, Badr El-Din NK. Royal jelly, a possible agent to reduce the nicotine-induced atherogenic lipoprotein profile. Saudi Med J 1995;16:337–42. 259. Abou-Hozaifa BM, Roston AAH, El-Nokaly FA. Effects of royal jelly and honey on serum lipids and lipoprotein cholesterol in rats fed cholesterol-enriched diet. J Biomed Sci Ther 1993;9:35–44. 260. Cho YT. Studies on royal jelly and abnormal cholesterol and triglycerides. Am Bee J 1977;117:36–9. 261. Liusov VA, Zimin IU. Experimental rational and trial of therapeutic use of bee raising product in cardiovascular diseases. Kardiologia 1983;23:105–9 [in Russian]. 262. Vittek J. Effect of royal jelly on serum lipids in experimental animals and humans with atherosclerosis. Experientia 1995;51:927–35. 263. Earnest CP, Almada AL, Mitchell TL. High-performance capillary electrophoresis-pure creatine monohydrate reduces blood lipids in men and women. Clin Sci 1996;91:113–8. 264. Volek JS, Duncan ND, Mazzetti SA, et al. No effect of heavy resistance training and creatine supplementation on blood lipids. Int J Sport Nutr Exerc Metab 2000;10:144–56. 265. Pons P, Rodríquez M, Más R, et al. One-year efficacy and safety of policosanol in patients with type II hypercholesterolemia. Curr Ther Res 1994;55:1084–92. v 266. Aneiros E, Calderson B, Más R, et al. Effect of successive dose increases of policosanol on the lipid profile and tolerability of treatment. Curr Ther Res 1993;54:304–12. 267. Castano G, Canetti M, Moreira M, et al. Efficacy and tolerability of policosanol in elderly patients with type II hypercholesterolemia: a 12-month study. Curr Ther Res 1995;56:819–23. 268. Castano G, Tula L, Canetti M, et al. Effects of policosanol in hypertensive patients with type II hypercholesterolemia. Curr Ther Res 1996;57:691–5. 269. Menendez R, Arruzazabala L, Más R, et al. Cholesterol-lowering effect of policosanol on rabbits with hypercholesterolaemia induced by a wheat starch-casein diet. Br J Nutr 1997;77:923–32. 270. Heinecke JW, Rosen H, Suzuki LA, Chait A. The role of sulfur-containing amino acids in superoxide production and modification of low density lipoprotein by arterial smooth muscle cells. Biol Chem 1987;262:10098–103. 271. 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. 272. Woodside JV, Young IS, Yarnell JW, et al. Antioxidants, but not B-group vitamins increase the resistance of low-density lipoprotein to oxidation: a randomized, factorial design, placebo-controlled trial. Atherosclerosis 1999;144:419–27. 273. Endo A. Monacolin K, a new hypocholesterolemic agent produced by a Monascus species. J Antibiot (Tokyo) 1979;32:852–4. 274. Heber D, Yip I, Ashley JM, et al. Cholesterol-lowering effects of a proprietary Chinese red-yeast-rice dietary supplement. Am J Clin Nutr 1999;69:231–6. 275. Li C, Zhu Y, Wang Y, et al. Monascus purpureus-fermented rice (red yeast rice): a natural food product that lowers blood cholesterol in animal models of hypercholesterolemia. Nutr Res 1998;18:71–81. 276. Wang J, Lu Z, Chi J, et al. Multicenter clinical trial of the serum lipid-lowering effects of a Monascus purpureus (red yeast) rice preparation from traditional Chinese medicine. Curr Ther Res 1997;58:964–77. 277. Heber D, Yip I, Ashley JM, et al. Cholesterol-lowering effects of a proprietary Chinese red-yeast-rice dietary supplement. Am J Clin Nutr 1999;69:231–6. 278. 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. 279. Anderson JW, Davidson MH, Blonde L, et al. Long-term cholesterol-lowering effects as an adjunct to diet therapy in the treatment of hypercholesterolemia. Am J Clin Nutr 2000;71:1433–8. 280. Romero AL, Romero JE, Galaviz S, Fernandez ML. Cookies enriched with psyllium or oat bran lower plasma LDL cholesterol in normal and hypercholesterolemic men from Northern Mexico. J Am Coll Nutr 1998;17:601–8. 281. Agarwal RC, Singh SP, Saran RK, et al. Clinical trial of gugulipid new hypolipidemic agent of plant origin in primary hyperlipidemia. Indian J Med Res 1986;84:626–34. 282. Nityanand S, Srivastava JS, Asthana OP. Clinical trials with Gugulipid—a new hypolipidemic agent. J Assoc Phys India 1989; 37:323–8. 283. Singh RB, Niaz MA, Ghosh S. Hypolipidemic and antioxidant effects of Commiphora mukul as an adjunct to dietary therapy in patients with hypercholesterolemia. Cardiovasc Drugs Ther 1994;8:659–64. 284. Asgary S, Naderi GH, Sarrafzadegan N, et al. Antihypertensive and antihyperlipidemic effects of Achillea wilhelmsii. Drugs Exp Clin Res 2000;26:89–93. 285. Warshafsky S, Kamer R, Sivak S. Effect of garlic on total serum cholesterol: a meta-analysis. Ann Int Med 1993;119(7)599–605. 286. Silagy C, Neil A. Garlic as a lipid-lowering agent—a meta-analysis. J R Coll Phys London 1994;28(1):39–45. 287. Neil HA, 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. 288. McCrindle BW, Helden E, Conner WT. Garlic extract therapy in children with hypercholesterolemia. Arch Pediatr Adolesc Med 1998;152:1089–94. 289. Isaacsohn JL, Moser M, Stein EA, et al. Garlic powder and plasma lipids and lipoproteins. Arch Intern Med 1998;158:1189–94. 290. Berthold HK, Sudhop T, von Bergmann K. Effect of a garlic oil preparation on serum lipoproteins and cholesterol metabolism. JAMA 1998;279:1900–2. 291. Superko HR, Krauss RM. Garlic powder, effect on plasma lipids, postprandial lipemia, low-density lipoprotein particle size, high-density lipoprotein subclass distribution and lipoprotein(a). J Am Coll Cardiol 2000;35:321–6. 292. Lawson L. Garlic oil for hypercholesterolemia—negative results. Quart Rev Natural Med Fall 1998;185–6. 293. Lawson LD. Garlic powder for hyperlipidemia—analysis of recent negative results. Quart Rev Natural Med Fall, 1998;187–9. 294. Berthold HK, Sudhop T, von Bergmann K. Effect of a garlic oil preparation on serum lipoproteins and cholesterol metabolism. JAMA 1998;279:1900–2. 295. Silagy C, Neil A. Garlic as a lipid-lowering agent—a meta-analysis. J R Coll Physicians London 1994;28:39–45. 296. Silagy C, Neil A. Garlic as a lipid-lowering agent—a meta-analysis. J R College Phys London 1994;28:39–45. 297. Kono S, Shinchi K, Ikeda N, et al. Green tea consumption and serum lipid profiles: a cross-sectional study in Northern Kyushu, Japan. Prev Med 1992;21:526–31. 298. Yamaguchi Y, Hayashi M, Yamazoe H, et al. Preventive effects of green tea extract on lipid abnormalities in serum, liver and aorta of mice fed an atherogenic diet. Nip Yak Zas 1991;97(6):329–37. 299. Sagesaka-Mitane Y, Milwa M, Okada S. Platelet aggregation inhibitors in hot water extract of green tea. Chem Pharm Bull 1990;38(3):790–3. 300. Stensvold I, Tverdal A, Solvoll K, et al. Tea consumption. Relationship to cholesterol, blood pressure, and coronary and total mortality. Prev Med 1992;21:546–53. 301. Tsubono Y, Tsugane S. Green tea intake in relation to serum lipid levels in middle-aged Japanese men and women. Ann Epidemiol 1997;7:280–4. 302. Fintelmann V. Antidyspeptic and lipid-lowering effect of artichoke leaf extract. Zeitschirfit fur Allgemeinmed 1996;72:1–19. 303. Heckers H, Dittmar K, Schmahl FW, Huth K. Inefficiency of cynarin as therapeutic regimen in familial type II hyperlipoproteinemia. Atherosclerosis 1977; 26:249–53. 304. Englisch W, Beckers C, Unkauf M, et al. Efficacy of artichoke dry extract in patients with hyperlipoproteinemia. Arzneimittelforschung 2000;50:260–5. 305. Sauvaire Y, Ribes G, Baccou JC, Loubatieres-Mariani MM. Implication of steroid saponins and sapogenins in the hypocholesterolemic effect of fenugreek. Lipids 1991;26:191–7. 306. Bordia A, Verma SK, Srivastava KC. Effect of ginger (Zingiber officinale Rosc) and fenugreek (Trigonella foenumgraecum L) on blood lipids, blood sugar, and platelet aggregation in patients with coronary artery disease. Prostagland Leukotrienes Essential Fatty Acids 1997;56:379–84. 307. Sharma RD, Raghuram TC, Rao NS. Effect of fenugreek seeds on blood glucose and serum lipids in type I diabetes. Eur J Clin Nutr 1990;44:301–6. 308. Sharma RD, Sarkar DK, Hazra B, et al. Hypolipidaemic effect of fenugreek seeds: a chronic study in non-insulin dependent diabetic patients. Phytother Res 1996;10:332–4. 309. Sharma RD, Raghuram TC, Dayasagar Rao V. Hypolipidaemic effect of fenugreek seeds. A clinical study. Phyother Res 1991;5:145–7. 310. Prasanna M. Hypolipidemic effect of fenugreek: a clinical study. Indian J Phramcol 2000;32:34–6. 311. Sowmya P, Rajyalakshmi P. Hypocholesterolemic effect of germinated fenugreek seeds in human subjects. Plant Foods Hum Nutr 1999;53:359–65. 312. Araghiniknam M, Chung S, Nelson-White T, et al. Antioxidant activity of dioscorea and dehydroepiandrosterone (DHEA) in older humans. Life Sci 1996;11:147–57. 313. Kubo K, Nanba H. Anti-hyperliposis effect of maitake fruit body (Grifola frondosa). I. Biol Pharm Bull 1997;20:781–5. 314. Story JA. Alfalfa saponins and cholesterol interactions. Am J Clin Nutr 1984;39:917–29. One preliminary human trial found that 120 grams per day of heat-treated alfalfa seeds for eight weeks led to a modest reduction in cholesterol. 315. Malinow MR, Bardana EJ, Goodnight SH. Pancytopenia during ingestion of alfalfa seeds. Lancet 1981;i:615.
3. Omega-3 fatty acids protect bypass patients (2005)
Hypertension1. Hypertension Bibliography
Also see discussion of hypertension and research. 1. Page LB, Damon A, Moellering RC Jr. Antecedents of cardiovascular disease in six Solomon Islands Societies. Circulation 1974;44:1132–46.2. Stamler J, Rose G, Elliott P, et al. Findings of the international cooperative INTERSALT study. Hypertension 1991;17(1 Suppl):I9–15. 3. MacGregor GA, Markandu ND, Sagnella GA, et al. Double-blind study of three sodium intakes and long-term effects of sodium restriction in essential hypertension. Lancet 1989;2:1244–7. 4. Cutler JA, Follmann D, Allender PS. Randomized trials of sodium reduction: an overview. Am J Clin Nutr 1997;65(Suppl):643S–51S. 5. Cutler JA, Follmann D, Allender PS. Randomized trials of sodium reduction: an overview. Am J Clin Nutr 1997;65(Suppl):643S–51S. 6. Egan BM, Stepniakowski KT. Adverse effects of short-term, very-low-salt diets in subjects with risk-factor clustering. Am J Clin Nutr 1997;65(Suppl):671S–7S. 7. Margetts BM, Beilin LJ, Vandongen R, Armstrong BK. Vegetarian diet in mild hypertension: a randomised controlled trial. BMJ 1986;293:1468–71. 8. Cappuccio FP, MacGregor GA. Does potassium supplementation lower blood pressure? A meta-analysis of published trials. J Hypertens 1991;9:465–73. 9. Appel LJ, Moore TJ, Boarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med 1997;336:1117–24. 10. Svetkey LP, Simons-Morton D, Vollmer WM, et al. Effects of dietary patterns on blood pressure: a subgroup analysis of the Dietary Approaches to Stop Hypertension (DASH) randomized clinical trial. Arch Intern Med 1999;159:285–93. 11. Sachs FM, Svetkey LP, Vollmer WM, et al. Effects on Blood Pressure of Reduced Dietary Sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. N Engl J Med 2001;344:3–10. 12. Zein M, Areas JL, Breuss GH. Effects of excess sucrose ingestion on the lifespan of SHR. J Am Coll Nutr 1989;8:435 [abstract #42]. 13. Rebello T, Hodges RE, Smith JL. Short-term effects of various sugars on antinatriuresis and blood pressure changes in normotensive young men. Am J Clin Nutr 1983;38(1):84–94. 14. Preuss HG, Fournier RD. Effects of sucrose ingestion on blood pressure. Life Sci 1982;30:879–86. 15. Rachima-Maoz C, Peleg E, Rosenthal T. The effect of caffeine on ambulatory blood pressure in hypertensive patients. Am J Hypertens 1998;11:1426–32. 16. Hodgoson JM, Buddey IB, Burke V, et al. Effects on blood pressure of drinking green and black tea. J Hypertens 1999;17:457–63. 17. Jee SH, He J, Whelton PK, et al. The effect of chronic coffee drinking on blood pressure. A meta-analysis of controlled clinical trials. Hypertension 1999;33:647–52. 18. Wakabayashi K, Kono S, Shinchi K, et al. Habitual coffee consumption and blood pressure: a study of self-defense officials in Japan. Eur J Epidemiol 1998;14:669–73. 19. Rossner S, Andersson IL, Ryttig K. Effects of a dietary fibre supplement to a weight reduction programme on blood pressure. A randomized, double-blind, placebo-controlled study. Acta Med Scand 1988;223:353–7. 20. Eliasson K, Ryttig KR, Hylander B, Rossner S. A dietary fibre supplement in the treatment of mild hypertension. A randomized, double-blind, placebo-controlled trial. J Hypertens 1992;10:195–9. 21. Schlamowitz P, Halberg T, Warnoe O, et al. Treatment of mild to moderate hypertension with dietary fibre. Lancet 1987;2:622–3. 22. Fehily AM, Burr ML, Butland BK, Eastham RD. A randomised controlled trial to investigate the effect of a high fibre diet on blood pressure and plasma fibrinogen. J Epidemiol Community Health 1986;40:334–7. 23. Swain JF, Rouse IL, Curley CB, Sacks FM. Comparison of the effects of oat bran and low-fiber wheat on serum lipoprotein levels and blood pressure. N Engl J Med 1990;322:147–52. 24. Grant ECG. Food Allergies and migraine. Lancet 1979;1:966–9. 25. Pirkle JL, Schwartz H, Landis JR, et al. The relationship between blood lead levels and blood pressure and its cardiovascular risk implications. Am J Epidemiol 1985;121(2):246–58. 26. Wu TN, Shen CY, Ko KN, et al. Occupational lead exposure and blood pressure. Int J Epidemiol 1996;25:791–6. 27. Narkiewicz K, Maraglino G, Biasion T, et al. Interactive effect of cigarettes and coffee on daytime systolic blood pressure in patients with mild essential hypertension. J Hypertens 1995;13:965–70. 28. Keil U, Liese A, Filipiak B, et al. Alcohol, blood pressure and hypertension. Novartis Round Symp 1998;216:125–44 [review]. 29. Kukkonen K, Rauramaa R, Voutilainene E, Lansimies E. Physical training of middle-aged men with borderline hypertension. Ann Clin Res 1982;14(Suppl 34):139–45. 30. Young DR, Appel LG, Jee SH, Miller ER III. The effect of aerobic exercise and T’ai Chi on blood pressure in older people: results of a randomized trial. J Am Geriatr Soc 1999;47:277–84. 31. Kelley GA, Kelley KS. Progressive resistance exercise and resting blood pressure. A meta-analysis of randomized controlled trials. Hypertension 2000;35:838–43. 32. Alderman MH. Nonpharmacologic approaches to the treatment of hypertension. Lancet 1994;334:307–11 [review]. 33. Stevens VJ, Obarzanek E, Cook NR, et al. Long-term weight loss and changes in blood pressure: results of the Trials of Hypertension Prevention, Phase II. Ann Intern Med 2001;134:1–11. 34. He J, Whelton PK, Appel LJ, et al. Long-term effects of weight loss and dietary sodium reduction on incidence of hypertension. Hypertension 2000;35:544–9. 35. Folkers K, Drzewoski J, Richardson PC, et al. Bioenergetics in clinical medicine. XVI. Reduction of hypertension in patients by therapy with coenzyme Q10. Res Commun Chem Pathol Pharmacol 1981;31:129–40. 36. Langsjoen P, Langsjoen P, Willis R, Folkers K. Treatment of essential hypertension with coenzyme Q10. Mol Aspects Med 1994;15 Suppl:s265–72. 37. Digiesi V, Cantini F, Oradei A, et al. Coenzyme Q10 in essential hypertension. Molec Aspects Med 1994;15 Suppl:s257–63. 38. Digiesi V, Cantini F, Brodbeck B. Effect of coenzyme Q10 on essential arterial hypertension. Curr Ther Res 1990;47:841–5. 39. Singh RB, Niaz MA, Rastogi SS, et al. Effect of hydrosoluble coenzyme Q10 on blood pressures and insulin resistance in hypertensive patients with coronary artery disease. J Hum Hypertens 1999;13:203–8. 40. Morris MC, Sacks F, Rosner B. Does fish oil lower blood pressure? A meta-analysis of controlled trials. Circulation 1993;88:523–33. 41. Mori TA, Bao DQ, Burke V, et al. Docosahexaenoic acid but not eicosapentaenoic acid lowers ambulatory blood pressure and heart rate in humans. Hypertension 1999;34:253–60. 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. Indigestion1. Indigestion (2005): Heartburn Remedies That Kill
The Journal of the American Medical Association now reports that the use of antacid preparations (Prilosec, Prevacid, Nexium, Pepcid, Zantac) also inhibit stomach acidity (production of hydrochloric acid) and makes people more prone to deadly Clostridium difficile infections and diarrhea. More alarming, the Centers for Disease Control reports that more and more cases of Clostridium difficile are being reported by non-hospitalized healthy adults. Could this rise in C. difficile infection rates be among the users of heartburn remedies? It seems likely. For the complete report, go to http://www.knowledgeofhealth.com/report.asp?story=The%20Heartburn%20Remedy%2 0That%20Kills Editor's Note: Try digestive enzymes during meals.
2. 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. Leber's Hereditary Optic Neuropathy1. 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. Light Sensitivity1. Improve Night Vision with Herbal Extract
2. 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 Degeneration1. 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.
2. Antioxidants (1996) & macular degeneration
See more about macular degeneration treatment and information. 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
3. Antioxidants (1997) and angiogenetic 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 angiogenetic 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.
4. Antioxidants (2001) and Zinc - AREDS Study
See more about macular degeneration treatment and information. 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.
5. Antioxidants (2002) Lutein, Zeaxanthin and Macular Degeneration Study
See more about macular degeneration treatment and information. 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.
6. 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."
7. Antioxidants (2008) and Macular Degeneration Prevention Study
See more about macular degeneration treatment and information. 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.
8. AREDS Study (2001)
See more about macular degeneration treatment and information. NATIONAL INSTITUTES OF HEALTH
9. 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.
10. Bilberry extract (2005) Dietary supplementation with bilberry extract prevents macular degeneration and cataracts in senesce-accelerated OXYS rats.
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.
11. 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
12. Carotenoids (1994), vitamins A, C, and E in diet
Learn more about macular degeneration treatment and information. Also see information on food sources for dietary nutrients. Dietary carotenoids, vitamins A, C, and E, and advanced age-related macular degeneration. A study on the impact of diet on 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. 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. JAMA (The Journal of the American Medical Association) 272: 1413-1420 (1994).
13. Carotenoids (1995) antioxidants & AMD
See more about macular degeneration treatment and information. 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. DM Snodderly, Am J Clin Nutr 1995 Dec;62(6 Suppl):1448S-1461S
14. 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.
15. CoQ10 (2003) Intake May Improve Retinal Function in Those with Macular Degeneration
Learn more about macular degeneration including nutritional recommendations and prevention recommendations. In the journal Ophthalmologica, Dr. Janos Feher, a researcher at the University of Rome, Italy, reported that CoQ10 may improve retinal function in patients with age-related macular degeneration by improving the performance of mitochondria in the retinal pigment epithelium. 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.
16. DHEA (2006) Age-related Macular Degeneration and DHEA
Learn more about macular degeneration treatment and information. Study suggests correlation between reduced blood serum levels of DHEA and increased severity of macular degeneration.
17. 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].
18. 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)
19. Essential Fatty Acids (2001) and macular degeneration
Learn more about macular degeneration treatment and information. Fish Protect Against Macular DegenerationEating 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
20. Exercise (1990) & Macular Degeneration Prevention
Learn more about macular degeneration treatment and information. Summary of 15 year cumulative study on exercise and macular degeneration M D Knudtson, R Klein and B E K Klein
21. Fat (2009) & Macular Degeneration
Learn more about macular degeneration treatment and information. 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
22. Fish Consumption (2000), Cholesterol and Incidence of AMD
See more information about macular degeneration treatment options Those consuming fish more than once per week were only 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
23. Fish Oil (2000) Essential Fatty Acids
Learn more about macular degeneration treatment and information. According to a 2000 study in the Eating fish as seldom as one to three times a month may cut the risk of developing age-related (AMD). In research being done by Australian researchers, they have been studying more than 3,600 people aged 49 and older. They 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
24. 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].
25. 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.
26. Glutathione - (1993) - Macular Degeneration
27. Glutathione and Macular Degeneration (2002)
28. 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.
29. Higher Omega-3 Intake Reduces Risk of Developing Macular Degeneration (Study Oct. 2009)
A new study has investigated whether higher omega-3 intake is associated with a reduced likelihood of developing AMD. This study shows the progression to advanced AMD in 1837 people at moderate to high risk of the condition. Baseline data was on Omega-3 intake with a validated food-frequency questionnaire. Participants who reported the highest omega-3 consumption were 20% less likely than their peers to develop AMD. The 12-year incidence of AMD in participants at moderate to high risk of these outcomes was lowest for those reporting the highest consumption of Omega-3. Assuming these results are generalizable, they may guide the development of low-cost and easily implemented preventive interventions for progression to advanced AMD. Ref: http://www.ajcn.org/cgi/content/abstract/ajcn.2009.27594v1
30. 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, optic neuropathy and ocular complications from behcet disease. - 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. The following also affect homocysteine levels in the blood: aging, excessive stress, deficiencies in choline, taurine, n-acetyl-cysteine. Eye Related 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 [abstract]
31. 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.
32. Inflammation and Macular Degeneration
33. Inflammation and Risk of Developing Age-related Macular Degeneration
This study also suggests that anti-inflammatory agents may play an important role in preventing AMD.
34. Inflammation and Risk of Developing Age-related Macular Degeneration (2005)
35. Intake of carotenoids and reduced risk of macular degeneration
36. Laser therapy improves vision in patients with Age-related Macular Degeneration
37. 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.
38. 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>
39. Low fat diet and omega-3 oils
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.
40. Low level of antioxidants with exposure to blue light increases risk of macular degeneration, 2008 study suggests.
41. Low Melatonin Levels May Increase Risk of Macular Degeneration (Study2009)
Study investigated melatonin levels in age-related macular degeneration (AMD) patients by measurement of 6-sulfatoxymelatonin levels (aMT6s), the major metabolite of melatonin in urine, and compare it with a group of age-and gender-matched controls. The first urine of the morning was collected from 43 AMD patients and 12 controls who did not have AMD. The level of aMT6s in specimens was measured by a commercial 6-sulfatoxymelatonin ELISA kit. The assay was performed by researchers, who were masked to the clinical information. To adjust for variation in the diluteness of urine, urinary creatinine level was measured and aMT6s levels were expressed as aMT6s/creatinine. The level of urinary aMT6s/creatinine (mean+/-SD) in AMD (6.24+/-3.45 ng aMT6s/mg creatinine) was significantly lower than that of the controls (10.40+/-4.51, p=0.0128). After adjustment for various factors (age, smoking, cancer, and coronary heart disease) that may influence the aMT6s level, the odds-ratio of urinary aMT6s comparing AMD patients to controls was 0.65 (95% confidence interval=0.48-0.88, p=0.0036), 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. This difference between AMD patients and controls is present after adjustment for the factors of age, smoking, and histories of cancer and coronary heart disease," wrote R. Rosen and colleagues (see also Age Related Macular Degeneration). The researchers concluded: "The significance of this result and the role of melatonin in the occurrence of AMD require further investigation." Rosen and colleagues published their study in Molecular Vision (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)
43. Lutein (1992) macular degeneration and cataracts
44. Lutein (1997) AMD blue light
45. Lutein (1997) Spinach and Corn in Diet
46. Lutein (1999) Dietary modification with lutein rich food
Learn about macular degeneration treatment and information. (PRESS RELEASE Reprinted from AOL News) DIETARY MODIFICATION WITH A LUTEIN-RICH FOOD REVERSES ARMD VISION LOSS, ACCORDING TO OPTOMETRIC RESEARCHER DR. STUART RICHER
47. Lutein (1999) from Spinach and Supplements
48. Lutein (1999), Zeaxanthin& the Retina - Macular Degeneration (AMD)
49. Lutein (2004) and AMD
50. Lutein (2004) and dry AMD
51. Lutein and Prevention of Macular Degeneration
52. Lutein and Zeaxanthin (2003) & Age-Related Macular Degeneration
From the Medical Research Council Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, United Kingdom. PURPOSE. To investigate the relation between plasma concentrations of lutein and zeaxanthin and age-related macular degeneration in a group of elderly men and women. METHODS. The Wisconsin Age-Related Maculopathy Grading System was used to grade features of early and late macular degeneration in 380 men and women, aged 66 to 75 years, from Sheffield, United Kingdom. Fasting blood samples were taken to assess plasma concentrations of lutein and zeaxanthin. RESULTS. Risk of age-related macular degeneration (early or late) was significantly higher in people with lower plasma concentrations of zeaxanthin. Compared with those whose plasma concentrations of zeaxanthin were in the highest third of the distribution, people whose plasma concentration was in the lowest third had an odds ratio for risk of age-related macular degeneration of 2.0 (95% confidence interval [CI] 1.0–4.1), after adjustment for age and other risk factors. Risk of age-related macular degeneration was increased in people with the lowest plasma concentrations of lutein plus zeaxanthin (odds ratio [OR] 1.9, 95% CI 0.9–3.5) and in those with the lowest concentrations of lutein (OR 1.7, 95% CI 0.9–3.3), but neither of these relations was statistically significant. 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
53. Lutein research -1993
54. Lutein Research-1997 - Dietary increase in macular pigment density
55. Lutein Research-1997 & AMD risks
56. Lutein research-1998
It appears that people lose visual sensitivity before the worst stages of disease. But with the right nutritional program, you might prevent the low macular pigment group from getting worse, and in the best cases even recover some of the lost function. Schepens Eye Research Institute , An Affiliate of Harvard Medical School, “Improved Nutrition Could Prevent Vision Loss, Schepens Study Finds,” February 1998.
57. 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.
58. Lutein, Zeaxanthin and AMD 2007 Study
59. 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.
60. Lutein, Zeaxanthin and Macular Degeneration 2008 Study
61. Lutein/Zeaxanthin and AMD Risk Reduction Age-Related Eye Disease 2008 Study (CAREDS)
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.
Reference:
62. Lycopene and Macular Degeneration
63. Macular carotenoids: lutein and zeaxanthin.
64. Macular degeneration & leafy greens
65. Macular Degeneration (2005): Heavy Cigarette Smoking Increases Risk
CAMBRIDGE, England, Dec. 20, 2005 - Smoking can contribute to age-related macular degeneration, according to investigators here. Long-term heavy smokers have a sharply increased risk -- between 2.5- and 3.5-fold -- of losing vision from age-related macular degeneration, according to medical geneticist John R.W. Yates, Ph.D., of the University of Cambridge. The study "provides strong support for a causal relation between smoking and age-related macular degeneration," Dr. Yates and colleagues concluded in a study published in the January issue of the British Journal of Ophthalmology. For full article, go to http://www.medpagetoday.com/PublicHealthPolicy/PublicHealth/tb/2359 Editor's Note2: Some research suggests that smokers should not supplement with betacarotene as it may increase chances for lung cancer.
66. Macular Degeneration (2005): Omega-3 Fatty Acid Study
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
67. Macular Degeneration (2005): Secondhand Smoking
There is mounting evidence indicating that cigarettes are not only bad for smokers but those around them. Now a new study from Cambridge University says secondhand smoke can cause vision problems. Secondhand smoke nearly doubles the risk of developing age related macular degeneration and the risk is much higher for smokers. Researchers found smoking a pack a day for 40 years tripled their risk of vision loss. Macular Degeneration Disease is the leading cause of partial blindness in the United States.
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
The results of the study indicated that high intake of vegetable, monosaturated 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
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
72. Macular Degeneration and Vitamin E and Zinc Deficiency
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. Macular Degeneration, 2005: acetyl-L-carnitine, omega-3 fatty acids, coenzyme Q10 may help reduce drusen
The aim of this randomized, double-blind, placebo-controlled clinical trial was to determine the efficacy of a combination of acetyl-L-carnitine, n-3 fatty acids, and coenzyme Q10 (Phototrop) on the visual functions and fundus alterations in early age-related macular degeneration (AMD). One hundred and six patients with a clinical diagnosis of early AMD were randomized to the treated or contro l groups. 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 mean change in all four parameters of visual functions showed significant improvement in the treated group by the end of the study period. In addition, in the treated group only 1 out of 48 cases (2%) while in the placebo group 9 out of 53 (17%) showed clinically significant worsening in VFMD. Decrease in drusen-covered area of treated eyes was also statistically significant as compared to placebo when either the most affected eyes or the less affected eyes were considered. These findings strongly suggested 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.
74. 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.
75. 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: 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.
76. Mesozeaxanthin Supplementation Effective in Raising Macular Pigment Density 2007 Study
Methods
Results 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.
Conclusion We have shown for the first time 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.
Reference:
77. More good fat, less bad, reduces age-related macular degeneration risk 2009 Studies
Two reports published in the May, 2009 issue of the American Medical Association journal Archives of Ophthalmology reveal a protective effect for omega-3 fatty acids, fish, nuts and olive oil, and an adverse effect for trans fatty acids, on the risk of developing age-related macular degeneration (AMD), a leading cause of vision loss in older individuals. In the first study, Jennifer S.L. Tan, MBBS, BE at the University of Sydney, Australia and her colleagues evaluated data from 2,454 participants 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 percent lower adjusted risk of developing early AMD compared with those who consumed less. In the second article, Elaine W. T. Chong, MD, PhD, of the Centre for Eye Research Australia and her associates evaluated data from 6,734 men and women aged 58 to 69 who participated in the Melbourne Collaborative Cohort Study. Dietary questionnaires completed between 1990 and 1994 were analyzed for the intake of various foods and individual fatty acids. Follow up examinations conducted between 2003 and 2006 detected 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 those whose intake was categorized as among the top 25 percent of participants having a 76 percent greater risk than those whose intake was among the lowest fourth. Olive oil emerged as protective against late disease. When those who reported consuming at least 100 milliliters per week olive oil were compared with those who consumed less than 1 milliliter per week, they were found to have a 52 percent lower risk of late AMD. For early AMD, those whose omega-3 fatty acid intake was among the top 25 percent had a 15 percent lower risk compared with those whose intake was among the lowest quarter. 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 associated with 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 conclude.
78. neovascular age-related macular degeneration (2004) and hyperhomocysteinemia associated
79. Nutrients (2006) Macular Degeneration: Associations Between Intermediate Age-Related Macular Degeneration and Lutein and Zeaxanthin
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 and vitamin D linked to 40% reduced risk of macular degeneration (2007)
Study shows that consumption of omega-3 fatty acids and omega-3 rich fish could slash the risk of developing age-related macular degeneration (AMD) by 40 per cent. This study adds further support for increasing the ratio of omega-3 to omega-6 fatty acids with the finding that arachidonic acid (AA, omega-6 fatty acid) is associated with an increased risk of AMD. Ref: "Association Between Vitamin D and Age-Related Macular Degeneration in the Third National Health and Nutrition Examination Survey, 1988 Through 1994" Authors: N. Parekh, R.J. Chappell, A.E. Millen, D.M. Albert, J.A. Mares Archives of Ophthalmology May 125, 2007 Volume 125, Pages 671-679
82. 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 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 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.
83. 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.
84. 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.
85. 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
86. Omega-3 fatty acids protective against advanced age-related 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 May, 2007 issue of the American Medical Association journal Archives of Ophthalmology. 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. 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."
87. Omega-3 linked with Protection from Macular Degeneration
88. Plasma homocysteine and total thiol content in patients with exudative age-related macular degeneration.
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. PURPOSE: Exudative age-related macular degeneration (ARMD) is one of the debilitating ocular complications, which results in permanent blindness. Elevated homocysteine (Hcys) levels have been associated in the development of several vascular diseases. Vascular and oxidative stress theories have been implicated for the development of choroidal neovascularization in exudative ARMD. The aim of the present study was to investigate the possible role of plasma Hcys and thiol content (tSH) as a risk factor for the development of exudative ARMD. METHOD: A total of 16 patients with exudative ARMD and 20 age-matched controls were recruited for the study. Plasma Hcys levels were analysed using Reverse Phase High Performance Liquid Chromatography. Plasma glutathione (GSH) content was determined using o-phthalaldehyde (OPA) derivatization and subsequent detection by fluorimeter. Plasma tSH levels were determined by using thiol-specific reagent dithionitrobenzoic acid (DTNB) spectrophotometrically. RESULTS: Plasma Hcys levels in exudative ARMD were elevated three-fold (18+/-5.0 muM) when compared to healthy controls (6.7+/-1.8 muM). There was a two-fold decrease in the GSH and tSH in exudative ARMD when compared with controls. Negative correlation was observed between diminished tSH and Hcys levels (r=-0.4837, P=0.05). Similarly plasma Hcys levels negatively correlated with GSH content (r=-0.6620, P<0.05). CONCLUSION: Results from our present study revealed that there is an elevated Hcys level and diminished thiol pool content in exudative ARMD that are significant.Eye advance online publication, 1 April 2005; doi:10.1038/sj.eye.6701853. PMID: 15803172 [PubMed - as supplied by publisher]
89. 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. Tthe 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).
90. Poor Circulation and Aged Related Macular Degeneration Study 2009
91. Prevention and remediation of macular degeneration
92. Pro-vitamin A and E
93. Refined Carbohydrates Diet (2006), Cataracts and Macular Degeneration
Learn more about macular degeneration treatment and information and cataracts information. For the past decade epidemiologic studies and clinical trials have been suggesting that diets high in the full-spectrum of vitamins, minerals and antioxidant nutrients lower the risk of degenerative eye diseases. Studies published in the 2006 April and May issues of The American Journal of Clinical Nutrition now suggest an association between consumption of high glycemic carbohydrate foods and both cortical and nuclear lens opacities and macular degeneration. April 2006 Journal of Clinical Nutrition Study Design 1036 eyes from 526 Boston-area participants without a previous ARMD diagnosis were included in this study. 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. Results and Conclusion After multivariate adjustment, 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 Design A food-frequency questionnaire was used to obtain dietary information from 3377 participants in the Age-Related Eye Disease Study (AREDS). The aim was to test whether glycemic index (GI) was associated with the presence of cortical or nuclear opacities. Results and Conclusion The participants with the highest dietary intake of high glycemic foods had the highest prevalence of nuclear and cortical opacities, respectively. This study is one of a few studies reporting the association between carbohydrate nutrition in non-diabetic persons and lens opacities, and it is the first study that has indicated a solid relationship between dietary GI and the risk of nuclear cataract. References: 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 [abstract] 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.abstract]
94. Resveratrol(2005) reduces oxidation and proliferation of human retinal pigment epithelial cells via extracellular signal-regulated kinase inhibition.
95. Serum anti-oxidants
96. Smoking and carotenoids
97. 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.
98. Statins May Increase Chances of Getting Macular Degeneration
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]
99. Stem Cell Transplants Show Some Success in Restoring Vision
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