Natural Foods Merchandiser

Brain Food

Could something as simple as eating fish, savoring a glass of wine or enjoying a garlic-rich salad help stave off dementia and Alzheimer?s disease? A number of studies suggest that yes, certain foods and nutritional supplements may act as brain foods, lowering the risk of these diseases by helping to prevent vascular damage and neuronal death.

When it comes to concerns about aging, Alzheimer?s disease is right up there. The Alzheimer?s Association estimates about 4.5 million Americans have the condition. It affects 6 percent to 8 percent of people older than 65.1 It is the most common cause of mental deterioration, or dementia, among the elderly. Dementia is medically described as a broad impairment of intellectual function that is progressive and interferes with normal social and occupational activities. Alzheimer?s disease is the most common and severe form of dementia. To stave off dementia, several promising approaches are available.

Homocysteine, cell death and dementia
Vascular health plays an important role in brain health and in preventing Alzheimer?s disease. The amino acid homocysteine increases reactive oxygen species. These free radicals damage blood vessels, a condition that triggers blood clots and leads to heart attacks and stroke. Atherosclerosis (plaque build-up that restricts arterial passageways) and high blood homocysteine levels also increase stroke risk. A stroke deprives the affected areas of the brain of oxygen and nutrients. The result is stroke-associated neuronal death, which can cause vascular dementia and Alzheimer?s.2,3

Homocysteine also causes breaks in DNA and induces apoptosis, a programmed cell suicide that is the major cause of neuronal death in patients with dementia and Alzheimer?s disease.3 Dead neurons can no longer communicate with one another or receive and store information; the gradual loss of functional neurons in areas of the brain responsible for thinking, learning and memory leads to dementia and Alzheimer?s disease. High homocysteine levels double the risk of dementia and Alzheimer?s disease.2 Researchers at Boston University followed 1,092 subjects without dementia, mean age 76 years, for an average of eight years. Dementia developed in 111 subjects, vascular dementia in 11 subjects, other non-Alzheimer?s disease dementia in 17 subjects and Alzheimer?s in 83 subjects. There was a strong association between increased plasma homocysteine, above the mean level of 9 micromoles/L in the general population, and risk of dementia and Alzheimer?s disease.

Hyperhomocysteinemia (plasma homocysteine levels higher than 14 micromoles/L, in this study) doubled the risk.2

Reducing homocysteine
Homocysteine toxicity is generally preventable and reversible with vitamins B6, B12 and folic acid.2 People older than 50 should get 1.7 mg per day of vitamin B6, 2.4 mcg per day of vitamin B12 and 400 mcg per day of folic acid. Therapeutic doses can be customized for those with high plasma homocysteine levels. At a conference last summer, researchers shared results of a three-month study involving 353 subjects with hyperhomocysteinemia (plasma levels higher than 16 micromoles/L) taking 5 mg of folic acid, 50 mg vitamin of B6 and 0.4 mg of vitamin B12 daily. Supplementation reduced homocysteine levels by 30 percent to 40 percent compared with placebo.4

In another small study, nine of 31 patients with dementia and hyperhomocysteinemia were treated with 50 mg of vitamin B1, 50 mg of vitamin B6, 5 mg of folic acid and 0.05 mg of vitamin B12. After four weeks, serum homocysteine concentrations returned to normal in all nine patients, dropping from 17.3 to 10.7 micromoles/L.5

Vitamin B12 is particularly important for vegetarians and vegans, a demographic at high risk for vitamin B12 deficiency, anemia, high homocysteine levels and irreversible neurological damage. In a one-year study of healthy vegetarians, researchers found an inverse relationship between plasma vitamin B12 and the amount of animal products they consumed. The vegans among them had the lowest vitamin B12 levels and the highest concentrations of plasma homocysteine. Those who took vitamin supplements had vitamin B12 concentrations similar to nonvegetarians. The researchers also found vitamin B12 levels declined and homocysteine levels increased with age.6

Oxidative stress and Alzheimer?s disease
Oxidative stress, produced by excess free radicals and inadequate antioxidants, is a major contributor to Alzheimer?s disease. The free radical damage causes cell membrane peroxidation, which damages DNA and kills neurons via apoptosis. A major source of oxidant stress linked to Alzheimer?s disease development is beta-amyloid peptide, a free-radical producer that accumulates as deposits in the brain (senile plaques) and triggers apoptosis in critical areas of the brain such as the hippocampus, the area governing learning and memory.7

Antioxidants from food and supplements prevent oxidative damage and can help protect brain cells against apoptosis. In some cases, antioxidants have been proven clinically to reduce the risk of Alzheimer?s disease.8 The most beneficial appear to be vitamins C and E.

In a 10-year study, investigators followed 5,395 men and women free of dementia who were at least 55 years old and assessed both dietary intake of antioxidants from food and the onset of dementia or Alzheimer?s disease. Following an average six-year follow-up, it was found that 197 developed dementia, of whom 146 had Alzheimer?s disease. When adjustments were made for a large number of variables, including sex, age, smoking habits and mental examination scores, high dietary intakes of vitamins C and E were associated with a reduced risk of Alzheimer?s disease. Those with the highest vitamin E intakes (more than 15.5 mg daily) were 43 percent less likely to develop Alzheimer?s disease; those with the highest vitamin C intake (more than 133 mg daily) were 34 percent less likely to develop the disease.9

Data from the long-term Framingham study involving 14,968 women ages 70 to 79 also showed a relationship between vitamins C and E supplements and cognition. Investigators compared results of cognitive function tests from those taking up to 600 mg of vitamin E and up to 1,300 mg of vitamin C, those taking one vitamin or the other, and past antioxidant users, with cognitive results of women who never used either supplement. The women who took vitamins C and E had better overall cognitive performance than did those who had never taken either vitamin. Researchers say the vitamin users were the equivalent of two years younger as a result of their supplementation. There was no cognitive benefit to taking very high doses—more than 600 mg of vitamin E or 750 mg of vitamin C.10

Vitamin E also appears to slow declining cognition. In a two-year double-blind, placebo-controlled multicenter study, researchers evaluated the effects of 2,000 IU of vitamin E daily, 10 mg of the drug selegiline daily or both on 341 patients with moderately severe Alzheimer?s disease. Researchers assessed loss of ability to perform basic activities in daily life, severe dementia or the need to be institutionalized, and duration to death. Vitamin E was most effective in reducing the risk of all endpoints in the Alzheimer?s disease patients. Compared with placebo, vitamin E users reduced their risk by 53 percent, and selegiline users by 43 percent. Those who took both only reduced their risk by 31 percent.11

Antioxidants may protect cognition, but antioxidant levels naturally decrease with age. To prevent dementia, people should maintain adequate antioxidant intake. Researchers in Italy found lower plasma levels of uric acid; superoxide dismutase (SOD); vitamins A, C and E; and carotenoids (lutein, zeaxanthin, beta-cryptoxanthin, lycopene and alpha- and beta-carotene) in 25 elderly patients with mild cognitive impairment and 63 patients with Alzheimer?s disease, compared with 53 controls who had normal levels and were free of dementia or Alzheimer?s disease. The authors suggest ?an increased intake of antioxidants in patients with mild cognitive impairment could be helpful in lowering the risk of conversion to dementia.?12

Phytochemical neuroprotection
Phytochemicals, including flavonoids, other polyphenols and organosulfur compounds, have neuroprotective effects, as shown experimentally in cell and animal studies. Observational studies in humans on the beneficial effects of diets rich in vegetables and fruit cannot be related to any specific phytochemical, however. With the exception of studies on Ginkgo biloba, clinical trials testing the effects of phytochemicals on cognition are limited. Indirectly, though, antioxidants reduce stroke risk by improving circulation and helping prevent atherosclerosis, both factors in preventing neural death and dementia.

Ginkgo (Ginkgo biloba) has been shown to improve cognition in people with certain forms of dementia.13 In a double-blind, randomized, placebo-controlled multicenter study, 202 patients with severe dementia, some with Alzheimer?s disease, received 120 mg of standardized ginkgo extract daily for 52 weeks. Patients taking ginkgo showed improved performance and social functioning compared with those on placebo. The authors suggest the effects were attributable to ginkgo?s antioxidant effects.13

Curcumin, a component of the spice turmeric, is a potent polyphenolic antioxidant with anti-inflammatory effects. Studies on an Alzheimer?s disease mouse model show dietary curcumin reduced oxidative damage and decreased beta-amyloid peptides in the brain by 43 percent to 50 percent. In studies on a neuron cell model, curcumin was more effective than alpha-tocopherol in preventing beta-amyloid toxicity.14

Resveratrol, a natural polyphenol found in grapes (mostly in the skin) is cardioprotective and may play a role in lowering Alzheimer?s disease risk. Moderate intake of resveratrol-rich red wine is a good way to get this antioxidant, as well as a wide range of flavonoids. Studies in cell cultures show resveratrol?s neuroprotective effects on cells may be attributable to its antioxidant effect and its ability to prevent neuronal death.15

Green and black tea (Camellia sinensis) contain catechins, which have active oxygen-scavenging effects. Results of studies in cell cultures show tea catechins protect brain cells of newborn mice from death by oxygen radicals; furthermore, injecting a particular catechin into mice improved memory impaired by a previous injection of a free radical-producing compound, suggesting tea may be ?useful for protecting humans from senile disorders such as dementia.?16

In a small study involving 19 people, investigators found drinking 400 mL of black tea or coffee three times daily increased alertness and information processing within 10 minutes after consumption, compared with those who took a caffeine-free placebo. The effects of tea and coffee were similar in all measures and not due entirely to caffeine.17

Aged garlic extract (kyolic), an odorless form of organic garlic, is rich in water-soluble organosulfur compounds with antioxidant activity, such as S-allyl cysteine, that are low or absent in fresh garlic.18 Aged garlic extract is antiatherosclerotic and as such can potentially help against stroke, dementia and Alzheimer?s disease. Aged garlic extract protects blood vessels by inhibiting the stickiness and aggregation of blood platelets that lead to clots. Results of a recent clinical study showed aged garlic extract prevents plaque build-up in arteries, an important factor in preventing heart disease and stroke.19 Human studies show it reduces cholesterol, decreases blood pressure and increases blood circulation,20 factors that may help prevent stroke and the dementia that can follow. Results of experimental studies show aged garlic extract is also neuroprotective—it reduces homocysteine,21 prevents beta-amyloid neurotoxicity,22 protects neurons from apoptosis23 and improves learning and memory in senility-prone mice.24

Omega-3 fatty acids and weekly fish consumption also reduce the incidence of Alzheimer?s disease. Researchers compared fish-eating patterns of 815 men and women, ages 65 to 94, who were unaffected by Alzheimer?s disease, and checked for the condition approximately four years later. People who ate at least one serving of fish a week had a 60 percent lower risk of Alzheimer?s compared with those who rarely or never ate fish. Dietary intake of omega-3 fatty acids, calculated from their content in marine food, had a similar risk-lowering effect. People who consumed the highest amounts (median 1.75 g daily) had a 70 percent reduced likelihood of developing Alzheimer?s compared with those getting the least (median 0.9 g daily).25

Food for a healthy brain
Food and supplements play an important role in protecting the brain against dementia and Alzheimer?s disease by battling free radical damage and moderating homocysteine levels. Future large, long-term human prospective studies on the association between specific items in our diet and changes in cognitive function will help to determine the most effective brain foods for preventing impairment. In the meantime, urge your customers to maintain an antioxidant-rich diet that includes phytochemicals, protective B vitamins and fish.

Carmia Borek, Ph.D., is a professor in the department of community health at Tufts University School of Medicine, Nutrition and Infectious Disease Unit. She?s an internationally known researcher on antioxidants in disease prevention and therapy.

1. Nourhashemi F, et al. Alzheimer disease: protective factors. Am J Clin Nutr 2000;71:S643-9.
2. Sehardi S, et al. Plasma homocysteine as a risk factor for dementia and Alzheimer?s disease. N Engl J Med 2002;346:476-83.
3. Behl C, Moosmann R. Oxidative nerve cell death in Alzheimer?s disease and stroke: antioxidants as neuroprotective compounds. Biol Chem 2002;383:521-36.
4. den Heijer M, Brouwer IA, et al. Vitamin supplementation reduces blood homocysteine levels: a controlled trial in patients with venous thrombosis and healthy volunteers. Arterioscler Thromb Vasc Biol 1998;18:356-61.?
5. Lebelhuber F, et al. Homocysteine and B vitamins in dementia. J Neural Trans 2000;107:1469-74.
6. Herrmann W, et al. Vitamin B12 status, particularly holotranscobalamin II and methylmalonic acid concentrations, and hyperhomocysteinemia in vegetarians. Am J Clin Nutr 2003;78:131-6.
7. Butterfield DA. Amyloid beta-peptide (1-42) induced oxidative stress and neurotoxicity: implications for neurodegeneration in Alzheimer?s disease brain. A review. Free Radic Res 2002;36:1307-13.
8. Grundman M, et al. Antioxidant strategies for Alzheimer?s disease. Proc Nutr Soc 2002;61:191-202.
9. Engelhart MJ, et al. Dietary intake of antioxidants and risk of Alzheimer?s disease. JAMA 2002;287:3223-9.
10. Grodstein F, et al. High-dose antioxidant supplements and cognitive function in community-dwelling elderly women. Am J Clin Nutr 2003;77:975-84
11. Sano M, et al. A controlled trial of selegiline, alpha-tocopherol or both as treatments for Alzheimer?s disease. The Alzheimer?s Disease Cooperative Study. N Engl J Med 1997;336:1216-22.
12. Rinaldi P, et al. Plasma antioxidants are similarly depleted in mild cognitive impairment and in Alzheimer?s disease. Neurobiol Aging 2003;24:905-15.
13. Le Bars PL, et al. A placebo-controlled double-blind randomized trial of an extract of Ginkgo biloba for dementia. JAMA 1997;278:1327-32.
14. Lim GP, et al. The curry spice curcumin reduces oxidative stress and amyloid pathology in Alzheimer transgenic mouse. J Neurosci 2001;21:8370-7.
15. Savakan E, et al. Red wine ingredient resveratrol protects from beta-amyloid neurotoxicity. Gerontology 2003;49:380-3.
16. Matsuoka Y, et al. Ameliorative effects of tea catechins on active oxygen related nerve cell injuries. J Pharmachol Exp Ther 1995;274:602-8.
17. Hindmarch I, et al. The effects of black tea and other beverages on aspects of cognition and psychomotor performance. Psychopharmacology (Berl) 1998;139:230-8.
18. Borek C. Antioxidant health effects of aged garlic extract. J Nutr 2001;131:S1010-5.
19. Budoff MJ, et al. Antiatherosclerotic effects of aged garlic extract (Kyolic) in bypass surgery patients analyzed by computer tomography. Presentation at Experimental Biology 2003, San Diego, Calif., 2003 Apr.
20. Yeh YY, et al. Garlic extract reduces plasma concentration of homocysteine in rats rendered folic acid deficiency. FASEB J 1999;13(4):A232;209.12.
21. Brenya G, et al. Effect of aged garlic extract on the cytotoxicity of Alzheimer beta-amyloid peptide in neuronal PC12 cells. Nutri Neurosci 1999;3:139-42.
22. Brown CL, Gebu ET. The effect of aged garlic extract on caspase-3 activity in PC12 cells. Presentation at Experimental Biology 2003, San Diego, Calif., 2003 Apr.
23. Moriguchi T, et al. Anti-aging effect of aged garlic extract in the inbred brain atrophy mouse model. Clin Exp Pharmachol Physiol 1997;24: 235-42.
24. Morris MC, et al. Consumption of fish and n-3 fatty acids and risk of incident Alzheimer?s disease. Arch Neurol 2003;60:940-6.

Natural Foods Merchandiser volume XXV/number 3/p. 114, 116-117

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