Feed your brain


What causes the brain to be especially vulnerable to mercury toxicity is its total dependence on critical energy supplies, and its high content of polyunsaturated fatty acids that are known to be susceptible to oxidation injury (lipid peroxidation). The brain utilizes energy at an enormously high rate, consuming 25 percent of all the bloods' glucose and 20 percent of all the oxygen, even though it comprieses only 2 percent of the body's weight. even in the deepest of comas, the brain's metabolic rate is slowed by only 50 percent.

Health and Nutrition Secrets (that can save your life), Dr Russell L. Blaylock, MD

Dietary intake of antioxidants from food sources may reduce the risk of developing Alzheimer's disease, two new studies have suggested (JAMA 2002;287:3223-9, 3230-7).
Both studies found that the benefit was present when the intake was from food sources rather than from supplements.

The studies were conducted because it has been suggested that oxidative stress has a mechanistic role in the development of Alzheimer's dementia. Several lines of evidence previously implied that oxidative damage to lipid membranes could disrupt normal neuronal and glial cell functioning, leading to the formation of amyloid plaques and to neuronal cell death.

Hence, it was hoped that dietary intake of antioxidants such as vitamins E and C and b carotene might inhibit the production of free radicals and reactive oxygen species.

Working independently on two continents, researchers in Rotterdam, the Netherlands, and in Chicago, Illinois, found evidence to support these theories.

Drs Marianne Engelhart and Mirjam Geerlings and colleagues from the Erasmus Medical Center in Rotterdam led the Rotterdam study, a population based prospective cohort study that examined the effect of dietary intake of vitamins C and E on the risk of incident Alzheimer's disease.

The Rotterdam study, conducted from 1990 to 1999, enrolled 5395 people aged 55 and over who were free of dementia at baseline, could give a reliable dietary history, and were not living in an institution. The mean age of the participants at baseline was 67.7 years (59% were women). They were followed up for an average of six years.

Dietary consumption of antioxidants was assessed by means of a self administered "food frequency" questionnaire, which evaluated dietary consumption of 139 food items and the use of vitamin supplements. The researchers evaluated the association between dietary intake of antioxidants and the development of Alzheimer's disease using Cox proportional hazards analysis.

Adjustments were made for age, sex, mental status, alcohol intake, education, smoking habits, body mass index, total energy intake, presence of carotid plaques, and the presence of the apolipoprotein e4 allele, which is associated with an increased risk of Alzheimer's disease.

At six years' follow up, high intakes of vitamins C and E were associated with a lower risk of the disease (rate ratios per 1 SD increase in intake were 0.82 (95% confidence interval 0.68 to 0.99) and 0.82 (0.66 to 1.00) respectively).

Good sources of vitamin C are citrus fruits, kiwi, sprouts, broccoli, and cabbage, while important sources of vitamin E are grains, nuts, milk, and egg yolk, the authors say.

In the Chicago study Drs Martha Morris and Denis Evans of Rush-Presbyterian Hospital conducted a similar prospective cohort study involving 815 men and women aged 65 and older. These patients were followed for an average of 3.9 years and included both African Americans and white Americans.

Alzheimer's disease developed in 131 subjects. When factors such as age, education, and presence of apolipoprotein e4 allele were taken into account, the group with the highest vitamin E intake had a 70% lower risk of developing the disease than those with the lowest vitamin E intake.

Neither this study nor the Rotterdam study found a benefit from consuming supplement sources of the vitamins, even though a higher dose is available in the supplements.

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