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Nutritional Supplementation and Alzheimer's Disease
By David Perlmutter, MD

As we move forward into the 21st century, we are witnessing a staggering increase in dementing illnesses. Approximately 4.5 million Americans have Alzheimer's disease. By the year 2030, it is estimated that this number will approach 9 million.

A 1999 report from the Department of Neurology and Clinical Chemistry at the University of Heidelberg, revealed that after Alzheimer's disease, the second most frequent cause of dementia in the elderly, was so called "vascular dementia", or brain dysfunction, a result of disease of the small blood vessels. Even more striking, was the finding of elevation of a particular chemical in the blood of these individuals called homocysteine. Blood homocysteine levels are directly related to intake of the B-complex group of vitamins, specifically, vitamin B6, and vitamin B12, as well as folic acid. The conclusion of the report provided very strong support for the effectiveness of dietary supplementation with the B-complex group of vitamins in reducing risk of dementia.

To be effective, therapy for Alzheimer's disease must achieve four tasks—reduce inflammation, limit damaging effects of free radicals, enhance neuronal function, and reduce homocysteine.

REDUCING INFLAMMATION
Essential Fatty Acids
Omega 3 and 6 essential fatty acids (EFAs) are key to reducing inflammation and are an integral part of our protocol for Alzheimer's disease. The best source of omega-3 fats are fish oils, the potency of which is determined by its DHA content. The greatest sources for omega-6 oils are borage seed oil and evening primrose oil. Potency of the omega-6 group is determined by the content of GLA. Zinc, magnesium, and vitamin B3 and vitamin B6 enhance the anti-inflammatory effects of both of these essential fatty acids.

LIMITING FREE RADICAL ACTIVITY
Vitamin E
The utilization of antioxidants to limit the activity of free radicals as therapy for Alzheimer's disease has been extensively evaluated over the past decade. Perhaps the most widely studied is vitamin E—a good candidate not only because of its powerful antioxidant activity, but also because of its high fat solubility. This feature is crucial since not only is the brain more than 60% fat, but it is the fat component that is at the highest risk for free radical damage.

Ginkgo Biloba
Perhaps the most convincing validation of Ginkgo Biloba's effectiveness may be found in a 1997 study published in the Journal of the American Medical Association. The progress of over 200 Alzheimer's patients was evaluated over a 1-year period. Half the group received Ginkgo Biloba, while the other half received a placebo. At the completion of the study, the placebo group showed a progressive decline in mental function on a standardized psychological test, while the group receiving Ginkgo, on average, actually improved. The authors concluded that Ginkgo Biloba was, "safe and appears capable of stabilizing and, in a substantial number of cases, improving the cognitive performance and the social functioning of demented patients for 6 months to 1 year."

Alpha Lipoic Acid
Lipoic Acid is a powerful anti-oxidant that is rapidly absorbed from the gut and readily enters the brain to protect neurons from free radical damage. Further antioxidant protection is derived from its ability to recycle vitamin C and vitamin E, and regenerate glutathione, one of the brain's most important antioxidants.

N-Acetyl-Cysteine (NAC)
In addition to increasing glutathione, NAC has an important antioxidant role in and of itself. One of the most damaging free radicals implicated in Alzheimer's disease is nitric oxide. Nitric oxide production is directly reduced by NAC.

Vitamin D
Vitamin D has been shown to have even more potency as an antioxidant when compared to vitamin E. Remarkably, in a Japanese study published in 1998, it was found that moderate to severe deficiencies of vitamin D were found in 80% of Alzheimer's patients studied.

ENHANCING NEURONAL FUNCTION


Coenzyme Q10 (CoQ10)
Coenzyme Q10 supplementation has been shown to enhance energy production in brain neurons and thus improve function. This powerful antioxidant has also demonstrated its ability to reduce the progression of Parkinson's disease by more than 40%. Isn't it then critically important to recognize that two of the most widely prescribed cholesterol lowering drugs, pravastatin (Pravachol®) and lovastatin (Mevacor®), can significantly lower serum coenzyme Q10 levels?

Acetyl-L-carnitine
Acetyl-L-carnitine is readily converted into an important neurotransmitter (brain chemical messenger) known as acetylcholine, proven to be profoundly deficient in the brains of Alzheimer's patients. Its second task is to facilitate the removal of the toxic by-products of brain metabolism.

Phosphatidylserine
Phosphatidylserine is one of the key constituents of neuronal membranes—the site where brain cells both receive and transmit chemical messages. Abnormalities of the neuronal membrane have been linked to age-related functional changes in brain performance.

Vitamin B-12
Standard medical texts have long reported that vitamin B-12 is a critical factor for preservation of normal brain function. Its deficiency is associated with confusion, depression, mental slowness, memory difficulties, and abnormalities of nerve function. Several studies have demonstrated that patients suffering from Alzheimer's disease generally have significantly lower blood levels of vitamin B-12 compared to age-matched, non-afflicted individuals. B12 helps prevent the accumulation of homocysteine, which, when elevated, markedly increases the risk for Alzheimer's disease as described above.

Folic Acid
Folic acid levels are often markedly depressed in patients suffering from dementia or confusional states. Deficiency of folic acid is associated with apathy, disorientation, memory deficits, and difficulties with concentration. Several studies have correlated low folic acid levels with dementia. Again, the mechanism may involve elevation of homocysteine since like vitamin B12, folic acid helps lower this blood vessel damaging amino acid.


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