Alzheimer's Disease (AD) is a progressive degenerative brain disease that gradually destroys a person's memory and ability to learn, reason, make judgments, communicate and carry out daily activities. AD currently (in 2005) affects 4.5 million Americans. One in 10 persons over age 65 has AD, and nearly half of those over 85 have it. The longer that you live, the greater your risk of developing AD.
There are few epidemiologic studies examining diet and it's effect on developing Alzheimer's Disease. Currently, no single nutritional component heas clearly been proven to cause or prevent Alzheimer's disease, however interestiong associations have been seen. Evidence from early studies reflects a pattern of dietary associations very similar to the more established dietary risk factors for cardiovascular diseases, (including heart disease). Patients who adopt these prudent dietary practices and modifications will reduce their risk for heart disease and may also reduce their risk of developing Alzheimer's disease.
Antioxidant Nutrients
The best evidence of Alzheimer's disease prevention involves the antioxidant nutrients, vitamins C and E. Patients with Alzheimer's disease develop amyloid beta (A-beta) plaques, an abnormal accumulation of A-beta protein outside neurons (nerve cells), and they develop abnormal neurofibrillary tangles within the cells. Numerous animal and laboratory studies have shown that Alzheimer's disease involves both oxidative and inflammatory processes, although it is not known whether these processes are a cause or effect of the disease or both. The ultimate result, however, is disruption of nerve cell functioning and signaling, leading to an insidious decline of cognitive ability and ultimately to neuronal cell death.
Free Radicals and Alzheimer's Disease
The brain (as well as the heart and liver) is a site of high metabolic activity that generates free radical molecules. Free radicals molecules with unpaired electrons that are highly reactive and thus toxic and destructive to cell tissue. Free radicals denature cells, or irreversabily change their nature. Much like a hot skillet irreversibly changes the liquid egg white into a white solid, so do free radicals irreversibly change the cells with which they come into contact. Infection, cell injury, hypoxia, x-rays, xenobiotics, and environmental toxins, such as smoking and pollution, all generate free radicals within the body. The body possesses natural defense mechanisms to combat oxidative stress, including antioxidant proteins and nutrients. Vitamin E is a potent chain-breaking antioxidant that resides within cell membranes, where it can neutralize free radicals as they are generated. Vitamin E also has anti-inflammatory properties. Vitamin C, a less potent antioxidant than vitamin E, is water soluble and therefore circulates within the plasma (liquid portion of the blood). Vitamin C additionally can restore vitamin E to its antioxidant capacity. The primary antioxidant which benefits this process of restoring other antioxidants such as C and E is the potent antioxidant glutathione. Antioxidants work by generously donating an electron from their prolific outer shells, without becoming a free-radical themselves. Thus, they can quench a free radical reaction like cold water can stifle a smoldering fire. Glutathione is the most complex of antioxidants and is called the "master antioxidant" because it is many times more potent than vitamin C and E, and can re-charge both of these antioxidants, allowing them to continue their important protective functions within the body.
Animal and laboratory studies have demonstrated that the antioxidant nutrients (more data is available on the roles of vitamin E and glutathione than vitamin C), protect the brain from damage due to oxidative and inflammatory mechanisms.[1,2] Rodents who were fed antioxidant-supplemented diets had superior learning acquisition and memory retention compared with rodents on control diets. At death, the brains of the antioxidant-fed rodents exhibited less neuronal cell loss and less evidence of oxidative damage and inflammation.[3,4]
The available evidence from human studies is limited and not altogether consistent. Two prospective studies, 1 of Chicago, Illinois, residents[5] and 1 in Rotterdam, The Netherlands,[6] found a lower risk of Alzheimer's disease with a higher food intake of vitamin E. However, another prospective study conducted in New York found no association.[7] Vitamin E intake in the New York study may have been too low to provide a neuroprotective benefit; the median of 7 IU/d for persons in the top third of intake was comparable to the lowest intake levels in the Chicago and Rotterdam studies.
Of the 3 trials, only the Rotterdam study found a reduced risk of Alzheimer's disease with high food intake of vitamin C. However, the Chicago study found that participants with the highest food intake of vitamin C were more than twice as likely to have a history of stroke or hypertension, and these persons may have increased their fruit consumption as a recent preventive measure, thus obscuring a potential protective association with Alzheimer's disease.
Supplements vs Dietary Vitamins
In none of the 3 prospective studies was vitamin E and vitamin C supplement use associated with less risk of Alzheimer's disease. Two other prospective studies[8,9] examined vitamin supplement use in relation to Alzheimer's disease, and only 1 of these[8] found evidence of reduced risk. There are several plausible explanations for the absence of association with vitamin E supplements. Vitamin E supplements have traditionally contained only alpha-tocopherol, the most biologically active form of vitamin E; however, gamma-tocopherol is the more abundant form in the US diet. Whereas alpha-tocopherol is the more potent antioxidant, gamma-tocopherol also has anti-inflammatory properties.[10] Recent studies indicate that the combined intake of the 8 different tocopherol forms reduces oxidative stress and inflammation to a greater degree than alpha-tocopherol alone.[11]
Another explanation for the absence of association with vitamin E supplements is that food intake may be a better indicator of long-term exposure to vitamin E. In addition, the study findings could be biased if many study participants initiated vitamin supplement use because of developing problems in cognition.
In summary, the strongest evidence for antioxidant protection against Alzheimer's disease rests with high food intake of vitamin E. The richest food sources of vitamin E include vegetable oils, margarine, nuts (especially almonds), and seeds (especially sunflower seeds). Moderate amounts of vitamin E are found in whole grains, egg yolk, and a limited number of vegetables (eg, collard greens) and fruits (eg, avocados, apples, melon).
Diet, Supplements and Alzheimer's Disease
Source: Martha Clare Morris, ScD, Associate Professor of Internal Medicine and the Rush Institute for Healthy Aging, Rush University Medical Center, Chicago, Illinois, Medscape General Medicine™ 1/15/2004
