Alzheimer’s disease and Nutrition

A progressive, degenerative disease of the brain and the leading cause of SENILITY in the United States. About 4 million Americans have Alzheimer’s disease, roughly 10 percent of the U.S. population over the age of 65 and nearly half of the population over 85. The disease can also strike younger adults (a small percentage of people in their 30s and 40s have Alzheimer’s). On average, a person lives between eight and 20 years after the onset of symptoms, which include short-term memory loss, difficulty performing simple tasks, and disorientation to time and place. Alzheimer’s disease results from the death of nerve cells in the forebrain and the hippocampus responsible for memory and learning. Patients also have a deficiency of ACETYLCHOLINE, a NEUROTRANSMITTER made by neurons that helps carry nerve impulses between cells. Currently, diagnosis of Alzheimer’s disease is very difficult, yet a comprehensive diagnosis is critical in treating the senile patient. Symptoms occurring before the age of 65 are designated early-onset Alzheimer’s; after 65, it is called late-onset Alzheimer’s.
Despite intensive research over the last decade, it is not known whether Alzheimer’s disease is a function of AGING, or whether it is the result of a specific disease process. Alzheimer’s seems to be a multifaceted disease, with environmental and genetic factors contributing. There is an association with Down’s syndrome and thyroid disease. Smoking a pack of cigarettes a day increases the odds of developing Alzheimer’s disease. Diet also plays a part. A healthy diet with low fat intake may reduce the risk of developing Alzheimer’s disease; studies also suggest that a high-fat diet during early and mid-adulthood may be associated with an increased risk of developing Alzheimer’s, especially in people with a genetic marker called apoE-4. In a retrospective study that examined food eaten by 304 men and women (72 with Alzheimer’s disease and 232 healthy individuals), researchers found that people with the apoE-4 gene who also ate the most fat were seven times more likely to develop Alzheimer’s than were people with the marker who ate lower-fat diets. In a separate 2000 study of Americans between the ages of 40 and 50, those who carried the apoE-4 gene and whose diet consisted of 40 percent fat calories had 29 times the risk for Alzheimer’s compared to non-apoE-4 carriers on the same high-fat diet.
Some population studies have reported an association between low-fat diets and a lower incidence in Alzheimer’s. For example, in China and Nigeria, where fat intake is low, the risk of developing Alzheimer’s is 1 percent at age 65 compared to 5 percent in the United States. In the Netherlands researchers reported an association between dementia and diets high in total fat, saturated fat, and cholesterol.
Scientists have identified four genes that increase the risk of developing Alzheimer’s. APOE-4 is implicated in late-onset cases. This gene can be passed down from one or both parents. Patients who have one copy of the gene have a three times greater risk of developing the disease than do patients who do not. Patients who inherit two copies have an eight times greater risk of developing Alzheimer’s. The other three genes—presenilin 1, presenilin 2, and amyloid precursor protein—are associated with early-onset cases. Nearly everyone who carries one or more of these genes will develop early-onset Alzheimer’s.
Another hypothesis for Alzheimer’s links
chronic CALCIUM deficiency to increased uptake of ALUMINUM and silicon by the brain. Aluminum concentrates in the brains of patients with the disease; whether this is a cause or an effect is unknown. In postmenopausal women, estrogen (hormone) replacement therapy may help prevent Alzheimer’s. The importance of estrogen in brain health is gradually being recognized. Alternatively, there may be alterations in nerve cell membranes. Other evidence links immune system activation with the disease process.
Research points to the following possible causes of senility: exposure to toxins, oxidative damage due to FREE RADICALS, abnormal protein metabolism, slow viruses, the narrowing by cholesterol deposits of arteries feeding the brain, ZINC and VITAMIN B12 deficiencies, head trauma, and adverse drug reactions that decrease blood and oxygen supply to the brain.
Clinical trials of an experimental vaccine for the disease, called AN-1792, were halted abruptly in early 2002 when several participants developed brain inflammation after taking it. The drug was a form of beta-amyloid, a protein fragment found in the amyloid plaques that grow over the brain tissue of Alzheimer’s patients. Researchers had hoped exposure to the protein would trigger participants’ IMMUNE SYSTEMs to produce antibodies to the amyloid plaques.
Experiments in mice have shown that FOLIC ACID—a vitamin found in high amounts in dark green, leafy VEGETABLES, CITRUS FRUITS and JUICES, whole wheat BREAD, and dry BEANS—may help ward off Alzheimer’s disease. Since 1998 the U.S.
FDA has required the addition of folic acid to enriched breads, CEREALS, FLOURS, CORNMEAL, PASTA, RICE, and other GRAIN products.
There is limited evidence that antioxidants may help fight or prevent some of the brain cell damage in Alzheimer’s disease that may be attributed to free radicals, thus slowing the progression of the disease. In particular, some evidence suggests that vitamin C or vitamin E supplements can slow the course of Alzheimer’s over several years. In a National Institute on Aging study, the antioxidant vitamin E delayed by six months the progression of some symptoms of Alzheimer’s disease. In another National Institute on Aging study, people in the middle to late stages of Alzheimer’s who took vitamin E at levels 70 times higher than the recommended daily dose noticed some beneficial effects. At a dose of 2,000 IU daily, vitamin E was able to slow the expected rate of decline compared to patients who did not take the vitamin. Other studies suggest that taking antioxidants (vitamins C and E) might significantly lower the risk of developing Alzheimer’s. In one preliminary Massachusetts study, none of the 50 subjects who used either vitamin C or E developed Alzheimer’s at follow-up studies. In a Dutch study of 5,000 people, a diet high in antioxidants reduced the risk of developing Alzheimer’s.
Other antioxidants, such as GINKGO biloba and PHOSPHATIDYLSERINE, melatonin, flavonoids (chemicals found in many plants, including fruits and vegetables), and carotenoids (pigments found in plants such as carrots) also may help ease symptoms of Alzheimer’s disease. Small studies of ginkgo did find slight improvement among patients with Alzheimer’s who took the herb. Although German physicians have approval to use ginkgo to treat Alzheimer’s, and it has been used for thousands of years in Chinese medicine, North American physicians disagree as to its benefits as a memory treatment.
According to several studies, eating plenty of dark-colored fruits and vegetables may slow brain aging. Extracts of blueberries and strawberries reversed age-related decline in lab animal brain function. Blueberries may be the best anti-Alzheimer’s antioxidant of all. When Tufts University researchers analyzed more than 40 fruits and vegetables, they found that raw blueberries contained the highest level of antioxidants (nearly 60 times the recommended daily levels)—more than blackberries, beets, spinach, and garlic. Animals fed an antioxidant-rich blueberry extract diet showed fewer age-related motor changes and outperformed their study counterparts on memory tests. Some studies on wine have reported a lower risk, but they have not been consistent. It might be that wine may increase even more risk of developing Alzheimer’s for people who carry the apoE-4 gene that has been linked to Alzheimer’s—while protecting people who do not carry the gene. However, supplements containing high doses of antioxidants can cause adverse effects. In addition, high doses of vitamin E are potentially harmful if combined with blood-thinning drugs. No one should take these or any supplements without consulting a doctor.
It is safer to consume antioxidants as part of a healthy diet; antioxidants are found in most dark colored fruits and vegetables, whole grains, legumes, nuts, and wheat germ.
Nutritional approaches to treatment employ CHOLINE and LECITHIN (phosphatidylcholine) supplements. The rationale for their use is based on the fact that the brains of diseased patients do not make enough acetylcholine, and supplying this building block could boost acetylcholine production. Results of clinical studies have not shown consistent improvements. Researchers have used drugs that help maintain acetylcholine levels with mixed results. A growth promoter called nerve growth factor may enhance brain function in aged experimental animals. Preliminary research suggests that GINKGO biloba, a leaf extract, is known to have antioxidant and anti-inflammatory properties and to enhance NEUROTRANSMITTER function, alleviates the symptoms of Alzheimer’s disease. Scientists are currently studying whether a lowfat, high-fiber diet may reduce the risk of developing Alzheimer’s disease just as it lowers the risk of other diseases associated with aging, like cardiovascular disease and cancer. Finnish researchers who studied 1,500 patients for 21 years found that subjects with high CHOLESTEROL and high blood pressure had a corresponding higher risk of developing Alzheimer’s. French researchers noted a link between high blood pressure and Alzheimer’s risk.