Vitamin E as an Antioxidant-Alzheimer's Disease-Part XIX pf a XXVIII Series of Articles on AD

(4/28/08) Valory Pavlik, PhD, and Rachelle Doody, MD from Baylor College of Medicine, in Houston, Texas, presented the results of their study of the role of high doses of Vitamin E at the American Academy of Neurology 60th annual meeting, . The researchers found that a dose of 2000 IU/day in Alzheimer's disease treatment regimens lowered mortality rate by 26% when compared with subjects who did not take the vitamin supplement.

Dr. Pavlik is quoted as saying ""We think this study is reassuring in that rather than causing harm, treatment with vitamin E appears to be protective when you measure outcomes in terms of overall survival. It also suggests additional research on the use of vitamin E and treatment of Alzheimer's disease is warranted."

Dr Doody stated: ""Our research suggests AD patients who persist with their antidementia therapy from the beginning of the disease to the end and who also take high-dose vitamin E are more likely to live longer at a higher level of ability."

This study is opposed to the recent meta-analysis of role of Vitamin E, which suggested that it may have a negative outcome in cardiovascular patients and was Dr. Pavlik's motivation to do this study with AD subjects.

The population studied were 847 probable AD patient's who attended the center during 1990 to 2004 where the researchers were employed. Less than 10% of the group took vitamin E alone, and approximately 15% of the study cohort did not take the vitamin. The average follow-up period was 4.9 years, with a range of 1 to 15 years.

The study also suggested, but not at a statistically significant level, that patients taking cholinesterase inhibitors alone compared with those taking no drug had a slightly higher-than-average mortality rate. This bears more investigation, needing more subjects to improve the statistical findings of this study.

(7/28/02)- Researchers at Case Western University concluded that individuals who eat a diet that is low in fat and high in antioxidants like vitamins C and E, fish, vegetables and whole grains did reduce the risk of suffering from Alzheimer's disease.

The researchers looked at the diets of 96 Alzheimer patients and compared it to the diets of almost 190 people who did not suffer from Alzheimer's. This point became even more obvious for individuals who had the Apo-e4 gene that has been linked to the disease.

Studies now point to the fact that besides age and genetic structure, diet, exercise, blood pressure and even cholesterol level may play a significant role in connection with Alzheimer's disease. Finnish researchers who have studied almost 1,500 individuals for an average of 21 years have found that high cholesterol and blood pressure appear to increase the risk of the disease even more than carrying the Apo-e4 gene. Their study also found a high correlation between high blood pressure and Alzheimer's disease.

Two population-based studies mentioned in the June 26, 2002 issue of Journal of the American Medical Association (JAMA) suggest that vitamin E in its natural form (nuts, leafy green vegetables etc.) reduce the risk of Alzheimer’s disease.

These are some of the latest studies reported in first line professional journals to be added to the preventative/protective armentarium stemming from many of the Alternative and Complementary Medicine advocates of the role of vitamin E as an antioxidant. Mainstream researchers are now looking into the effects of vitamin E, especially its neuroprotective effects. With Alzheimer’s disease expected to rise precipitously, vitamin E has become a pivotal "player" in both the prevention and treatment of the disease

An overall increase in oxidative stress is thought to be associated with the natural aging process and age-related diseases such as cardiovascular disease, diabetes, and a variety of different malignancies. Oxidative stress is defined as the balance between the production of harmful free radicals and protective antioxidants.

Stress decreases the survival, size and neurogenesis of neurons in the hippocampus. Stress decreases the expression of brain-derived neurotrophic factor (BDNF), an effect that could contribute to the atrophy and death of vulnerable neurons in the hippocampus, which may be associated with cognitive impairment.

While the many studies of the role of vitamin E are not definitive, they lend credence to the use of natural vitamin E as a preventative factor in dealing with diseases associated with oxidative stress. Vitamin E is a compound present naturally in the diet, or added to it, which lowers the rate of production of deleterious changes by free radical reactions without significantly impairing the essential reactions involved in body maintenance and function.

Free radicals are produced from exogenous sources and are also produced as a by-product of natural cellar metabolism and are capable of causing widespread damage. Two to three percent of the human body’s oxygen is transformed into free radicals. In general, damage from free radicals has been associated with tissue degeneration resembling that of aged tissue as well as with lower intracellular energy levels (i. e. decreases in adenosine triphosphate).

Fruit flies with heightened expression of protective enzyme superoxide dismutase or catalase have been found to live longer than genetically unaltered flies. As yet, however, no research has been able to demonstrate direct linkage of decreased free radical production to an increased life span, despite the claims made by some products found in stores that specialize in nutritional supplements.

The JAMA study, mentioned above, was conducted by Martha Clare Morris, Sc.D., of the Rush Institute for Healthy Aging at Rush-Presbyterian-St. Luke’s Medical Center, Chicago, IL, Denis A. Evans, M.D., and colleagues. The National Institute on Aging (NIA) at the National Institutes of Health supported this study.

The June 26 issue of JAMA includes similar findings from scientists in The Netherlands, who also reported a link between high dietary intake of vitamins C and E and protection against AD in certain people. In addition, the journal contains an editorial on the epidemiological study of dietary intake of antioxidants and the risk of AD by Daniel J. Foley, M.S., of the NIA’s Laboratory of Epidemiology, Demography, and Biometry, and Lon White, M.D., Pacific Health Research Institute, Honolulu.

Morris et al looked at the effect of certain risk factors (age, gender, education, genetic risk) on the outcome of the study. . Only the presence or lack of apoE-e4, one form of a protein associated with increased risk of late-onset AD, seemed to matter. Statistical analysis indicated the protective effect of vitamin E from food was strongest among people who did not have the apoE-e4 risk factor allele. "Dietary vitamin E may protect against Alzheimer’s disease," says Morris, "but the protection may only occur among people without the apoE-e4 allele." The other apoE alleles may be the necessary conditions for vitamin E to be effective in preventing/postponing the onset of Alzheimer’s disease.

The head of the Dementias of Aging Branch at the NIA, Neil Buckholtz, Ph.D, states "This and a number of important population studies have pointed to vitamin E as possibly protective against oxidative damage or other mechanisms associated with cognitive decline and dementia. The only way this association can really be tested is through clinical studies and trials now underway. These will help us determine whether vitamin E in food or in supplements -- or taken together -- can prevent or slow down the development of mild cognitive impairment or AD."

These population-based studies do not propose that people run out and stock up on vitamin E. In fact, the Morris study only looked at natural occurring vitamin E, not the capsules or gels found in natural food stores. There may be a different isomer of tocopherol found in natural foods that are not present in the vitamin E supplements.

Nor have there been clinical trials to test the notion of the neuroprotective effects of vitamin E. They are now in the research clinical pipeline. The other factor to be aware of relates to the dosage and safety of antioxidants. Studies have suggested that dosage of more than 2000 International Units daily may be associated with increased bleeding. It is a good idea to consult with your physician when taking vitamin E.

The brouhaha surrounding vitamin E brought to mind a book (Clinical Judgment) written by Dr. Alvan Feinstein, an authority on the clinical use of statistics in which he wrote: "At a time of potent drugs and formidable surgery, the exact effects of ,any therapeutic processes are dubious and shrouded in dissension." The same could be said of the supplement vitamin E.

Controversy exists about certain treatments in main line medicine as well as challenges to alternative medicine treatments. Authoritative opinions in medicine have been reversed. It is time all energies move in the direction of trying to understand how much of what medicine does, be it pharmaceutical drugs or alternative medicines, is effective, and how much can be improved. The answer to oxidative stress may lie in alternative medicines. We now await the results of clinical trials to show us the direction to take.

See: Alzheimer's Disease Part I-Medications for Alzheimer's.
See: Alzheimer’s Disease Part II- Selegiline and AD.
See: Alzheimer's Disease Part III- Use of Gingko Biloba in memory problems of Alzheimer patients.
See: Alzheimer's Disease PartIV-Alternative Treatment.
See: Alzheimer's Disease Part V-Possible New Drugs for Alzheimer's Disease Treatment.
See: Alzheimer's Part VI -Early Diagnosis.
See: Alzheimer's Part VII -New Medication-Metrifonate
See: Alzheimer’s Disease Part VIII  - Implications of Longer Life Expectancies
See:  Alzheimer’s Disease Part IX-  -Estrogen and Alzheimer’s Disease
See:  Alzheimer’s Disease Part X-- -Pocket Smell Test
See:  Alzheimer’s Disease Part XI - Ethical Care
See: Alzheimer's Disease Part XII- MAO
 See: Alzheimer's Disease Part XIII-Possible Screening for ADt
See: Alzheimer's Disease Part XIV-Donepezil
See" Alzheimer's Disease Part XV-Cerebroylsin
See: Alzheimer's Disease Part XVI-MCI
See: Alzheimer's Disease Part XVII-Research Summary
See: Alzheimer's Disease Part XVIII- NSAIDs
See: Alzheimer's Disease-Part XX-Clinical Trials
See: Alzheimer's Disease Part XXI-The Brain
See Dementia with Lewy Bodies- Part XXII-by Gourete Broderick
See: Alzheimer's Disease-Part XXIII-HMG
See: Alzheimer's Disease-Part XXIV-A Prequel
See: Alzheimer's Disease-Part XXV-Psychosis
See: Alzheimer's Disease-Part XXVI-Amyloid-beta Hypothesis Controversy
See: Alzheimer's Disease-Part XXVII- AD and Diabetes
See: Alzhemeir's Disease-Part XXVIII - Insulin and AD


Harold Rubin, MS, ABD, CRC, Guest Lecturer
April 28, 2008

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