Antioxidants: Theory vs. Reality in Alzheimer's Disease

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AUTHOR:
Alvin B. Lin, MD, FAAFP

Associate Professor of Family and Community Medicine, University of Nevada School of Medicine

Adjunct Professor of Family Medicine and Geriatrics, Touro University Nevada College of Medicine

Advisory Medical Director, Infinity Hospice Care

Medical Director, Lions HealthFirst Foundation

Dr. Lin maintains a small private practice in Las Vegas, NV. The posts represent the views of Dr. Lin, and in no way are to be construed as representative of the above listed organizations. Dr. Lin blogs about current medical literature and news at http://alvinblin.blogspot.com/.

Oxidation was originally defined as the process in which at least one electron is lost when oxygen interacts with another substance. Rust is a prime example of this phenomenon. Free radicals are chemicals that steal an electron from other substances, leading to atomic, then molecular, and then cellular damage, resulting in clinical disease, and finally aging. At least that's what the proponents of free radical theory would have us believe since antioxidants, which should theoretically slow the oxidation process, should improve health. Thus, dietary supplement manufacturers recommend that we consume handfuls of pills packed full of antioxidants in order to improve our health. The basis of their claims? Observational data associating that diets high in antioxidants, eg fruits and vegetables, are associated with better health. Unfortunately, the truth isn't always so straightforward and reality doesn't always follow theory.

For instance, in a randomized double-blind, placebo-controlled study published online earlier this week in Archives of Neurology, the authors concluded that antioxidant supplements had no effect on cerebrospinal fluid markers of Alzheimer's disease. Now before you empty out your medicine cabinet and throw out all your expensive supplements, take a minute to evaluate the study. The authors randomized 78 men and women , average age 72 years to either vitamin E (alpha tocopherol) 800 IU daily, plus vitamin C 500 mg daily, plus alpha lipoic acid 900 mg daily or to coenzyme Q10 400 mg three times daily or to placebo for 16 weeks, during which they had to submit themselves for serial lumbar punctures (spinal taps) at the start and end. In case you're wondering, everyone had to take something three times daily so they had no idea what they received if anything.

So we could posit that perhaps the vitamin E/vitamin C/ALA dose was not high enough but other studies have demonstrated an increase mortality at these higher doses. Less problematic would be to claim that alpha tocopherol is not the best tocopherol to represent vitamin E. Higher levels of coQ10 have been studied in Parkinson's disease and amyotrophic lateral scelrosis without either benefit or harm, so it's not clear why a higher dose was not used for this study (besides cost). Finally, one could argue that perhaps 16 weeks isn't nearly enough time to demonstrate any benefit in CSF markers. However, the authors uncovered a disheartening decrease in cognitive function in the group randomized to E/C/ALA.

Bottom line? I can't recommend that any of my patients take E/C/ALA or high dose coQ10 in an attempt to prevent or slow down progression of Alzheimer's disease. However, the data still stands demonstrating benefit from dietary antioxidants. Similar findings exist between antioxidants (dietary vs supplemental) and stroke risk. As my other sister-in-law is fond of saying, choose wisely!