Townsend Letter for Doctors and Patients
Alternative Medicine Conference Calendar
Check out recent tables of contents
From the Townsend Letter for Doctors & Patients
July 2002

Alzheimer's Disease — A Functional Approach
by David Perlmutter, MD, Board-Certified Neurologist

(adapted from the book

Advertise with TLDP!
Order this issue!
Search our site

As the 20th century comes to a close, we are witnessing a staggering increase in dementing illnesses. At present, approximately 4.5 million Americans have Alzheimer's disease. By the year 2030, it has been estimated that this number will approach 9 million. Prevalence of Alzheimer's disease has been estimated to be 50% in individuals 85 years or older – the most rapidly growing segment of our population. Estimates of annual costs for the care of these patients approach $60 billion in the US alone.1 Any effective treatment that could delay the onset of Alzheimer's by just 5 years would reduce the cost to society by as much as $30 billion annually.2 But the emotional costs borne by families and caregivers are immeasurable.

In our magic-bullet society where physicians and patients alike are programmed to turn to the pharmaceutical industry to cure our ills, it appears that we have come up empty-handed when confronted by dementia. Nevertheless, our medical journals continue to display large compelling advertisements extolling the effectiveness of various so-called "Alzheimer's drugs.” But in a recent issue of Archives of Neurology (June 1999), the lack of usefulness of any of these drugs was eloquently described in a guest editorial by Dr. William Pryse-Phillips.3

Tacrine (Cognex®), one of the most promoted dementia drugs in the United States might reduce the "likelihood of nursing-home placement.” But, as Dr. Pryse-Phillips reported, "the drug's adverse effects on the liver and high drop-out rate were recurrent problems. While tacrine is accepted in the United States and in some European countries, evaluation by the Canadian Health Protection Branch led to its rejection on the grounds that the benefits did not translate into sufficient functional improvement to offset its potential risks (such as effects on the liver), an opinion strengthened by an assessment that concluded that it showed no clear evidence of efficacy or effectiveness.”4 In addition to Canada, several other countries have rejected tacrine, again because of its lack of clinical effectiveness and significant risk of potentially dangerous side effects.

The latest and most highly touted Alzheimer's drug, donepezil (Aricept®), has provided physicians yet another opportunity to convince themselves that they are "treating” a specific illness – in this case Alzheimer's disease. But the truth is that donepezil is essentially useless. As Dr. Pryse-Phillips reported, "Donepezil may improve certain neuro-psychological test scores, but its clinically meaningful benefits in treatment of Alzheimer's disease seem to be minimal.”5 This revelation should hit home to prescribing physicians, especially in light of the potential for adverse reactions to this drug including depression, vomiting, dizziness, and insomnia.

What then explains the tens of thousands of prescriptions written each year for these drugs? The answer lies squarely in the over $5-billion spent by pharmaceutical companies promoting their wares. Pharmaceutical advertising targeted at physicians, is so persuasive that the information presented is generally accepted as scientific fact. As an article in a recent Consumer Reports entitled Pushing Drugs to Doctors revealed, "A landmark 1982 study by Dr. Jerry Avorn of Harvard showed that doctors' opinions of two popular, heavily advertised drugs, came straight from the ads and sales pitches. The doctors believed they'd gotten their information from objective scientific sources, but those sources, in fact, had said all along that the drugs were not effective for their advertised uses.”6

Our society focuses on treating medical problems with precious little attention paid to disease prevention. Indeed, it is the general purpose of this text to provide techniques designed to effect improvements in various neurodegenerative conditions, or at least slow the rate of an individual's decline. But it seems appropriate to first explore some of the emerging theories surrounding the causes of Alzheimer's disease.

Electromagnetic Fields

In these days of hand-held cellular phones, personal computers, and an abundance of other electronic devices, the general public seems to be at least marginally concerned about the possible health risks of electromagnetic radiation exposure as evidenced by articles appearing not only in alternative medical publications, but in mainstream journals as well.

In 1995, attention was drawn to the possible link between electromagnetic radiation and Alzheimer's disease following a landmark publication in the American Journal of Epidemiology by researchers at the University of Southern California School of Medicine.7 Subsequently, these researchers confirmed a direct relationship between occupations exposing individuals to higher levels of electromagnetic radiation and the risk of developing Alzheimer's disease. Their report, published in the December 1996 issue of Neurology, revealed a substantial increased risk of developing Alzheimer's disease in individuals whose occupations exposed them to higher than average levels of electromagnetic radiation. The occupations determined to be "high risk” with respect to exposure included electrician, machinist, machine operator, seamstress, sewing factory worker, sheet metal worker, typist, keypunch operator, welder, machine shop worker, and several others. The risk of developing Alzheimer's disease in these individuals was calculated to be as much as four times higher than the general population. Subjects evaluated were at least 65 years of age at the time of their first examination and their recorded occupations reflected what they had been doing up to 40 years prior to their evaluation and diagnosis of Alzheimer's disease.8

It is critical to recognize that the data used in this research reflected levels of electromagnetic exposure long before our population began using "cell-phones,” personal computers, and the like.

How exposure to electronic devices may lead to Alzheimer's disease is unclear. Several authors have indicated that the electromagnetic radiation produced by electronic equipment enhances the formation of beta amyloid, a protein known to be prevalent in the brains of Alzheimer's patients.9 Exactly how electromagnetic radiation increases beta amyloid is unclear, but it is clear that this protein enhances brain inflammation, now known to be the primary cause of brain degeneration in this disease.10

Perhaps because influences like electromagnetic radiation and toxic chemicals in the environment cannot be seen or perceived, there is reluctance by mainstream medicine to recognize potential health risks associated with these factors. Typically, when these topics are raised, a common response by defenders of the status quo seems to be "There is no peer-reviewed literature supporting these outlandish claims.” But in reality, that is simply not the case. The journal in which this research was published is the "Official Journal of the American Academy of Neurology,” perhaps the most well-respected peer-reviewed journal dealing with neurologic disease in the world. Somehow it seems that articles linking environmental factors with disease, much like research dealing with the impact of nutrition on health, are generally overlooked in favor of concentrating on pharmaceutical approaches to treating the illnesses they cause.


Another generally unnoticed but certainly important risk factor for the development of Alzheimer's disease is exposure to aluminum. This relationship has not escaped the eyes of the manufacturers of various consumer products as we now see a proliferation of advertisements for everything from aluminum-free antiperspirants and shampoos, to ads claiming a specific antacid is better than the next as it contains "no aluminum.” But is the threat of aluminum anything more than what we read in health-food store shopping bag stuffers?

In actuality, the science relating Alzheimer's and aluminum appears in our most highly respected medical journals. Reporting in the journal Neurology in 1996, researchers from the University of Toronto found an astounding 250% increased risk of Alzheimer's disease in individuals drinking municipal water high in aluminum for a 10 or more year period of time. Alzheimer's risk increased by 70% in those exposed to municipal drinking water containing only minimally increased amounts of aluminum – water consumed by an alarming 19% of the Ontario population. Based upon their findings and the many scientific reports of elevated levels of aluminum in the brains of Alzheimer's patients, the authors concluded, "The findings from epidemiological studies, coupled with the large body of experimental evidence of aluminum neurotoxicity and elevated concentration in Alzheimer's disease affected brain, argue that priority should be given to consideration of lowering, and maintaining, acceptable limits of residual aluminum in drinking water…particularly for older age groups at risk for Alzheimer's disease.”11

One could certainly argue the rationale for reducing aluminum exposure "particularly for older age groups at risk for Alzheimer's disease” since aluminum accumulates over many years regardless of age, and we will all be members of the "older age group” eventually. But nevertheless, studies like these are a wake-up call alerting us that diseases like Alzheimer's are not random events, but are, at least to some degree, diseases brought about by factors over which we have control.

The likelihood of Alzheimer's disease being related to aluminum is further strengthened by a report in the journal The Lancet which described actual slowing of progression of dementia in Alzheimer's disease following administration of desferoximine, a chemical known to enhance aluminum excretion.12_

How aluminum increases Alzheimer's risk is now fairly well understood. Like other metals, aluminum directly enhances the formation of dangerous free radicals, leading to progressive damage of the delicate cell membranes surrounding neurons.13 Eventually, this cumulative damage hampers neuronal function which manifests as failure in such areas as memory and reasoning – characteristics commonly associated with Alzheimer's disease.

The damaging effects of free radicals produced by the presence of aluminum can be significantly reduced by the administration of melatonin, a powerful brain antioxidant.14 Melatonin is produced by the pineal gland, a small almond shaped structure situated in the back of the brain. The production of this important hormone rapidly declines with age. In addition, melatonin production is extremely light-sensitive, being produced almost exclusively during darkness.

In an intriguing report from South Africa, researchers tried to explain why Alzheimer's disease is exceedingly rare in rural Africa, while prevalent in more developed areas. They reasoned that, "Since melatonin is produced by the pineal gland only in the dark, the excess of electric light in developed countries may help explain why Alzheimer's disease is more prevalent in these countries than in rural Africa.”15

In an article appearing in the Townsend Letter for Doctors in 1993, Dr. Michael A. Weiner, executive director of the Alzheimer's Research Institute summarized our present understanding of the dangers of aluminum exposure stating, "aluminum has been known as a neurotoxic substance for nearly a century. The scientific literature on its toxic effects has now grown to a critical mass. It is not necessary to conclude that aluminum causes Alzheimer's disease to recommend that it be reduced or eliminated as a potential risk. It is the only element noted to accumulate in the tangle-bearing neurons characteristic of the disease and is also found in elevated amounts in four regions of the brain of Alzheimer's patients.”16

Aside from municipal drinking water, other potential sources for aluminum exposure are many and include nondairy creamers, self-rising flours, cake mixes, and various processed foods, especially individually wrapped cheese slices. We are able to excrete about 20 milligrams of ingested aluminum each day,17 but this amount can be greatly exceeded by even a single antacid tablet which may provide as much as 200 milligrams of aluminum. Other medications high in aluminum include many buffered analgesic products. A list of various aluminum containing medications is found below



In this context, efforts aimed at preventing dementia would certainly seem to take on more importance. In an interesting report appearing in The Lancet, May 8, 1999, from the Department of Neurology and Clinical Chemistry at the University of Heidelberg, researchers revealed that the second most frequent cause of dementia in the elderly population after Alzheimer's disease was so called "vascular dementia,” or brain dysfunction as a consequence of disease of the small blood vessels. What was more striking, was the finding of elevation of a particular chemical in the blood of these individuals called homocysteine.18_ Blood homocysteine levels are directly related to intake of the B-complex group of vitamins, specifically, vitamins B6, and 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 terms of reducing risk of dementia. As the author stated "we speculate, therefore, that progression of vascular dementia in patients with identified hyperhomocysteinemia (elevated homocysteine) could be prevented by vitamin supplementation.”19

But apart from vascular dementia, elevation of homocysteine has even more important implications. New research has found that elevation of this blood chemical is directly related to the risk of Alzheimer's disease – the most common dementing illness. In a 1998 article published in Archives of Neurology, researchers noted a 200% increased risk of Alzheimer's disease in individuals with elevation of blood homocysteine levels.20 And again, elevated homocysteine can almost always be normalized with simple vitamin therapy!

More distressing is the fact that levels of brain-damaging homocysteine can be increased by some commonly used medications including L-dopa 21_ (Sinemet®), the mainstay treatment for Parkinson's disease, as well as antibiotics containing trimethoprim 22_ (Bactrim® and Septra®).

While the idea that the process of inflammation accounts for the tissue destruction in diseases like arthritis is widely recognized, accepting the role for inflammation in Alzheimer's is somehow more difficult. Nevertheless, the current understanding of Alzheimer's disease holds that:

Symptoms of Alzheimer's disease result from failure of neurons damaged or destroyed by free radicals generated by inflammation.23

This thesis is supported by many studies demonstrating higher levels of inflammation-specific chemicals known as cytokines in brains of Alzheimer's patients, as well as the finding of reduced risk of the disease in individuals having a history of treatment with the common class of arthritis medicines known as nonsteroidal anti-inflammatory drugs (NSAIDs) or aspirin. In a 1997 publication in the journal Neurology, researchers from the Johns Hopkins School of Medicine reported a relative risk of Alzheimer's disease of only 40% of normal in individuals reporting 2 or more years of using NSAIDs. Risk was 74% of normal in aspirin users, while there was an actual increase in risk of Alzheimer's (35% above normal) in the group taking acetaminophen (the active ingredient in Tylenol®) for two years or more.25 Why acetaminophen might actually increase the risk of Alzheimer's disease may relate to its effect on an important antioxidant, glutathione. Glutathione serves as one of the primary brain antioxidants so its deficiency could potentially allow increased free radical damage. Acetaminophen has been shown to reduce glutathione production, thus paving the way for enhanced brain destruction by free radicals.26

The role of inflammation in Alzheimer's goes far beyond simple consideration of whether someone has taken a specific arthritis drug in the past or not. Inflammation may actually represent the mechanism linking specific dietary patterns to either the development of the disease or enhancing its progression. In a compelling 1998 report appearing in the journal Medical Hypothesis entitled "Could diet be used to reduce the risk of Alzheimer's disease?” Dr. P.E. Newman describes how a specific breakdown product of dietary fat, arachidonic acid, profoundly enhances inflammation.27 Indeed, it is the inhibition of the formation of arachidonic acid that explains the function of various anti-inflammatory drugs. Dr. Newman then reveals how other dietary fats, namely the essential fatty acids from the omega-3 and omega-6 groups, have just the opposite effect – they actually reduce the inflammatory process.

Inflammation-causing arachidonic acid is found in abundance in meats, meat products, and eggs. It is efficiently absorbed from the gut and is incorporated into the membranes of cells more readily than any other fatty acid. As Dr. Newman stated, "It has been estimated that persons eating a typical Western diet take in between 200 and 1000 mg per day of arachidonic acid in their food. As the normal requirement of arachidonic acid is only about 1 mg per day… it is easy to understand why over the years persons in the industrialized countries build up excessive pools of arachidonic acid and why older persons in such societies tend to develop …rheumatoid arthritis, atherosclerosis, certain neoplasms (cancers), psoriasis, and why not, Alzheimer's disease.”28

This offers a strong and sound argument against meat and egg consumption, and supports the use of essential fatty acid supplements (see below) combined with diets rich in fish, vegetables and grains - natural sources of the inflammation reducing omega-3 and omega-6 oils.

Powerful Therapy

Effective therapy for Alzheimer's disease must accomplish three tasks – reduce inflammation, limit the damaging effects of free radicals, and enhance neuronal function.

Reducing Inflammation

Essential Fatty Acids

Manipulation of dietary fats is a proven therapy to reduce inflammation. Dietary changes designed to reduce arachidonic acid (less meat and eggs), while increasing omega-3 and omega-6 levels have been demonstrated to be effective in a variety of inflammatory conditions including arthritis, psoriasis, inflammatory bowel diseases and multiple sclerosis. This is why essential fatty acid supplementation is an integral part of any nutritional protocol for Alzheimer's disease. The best source for omega-3 fats are fish oils, the potency of which is determined by its DHA content. Flaxseed oil is another source for omega-3's, but provides considerably less DHA compared to supplements derived from fish oil.

The best 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 vitamins B3 and B6 enhance the anti-inflammatory effects of both of these essential fatty acids. An accurate level of both the inflammation enhancing fatty acids and those which reduce this activity can be easily assessed using a simple blood test, the Essential Fatty Acid Panel, from Great Smokies Diagnostic Laboratory in Asheville, North Carolina (see below).

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 highest risk for free radical damage.

Based upon these characteristics, vitamin E would seem the ideal candidate for Alzheimer's disease therapy and as such was the subject of a landmark study published in the New England Journal of Medicine in 1997. In this study, patients were given Vitamin E, selegiline (another so-called "Alzheimer's drug”), both, or placebo for two years. At the end of the study data was compiled assessing such parameters as being institutionalized, loss of ability to perform activities of self-care, "severe” dementia, and death. The compelling results clearly demonstrated that the group taking vitamin E did best in all areas including longevity and cognitive function – better than the prescription medication.29

The other important role for vitamin E is that it serves to protect dietary essential fatty acids from being rendered less effective by oxidation. Vitamin E must always be included in any nutritional program utilizing essential fatty acid supplementation as described above.

Ginkgo biloba

The therapeutic use of Ginkgo biloba goes back centuries and is described in traditional Chinese pharmacopoeia. In France, extracts of Ginkgo biloba are administered orally and intravenously and are among the most commonly prescribed pharmaceutical drugs as they are in Germany where Ginkgo is licensed for the treatment of a variety of brain disorders including headache, tinnitus, vertigo and memory disorders.

Perhaps the most convincing validation of the effectiveness of Ginkgo biloba comes from a 1997 publication entitled: A Placebo-Controlled, Double-blind, Randomized Trial of an Extract of Ginkgo Biloba for Dementia, published in none other than the Journal of the American Medical Association. In this study, 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. The results were dramatic. 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. Similar results were also noted in independent evaluations of social skills. 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.”30 The effectiveness of Ginkgo biloba may be explained by several mechanisms including increasing blood flow, improving cerebral metabolism, and perhaps most importantly, its antioxidant potential, reducing the damaging activity of free radicals.31

Alpha Lipoic Acid

In the next decade, lipoic acid will clearly rank as one of the most important discoveries in the treatment of neurodegenerative diseases. New research is being published almost every day describing the vast potential of this nutrient, and with good reason. 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 vitamins C and E, and regenerate glutathione, one of the brain's most important antioxidants.

The brains of Alzheimer's patients have been shown to contain significantly elevated levels of iron, a "catalyst” which enhances free radical production.32 Lipoic acid acts as a powerful metal chelator. It binds several potentially toxic metals in the body including cadmium and free iron, and facilitates their excretion. This is another important reason why lipoic acid should be a part of any nutritional protocol for Alzheimer's disease.

N-Acetyl-Cysteine (NAC)

As mentioned above, glutathione is one of the most important brain antioxidants. Deficiency of glutathione activity has been described in various neurodegenerative conditions. To be effective, glutathione must be administered intravenously. Fortunately, glutathione production can be enhanced by the oral administration of NAC.

In addition to increasing glutathione, NAC has an important antioxidant role in and of itself. One of the most notorious free radicals implicated in Alzheimer's disease is nitric oxide. Nitric oxide is formed by the activation of an enzyme, nitric oxide synthase. NAC has the unique ability to reduce the activity of nitric oxide synthase and thus reduce the generation of nitric oxide.33 The overall effect is a marked lowering of free radical activity, thus creating a less hostile environment for delicate brain tissue.

Vitamin D

Typically regarded as having utility only in preserving bone density, vitamin D has recently been demonstrated to have profound antioxidant activity. Like vitamin E, it is highly fat-soluble, making it an ideal candidate as a brain protecting free radical scavenger. In fact, 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. Unfortunately, the authors failed to recognize the potency of vitamin D as an antioxidant and focused their comments exclusively on its role in bone health.34

Enhancing Neuronal Function

Coenzyme Q10 (CoQ10)

Coenzyme Q10 is a critical transporter of electrons in the process of energy production in every living cell. As such, deficiencies of CoQ10 function have profound effects on cellular activity and viability. CoQ10 supplementation has been demonstrated to enhance energy production in brain neurons and thus improve function.35 In addition, new research demonstrates a direct correlation between CoQ10 levels and longevity in a variety of animal species.36_ This likely stems not only from CoQ10's role in enhancing energy production, but its significant antioxidant activity as well. 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?

Nicotinamide Adenine Dinucleotide (NADH )

Like CoQ10, NADH is both an essential ingredient for the chemical reactions powering all living cells and a powerful antioxidant. Because defects of cellular energy production and free radical damage are two of the fundamental mechanisms underlying Alzheimer's disease, NADH would seem to be a perfect candidate for clinical study. In a 1996 article appearing in Annals of Clinical and Laboratory Science, Dr. Jörg Birkmayer reported a significant improvement in cognitive performance as measured on a standardized mental performance test in a group of Alzheimer's patients given NADH. Those not receiving the supplement continued to deteriorate. Dr. Birkmayer noted that in addition to increasing cellular energy production, NADH also enhanced the production of two important brain chemicals, dopamine and noradrenaline – both noted to be deficient in Alzheimer's patients. As he stated, "The concept of using NADH as an anti-dementia agent follows a strategy which differs from the approaches mentioned previously. The NADH seems to act in two ways. One is the stimulation of the endogenous biosynthesis of dopamine and noradrenaline. The other is an increase in energy production of cells in the brain and in the periphery.”38


Acetyl-L-carnitine functions primarily as a shuttle, transporting critical fuel sources into the mitochondria, the energy producing machinery of the neuron. Its second task is to facilitate the removal of the toxic byproducts of brain metabolism. Because of these functions, acetyl-L-carnitine has a pivotal role in facilitating the fundamental processes necessary for brain cell survival.

In addition, acetyl-L-carnitine is readily converted into an important neurotransmitter (brain chemical messenger) known as acetylcholine, which is known to be profoundly deficient in the brains of Alzheimer's patients.

It is for these reasons that acetyl-L-carnitine has been so extensively evaluated in dementia studies. In a report entitled "A 1-year multicenter placebo-controlled study of acetyl-L-carnitine in patients with Alzheimer's disease” which appeared in the journal Neurology, researchers at the University of California, San Diego found a striking reduction in the rate of mental decline in younger Alzheimer's patients taking acetyl-L-carnitine over the 1 year evaluation.39


Over the past 2 decades extensive medical literature has appeared describing the important role of lecithin in preserving normal brain function. More recent research has revealed that the beneficial action of lecithin is, for the most part, due to one of its components, 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. Another important membrane in nerve cells requiring adequate phosphatidylserine is that which surrounds the energy-producing structures, the mitochondria. Adequate phosphatidylserine is a basic requirement to maintain vital energy production of the mitochondria, ensuring optimal function of the brain.

These important functions of phosphatidylserine have prompted vigorous research into its therapeutic potential in dementia. In a 1991 article entitled, Effects of phosphatidylserine in age-associated memory impairment, appearing in the journal Neurology, researchers from Stanford University treated 149 memory impaired patients with phosphatidylserine for 12 weeks and observed a marked improvement on performance tests related to memory and learning compared to a similar group receiving a placebo. The authors stated, "These results suggest that the compound may be a promising candidate for treating memory loss in later life.”40

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.41 Perhaps its most important function is its role in the maintenance of myelin, the protective, insulating coat surrounding each neuron. New research reveals that B12 helps prevent the accumulation of the brain damaging amino acid 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.42 Again, the mechanism may involve elevation of homocysteine since like vitamin B12, folic acid helps lower this blood vessel damaging amino acid.


The science relating electromagnetic radiation exposure to Alzheimer's disease is sound. Reducing the risk of Alzheimer's disease involves a recognition and avoidance of potential sources of electromagnetic radiation like hand-held cellular telephones, electric blankets, hand-held hair dryers, clock-radios on the night stand near the head, and desktop computers, to name but a few.

The relationship between Alzheimer's disease and aluminum is supported by several observations including worldwide epidemiological reports, the presence of extremely high brain aluminum levels in Alzheimer's patients, and studies revealing that aluminum increases damaging free radicals. Many municipal water utilities add aluminum sulfate to public water sources to help remove fine particulate matter. This is a strong argument in favor of drinking bottled water. Avoid medications containing aluminum (see below). Read ingredient labels of food products to help avoid aluminum consumption. Food cooked in aluminum cookware can absorb substantial amounts of aluminum. Choose glass or stainless steel. And remember that melatonin can limit aluminum's damaging effects.

Avoid medications containing acetaminophen as it reduces the availability of the important antioxidant glutathione. Research shows increased risk of Alzheimer's in those taking acetaminophen with decreased risk in individuals choosing nonsteroidal anti-inflammatory drugs or aspirin. So choose Advil® or aspirin over Tylenol® as an analgesic.

Meat and eggs are rich inflammation-producing fatty acids. And it is this inflammation that leads to the enhanced production of brain damaging free radicals. The best diet is vegetarian with added fish. Supplementation with oils rich in appropriate essential fatty acids can remarkably reduce inflammation – reducing free radical production.

Appropriate antioxidants and cellular energizers, substantiated by research published in the most well-respected scientific and medical journals, have important roles in any treatment plan for this disease.

Alzheimer's Protocol

Vitamin B12 1cc (1000mcg) injected IM daily for 5 days, then twice weekly (see above)

Essential fatty acids: daily dose Linolenic acid –

best choice EPA / DHA fish oil providing--- DHA 500 mg

- or - Flaxseed oil 2 tablespoons

and Linoleic acid: Evening Primrose oil, or Borage oil, or Black Currant oil providing GLA 300 mg

Vitamins and Antioxidants

B3 100 mg

B6 100 mg

Vitamin C 800 mg

Vitamin E 400 IU

Alpha lipoic acid 80 mg

N-Acetyl Cysteine 400 mg

Ginkgo Biloba 60 mg

Vitamin D 400 IU

Melatonin 3 mg at bedtime

Cellular Energizers

Coenzyme Q10 60 mg

NADH 5 mg (twice daily)

Phosphatidylserine 100 mg

Acetyl-L-carnitine 400 mg


Magnesium 400 mg

Zinc 20 mg

Note: The above described recommendations for essential fatty acids can be modified based on the degree of imbalance revealed in a simple blood test, the Essential Fatty Acid Panel, available from: Great Smokies Diagnostic Laboratory; 63 Zillicoa Street; Asheville, North Carolina 28801-9801 USA; 800-522–4762

Antacids with Aluminum

Maalox tablets

Mintox Tablets

RuLox #1 tablets

RuLox #2 Tablets

Extra Strength Maalox Tablets


Duracid Tablets

Titralac Extra Strength Tablets

Marblen Tablets

Alkets Tablets

Mi-Acid Gelcaps

Mylanta Gelcaps

Myalgen Gelcaps

Calglycine Antacid

Titralac Tablets

Alenic Alka Tablets

Foamicon Tablets

Genaton Tablets

Gaviscon Tablets

Double Strength Gaviscon-2 Tablets

Gaviscon Extra Strength Relief Formula Tablets

Extra Strength Alenic Alka Tablets

Extra Strength Genaton Tablets

Almacone Tablets

Mylanta Tablets

RuLoxPlus Tablets

Magalox Plus

Gelusil Tablets

Maalox Plus Tablets

Mintox Plus Tablets

Extra Strength Maalox Plus Tablets

Mylanta Double Strength Tablets

Tempo Tablets

Analgesics with Aluminum

Buffets II Tablets

Vanquish Caplets

Cope Tablets

Analgesics without Aluminum

Bayer Select Maximum Strength Headache Caplets

Anacin Caplets and Tablets

Anacin Maximum Strength Tablets

From: Drug Facts and Comparisons® 1999 Edition

Alzheimer's Disease – A Functional Approach

Adapted from the book

by David Perlmutter, MD Board-Certified Neurologist

ISBN: 0-9635874-1-2,


David Perlmutter, MD

800 Goodlette Rd. N. #270

Naples, Florida 33940 USA


Fax 941-649-6370


1. Cumings J.L., Current Perspectives in Alzheimer's disease. Neurology 51 (suppl. 1): S1,1998

2. Martin, J.B., Molecular Basis of the Neurodegenerative Disorders. N Eng J Med 340(25): 1970-80,1999

3. Pryse-Phillips, W., Do We Have Drugs for Dementia? Arch Neurol 56:735-737, 1999

4. Ibid.

5. Ibid.

6. Avorn, J., In: Pushing Drugs to Doctors. Consumer Reports, Feb.: p 88,1992

7. Sobel, E., Davanipour, Z., Sulkave, R., et al., Occupations with exposure to electromagnetic fields: a possible risk factor for Alzheimer's disease. Am J Epidemiol 142:515-524, 1995

8. Sobel, E., Dunn, M., Davanipour, Z., et al., Elevated risk of Alzheimer's disease among workers with likely electromagnetic field exposure. Neurology 47:1477-81, 1996

9. 1594

10. Floyd, R.A., Neuroinflammatory Processes are Important in Neurodegenerative Diseases: An Hypothesis to Explain the Increased Formation of Reactive Oxygen and Nitrogen Species as Major Factors Involved in Neurodegenerative Disease Development. Free Radical Biology and Medicine 26 (9/10): 1346-55, 1999

11. McLachlan, D.R.C., Bergeron, C., Smith, J.E., et al., Risk for Neuropathologically confirmed Alzheimer's disease and residual aluminum in municipal drinking water employing weighted residential histories. Neurology 46: 401-405, 1996

12. Crapper McLachlan, D.R., Dalton, A.J., Kruck, T.P. et al., Intramuscular desferrioxamine in patients with Alzheimer's disease. Lancet 337(8753): 1304-1308, 1991

13. Janetzky, B., Reichmann, H., Youdim, M.B.H., Iron and Oxidative Damage in Neurodegenerative Diseases, in Mitochondria and Free Radicals in Neurodegenerative Diseases. Beal, M.F.(ed.),New York, Wiley-Liss Pub. 1997

14. Daniels, W.M., van Rensberg, S.J., van Zyl, J.M., et al., Melatonin prevents beta-amyloid induced lipid peroxidation. J Pineal Res 24(2):78-82, 1998

15. van Rensberg, S.J., Daniels, W.M., Potocnik, F.C., et al., A new model for the pathophysiology of Alzheimer's disease. Aluminum toxicity is exacerbated by hydrogen peroxide and attenuated by an amyloid protein fragment and melatonin. S Afr J Med 87(9):1111-1115, 1997

16. Weiner, M.A., Evidence points to aluminum's link with Alzheimer's disease. Townsend Letter for Doctors 124:1103, 1993

17. Birchall, J.D., Chappel, J.S., Aluminum, Chemical Physiology and Alzheimer's Disease. Lancet 2(8618):1008-10, 1988

18. Faßender, K., Mielke, O., Bertsch, T., et al., Homocysteine in cerebral macroangiography and microangiopathy. Lancet 3531586-87, 1999

19. Ibid.

20. Clarke, R., Smith, A.D., Jobst, K.A., et al., Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer's disease. Arch Neurol 55:1449-55, 1998

21. Müller, T., Werne, B., Fowler, W., et al., Nigral endothelial dysfunction and Parkinson's disease. Lancet 354, 126-127, 1999

22. Smulders, Y.M., de Man, A.M.E., Stehouwer, C.D.A., Trimethoprim and fasting homocysteine. Lancet 352:1827-28, 1998

23. Floyd, R.A., Neuroinflammatory Processes are Important in Neurodegenerative Diseases: An Hypothesis to Explain the Increased Formation of Reactive Oxygen and Nitrogen Species as Major Factors Involved in Neurodegenerative Disease Development. Free Radical Biology and Medicine 26 (9/10): 1346-55, 1999

24. Ibid.

25. Stewart, W.F., Kawas, C., Corrada, M., Risk of Alzheimer's disease and duration of NSAID use. Neurology 48: 626-632, 1997

26. Vendemiale, G., Grattagliano, I., Altomare, E., et al., Effect of acetaminophen on hepatic glutathione compartmentation and mitochondrial energy metabolism in the rat. Biochem Pharmacol 25:52 (8): 1147-54, 1996

27. Newman, P.E., Could diet be used to reduce the risk of developing Alzheimer's disease? Med Hypothesis 50:335-37, 1998

28. Ibid.

29. Sano, M., Ernesto, C., Thomas, R.G., et al., A controlled trial of selegeline, alpha-tocopherol, or both as treatment for Alzheimer's disease. N Engl J Med 336:1216-22, 1997

30. Le Bars, P., Katz, M.M., Berman, N., et al., A Placebo-Controlled, Double-blind Randomized Trial of an Extract of Ginkgo Biloba for Dementia. JAMA 278(16):1327-32,1997

31. Ibid.

32. Janetzky, B., Reichmann, H., Youdim, M.B.H., Iron and Oxidative Damage in Neurodegenerative Diseases, in Mitochondria and Free Radicals in Neurodegenerative Diseases. Beal, M.F.(ed.),New York, Wiley-Liss Pub. 1997

33. Pahan, J., Sheikh, F.G., Namboodiri, A.M.S., N-acetyl cysteine inhibits induction of NO production by endotoxin or cytokine stimulated rat peritoneal macrophages, C6 glial cells and astrocytes. Free Radical Biology and Medicine 24(1): 39-48, 1997

34. Stao, Y., Asoh, T., Oizumi, K., High prevalence of vitamin D deficiency and reduced bone mass in elderly women with Alzheimer's disease. Bone 23(6):555-557, 1998

35. Shults, C.W., Beal, M.F., Fontaine, K. et al., Absorption, tolerability and effects on mitochondrial activity of oral coenzyme Q10 in parkinsonian patients. Neurology 50: 793-795,1998

36. Lass, A., Sohal, R.S., Comparisons of Coenzyme Q bound to mitochondrial membrane proteins among different mammalian species. Free Radical Biology and Medicine 27(1/2):220-26,1999

37. Mortensen, S.A., Leth, A., Agner, E., Dose-related decrease of serum coenzyme Q10 during treatment with HMG-CoA reductase inhibitors. Mol Aspects of Med 18(Suppl.) S137-44, 1997

38. Birkmayer, J.G.D., Coenzyme Nicotinamide Adenine Dinucleotide – New Therapeutic Approach for Improving Dementia of the Alzheimer Type. Ann Clin and Lab Science 26(1):1-9, 1996

39. Thal, L.J., Carta, A., Clarke, W.R., et al., A 1-year multicenter placebo-controlled study of acetyl-L-carnitine in patients with Alzheimer's disease. Neurology 47:705-711, 1996

40. Crook, T.H., Tinklenberg, J., Yesavage, J., Effects of phosphatidylserine in age-associated memory impairment. Neurology 41:644-49, 1991

41. Clarke, R., Smith, A.D., Jobst, K.A., et al, Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer's disease. Arch Neurol 55:1449-55, 1998

42. Ibid.

Visit our pre-2001 archives

Search our pre-2001 archives for further information. Older issues of the printed magazine are also indexed for your convenience.
1983-2001 indices
; 1999-Jan. 2003 indices
Once you find the magazines you'd like to order, please use our convenient form, e-mail, or call 360.385.6021 (PST).

© 1983-2002 Townsend Letter for Doctors & Patients
All rights reserved.
Web site by Sandy Hershelman Designs
February 22, 2003