Alzheimer’s Disease — A Functional Approach

[Guest guest]

http://www.townsendletter.com/July_2002/alzheimers0702.htm

 

 

 

 

 

Alzheimer’s Disease – A Functional Approach

 

Adapted from the book BrainRecovery.com

 

 

 

 

Alzheimer’s Disease — A Functional Approach

by David Perlmutter, MD, Board-Certified Neurologist

 

 

(adapted from the book BrainRecovery.com)

 

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.

 

 

 

 

 

 

Aluminum

 

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

 

..

 

 

 

 

Homocysteine

 

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

 

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

 

 

 

 

Phosphatidylserine

 

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.

 

 

 

 

 

 

Summary

 

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

 

 

 

 

Minerals

 

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

 

Acid-X

 

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

 

Drug Facts and Comparisons® 1999 Edition

 

 

 

Alzheimer’s Disease – A Functional Approach

 

Adapted from the book BrainRecovery.com

 

by David Perlmutter, MD Board-Certified Neurologist

 

ISBN: 0-9635874-1-2, www.BrainRecovery.com

 

 

 

 

 

 

 

Correspondence:

 

David Perlmutter, MD

 

800 Goodlette Rd. N. #270

 

Naples, Florida 33940 USA

 

941-649-7400

 

Fax 941-649-6370

 

 

 

 

 

 

References

 

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.

 

 

 

 

by David Perlmutter, MD Board-Certified Neurologist

 

ISBN: 0-9635874-1-2, www.BrainRecovery.com

 

 

Gettingwell- / Vitamins, Herbs, Aminos, etc.

 

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Or, go to our group site: Gettingwell

 

 

 

 

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