Alzheimer and 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, the American Journal of Epidemiology, researchers at the University of Southern California School of Medicine confirmed a direct relationship between occupations exposing individuals to higher levels of electromagnetic radiation and the risk of developing Alzheimer's disease. 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.

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. It is clear that this protein enhances brain inflammation, now known to be the primary cause of brain degeneration in this disease.

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 illness they cause.

Alzheimer and Aluminum

Another generally unnoticed but certainly important risk factor for the development of Alzheimer's disease is exposure to aluminum. The science relating to Alzheimer's and aluminum appears in our most highly respected medical journals. Reporting in the journalNeurology 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. "The findings from epidemiological studies, coupled with the large body of experimental evidence of aluminum neurotoxicity and elevated concentration in the Alzheimer's disease affected brain, argue that priority should be given to consideration of lowering, and maintaining, acceptable limits of residual aluminum. 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.

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.

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. Eventually this cumulative damage hampers neuronal function in such areas as memory and reasoning-characteristics commonly associated with Alzheimer's disease.

The damaging effect of free radicals produced by the presence of aluminum can be significantly reduced by the administration of melatonin, a powerful brain antioxidant. 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 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."

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 to be a neurotoxic 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 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."

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

Antiacids with Aluminum

• Acid-X
• Alenic Alka tablets
• Alkets tablets
• Almacore tablets
• Calglycine Antacid
• Duracid Tablets
• Extra Strength Alenic Alka tablets
• Extra Strength Genaton tablets
• Extra Strength Maalox tablets
• Foamicon tablets
• Gaviscon Extra Strength Relief Formula Tablets
• Gaviscon tablets
• Gelusil tablets
• Genaton tablets
• Mylanta
• RuLox #1 tablets
• RuLox #2 tablets
• RuLox Plus tablets
• Gaviscon-2 Double Strength tablets
• Mylanta gelcaps
• Mylanta Double Strength tablets
• Myalgen gelcaps
• Mintox tablets
• Mintox Plus tablets
• Mi-Acid gelcaps
• Maalox Plus Extra Strength tablets
• Maalox Plus tablets
• Maalox tablets
• Marblen tablets
• Megalox tablets
• Tempo tablets
• Titralac Extra Strength tablets
• Titralac 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

Alzheimer and Homocysteine

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. 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.

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 the Archives of Neurology, researchers noted a 200% increased risk of Alzheimer's disease in individuals with elevation of blood homocysteine levels. 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 (Sinemet®, the mainstay treatment for Parkinson's disease) as well as antibiotics containing trimethoprim (Bactrim® and Septra®).

The current understanding of Alzheimer's holds that symptoms of Alzheimer's disease result from failure of neurons damaged or destroyed by free radicals generated by inflammation. This thesis is supported by many studies demonstrating higher levels of inflammation-specific chemicals known as cytokines in brains of Alzheimer's patients.

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. 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 the cells more readily than any other fatty acid.

As Dr. Newman stated, "It has been estimated that the persons eating a typical Western diet take in between 200-1000 mg per day of arachidonic acid in their food. As the normal requirement of arachidonic acid is only 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."

This offers a strong and sound argument for the use of essential fatty acid supplements combined with diets rich in fish, vegetables and grains-natural sources of the inflammation reducing omega-3 and omega-6 oils.

Powerful Alzheimer Therapy

Effective therapy for Alzheimer's disease must accomplish three tasks:

• Reduce Inflammation
• Limit the Damaging Effects of Free Radicals
• Enhance Neuron Function.

1 - Reducing Inflammation

Essential Fatty Acids

Manipulation of dietary fats is a proven therapy to reduce inflammation. Increasing omega-3 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.

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.

2. Limiting Free Radical Activity

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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.

In a study published in the New England Journal of Medicine in 1997, 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 were 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 the group taking vitamin E did best in all areas including longevity and cognitive function-better than the prescription medication.

Gingko Biloba

The therapeutic use of Gingko biloba goes back centuries and it is described in traditional Chinese pharmacopoeia. Perhaps the most convincing validation of the effectiveness of Gingko biloba comes from a 1997 publication entitled:

 

A Placebo-Controlled, Double-blind, Randomized Trial of an Extract of Gingko biloba for Dementia, published in none other than the Journal of the American Medical Association. 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 Gingko, on average, actually improved. The effectiveness of Gingko 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.

Alpha Lipoic Acid

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. 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 part of any nutritional protocol for Alzheimer's disease.

N-Acetyl-Cysteine (NAC)

As mentioned above, glutathione is one of the most important brain anti-oxidants. 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 role in and of itself. One of the most notorious free radicals implicated in Alzheimer's disease is nitric oxide. NAC has the unique ability to reduce the activity of nitric oxide synthase and thus reduce the generation of nitric oxide.

Vitamin D

Vitamin D has recently been demonstrated to have profound antioxidant activity. 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.

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3. Enhancing Neuronal Function

Enhancing Neuronal Function is the third component of Effective treatment for Alzheimer's disease.

Coenzyme CoQ10 (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. 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 anti-oxidant. In a 1996 article appearing in the 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. "...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 an in the periphery."

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 survival.

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

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 journalNeurology 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.

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. Adequate phosphatidylserine is a basic requirement to maintain vital energy production of the mitochondria, ensuring optimal function of the brain. In a 1991 article entitled,Effects of phosphatidylserine in age-associated memory impairment, appearing in the journal Neurology, researchers from Stanford University stated that the results from treating memory impaired patients "suggest that the compound may be a promising candidate for treating memory loss in later life."

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. New research reveals that B-12 helps prevent the accumulation of the brain damaging amino acid homocysteine, which, when elevated, markedly increases the risk for Alzheimer's disease.

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. Again, the mechanism may involve elevation of homocysteine since like vitamin B-12, folic acid helps lower this blood vessel damaging amino acid.

DMAE

DMAE is one of the most important nutrients for the brain because it can enhance production of one of the brain's important neurotransmitters, acetylcholine, which controls memory, heart muscles, lungs and digestion.

Because acetylcholine is unable to cross the blood-brain barrier, it must be produced within the brain from its precursor, choline. However, choline cannot cross the blood-brain barrier until it has been converted by the liver into its lipid soluble form. If sufficient choline is not available or if the body's ability to produce this form of choline is less than ideal, acetylcholine levels are likely to be low. DMAE, which is basically a choline molecule with one methyl group missing from the nitrogen, readily crosses the blood-brain barrier. Once inside the brain, it is easily converted first to choline, then to acetylcholine. Studies indicate that DMAE can elevate mood and promote more restful sleep, as well as enhance memory, mental focus, clarity or thought and muscle tone.

Huperzine (HupA)

The alkaloid compound huperzine A (HupA) is a traditional Chinese herbal remedy prepared from the moss Huperzia serrata. The purified compound has been used in China for several years as a prescription drug for treating dementia.

HupA appears to be a potent inhibitor of acetylcholinesterase (AChE), the enzyme that breaks down acetylcholine. Biopsy and postmortem studies show substantial loss of presynaptic cholinergic neurons in brains of Alzheimer's patients indicating that whatever acetylcholine is produced in the brains of these patients is quickly broken down by AChE. This acetylcholine shortage may contribute to memory loss and other cognitive defects.

HupA may also protect neurons. In studies using cultures of cells from the hippocampus and cerebellum of rat embryos, HupA decreased neuronal cell death caused by toxic levels of glutamate.

Vinpocetine

Vinpocetine, from Periwinkle, facilitates cerebral metabolism by improving cerebral microcirculation, stepping up brain cell ATP production and increasing utilization of glucose and oxygen. Vinpocetine is a derivative of vincamine, which is an extract of periwinkle. Although these substances have many similar effects, Vinpocetine has more benefits and fewer adverse effects.

Vinpocetine is often used for treatment of cerebral circulatory disorders such as memory problems, acute stroke, aphasia (loss of the power of expression), apraxia (inability to coordinate movements), motor disorders, dizziness and headache. It is also used to treat opthalmological diseases of various origin and sensorineural hearing impairment.

Alzheimer Treatment - Summary

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

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

Appropriate anti oxidants 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.

"Gluten sensitivity is common in patients with neurological disease of unknown cause and may have aetiological significance" Lancet, 347:369-371(1996).

Suggested Alzheimer Nutritional Supplementation

Suggested Alzheimer Nutritional Supplementation:

Preventative Maintenance

• Ceralin Forte - 3 capsules daily
  Ceralin Forte is formulated to provide well-rounded support for brain and nerve protection, addressing multiple pathways involved in neurological health.
• Wellness EssentialsTM - 1 packet twice daily.
  Daily foundation nutrition plus advanced detox support.

Therapeutic Nutritional Support Protocol - Add to Above

• Ceriva - 2 softgels daily.
  Ceriva is formulated to support healthy cognitive function in those concerned about maintaining their memory by beneficially modulating acetylcholine.
• Memories - 2-4 Tablets Daily 
  Healthy brain function support
• CoQ10ST-100 - 1-2 capsules daily.
  Stabilized, Highly Absorbable Coenzyme Q10 with Natural Vitamin E
• Meta Lipoate 300 - 2-4 tablets daily.
  Premium-grade, purity-controlled alpha-lipoic acid.
• GLA Forte - 1-2 capsules daily. Potent source of omega-6 fatty acids.
• BenesomTM - 1 to 2 tablets one hour before bedtime.
  Benesom is formulated to promote a restful, relaxed state and relieve occasional sleeplessness by beneficially modulating the metabolism of melatonin and

Dietary Suggestions

• Anti-Inflammatory Diet

Alzheimer References

1. van Rensberg, S.J., Daniels, W.M., Potocnik, F.C., et al. A new model for the pathophysiology of Alzheimer's disease. Aluminum toxicity us exacerbated by hydrogen peroxide and attenuated by an amyloid protein fragment and melatonin. S Afr J Med87(9):1111-1115;1997.
2. Weiner, M.A., Evidence points to aluminum's link with Alzheimer's disease. Townsend Letter for Doctors 124:1103; 1993.
3. Birchell, J.D., Chappel, J.S., Aluminum, Chemical Physiology and Alzheimer's Disease. Lancet 2(8618):1008-1010; 1988.
4. Faßender, K., Mielke, O., Bertsch, T. et al. Homocysteine in cerebral macroangiography and microangiography. Lancet 353:1586-1587; 1999.
5. 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.
6. Müller, T., Werne, B., Fowler, W., et al. Nigral endothelial dysfunction and Parkinson's disease. Lancet 354:126-127; 1999.
7. Smulders, Y.M., de Man, A.M.E., Stehouwer, C.D.A. Trimethoprim and fasting homocysteine Lancet 352: 1827-1828; 1998.
8. Floyd, R.A. Neuroinflammatory processes are important in neurodegenerative disease: A 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.
9. Newman, P.E., Could diet be used to reduce the risk of developing Alzheimer's disease? Med Hypothesis 50:335-37; 1998.
10. Sano, M., Ernesto, C., Thomas, R.G., et al. A controlled trial of selegeline, alpha-tocopherol, or both as treatment for Alzheimer's disease. New Engl J Med 336:1216-22;1997.
11. Janetsky, 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.
12. Pahan, J., Sheikh, F.G., Namboodiri, A.M.S., N-acetylcysteine inhibits induction of NO production by endotoxin or cytokine stimulated rat perionel macrophages, C6 glial cells and astrocytes. Free Radical Biology and Medicine 24(1):39-48; 1997.
13. 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.
14. Shults, C.W., Beal, M.F., Fontaine, K., et al. Absorption, tolerability and effects on mitochondrial activity of oral coenzyme Q10 in Parkinson's patients. Neurology 50:793-795; 1998.
15. Birkmayer, J.G.D. Coenzyme Nicotinamide Adenine Dinucleotide-New Therapeutic Approach for Improving Dementia in Alzheimer Type. Ann Clin and Lab Science 26(1):1-9;1996.
16. 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.
17. Crook, T.H., Tinklenberg, J., Yesavage, J. Effects of phosphatidylserine in age-associated memory impairment. Neurology 47:705-711; 1996.
18. Clarke, R., Smith, A.D., Jobst, K.A. et al. Folate, vitamin B-12, and serum total homocysteine levelsin confirmed Alzheimer's disease. Arch Neurol 55:1449-55; 1998.