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Alzheimer's disease on the rise
Should we be worried about 10% rise in the incidence of Alzheimer's disease in the U.S. in as little as 5 years (Alzheimer's Association), as reported in a recent Times Magazine article? Not only that it becomes more widespread, it is more and more beginning to affect not just the elderly, but mid-age folks as well.
The question, of course, is not should we be worried, but what should we do about it. The article ends by putting all the hope in new drugs to slow down this alarming trend. According to it, as many as nine Alzheimer's drugs are in late-stage clinical trials.
While the article also states that no one knows what causes crippling memory loss brought on by Alzheimer's, this is not quite correct. In any particular case, there may be - and likely so - more than a single cause, and the mechanism is complex. Likewise, the mechanism may differ from one person to another. But important pieces of the puzzle are already known for quite some time.
As with any other illness, causes of Alzheimer's result from body malfunction; thus they can be traced to
genetics, nutrition and/or toxicity.
Here are the main outlines.
In the case of aluminum, it is not necessarily body contamination itself that causes neural damage; for instance, faulty magnesium distribution, can lead to a local (hippocampus) magnesium depletion and subsequent accumulation of aluminum inside neurons. These neurons now can't efficiently detoxify ammonia, which accumulates and finally kills the neuron (Glick, Durlach, Deloncle et al, 1990).
Such toxic re-distribution of minerals within neurons could be caused by altered albumin species (protein molecules), or a mere leakage of serum proteins through diseased, free-radical and/or homocysteine damaged blood vessel walls. Thus, vascular disease risk factors are also contributing risk factors for Alzheimer's-like symptoms. This explains the efficiency of antioxidants, as well as B-vitamins (particularly B9 and B12, often correcting elevated homocysteine) in slowing down and, sometimes, reversing Alzheimer's symptoms.
It is worthy to note that the blood-brain barrier, represented by brain's endothelial capillary wall tightly filled with cells - so that the only way for any molecular or sub-molecular structure to get through it is either by slow passive diffusion of fat-soluble compounds (since cellular walls are made of fatty acids), or carrier-mediated transport for water-soluble ones - appears to be significantly more porous/permeable in the hypothalamus area than the rest of brain's epithelium. That would make this area - neighboring the part of brain whose deterioration seems to be directly implicated in Alzheimer's, hippocampus - most exposed to damage from a variety of toxic substances that find their way into the body.
More than twenty years ago, researchers were able to reverse early stages of Alzheimer's with phosphatidyl choline (the most bio-active component of lecithin) supplementation; this phospholipid is needed for the formation of acetylcholine (major body neurotransmitter), known to be low in Alzheimer's disease. The likely main reason of low p-choline levels is free radical damage from processed foods and toxic chemicals, depleting its body supply12, already diminished by nutritionally poor diets based on processed foods.
However, phosphatidyl choline supplementation is not necessarily beneficial for treating Alzheimer's, since acetylcholine synthesis depends on the particular enzyme (acetylcholine transferase), which can be inactivated by pesticides, lack of vitamin C, or some other factor.
Damage to the brain cells caused by toxins and free radicals results in accumulation of the special form of protein - amyloids - which also could cause symptoms of Alzheimer's (although it is not quite clear if it is actually causing the symptoms, or is merely damage follow-up, because it is a substance that normally forms inside dying cells).
Presence of metals in your mouth, such as dental materials (amalgams, bridges, crowns, etc.) and compounds, can generate electricity that disturbs subtle neural currents essential for proper brain functioning.
The latest factor linked to Alzheimer's symptoms is elevated glucose level (diabetes). Since insulin-dependent cells become unable to effectively use glucose, they become energy deficient, sluggish and, ultimately, inflamed. This, in turn, results in amyloid plaque buildup. The mechanism is not positively determined, but it is thought to be triggered by reduction in the cellular synthesis of acetylcholine (as mentioned, other factors also can affect its synthesis).
In the similar manner, development of Alzheimer's can result from any form of mitochondrial dysfunction.
In light of this, report of a diagnosed Alzheimer's dementia reversed to age-related memory loss by a 2-year treatment consisting of selected supplements combined with gluten-free diet (R. L. Hoffman) don't come as a surprise. Vitamin B6/9/12 supplementation lowered homocysteine blood level, and may have remedied vascular dementia caused by it. High-dose supplementation of inositol - needed for body's synthesis of lecithin - may have improved acethylcholine production. Antioxidant cocktail may have helped by suppressing inflammatory process, and mitochondrial enhancers like CoQ10, NADH and carnitine by strengthening the overall cellular function.
In addition to their individual effects, these and other included nutrients (thiamine, DHA, DHEA, Ginko biloba, and others) have likely had a higher-level synergistic beneficial effect.
It certainly warrants more research and studies along these lines. We shouldn't expect that from pharmaceutical companies, who are chasing high profits in selling high-cost patentable medications, merely suppressing the symptoms. It is the government, through its public health institutions, that should take this initiative.
Most of the factors contributing to Alzheimer's disease were known for a long time; as long as over quarter of a century, which is when Tom Warren wrote his inspiring book, "Beating Alzheimer's" (1991). The author succeeded in reversing his Alzheimer's and recovering, through excruciating process of identifying and eliminating toxins accumulating in his brain, as well as nutritional deficiencies contributing to the disease.
Apparently, the main culprit in his case was mercury evaporating from dental amalgams into his brain. Very low mercury levels have caused Alzheimer-like neural changes in both, laboratory brain tissue cultures and experimental animals (Haley, 2002).
Sadly, those early leads were not followed upon. The main incentive for funding medical research is either focused public concern or big profit expectations. There is no focused public concern about Alzheimer's, and there is no big profits in determining its causes and drug-free treatment to the disease.
So, while the Congress reportedly considers research funding that would include Alzheimer's, even if it passes, the powerful pharmaceutical lobby will likely see that it is directed toward development of new drugs. Never mind that limiting the action to medicating Alzheimer's symptoms - as opposed to prioritizing healing and prevention - is evidently a losing battle.
As for the medical establishment, it moves - expectedly - pretty much along the lines set by pharmaceutical industry. When Tom Warren's neurologist had to face that Tom's brain was disease free after being positively diagnosed with Alzheimer's, his reaction was that Tom
never really had it.
The reason: by its medical definition, Alzheimer's is an incurable memory disease.
As absurd as it is, this "point of view" of the medical establishment hasn't changed much. There is a rationale for it: it is much easier to say that reversed Alzheimer's disease hasn't actually been Alzheimer's, than to accept that you and your entire concept of medicine are a failure. R