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ALZHEIMER'S DISEASE:  Nutritional Causes, Prevention and Therapies   
   
Named after Dr. Alois Alzheimer, who identified this form of dementia in 1906, Alzheimer's Disease
is a progressive form of degenerative brain disease that generally leads to confusion, memory loss,
agitation, apathy, depression, problems with perception, speech, trouble moving, and fearing things
that are not there.  Up to 70% of dementias are due to Alzheimer's disease, with the diagnosis usually
being made by ruling out other causes of dementia.

Alzheimer's disease (AD) occurs almost as often in men as it does in women, whereby early onset
of AD appears before age 60, and late onset AD - the most common form of the disease - develops
in people 60 and older.  Several factors are believed to be involved in the development of Alzheimer's
disease, but none have been proven conclusively as of yet.

Neurochemical causes are thought to include lack of substances used by the nerve cells to transmit
nerve impulses (neurotransmitters), including acetylcholine, serotonin, somatostatin, substance P,
GABA, norepinephrine, or they are comprised of elevated concentrations of extra-cellular glutamate,
which are highly toxic to neurons. As a result, some researchers believe glutamate-rich food sources,
such as MSG, to be of concern.  The antiglutamatergic drug
Memantine (Axura, Namenda) aims to
restore a proper balance in the glutamate-NMDA system when it has become overstimulated by
glutamate.

Environmental causes to promote Alzheimer's disease include above-normal exposure to iron, zinc,
copper, manganese, Aluminum and other substances.  High aluminum (aluminium) intake in particular
inhibits choline transport and reduces neuronal choline acetyltransferase.  This may contribute to the
acetylcholine deficiency, which is a key component of Alzheimer's disease.  In some municipalities,
drinking water contains very high levels of added aluminum.

Infectious causes include Amyloid or Prion (virus-like organisms) infections, that affect the brain and
spinal cord / central nervous system, and derived from a scrapie-like factor, a disease affecting sheep.
Other risk factors include a family history of Alzheimer's disease (there is a 5-10% inherited predispo-
sition to the development of AD), a mutation of the APOE gene, Parkinson's disease, alcohol abuse,
apolipoprotein E-4, depression, head trauma (boxing), free radical damage (oxidative stress), lack of
mental stimulation (reading, problem solving, gardening), and long-term electromagnetic exposure.

Some research is underway trying to slow the progression of Alzheimer's disease by using a course
of common Antibiotics following the discovery of an increased incidence of chlamydia pneumoniae
infection in the brains of deceased Alzheimer's patients. Chlamydia pneumoniae and mycoplasma
pneumoniae have also been found with some forms of asthma, heart disease, and multiple sclerosis.

Dietary factors implicated with Alzheimer's disease include the presence of AGEs (advanced glycation
end products), as well as possible nutritional deficiencies that may include Vitamin A, Vitamin C & E,
Vitamin B6 & B12, DHA / w3 EFAs (i.e. cold water fish), and folate, although no reliable studies have
confirmed a definite link.  Whatever the cause, the lesions and the damaged neurons eventually reduce
blood flow to affected areas of the brain, causing hypoxic ischemia (oxygen deprivation).

Many of the studies done on Ginkgo Biloba in regard to Alzheimer's disease showed that it had some
ability to improve the cognitive performance and the social functioning of demented patients, at least at
an early stage of the disease.  At the same time, rats that were given gingko biloba lived longer then
those that were not.  In one study, the type of effects produced by ginkgo biloba in elderly dementia
patients were similar to those induced by a class of drugs called
Cholinesterase inhibitors - used to
treat Alzheimer's disease - which includes rivastigmine (Exelon), donepezil (Aricept), and galantamine
(Reminyl).  Because of the potential to cause liver damage, tacrine (Cognex) - another cholinesterase
inhibitor - is not much used any longer in the treatment of Alzheimer's disease.

On a cautionary note, a couple of previously well controlled patients developed seizures within two
weeks after starting to take ginkgo biloba, although they became seizure-free again after discontinuing
the herb.  Other potential side effects from taking ginkgo biloba include irritability, restlessness, gastro-
intestinal discomfort, skin rash, bleeding and headaches.

The question remains:  Unless there is a treatment that is able to halt the progression of this disorder
in its early stages, what are the advantages of taking a drug that is only able to slow the advancement
of Alzheimer's disease and prolong the inevitable?
  
 ***
  
When measuring nutritional aspects, or intracellular chemistry of patients meeting a diagnostic criteria
of Alzheimer's disease, they comprise abnormal
Sulfur levels, which is also seen in patients suffering
from Lou Gehrig's disease, or ALS (amyotrophic lateral sclerosis).  ALS patients however present with
elevated sulfur levels and above-normal selenium levels, while Alzheimer's disease patients present
with very deficient sulfur levels and below-normal, to very low selenium levels.  Following is a typical
cellular profile of someone suffering from moderate, or mid-stage Alzheimer's disease:
  
average intracellular profile of Alzheimer's disease patients
Both - sulfur and selenium - affect the central nervous system, provoking an inflammatory response as
a result of excessive uptake / retention (such as with ALS), and provoking a degenerative response as
a result of insufficient uptake / retention (such as with Alzheimer's disease).  Subsequently, dietary and
supplemental sources of sulfur should be adjusted accordingly when dealing with either condition.

The positive response to sulfur-raising therapy I have observed in patients suffering from Alzheimer's
disease has been inversely proportional to the progression of the disease, with sulfur levels of every
patient tested having been from significantly below-normal in early stages, to totally deficient - or no
longer being measurable, with late-stage cases.  On the other hand, not much of a variation in regard to
sulfur levels was observed with the types of dementias associated with Vascular / Cerebral Sclerosis,
or for instance Lewy Body dementia.

Interestingly, sulfur is a very potent aluminum antagonist, which should satisfy those individuals who
maintain that aluminum is a significant factor with Alzheimer's disease.  Likewise, whenever people
- young or old - suffer from a "foggy mind," concentration problems, and/or poor memory, a majority of
them show below normal sulfur activity, including many children or adults diagnosed with ADD / ADHD
,
or those who have actually tested for elevated levels of aluminum.  Municipalities that in addition to
fluoride and chlorine also add aluminum to drinking water certainly do not help those people struggling
to maintain adequate sulfur levels.

Another potent dietary sulfur antagonist is Copper, which is found in a variety of commonly consumed
"addictive" foods and beverages such as coffee, cola, chocolate and cocoa products, as well as wheat
germ, shellfish, soybeans, nuts, liver, and many other sources.  A high copper / low sulfur status not only
provides a biochemical platform that encourages the development of Alzheimer's disease, but also
some forms of arthritis and vascular degeneration.

While some drugs or antibiotics may slow - or if it should happen - halt the progression of Alzheimer's
disease, sulfur supplementation has the potential of not only preventing, but actually reversing the
condition, provided it has not progressed to a stage where much damage has been done to the brain.

I believe one major reason for the increase in Alzheimer's disease over the years has been the bad
reputation
Eggs have been getting in respect to being a high source of cholesterol, despite the fact of
dietary cholesterol having little impact on serum cholesterol - which is now also finally acknowledged by
mainstream medicine.  In the meantime, a large percentage of the population lost out on an excellent
source of sulfur and a host of other essential nutrients by following the nutritional misinformation spread
on eggs.  Of course, Onions and Garlic are another rich source of sulfur, but volume-wise, they cannot
duplicate the amounts obtained from regularly consuming eggs.

MSM (methyl sulfonyl methane) is another organic source of sulfur that is found in a variety of uncooked
and unprocessed foods (eggs, milk, seafood, meats, cabbage, onions...).  Its supplemental form was
previously only used in veterinary medicine, but once approved for humans, it gained great popularity
among arthritis sufferers.
Its availability for patients with low sulfur levels and corresponding memory / concentration problems -
among other conditions - all the way to early or moderate stages of Alzheimer's disease has become a
major turning point in the successful treatment of low sulfur-related diseases, especially for patients who
could not tolerate dietary sources of sulfur.

Nevertheless, in addition to supplementing MSM, I still recommend the regular consumption of eggs,
garlic and onions (when tolerance is not a problem) for patients whose sulfur levels test below normal
for their many extra nutritional benefits. ¤

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Copyright © 2000-2008  Ronald Roth           Acu-Cell Disorders: Alzheimer's Disease
  
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