Alzheimer’s is a largely age-dependent disease. It is estimated that 2% to 5% of people over 65 years of age and up to 20% of those over 85 years of age have Alzheimer’s telltale signs.
Dr. Harold Foster provides a detailed explanation about this terrible disease in his book “What Really Causes Alzheimer’s.” Dr. Foster outlines which contaminants to avoid and what options to consider for preventing and even reversing the formation of destructive plaques and neurofibrillary tangles that inhibit brain function.
While toxic aluminum does accumulate in the brain and is known to cause nerve damage, there seem to be a number of contributing factors, such as impaired detox mechanisms and missing minerals in foods, notably magnesium.
Dr. Foster discusses what happens in the brain to cause loss of myelin tissue, and which minerals are missing from our western diet, worsening the problem. He points to a possible preventive strategy, but in the end, it is our own choice. Is our health going to be more important to us than industrial production including the attendant pollution?
An Executive Summary of Dr. Foster’s Book: What Really Causes Alzheimer’s Disease
|There is currently a global Alzheimer’s disease pandemic, involving tens of millions of victims. This book shows what to do about it, including memory loss issues. This book suggests how to reverse memory loss in the early stages of Alzheimer’s disease.
There is currently a global Alzheimer’s pandemic involving tens of millions of victims. In the USA alone, the number of those affected is expected to reach 14 million by 2050. This suffering and the financial costs associated with it are unnecessary. Alzheimer’s disease is caused by aluminum and is particularly common in those carrying the APO E4 allele(s), who are more susceptible to this toxic metal because they are less capable than the general population of removing brain beta-amyloid and tau proteins. As a consequence, such individuals are at higher risk of developing Alzheimer’s disease, as these abnormal proteins build up in the brain and form neuritic plaques and neurofibrillary tangles. Naturally, this process occurs more often and most rapidly in regions that promote the deposition of beta-amyloid and tau. Such “harmful” environments are those in which drinking water is acidic, high in monomeric aluminum, and lack magnesium, calcium, and silicic acid. Under these circumstances, aluminum enters the brain and impairs various enzymes, including choline acetyltransferase, calcium/calmodulin kinase II, alkaline phosphatase, and phospholipase.
The result of this process is the abnormal brain pathology seen in Alzheimer’s disease patients and the disrupted biochemistry associated with it. In an earlier publication, I called this explanation of the downward spiral, known as Alzheimer’s disease, Foster’s Multiple Antagonist Hypothesis.
Retrogenesis, the loss of abilities in cognition, coordination, behaviour, language, and feeding in the reverse order that they were acquired, occurs in Alzheimer’s disease. This is, in part, because aluminum inhibits at least three membrane-bound enzymes, Na+K+ ATPase, acetylcholinesterase, and, most interestingly, the myelin-specific enzyme 2’3’-cyclic nucleotide phosphohydrolase. As a result, it can cause rapid thinning of the myelin sheath and increase its susceptibility to oxidative stress. It seems very likely that these destructive processes are linked to demyelinization and so to associated retrogenesis.
The APO E4 allele plays a key role in promoting Alzheimer’s disease because of the inefficiency with which those possessing this genetic aberration can remove brain beta-amyloid and tau. Genetically, however, there is more to Alzheimer’s disease than the APO E4 gene. To date, four genes have been identified as playing a role in either early- or late-onset Alzheimer’s disease: beta-amyloid precursor protein, presenilin-1, presenilin-2, and apolipoprotein E genes. Workers have linked most of these variants to familial early-onset Alzheimer’s, but the apolipoprotein E4 allele is a relatively common risk factor for developing late-onset Alzheimer’s disease.