Goschorska M, Baranowska-Bosiacka I, Gutowska I, Metryka E, Skórka-Majewicz M, Chlubek D. Potential Role of Fluoride in the Etiopathogenesis of Alzheimer’s Disease. Int J Mol Sci. 2018 Dec 9;19(12). pii: E3965. doi: 10.3390/ijms19123965.
The etiopathogenesis of Alzheimer’s disease has not been fully explained. Now, the disease is widely attributed both to genetic and environmental factors. It is believed that only a small percentage of new AD cases result solely from genetic mutations, with most cases attributed to environmental factors or to the interaction of environmental factors with preexistent genetic determinants. Fluoride is widespread in the environment and it easily crosses the blood⁻brain barrier. In the brain fluoride affects cellular energy metabolism, synthesis of inflammatory factors, neurotransmitter metabolism, microglial activation, and the expression of proteins involved in neuronal maturation. Finally, and of specific importance to its role in Alzheimer’s disease, studies report fluoride-induced apoptosis and inflammation within the central nervous system. This review attempts to elucidate the potential relationship between the effects of fluoride exposure and the pathogenesis of Alzheimer’s disease. We describe the impact of fluoride-induced oxidative stress and inflammation in the pathogenesis of AD and demonstrate a role for apoptosis in disease progression, as well as a mechanism for its initiation by fluoride. The influence of fluoride on processes of AD initiation and progression is complex and warrants further investigation, especially considering growing environmental fluoride pollution.
Brewer GJ. The Copper-2 Hypothesis for Causation of the Current Alzheimer’s Disease Epidemic. Chem Res Toxicol. 2017 Feb 6. doi: 10.1021/acs.chemrestox.6b00373.
Alzheimer’s disease, the most common cause of dementia, is at epidemic proportions (15 to 44% depending on age, of those age 65 to 84) in the U.S. and other developed countries, but remains relatively rare in undeveloped countries. Surprisingly, solid historical data reveals the epidemic is a creature of the last century. That is the disease was also rare in developed countries, until the 20th century. It is disappointing that these historical and demographic facts have been ignored by the Alzheimer’s disease scientific community. Disappointing because these facts clearly point at an environmental change in the 20th century in developed countries as a major factor in causing the epidemic. Some scientists have discarded the claimed rarity of the disease in the 19th century as incorrect, saying that Alzheimer’s disease is a disease of aging, and the increasing lifespan of people accounts for the current high prevalence of the disease. But this cavalier attitude ignores historical data indicating there were many elderly people in the 19th century that weren’t getting Alzheimer’s disease with any significant frequency. In this review, after documenting that the observed assertions about historical and demographic facts are correct, evidence is amassed that the main environmental culprit causing the Alzheimer’s epidemic is ingestion of divalent copper, or copper-2. The two sources of copper-2 ingestion are drinking water and multimineral supplement pills containing copper. The increase in copper plumbing use in developed countries parallels the increasing prevalence of Alzheimer’s disease. It has been shown that enough copper is leached from copper plumbing in most households to cause Alzheimer’s disease, using the Alzheimer’s disease animal model studies as a guide to toxic levels. It is relatively easy to avoid or greatly diminish copper-2 ingestion by not using copper containing supplement pills, and testing drinking water for copper levels. If the copper in water is too high, a simple device can be put on the tap to remove copper.
Brewer GJ Divalent Copper as a Major Triggering Agent in Alzheimer’s Disease. Journal of Alzheimer’s Disease 2015 Apr 8.
Alzheimer’s disease (AD) is at epidemic proportions in developed countries, with a steady increase in the early 1900 s, and then exploding over the last 50 years. This epidemiology points to something causative in the environment of developed countries. This paper will review the considerable evidence that that something could be inorganic copper ingestion. The epidemic parallels closely the spread of copper plumbing, with copper leached from the plumbing intodrinking water being a main causal feature, aided by the increasingly common use of supplement pills containing copper. Inorganic copper is divalent copper, or copper-2, while we now know that organic copper, or copper in foods, is primarily monovalent copper, or copper-1. The intestinal transport system, Ctr1, absorbs copper-1 and the copper moves to the liver, where it is put into safe channels. Copper-2 is not absorbed by Ctr1, and some of it bypasses the liver and goes directly into the blood, where it appears to be exquisitely toxic to brain cognition. Thus, while aggregation of amyloid-β has been postulated to be the cause of AD under current dogma, the great increase in prevalence over the last century appears to be due to ingestion of copper-2, which may be causing the aggregation, and/or increasing the oxidant toxicity of the aggregates. An alternative hypothesis proposes that oxidant stress is the primary injuring agent, and under this hypothesis, copper-2 accumulation in the brain may be a causal factor of the oxidant injury. Thus, irrespective of which hypothesis is correct, AD can be classified, at least in part, as a copper-2 toxicity disease. It is relatively easy to avoid copper-2 ingestion, as discussed in this review. If most people begin avoiding copper-2 ingestion, perhaps the epidemic of this serious disease can be aborted.
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