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03 octubre, 2014

#Alzheimers Caused by #Fluoride


New Insight: Alzheimer’s Disease Linked to Pineal Gland Calcification from Fluoride
by Christina Sarich

Alzheimer’s disease is running rampant throughout the modern world now, but even with pharmaceutical companies spending billions on drugs to ‘cure’ it, they have failed miserably. While the use of coconut oil for Alzheimer’s disease is proving beyond beneficial, the answer to really treating this disease may lie in the pineal gland and the decalcification of one of the most important elements of the endocrine system. 

For the past few decades, research into treating Alzheimer’s disease has been relegated to an assumption: that it is caused by the lack of the neurotransmitter, acetylcholine. In fact, most pharmaceuticals made to treat Alzheimer’s patients are acetylcholinesterase inhibitors (drugs that inhibit the enzyme that breaks this neurotransmitter down.) 

Big Pharma Fails to Treat Alzheimer’s
These drugs have produced only palliative results, if any, and many of them cause seizures or other neurological issues in the patients who take them. As Sayer Ji from GreenMedInfo so convincingly points out, Alzheimer’s drugs are nothing but patented xenobiotic chemicals, completely alien to human physiology. So – if this is the case, it makes sense to look deeper into the causes of such a prevalent disease which is said to be ‘bigger than cancer’ for the pharmaceutical markets. 

Despite failed trials, Big Pharma continues to invest heavily in ‘cures’ that may not do anything but worsen the disease. 

For instance, trials of Eli Lilly’s gamma-secretase inhibitor, semagacestat (LY450139), were halted due to below par results. Later, despite reports that results of solanezumab, a neuroprotector that binds to plaque and inhibits its formation, were positive, the company said that it was not going to the FDA for approval, but will conduct a third Phase III trial. The company has already failed three times at creating a “inhibitor that would address this disease effectively. 

These attempts are in the company of other failed pharmaceutical projects: 

  • In 2011, Bristol-Myers Squibb tried to develop a gamma-secretase inhibitor (BMS-708163. Test results were less than promising.
  • In 2012, Pfizer announced that it was abandoning further development of intravenous formulations of bapineuzumab, an anti-amyloid antibody, after the failure of its Phase II study.
  • In 2013, Baxter International reported that its immune-bolstering treatment had ended in a failure after trying to create a drug called Gammagard out of components of the human immune system. It also failed at removing amyloid plaques from the brain.
Research Reveals Link Between Calcification of the Brain and Alzheimer’s Disease
A new study looks at intracranial calcifications in the brains of Alzheimer’s patients. After noticing that the brain’s primary structures were negatively affected by calcification, namely the pineal gland, habenula, choroids plexus, superior sagittal sinus, basal ganglia, falx, dura mater, and tentorium cerebelli, as well as the petroclinoid ligaments, a promising new hypothesis was formed.

Removing calcification from the brain could treat the disease.
 
Alzheimer’s patients had highly calcified pineal glands, as do two-thirds of the adult population, and a likely cause of this calcification is fluoride.

“Fluoride is likely to cause decreased melatonin production and to have other effects on normal pineal function, which in turn could contribute to a variety of effects in humans.” (National Research Council 2006).

Alzheimer’s disease patients are commonly deficient in melatonin levels, likely due to the inability of their pineal gland to produce adequate quantities. The pineal gland is responsible for regulating melatonin and seratonin, which are precursors to N,N-Dimethyltryptamine, or DMT. Melatonin is secreted at night and our pineal gland is aided in this process by sleeping in complete darkness, which is how melatonin production is best synthesized. Our endogenous melatonin levels usually peak around 2 AM, and ceases when the sun comes up. 

By the time most people are 17 years old, their pineal glands are calcified, thus greatly reducing this gland’s ability to create melatonin. Their pineal glands will often appear as a lump of calcium during a magnetic resonance scan. Calcification is the buildup of calcium phosphate crystals in various parts of the body, a natural process caused primaily by nanobacteria. 

Nanobacteria are tiny microorganisms that form calcium phosphate shells around themselves, essentially to protect themselves from your immune system. It appears from the latest research that this may be the cause of much of disease. From arthritis, to stroke, from cancer to back pain – and now Alzheimer’s disease.

The International Center for Nutritional Research supports this new hypothesis that calcification of the pineal gland can be causing Alzheimer’s disease: 

“Fluoride does not accumulate in brain. Of all tissues, brain has the lowest fluoride concentration [Jenkins, 1991; Whitford, 1996; Ekstrand, 1996]. It is generally agreed that the blood-brain barrier restricts the passage of fluoride into the central nervous system. The human pineal gland is outside the blood-brain barrier [Arendt, 1995].
It is one of a few unique regions in the brain (all midline structures bordering the third and fourth ventricles) where the blood-brain barrier is weak. Cells in these regions require direct and unimpeded contact with blood[Rapoport, 1976]. Therefore, pinealocytes have free access to fluoride in the bloodstream. This fact, coupled with the presence of HA, suggest that the pineal gland may sequester fluoride from the bloodstream.” 

In fact, Alzheimer’s patients have been observed to have a higher degree of pineal gland calcification than patients with other types of dementia, and sleep disturbances have been identified as a primary cause of Alzheimer’s disease pathogenesis, due to the fact that wakefulness increases the the toxic Alzheimer’s disease associated brain protein — amyloid-β (Aβ), known as amyloid plaques - and sleep reduces Aβ. Melatonin has also been known to inhibit the progression of Aβ brain pathology as well as the formation of Aβ protein itself. 

So while pharmaceutical companies spend billions on ways to stop amyloid plaque buildup, they aren’t looking at the root cause of the calcification of the pineal gland which inhibits melatonin production, which is the body’s own natural way to inhibit amyloid plaques.

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