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Alzheimer's disease is expanding unchecked throughout the modern world, despite billions spent annually on pharmaceutical interventions. Could the calcification of the brain play a role?
Despite the multi-billion dollar successes of conventional pharmacological interventions for Alzheimer's disease, lackluster treatment outcomes have revealed them to be an abject failure. The ongoing hypothesis for the past few decades has been that Alzheimer's disease is caused by a lack of the neurotransmitter acetylcholine, but acetycholinesterase inhibitors (drugs that inhibit the enzyme that breaks this neurotransmitter down) have failed miserably to produce anything but momentary palliative improvements, if that. In addition, post-marketing surveillance data now clearly shows these drugs may actually cause new, more serious neurological problems, such as seizures.
And why should we surprised? We do not know of a disease in existence that is caused by a lack of a pharmaceutical agent. And what are Alzheimer's disease drugs but patented xenobiotic chemicals, completely alien to human physiology? Therefore, the answer is to look deeper at the underlying causes of Alzheimer's disease, and preventing, addressing and reversing them whenever possible -- the perennial goal of compassionate and logical medicine.
Pineal Gland Calcification and Alzheimer's Disease
A promising new perspective on Alzheimer's disease looks at the role of age-induced brain calcification in neurodegenerative diseases. So-called normal intracranial calcifications, which accumulate in the brain with age, are so prevalent today that the conventional medical establishment considers them non-pathological when not accompanied by overt evidence of disease. The primary brain structures affected are:
- Pineal gland
- Choroid plexus
- Basal ganglial calcification
- Falx, dura mater or tentorium cerevelli
- Petroclinoid liagaments
- Superior sagittal sinus
Pineal gland calcification is now found in two-thirds of the adult population. While related to neurological injury and innate repair processes, its exact causes in each individual case are complex and mostly unknown. However, one likely culprit is fluoride exposure. [See: Fluoride: Calcifier of the Soul]
One of the primary functions of the pineal gland is to secrete melatonin, a powerful sleep regulatory hormone and antioxidant, known to be protect against over 100 health conditions, including various lethal cancers. A recent study found that the degree of pineal gland calcification (and pineal cyst volume) in study participants correlated negatively with sleep rhythm disturbances; also, the less calcified their pineal glands were found to be the more melatonin was found in their saliva.
In connection with this finding, Alzheimer's disease patients are commonly deficient in melatonin levels, likely due to the inability of their pineal gland to produce adequate quantities.  Indeed, Alzheimer's patients have been found 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 driver of Alzheimer's disease pathogenesis, due to the fact that wakefulness increases the the toxic Alzheimer's disease associated brain protein -- amyloid-β (Aβ) -- and sleep reduces Aβ. Melatonin has also been identified to inhibit the progression of Aβ brain pathology as well as the formation of Aβ protein itself.
A 2009 study published in Medical Hypothesis sheds light on the mechanisms that may link pineal gland dysfunction with the etiology of Alzheimer's disease:
"[T]he presence of lesions in the pineal gland, which may be attributable to different causes (old age, or exposure to cytotoxic materials or environmental contaminants), would result in development of calcification, the extent of which would increase with more severe injury, with lower concentrations of crystallization inhibitors (pyrophosphate and phytate) and/or with reduced ability of the immune system. Calcification of the pineal gland would lead to a loss of function, decreasing the excretion of melatonin. This reduction in melatonin would both generate a further increase in oxidative injury (because of a fall in antioxidant capacity) and would be responsible for an increase in the deposition of b-amyloid protein, which is associated with the development of Alzheimer's disease. Therefore, a dearth of crystallization inhibitors could be a risk factor for development of Alzheimer's disease, and this hypothesis should be further evaluated."