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Alzheimer's Disease and Pineal Gland Calcification

  1. #1
    Join Date
    Mar 2012

    Exclamation Alzheimer's Disease and Pineal Gland Calcification

    Pineal Gland Calcification may be a cause of Alzheimer's, I haven't taken calcium supplements in years, but do take k2 and magnesium, melatonin at times for sleep, hopefully it's helping...more here.

    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
    • Habenula
    • 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.[1] 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.[2]

    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.[3] [4]

    Indeed, Alzheimer's patients have been found to have a higher degree of pineal gland calcification than patients with other types of dementia,[5] and sleep disturbances have been identified as a primary driver of Alzheimer's disease pathogenesis,[6] 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.[7]

    If brain calcification is one of the primary driver's of Alzheimer's disease, as proposed, then inhibiting calcification may be a viable strategy for prevention and treatment. A first line approach would be the avoidance of exposure to cytotoxic materials or environmental contaminants that damage the brain. Stress reduction would also be a viable strategy, as it has also been found in the animal model to produce increased pineal gland calcification.[8]

    There is also a possible role of excess inorganic calcium supplementation (in conjunction with magnesium deficiency) which may drive ectopic calcification, i.e. calcification of soft tissue such as the arteries, breast, prostate, joints, etc.

    Theoretically, any injurious vector – natural or unnatural, dietary or environmental, infectious or pharmaceutical – could contribute to brain damage and subsequent calcification. Here is a list on our database under the 'Adverse Pharmacological Actions' index of over 85 problem substances identified to have neurotoxic properties.

    This also means that beyond the use of targeted crystallization inhibitors such as pyrophosphate and the plant derived substance phytate (and possibly magnesium and vitamin K2), natural, preferably food-based, neuroprotective agents may also hold great promise in decelerating damage associated with calcification linked neurodegeneration.

  2. #2
    Join Date
    Apr 2018
    That is pretty interesting, especially the fluoride connection. I have always understood that high cholesterol could be a contributing factor. There's just so much we don't know about the disease. My FIL is in the later stage. He went downhill pretty rapidly, he was still driving just three years ago. We think he had it a lot longer than we thought.

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