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.”
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. 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.
Our database contains a list under the ‘Pharmacological Actions‘ index of 165 natural substances with neuroprotective properties, with 109 studies on curcumin, the primary golden hued polyphenol found in the spice turmeric, exhibiting a variety of brain supportive and protective functions. What makes turmeric (curcumin) all the more compelling is that there are 30 studies on our database already demonstrating its value specifically in Alzheimer’s disease.
Ultimately, conditions such as Alzheimer’s disease do not occur in a vacuum but reflect the overarching context of our bodily, psychological and environmental health as a whole. Simply adjusting brain metabolism from insulin-dependent glucose driven metabolism to a more fat based diet, could dramatically improve neurological health, and subsequently cognition and memory, as evidenced by dramatic improvements using simple interventions like coconut oil for Alzheimer’s disease patients. Simple evidence-based, relatively non-toxic interventions using spices like turmeric have also shown great promise in preliminary case studies.
For additional research on natural interventions for, and environmental contributing causes to, Alzheimer’s disease use our Health Guide: Alzheimer’s Disease.
 Liebrich LS, Schredl M, Findeisen P, Groden C, Bumb JM, Nölte IS. Morphology and function: MR pineal volume and melatonin level in human saliva are correlated. J Magn Reson Imaging. 2013 Nov 8. doi: 10.1002/jmri.24449. [Epub ahead of print] PubMed PMID: 24214660.
 Liu RY, Zhou JN, Van Heerikhuize J, Hofman MA, Swaab DF. Decreased melatonin levels in postmortem cerebrospinal fluid in relation to aging, Alzheimer’s disease, and apolipoprotein E-epsilon4/4 genotype. J Clin Endocrinol Metab 1999;84:323–7.
 kene DJ, Swaab DF. Melatonin rhythmicity: effect of age and Alzheimer’s disease. Exp Gerontol 2003;38:199–206.
 Lucey BP, Bateman RJ. Amyloid-β diurnal pattern: possible role of sleep in Alzheimer’s disease pathogenesis. Neurobiol Aging. 2014 May 15. pii: S0197-4580(14)00350-9. doi: 10.1016/j.neurobiolaging.2014.03.035. [Epub ahead of print] Review. PubMed PMID: 24910393.
 Pappolla MA, Simovich MJ, Bryant-Thomas T, Chyan YJ, Poeggeler B, Dubocovich M, et al. The neuroprotective activities of melatonin against the Alzheimer beta-protein are not mediated by melatonin membrane receptors. J Pineal Res 2002;32:135–42.
 J Milin. Stress-reactive response of the gerbil pineal gland: concretion genesis. Gen Comp Endocrinol. 1998 Jun;110(3):237-51. PMID: 9593645