Textbook of Clinical Nutrition and Functional Medicine, vol. 2: Protocols for Common Inflammatory Disorders (Inflammation Mastery & Functional Inflammology) by Alex Vasquez

Author:Alex Vasquez [Vasquez, Alex]
Language: eng
Format: azw3
ISBN: 9780990620440
Publisher: Alex Vasquez
Published: 2016-03-23T04:00:00+00:00

Intracellular Hypercalcinosis: A Functional Nutritional Disorder with Implications Ranging from Myofascial Trigger Points to Affective Disorders, Hypertension, and Cancer

This article was originally published in Naturopathy Digest in 2006 naturopathydigest.com/archives/2006/sep/vasquez.php

Introduction: Let us explore the possibility that elevated levels of calcium within the cell (intracellular hypercalcinosis) might predispose toward a wide range of clinical problems including migraine, hypertension, myofascial trigger points, inflammation, and cancer. Further, let’s review the data showing that several commonly employed nutritional interventions can be used synergistically to counteract and correct this problem. By the time readers complete this article, they will have 1) an understanding of this problem, 2) a protocol for how to correct this problem, and 3) be able to explain the biochemical rationale for using these nutritional protocols in patients who might otherwise be treated with drugs in general and calcium-channel-blocking drugs in particular.

Although prescription drugs are often used by medical doctors in a “willy-nilly manner” (according to Harvard Medical School Professor Dr. Jerry Avorn581), let’s assume for a moment that legitimate reasons exist for the widespread use of drugs that block calcium channels in cell membranes—the “calcium-channel-blocking drugs.” Although it is counterintuitive to promote health by interfering with the body’s natural function, calcium-channel-blocking drugs are routinely used in pharmaceutical medicine for a broad range of problems including hypertension, heart rhythm disturbances, bipolar disorder, and anxiety/panic disorders. Widespread medical use of calcium-channel-blocking drugs appears to validate the supposition that excess intracellular calcium is an important contributor to these and perhaps other problems. Therefore, if intracellular hypercalcinosis is the problem, then any safe and cost-effective treatment that can correct this problem should be met with the same widespread acceptance given to calcium-channel-blocking drugs, which are universally accepted and utilized in the allopathic “conventional medicine” society. At the very least, we can generally state that all phenomena that contribute to calcium deficiency result in an increase in intracellular calcium levels (the “calcium paradox”) due to the effect of parathyroid hormone, which specifically promotes calcium uptake in cells while mobilizing calcium from bone. Additionally, a few other nutritional influences (such as fatty acid imbalances) modulate cellular calcium balance, and these will be discussed in the section on clinical interventions.

The Problem of Excess Intracellular Calcium: Although the current author is the first to coin the phrase “intracellular hypercalcinosis”, several other authors have pointed to the problem of the “calcium paradox” and the means by which body-wide calcium deficiency can result in intracellular calcium overload, which triggers a cascade of events leading to adverse health effects. Most notably, the work of Takuo Fujita582,583 stands out in its clarity and specificity in linking intracellular hypercalcinosis with disorders such as hypertension, arteriosclerosis, diabetes mellitus, neurodegenerative diseases, malignancy, and degenerative joint disease.

Mechanisms by which intracellular hypercalcinosis contributes to disease have been defined, at least partially. However, we must remember that nutritional disorders never occur in isolation, and that the effects of intracellular hypercalcinosis observed clinically are overlaid with manifestations of the primary nutritional/metabolic disorder. Stated differently, contrary to what the pharmaceutical paradigm’s monotherapeutic

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