Each and every cell in our bodies contains hundreds of mitochondria. Mitochondria are the cellular power houses that produce energy for the cell. If the body runs out of food, mitochondria can convert our own muscle protein into energy. If lack of food continues to be a problem, mitochondria can convert fat into energy to save muscle tissue. Mitochondria are responsible for 90% of the energy production that cells, tissues, organs and bodies require for metabolism.

Thyroid hormones are responsible for metabolism and when thyroid hormones are given to animals, trillions of mitochondria increase in size and number. The total membrane surface of the mitochondria increases in almost direct proportion to the increased metabolic rate of the whole animal. The Textbook of Medical Physiology, states, “It seems almost an obvious deduction that the principal function of thyroxine (thyroid hormone) might be simply to increase the number and activity of mitochondria.”

It is interesting to note that mitochondrial DNA are inherited solely from the mother. The mother’s egg contains the entire set of DNA responsible for their production and this DNA is completely separate from the 46 chromosomes that define a person’s individuality. Men’s sperm contribute nothing towards mitochondria. This finding correlates with the fact that hypothyroidism is chiefly inherited from the mother.

Mitochondrial mutations appear to be largely responsible for the metabolic defects at the cellular level, which result in a hypothyroid-like condition. Modern thyroid blood tests do not detect this because thyroid hormone levels may be normal, but they are not high enough to stimulate the genetically defective mitochondria into normal activity. The increased basal temperature that results from administering desiccated thyroid is a direct result of enhanced mitochondrial activity.

There are receptors for thyroid hormones both on the surface and within every human cell. Around 100 different mutations have been found in one of the primary genes for thyroid receptors. Defective thyroid receptors may prevent a sufficient supply of hormones that are circulating in our blood from reaching the mitochondria and other crucial sites such as the nucleus of the cell. So, it appears that altered glycosylation is directly related to hypothyroidism. The cell surface sugar structures (cell receptors) and those glycoproteins within the cell are not constructed properly and thyroid hormone does not trigger the metabolic action to occur optimally and leads to the disease state with ramifications for other disease states over time. This and more information are available in a 2-hour class webinar.

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