thyroid
When there is a need for increased metabolism (such as the body being cold), the hypothalamus, stimulates the pituitary to produce Thyroid Stimulating Hormone (TSH) based upon the levels of T4 in circulation. The thyroid responds by producing T4 and T3 (named for how many molecules of iodine is on each). Most of the thyroid production is T4, (T3 accounts for only 7%). In order to be transported in the bloodstream, the T4 and T3 must be “bound” to proteins, when they are dropped off at the cells throughout the body they become active by dropping the protein, or they become “free”.

T3 is the most active form of the hormone that the body can use . This means that most of the T4 must be converted to T3 in order for effective utilization by the body. Approximately 60% of this happens in the liver. 20% is converted into reverse T3 (rT3) which cannot be used, and 20% becomes T3 sulfate and T3 acetic acid which has the potential to become activated to T3 in the intestines by healthy gut flora (good bacteria). Note: antibiotics do not discriminate between “good” and “bad” bacteria in the gut, which is why frequent use of these medications can impair thyroid function.

So do you see why it is possible to have symptoms of hypothyroidism when your TSH (the only marker typically checked for by traditional healthcare models) is completely normal? Only looking at TSH assumes ideal conversion of T4 to T3. Only looking at TSH ignores possible physiological stumbling blocks such as:
  • Gut dysfunction;
  • Estrogen dominance (ie birth control pills) creating too many thyroid binding proteins (think of the thyroid binding proteins as cabs transporting people around the city, but in this case they won’t let their passengers (T3) out);
  • Hypothalamus paraventricular defect leading to low TSH caused by Neurotransmitter production deficits, hormone imbalances, or cytokines;
  • Pituitary suppression caused by high levels of cortisol;
  • Autoimmune responses;
  • Down-regulation of the 5’ deiodinase enzyme responsible for converting T4 to the physiologically active form, T3. This can be due to a vast number or causes ranging from drug interactions to nutritional deficiencies to high cortisol levels, plus many more

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