Daily, I found myself with the issue of a patient who has been clinically diagnosed hypothyroidism and that brings “normal” clinical exams and therefore is not treated.
Thyroid is a gland that keeps fundamental hormones to our health and survival. The usual clinical exams can be in fact “good” and this does not mean that the patient does not have peripheral hypothyroidism. This happens because of the central level mechanism of regulation, hypophysis is a different mechanism from the peripheral level.
In fact, thyroid keeps mostly a pro-hormone (inactive hormone), the T4. This has then to be converted onto T3, an active hormone. All of the cells in our body have receptors for the thyroid hormones. This only happens also for another hormone, vitamin D.
There are factors that stimulate the production of thyroid hormones, like iron, iodine, tyrosine, zinc, selenium, vitamins E, B2, B3, B6, C & D.
Factors that inhibit this production, like stress, physical or emotional trauma, radiation, and other medications (lithium), fluorine, toxins (pesticides, plastics, mercury, cadmium and lead), the inflammatory and autoimmune diseases like the celiac disease for example, the low calories diets, the infections, which end up being stressful to the body, the hepatic and renal dysfunction, the depression, the obesity, the peripheral resistance to leptin and insulin, the diabetes, the chronic pain, the fibromyalgia and chronic fatigue…
In these situations, the inactive hormone will transform into another hormone that is also not active, but that competes with the active one in areas of connection, making this to not act, which means T4 (thyroxin) will not convert onto T3 (triiodothyronine) but acts in rT3 (reversed T3).
Nevertheless, in theses situations, the deiodinase 2, enzyme that coverts the T4 into T3 to the level of the hypophysis is inhibited.
If deiodinase 2 exists to the level of the hypophysis, it converts T4 into T3, as it is stimulated, the T3 will inhibit the TSH (thyroid’s stimulating hormone) and we’ll have a “normal” TSH. Many times, TSH is only the marker used! However, at peripheral level, for example, in these situations the deiodinase 1, that converts the T4 into T3 is inhibited to peripheral level and the patient has an intracellular hypothyroidism.
Also, the enzyme that converts the T4 into rT3 for example, does not exist on the hypophysis, as in these described situations, the body can be “full” of inactive hormones (rT3), but the hypophysis could have “normal” values as this depends on another regulating mechanism.
I tried to simplify but the system is in fact much more complex in order to comprehend globally what is happening and so that the patient can be treated in a convenient manner.
The alarm is that NORMAL CLINICAL EXAMS (the usually requested for the study of thyroid) DO NOT EXCLUD THE CELLULAR HYPOTHYRIODISM!