Stabilizing My Thyroid…

It has taken about eighteen months to get my thyroid dosage stabilized since I had to change  manufacturers. Since I am not able to metabolize copy-righted proprietary formulas like Synthroid, I have to take a bio-identical thyroxine supplement. I was able to take Armour thyroid derived from pig thyroids until they reformulated their tablets and I had an anaphylactic allergic reaction to the binders that they were using. According to the  hypoallergenic bio-identical thyroid supplement I am now taking, it is not unusual for  people who need thyroid medication to have allergic reactions to supposedly inactive ingredients in the tablets.

Getting the dose right, especially when switching medications, is a challenge. A ‘normal’ adult dose of levo-thyroxine is based on 1.6 micrograms per kilo of weight. I was taking 180 micrograms of Armor, which standard practice claims is enough for a 250-pound man. And that might be true. For decades, thyroid levels and dosages were based on a single study that looked at thyroid levels in the freshman class at Harvard before women were admitted.

However, women in general appear to need more thyroid than most men, and my particular ancestry seems to need more thyroid than most regardless of gender. The next range of thyroid supplementation ranges from 2-3mcg/k. That amount is currently recommended for those over twelve that have not completed growing

At 2.5 micrograms per kilo, the Armour I was taking was the right amount for a 160-pound woman with non-alcoholic fatty liver disease and serious malabsorption. Now I am taking 137 micrograms of Tyrosint. At 1.6 micrograms per kilo, that would be enough for a 190-pound man.

I am still carrying around several gallons of extra water with pitting edema and actually weigh 185 so I fit into the therapeutic format however briefly. More to the point is that at 2.5 mc/k, 137 mcg is also the right amount for a woman that weighs a hundred and thirty plus pounds, which is my usual pre-lightning strike pre metabolic acidosis pre-liver disease weight. Hopefully, that means that not only am I absorbing more of the thyroid medication I am taking, but the severity of my metabolic acidosis and non-alcoholic fatty liver disease are easing.

Getting those issues recognized, never mind treated has been a challenge, partly because I have such drastic reactions to the prescription medications I am offered. My reactivity should not be a surprise. According to the package insert in Tyrosint, some of the drugs that interfere with ‘thyroid absorption, synthesis, secretion, catabolism, protein binding and tissue response’ include antacids, salicylates (aspirin) and non-steroidal anti-inflammatory drugs (NSAID’s), cortisol and other steroids, antidepressants, anti-anxiety drugs, muscle relaxants, barbiturates, opiates and nicotine.

As usual, what I want to know is why so many MD’s and their primary care providers label me ‘non-compliant’ when I refuse to take the drugs they are hustling instead of noting that I have difficulty metabolizing thyroid on my chart. Some PCP’s have even gone so far as to tell me that I should stop taking supplemental thyroid because my blood tests are normal. Such idiocy should be considered mal-practice. If telling a diabetic that they should stop taking insulin because their blood sugar tests normal would get people’s licenses pulled, so should misleading patients about their thyroid medication.

Despite the massive denial in the medical industry, hypothyroidism is endemic right now. The reasons for that are unclear. We do know that fluoride, now added to most toothpaste and municipal water supplies  was once the treatment of choice for Grave’s disease or over-active thyroid because it interferes with our bodies ability to take up and use iodine. In my case, copper toxicity has been a factor (click here)

But, since the metabolic process that regulates thyroid production is so sensitive and complex, environmental factors are only one aspect to consider. The process starts with Thyrotropin Release Hormone (TRH) secreted from the hypothalamus. The amount of TRH released is very sensitive to adrenal stress. Assuming one’s adrenals are in good shape, TRH stimulates the pituitary to secrete Thyrotropin Stimulating Hormone (TSH) which in turn stimulates the thyroid itself to produce thyroxine.

Persuading our body to use levothyroxine is also complex. Getting it out of the blood stream and into the cell is an essential step. Then T3 and T4 must diffuse into the cell nucleus. Once there, T3 binds to thyroxine receptor proteins on the DNA itself.

There are different forms of thyroxine, numbered according to how many iodine ions are attached.  T4 has 4 iodine ions, T3 has three and so on. Some T3 molecules are right-handed while some are left-handed and noted as rT3. There is not a clear understanding of the way rT3 is metabolized or if it differs significantly from T3.

But, once bound to DNA, we know that T3 activates gene transcription so that messenger RNA can inform the cell what cyto-proteins it should synthesize. Cytokines alone have turned out to be key elements of treating and preventing many of our modern diseases including allergies, cancer, dementia, infertility, and more. In short, the effects of low thyroid levels are slow, insidious and widespread because thyroid hormones control cell metabolism through DNA and RNA transcription and protein synthesis.

Thyroid’s influence on intra-cellular protein synthesis is nothing to take lightly which is why I go to an endocrinologist to track my thyroid levels, not a primary care provider. Since the quality as well as the quantity of my life depends on my ability to face down the ignorance and arrogance of most primary care providers, I continue contemplating getting a ‘Non-Compliant and Proud of It’ button I can pull out and wear when I encounter the all too prevalent and blatant  ignorance and arrogance at the PCP’s office.

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