I have attempted for a long time to treat my chronic fatigue syndrome and Hashimoto's thyroiditis with NDT (natural dessicated thyroid) by following the usual regimen propagandized by Broda Barnes teachings offspring websites such as STTM. The result was always the same: I'd feel a lot better for a few days and then start developing horrible side effects - orthostatic tachycardia, facial swelling, extreme fatigue, depression, amotivation, and pronounced droopy eyelids, swollen veins and eye puffiness. I also noticed that while paradoxically my usually high heart rate would go up while standing due to drop in BP, it was actually lower than usual when I was laying. I finally got off all T3 and NDT and now only use a small dose of T4 but I still have some degree of cognitive dysfunction and low motivation. My research led me to trace amines and TAAR receptor.
It was very interesting to discover that 3-iodothyronamine, which is an endogenous trace amine produced from t3 and t3 hormones, acts as a hibernation-inducing molecule in animals (and a very recent metabolomics study by R. Naviaux described ME/CFS as a state of dauer or essentially "hibernatory hypometabolism" http://www.pnas.org/...37/E5472.full).It is associated with decrease in heart rate (negative chronotropic effect), ptosis (droopy eyelids) and drop in body temperature. This was really eye opening to me because up until now I could not understand how could high doses of thyroid hormone produce such a paradoxical response in me - lowered body temperature instead of high, weight gain instead of weight loss, and lowered heart rate instead of high heart rate. Now it makes sense: the effects of T1AM (3-iodothyronamine) were greater than the effects of increased T3 (and would become more pronounced later in the day as the T3 dose would begin to wear off).
Why did this happen to me and not to other people who seem to be able to tolerate high dose of thyroid for their fatigue and depression? Do I have a genetically abnormal TAAR receptor or an impairment in either synthesis or breakdown of trace amines? I am pretty sure I'm not the only one who experienced this paradoxical reaction, and I'm looking for other people who either already have some insights or have expertise in neurocheimstry, and are interested in exploring this further together, perhaps not only as potential side effect of high thyroid treatment regiments but also as an underlying mechanisms behind CFS and POTS. Not only TAAR is presumed to neuromodulate pretty much all of the other neurotransmitters (DA, NE, SE, Ach and possibly GABA), it also acts directly and indirectly on alpha1-adrenergic receptors and it also appears to be a potent modulator of immune system - which makes it a very good suspect for these conditions.
3-Iodothyronamine (T1AM) is an endogenous compound with chemical features that are similar to thyroid hormone. T1AM has a carbon skeleton identical to that of T4 and contains a single carbon-iodine bond. Theoretically, T1AM could be produced from T4 by enzymatic decarboxylation and deiodination. Recent studies show that T1AM and higher iodinated thyronamines are subject to similar metabolic processing as iodothyronines such as T4, suggesting a biological linkage between iodothyronines and iodothyronamines. In addition, single doses of T1AM administered to rodents induce a hypometabolic state that in certain ways resembles hibernation and is opposite to the effects of excess T4. This review will discuss the latest developments on this recently discovered thyroid hormone derivative.
https://www.ncbi.nlm...les/PMC2654747/
