frozenborderline
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@pattismith I never said lithium activates D1. I only know that it can activate D2 (the main dio in the CNS) based on the rodent study I linked earlier.
http://press.endocrine.org/doi/10.1210/endo.141.3.7358
Fourteen days of administration of two different dosages of lithium had opposing effects on 5′D-II activities (Fig. 5, right). The 0.15% lithium diet reduced 5′D-II activity in the cortex, whereas the 0.3% lithium diet enhanced it. T4 levels were significantly elevated after the low dose and significantly reduced after the high dose. Likewise, the serum concentrations of T4and T3 were enhanced after the 0.15% diet and lowered after the 0.3% diet (Table 1). The activities of 5D-III were, however, significantly reduced after administration of both dosages.
It is also possible that lithium inhibits both T3 and T1AM synthesis, therefore if you take T3+lithium, you end up with net gain minus T1AM effect.
I'm more convinced by what I observed personally than from what I've read.
The dose of lithium I took before my TSH levels began to go up was pretty high (I worked up to 20 mg of lithium orotate per day in divided doses). I would not be able to tolerate that dose without some thyroid onboard. I tried lithium before and while it calmed me it always worsened my CFS and gave me "leaden paralysis".
Initially, I took it with low dose levothyroxine, not T3. After a month on that regimen my T4 was borderline high (1.7) - very strange given how low the dose I was taking - but strangely my TSH also went up for the first time. There was a disconnect in the feedback mechanism which I could (Unfortunately, I got those through primary care doctor who failed to order T3. I began to have more energy and motivation and better sensory perception but it gave me severe psychological anxiety and palpitations so I stopped. Before lithium I could not tolerate T4 at all, it made me feel dreadful, so this was still a significant change.
I remember that when I combined lithium and T3 it had a very powerful amplification effect on T3. I pretty much had to discontinue T3 right away.
The other explanation is that lithium has direct effect on modulating TRH release (described here):
https://www.ncbi.nlm.nih.gov/pubmed/12401339
https://www.nature.com/articles/1380514.pdf?origin=ppub
Also, both lithium and carbamazepine decrease deoidonase 3.
https://www.ncbi.nlm.nih.gov/pubmed/8981386
I did look at that SPINA and while I misunderstood initially what TTSI stands for, I'm still trying to figure out why do did my body raised my TSH so much at the same time when it simultaneously more than doubled my thyroid resistance. I'm no longer taking lithium on a regular basis but the TSH trend continues. That makes me think that I'm actually hyperthyroid right now and the markedly increased resistance is a protective mechanism.
The other possible explanation I can think of right now is that there was some hypothalamic level response when I went on lithium because it caused functional iodine deficiency (lithium replace iodine). When I first got off lithium my T3 was naturally at 3.5 which never happened before. I had too much anxiety on that level. I suspect my ideal fT3 is 3.2. Very narrow range. Anything below that affects my mood, energy brain function. Anything above that gives fibromyalgia, anxiety and POTS.
I'm going to test myself for TSH receptor antibodies just to rule the concurrent processes going on that might be making thyroid regulation so tricky. If there are no antibodies then I will lean toward hypothalamic or genomic changes.
By the way I did find cases online about IVIG raising thyroid antibodies in patients, and one woman who had pre-existing Graves but was hypothyroid before IVIG wrote that it caused her to develop hyperthyroidism again.
do you think ivig should be avoided in people with possible thyroid issues but normal blood hormone levels?