A very interesting paper that re-confirms what so many here have said - hypothyroidism affects the heart. But with a concerning point that correcting that hypothyroidism rapidly actually damages the heart. Anyway, thankfully, you can follow the link to read the full paper. Though that doesn't say what the the optimum approach might be. And it is all from rats.
PLoS One. 2014 Oct 15;9(10):e109753. doi: 10.1371/journal.pone.0109753. eCollection 2014.
Hypothyroidism and its rapid correction alter cardiac remodeling.
The cardiovascular effects of mild and overt thyroid disease include a vast array of pathological changes. As well, thyroid replacement therapy has been suggested for preserving cardiac function. However, the influence of thyroid hormones on cardiac remodeling has not been thoroughly investigated at the molecular and cellular levels. The purpose of this paper is to study the effect of hypothyroidism and thyroid replacement therapy on cardiac alterations. Thirty Wistar rats were divided into 2 groups: a control (n = 10) group and a group treated with 6-propyl-2-thiouracil (PTU) (n = 20) to induce hypothyroidism. Ten of the 20 rats in the PTU group were then treated with L-thyroxine to quickly re-establish euthyroidism. The serum levels of inflammatory markers, such as C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL6) and pro-fibrotic transforming growth factor beta 1 (TGF-β1), were significantly increased in hypothyroid rats; elevations in cardiac stress markers, brain natriuretic peptide (BNP) and cardiac troponin T (cTnT) were also noted. The expressions of cardiac remodeling genes were induced in hypothyroid rats in parallel with the development of fibrosis, and a decline in cardiac function with chamber dilation was measured by echocardiography. Rapidly reversing the hypothyroidism and restoring the euthyroid state improved cardiac function with a decrease in the levels of cardiac remodeling markers. However, this change further increased the levels of inflammatory and fibrotic markers in the plasma and heart and led to myocardial cellular infiltration. In conclusion, we showed that hypothyroidism is related to cardiac function decline, fibrosis and inflammation; most importantly, the rapid correction of hypothyroidism led to cardiac injuries. Our results might offer new insights for the management of hypothyroidism-induced heart disease.
The thing that confuses me about this type of study is that they medically induced hypothyroidism with PTU. So what does that mean for people who do not have medically induced hypothyroidism?
Then they reversed the hypothyroid state with T4.
'The LT4 treatment for 1 week decreased the TSH levels to normal values that remained stable until the end of the protocol'
From the above it seems as if they only gave the T4 for one week and we don't know how much the dose they gave for that one week was in equivalent human terms - I.e. was it like a hypoT person suddenly taking 150mcg T4... Versus the low and slow approach that the majority of people take with starting doses and slow increases.
Then add in the fact it was all done on male rats... I don't know anything about whether we are similar enough to rats to be able to judge anything about that.
This bit is interesting:
'Our results might offer new insights for the management of hypothyroidism-induced heart disease.'
They did talk at one point about how T4 is given to people who've already had a attack (as part of their heart treatment) and who were not diagnosed hypoT pre-heart attack. So it seems as if they aim this info at them.... Rather than diagnosing hypothyroidism in its early stages, treating it and aiming to avoid the heart attack?!
As someone with a diagnosis of 'm.e' after twenty years being treated for hypo and now trying to address hidden hypo issues - perhaps obscured by a TSH of 0.01 or perhaps RT3 or some other issue the NHS does not deal with - I definitely observe how the heart is key to my illness. It just does not have the power it needs, and therefore my whole body does not have the power it needs. What interested me was when I bought NDT and read the American leaflet it gave more info about the way to use the medication than any previously read UK info pages, whether for T4 or UK T3. It made it very clear that because of the dangers to the heart it was imperative that dose increases happened gradually, very gradually, that the cells need time to almost soak up the new T3 on offer and only when saturated and start to struggle again should the dose be increased. I assume this ties in with these findings.
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