Hypothyroidism causes heart/kidney fibrosis, vitamin D prevents it
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If there is any doubt just how dangerous low metabolic rate can be, the study below should help dissipate such doubts. The study found that (sub)clinical hypothyroidism resulted in severe heart and kidney fibrosis, as well as muscle breakdown, in just 6 weeks after induction. The study induced the hypothyroidism pharmacologically, but the drug used to induce it is not known to cause such negative effects directly, so it was certainly the low metabolic rate that caused the organ dysfunction and whole-body degeneration. Remarkably, the oral administration of vitamin D managed to ameliorate and prevent most such dysfunction/degeneration, when administered over the same 6-week period. The human-equivalent doses were 15 IU / kg and 75 IU / kg body-weight daily, with the higher dose being more effective. The study is very new so I don’t yet have access to the full text, but when I managed to read it in full I will post the specific metrics of how effective vitamin D was.
http://dx.doi.org/10.1007/s00210-024-03593-8
“…There are several interactions between thyroid hormones (THs) and kidney and heart function. Consequently, THs deficit results in profound changes in renal and cardiac function regulation. Interestingly, emerging evidence suggests that vitamin D (Vit D) may benefit to fibrotic lesions in various tissues. Herein, this study was designed to investigate the potential impact of Vit D on renal and cardiac fibrosis in hypothyroid rats. Forty male Wistar rats were divided into four groups as follow: control, hypothyroid (0.05% PTU in drinking water), and hypothyroid + Vit D (PTU and doses of 100 or 500 IU/kg/day, by gavage) groups. After 6 weeks, biochemical parameters such as creatinine and urea in serum samples, and oxidative stress markers including malondialdehyde (MDA), total thiol groups, and superoxide dismutase (SOD) in renal and cardiac tissues homogenate were measured. Also, renal and cardiac fibrosis was evaluated histologically using Masson’s trichrome staining. Hypothyroidism significantly increased creatinine and urea. Also, in hypothyroid group renal and cardiac fibrosis as well as MDA were increased, while anti-oxidative markers including total thiol group and SOD were decreased. Administration of Vit D significantly improved these alterations in oxidative stress markers and fibrosis in renal and cardiac tissues. In conclusion, this study highlighted that Vit D supplementation reduced renal and cardiac fibrosis and improved oxidative stress. These results support the emerging experimental findings linking Vit D being introduced as a potential therapeutic agent.”
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It is good to know about vitamin D.
Peatbot.com: Based on the context provided, reducing cardiac fibrosis can be associated with the regulation of collagen gene expression and the influence of thyroid hormones. Here are some insights from the studies mentioned:
- Thyroid Hormone Treatment:
- The study by Yao and Eghbali (Cardiovasc Res 1992) suggests that thyroid hormone treatment can lead to decreased collagen mRNA and regression of cardiac fibrosis. In the tight skin mouse model, thyroid hormone treatment resulted in diminished collagen content and the disappearance of cardiac fibrosis. This indicates that thyroid hormone may play a significant role in preventing and regressing cardiac fibrosis through endocrine pathways.
- Negative Regulation by Thyroid Hormone Receptor:
- The study by Chen et al. (Mol Cell Endocrinol 2000) provides evidence that thyroid hormone receptors negatively regulate the pro-alphal(I) collagen gene expression. This suggests that maintaining adequate levels of thyroid hormones could potentially reduce collagen synthesis and thus cardiac fibrosis.
- Avoidance of Hypothyroidism:
- Hypothyroidism has been associated with increased myocardial fibrosis due to the lack of thyroid hormone, which leads to increased collagen synthesis. Ensuring proper thyroid function might help in reducing the risk of developing cardiac fibrosis.
These studies highlight the potential of thyroid hormones in managing cardiac fibrosis. However, it is important to consult with healthcare professionals for personalized medical advice and treatment options.
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I find this a classic example of misinterpretation of scientific studies.
And there are way too many to discuss each one of those in their wrong conclusions.D3 metabolism in rodents is known to be crucially different from D3 metabolism in humans.
It's beyond poor science to even directly convert these rodent findings to human equivalent doses.This just feels like science-spam.
The findings themselves and the priorly known implications of hypothyroidism may be valid.
The conclusions (and motives for funding such studies) with regard to "vitamin D prevents it" are not.
