This is a short interview of the author on a recent retrospective review that revealed no increase in cardiovascular events in men. The author rightly points out his data, which is quite different than the previous JAMA and PLOSone publications which showed an increase in cardiovascular events.
However, the lead author points out the main problem with comparisons: his study group was younger and healthier. So, the comparison is apples to oranges. Studies still point to increased risk of Testosterone therapy in men with pre-existing CVD. This new study does not refute this point at all.
Another serious flaw here, is that only Testosterone was followed. This logic is seriously flawed as I have previously documented. The author points out the flaw in the levels in the JAMA study post treatment. But he fails to account for the the lack of adequate pathway assessment i.e.aromatazation. Also, no inflammatory cytokine evaluation was performed in that study. Both of these should have been highlighted.
In contrast, a positive was the length of follow.
In this study, flu vaccine is found to reduce MI risk by 45%. Now, the take home point here is that those with cardiovascular compromise need to avoid the flu--not, that the flu vaccine by itself reduces the risk. The authors of this study fail to state the low success of the flu vaccine in the prevention of the flu. They also fail to state the increased inflammation as a result of the vaccine itself. A better approach would be to use natural therapies i.e.. vitamin D that have been shown to prevent the flu.
This is simply a public release prior to publication. Study found that Testosterone therapy in men with existing CAD did not increased adverse events; in fact, it appeared to decrease the adverse events when compared to that of the non-treatment group. Study not yet available to read the specific design, stats, and results which would be required to better analyze the actually results.
Thyroid hormone plays significant role in cardiac remodeling after acute myocardial infarction. Thyroid hormone, particularly T3 as the vast majority of T3 is produced in heart tissue via D1 enzymatic activity, improves cardiac contractility, reduces systemic vascular resistance, reduces cardiac work load, decreases blood pressure, improves cardiac metabolism, and thus improves outcomes post MI.
A good biomarker of intracardiac TH signaling would be helpful but has not been identified. In the absence of such a marker,
a rational, cautious therapeutic approach might be to restore and maintain over time biochemical euthyroidism as documented
by normal circulating levels of TSH, FT4, and FT3.
a low-T3 state resulting from altered peripheral TH metabolism secondary to caloric restriction is associated
with impaired cardiac contractility
Low-T3 syndrome is the central finding and defines the illness in a variety of acute and chronic severe nonthyroidal illnesses
with cardiac origin, including MI, HF, and surgically treated cardiac disease.1 Low circulating levels of T3 in the absence of primary thyroid hypofunction have been found in 20% to 30% of patients with
dilated cardiomyopathy.
Great review of the current understanding of thyroid hormone metabolism in cardiac tissue. Low T3 and increased rT3 (via increased D3 activity) is CLEARLY associated with poor cardiac performance and post MI and CHF is associated with poor outcomes. T3 is critical in cardiac remodeling and recovery post MI. T3 is actually a vasodilatory in the coronary arteries. Why a endocrinologist would call rT3 useless only points to their ignorance of the literature.
Life extesnsions rebuttal to recent JAMA study. There was several significant flaws in that study and thus limited evidence can be gained by that study. In fact, I find no useful clinical information from that study.
In the rebuttal, there are flaws. The reference the low serum T after treatment and correctly discuss aromatase activity. But they fail the mention that the less than optimal serum T is likely the result of the high aromatase activity in these men. Age, stress, and weight are primary causes of increases estrogen production in these men. These would be why likely high estrogen production occurred and less than optimal serum T resulted. And, increased E2 will cause an increase in CRP which can precipitate CVD events.
Androgen deprivation therapy increases fatal heart attack risk in those with prostate cancer. Also of note, the ADT therapy group did not provide a survival benefit over that of radiation alone.
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Wow, thyroid hormones play a significant role in cardiac remodeling post MI. Thyroid hormones, "promotes tissue growth and differentiation and favorably remodels cardiac cell while increases cellular survival..." How many people post-MI are having their thyroid evaluated, let alone correctly evaluated?
Animal model finds that Testosterone improves ventricular remodeling and function following myocardial infarction in male rats. This similar finding has been found in human studies as well.
Testosterone therapy was found to lower BNP in this rat study.
Only abstract available here, but EDTA chelation found to reduce risk of death, reinfarction, stroke, hospitalization, angina in individuals with diabetes and prior MI from 38% to 25%.
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Study finds increased risk of sudden MI in men with low Testosterone and elevated Estradiol. In converse, increased risk is associated with elevated Estradiol in women.
This study appears to fly in the face of the recent studies on the dangers of Testosterone therapy in those with comorbidities. This study was a retrospective cohort. The study found that men in the highest risk for MI, had a reduced MI risk with Testosterone therapy. Men in the lower risk quartiles had no such benefit. Of note, the frequency of injections suggests inadequate dosing i.e. 4.4 in first year and 8.2 in follow up. Most injection regimens will require at least monthly injections, though Testosterone pellets were used. Of special note, no mention of level testing of Testosterone prior to study and/or during study and follow up.