Here is a quote from the PLOS ONE study that, in my opinion, really broke down what they felt were the exact causes of increased heart risk associated with TRT use:
"Taken together, the evidence supports an association between testosterone therapy and risk of serious, adverse cardiovascular-related events–including non-fatal myocardial infarction–in men. However, there is some evidence that low endogenous testosterone levels may also be positively associated with cardiovascular events [16], [17]. But, as extensively reviewed by Xu et al. [5], effects of endogenous and exogenous testosterone may differ. Exogenous testosterone (TT) is associated with physiologic changes that predispose to clotting and thrombotic disorders including increased blood pressure [18], polycythemia [19], reductions in HDL cholesterol [18], [20], and hyperviscosity of the blood and platelet aggregation. [20]–[23]; TT also increases circulating estrogens [24], [25] which may play a role in the observed excess of adverse cardiovascular-related events, given that estrogen therapy has been associated with this excess in both men and women. [26]–[29] The mechanisms linking estrogens to thrombotic events may be related to markers of activated coagulation, decreased coagulation inhibitors, and activated protein C resistance [30]."
Looking at this, I know we have many ways to circumvent these issues through estrogen control and phlebotomy. Does anyone else see areas that may be concerning?
"Taken together, the evidence supports an association between testosterone therapy and risk of serious, adverse cardiovascular-related events–including non-fatal myocardial infarction–in men. However, there is some evidence that low endogenous testosterone levels may also be positively associated with cardiovascular events [16], [17]. But, as extensively reviewed by Xu et al. [5], effects of endogenous and exogenous testosterone may differ. Exogenous testosterone (TT) is associated with physiologic changes that predispose to clotting and thrombotic disorders including increased blood pressure [18], polycythemia [19], reductions in HDL cholesterol [18], [20], and hyperviscosity of the blood and platelet aggregation. [20]–[23]; TT also increases circulating estrogens [24], [25] which may play a role in the observed excess of adverse cardiovascular-related events, given that estrogen therapy has been associated with this excess in both men and women. [26]–[29] The mechanisms linking estrogens to thrombotic events may be related to markers of activated coagulation, decreased coagulation inhibitors, and activated protein C resistance [30]."
Looking at this, I know we have many ways to circumvent these issues through estrogen control and phlebotomy. Does anyone else see areas that may be concerning?
