Enjoy the nice literature summary. Still no concrete causation between clotting and AAS use and reinforces the YMMV principle. It’s great to not have any issues with long-term use of high dosages of AAS until it isn’t. I like the highlighted summary statement below:
In summary, the evidence presented herein leads to the conclusion that AAS excess may generate a prothrombotic state based on elevated platelet count, platelet agonists reactivity, and platelet activation with subsequent enhanced platelet aggregation. As noted, most of the reviewed human and animal studies revealed a stimulatory action of exogenous androgens on platelet function and count, whereas only a few others indicated a neutral, or even an inhibitory, effect. Regarding the influence of androgens in physiological doses on platelet function, researchers agreed on them having a beneficial effect. The heterogeneity of the findings results from imponderable factors, such as the various types of androgens used, the large variability in doses, time of intake, way of administration, or cycle of drug-use in athletes, as well as the variable number of subjects included in studies, the hemostatic status of the human subjects prior to treatment, or even their individual susceptibility to androgen intake or therapy.
Even if there is a comprehensive body of evidence suggesting the existence of a pro-aggregant effect of exogenous androgens, the link between AAS abuse and thrombosis remains to be more clearly established. This causal relationship must also refer to the influence of androgen excess over the humoral system of coagulation and fibrinolysis, another subject of debate. The gathered data in this area suggest that AAS abuse induces an overactivation of the hemostatic system, with both procoagulant and fibrinolytic effects . Depending on various exogenous or endogenous factors, at a certain moment the procoagulant action probably overcomes the fibrinolytic one. The coagulation abnormalities, especially when associated with increased platelet activity, may therefore lead to a thrombotic diathesis, which could explain the multitude of thromboembolic events reported so far in the AAS-abusing population.
Despite over fifty years of research on the thrombotic risk of androgens, the current state of knowledge in this regard is still scarce. Taking into account the fact that the prospective longitudinal studies in humans have unavoidable limitations, because of obvious ethical considerations, it is a certainty that at least more epidemiological studies with thrombosis outcome, and animal experiments with “real-life” AAS dosages are warranted, in order to elucidate the overall effect of supraphysiological androgens on hemostasis and to provide new compelling evidence for their claimed thrombogenic potential.