madman
Super Moderator
Conclusion
New clinical and translational studies suggest that testosterone in excess may in part convert to DHT and expose its deleterious effects, rather than the neuroprotective attributes of conversion of testosterone to estrogen. Atypically high and low DHT levels appear as risk factors for stroke. Insufficient data are available to reject a causal relationship between androgens or pro-androgenic steroids and incidences of acute cerebral infarction. Although testosterone supplementation may increase coronary artery noncalcified plaque volume, a risk factor for thrombosis and ischemic attack, significant changes in atherosclerotic intima thickening may also occur in major arterial locations. Long-term health benefits of androgens supplementation in androgen-deficient individuals in relation to cerebrovascular events are unknown. These concerns call into question the likelihood of distinct genetic biomarkers and predispositions (e.g. high metabolizers versus low metabolizers) that may influence the efficacy and safety of pharmacologic androgens. These hypotheses require further research to determine the relative/absolute HRs to complete risk stratifications of androgen use in the general population.
New clinical and translational studies suggest that testosterone in excess may in part convert to DHT and expose its deleterious effects, rather than the neuroprotective attributes of conversion of testosterone to estrogen. Atypically high and low DHT levels appear as risk factors for stroke. Insufficient data are available to reject a causal relationship between androgens or pro-androgenic steroids and incidences of acute cerebral infarction. Although testosterone supplementation may increase coronary artery noncalcified plaque volume, a risk factor for thrombosis and ischemic attack, significant changes in atherosclerotic intima thickening may also occur in major arterial locations. Long-term health benefits of androgens supplementation in androgen-deficient individuals in relation to cerebrovascular events are unknown. These concerns call into question the likelihood of distinct genetic biomarkers and predispositions (e.g. high metabolizers versus low metabolizers) that may influence the efficacy and safety of pharmacologic androgens. These hypotheses require further research to determine the relative/absolute HRs to complete risk stratifications of androgen use in the general population.