Testosterone supplementation did not show consistent benefit for cardiovascular risk , sexual function , mood and behavior , or cognition .
Studies that examined clinical cardiovascular endpoints have not favored testosterone therapy over placebo .
Testosterone is ineffective in treating erectile dysfunction and controlled trials did not show a consistent effect on libido .
Testosterone supplementation consistently increased muscle strength but did not have beneficial effects on physical function .
Most studies on mood-related endpoints found no beneficial effect of testosterone treatment on personality , psychological well-being , or mood .
Testosterone products are recommended by some prescribers in response to a diagnosis or presumption of " low testosterone " ( low-T ) for cardiovascular health , sexual function , muscle weakness or wasting , mood and behavior , and cognition .
Osteoprotegerin levels decrease during testosterone therapy in aging men and are associated with changed distribution of regional fat.
The cardiovascular effects of testosterone treatment are debated . Osteoprotegerin ( OPG ) is an independent marker of cardiovascular risk . We investigated the effect of testosterone therapy on OPG levels in aging men with low normal bioavailable testosterone levels . A r and omized , double-blinded , placebo-controlled study of 6 months testosterone therapy ( gel )  in 38 men aged 60 - 78 years with bioavailable testosterone < 7.3 nmol/l and waist circumference > 94 cm was performed .  Clinical evaluation , OPG , and C-reactive protein ( CRP ) measurements were carried out . Lean body mass ( LBM ) , total fat mass , and bone mineral density ( BMD ) were established by dual X-ray absorptiometry . Visceral adipose tissue ( VAT ) and subcutaneous adipose tissue ( SAT ) were measured by magnetic resonance imaging . Power calculation was based on an increase in LBM during testosterone therapy and responders were defined as testosterone treated patients with increased LBM ( Δ LBM positive ) , n=14 . Data are presented as median ( interquartile range ) . Testosterone therapy  decreased total fat mass and SAT , whereas VAT was unchanged ( n=38 ) . OPG levels decreased during testosterone therapy ( from 2.0 ( 1.9 - 2.5 ) to 1.9 ( 1.6 - 2.2 ) ng/ml , p<0.05 vs. placebo ) , whereas CRP levels were unchanged ( n=38 ) . In responders to testosterone therapy ( n=14 ) , ΔOPG levels were inversely associated with ΔSAT ( r= - 0.60 , p=0.03 ) and positively associated with ΔVAT ( r=0.56 , p=0.04 ) . OPG levels  decreased during testosterone therapy suggesting decreased cardiovascular risk . Decreased OPG levels were associated with changes in regional fat distribution and future studies are needed to further evaluate the association between OPG and regional fat mass distribution
Testosterone supplementation did not show consistent benefit for cardiovascular risk , sexual function , mood and behavior , or cognition .
Studies that examined clinical cardiovascular endpoints have not favored testosterone therapy over placebo .
Testosterone is ineffective in treating erectile dysfunction and controlled trials did not show a consistent effect on libido .
Testosterone supplementation consistently increased muscle strength but did not have beneficial effects on physical function .
Most studies on mood-related endpoints found no beneficial effect of testosterone treatment on personality , psychological well-being , or mood .
Testosterone products are recommended by some prescribers in response to a diagnosis or presumption of " low testosterone " ( low-T ) for cardiovascular health , sexual function , muscle weakness or wasting , mood and behavior , and cognition .