TL;DR: Testosterone replacement shifts the cytokine balance to a state of reduced inflammation and lowers total cholesterol in men with symptomatic androgen deficiency.
Abstract: Testosterone has immune-modulating properties, and current in vitro evidence suggests that testosterone may suppress the expression of the proinflammatory cytokines TNFalpha, IL-1beta, and IL-6 and potentiate the expression of the antiinflammatory cytokine IL-10. We report a randomized, single-blind, placebo-controlled, crossover study of testosterone replacement (Sustanon 100) vs. placebo in 27 men (age, 62 +/- 9 yr) with symptomatic androgen deficiency (total testosterone, 4.4 +/- 1.2 nmol/liter; bioavailable testosterone, 2.4 +/- 1.1 nmol/liter). Compared with placebo, testosterone induced reductions in TNFalpha (-3.1 +/- 8.3 vs. 1.3 +/- 5.2 pg/ml; P = 0.01) and IL-1beta (-0.14 +/- 0.32 vs. 0.18 +/- 0.55 pg/ml; P = 0.08) and an increase in IL-10 (0.33 +/- 1.8 vs. -1.1 +/- 3.0 pg/ml; P = 0.01); the reductions of TNFalpha and IL-1beta were positively correlated (r(S) = 0.588; P = 0.003). In addition, a significant reduction in total cholesterol was recorded with testosterone therapy (-0.25 +/- 0.4 vs. -0.004 +/- 0.4 mmol/liter; P = 0.04). In conclusion, testosterone replacement shifts the cytokine balance to a state of reduced inflammation and lowers total cholesterol. Twenty of these men had established coronary disease, and because total cholesterol is a cardiovascular risk factor, and proinflammatory cytokines mediate the development and complications associated with atheromatous plaque, these properties may have particular relevance in men with overt vascular disease.
TL;DR: Testosterone replacement therapy in hypogonadal men delays time to ischaemia, improves mood, and is associated with potentially beneficial reductions of total cholesterol and serum tumour necrosis factor α.
Abstract: Background: Low serum testosterone is associated with several cardiovascular risk factors including dyslipidaemia, adverse clotting profiles, obesity, and insulin resistance. Testosterone has been reported to improve symptoms of angina and delay time to ischaemic threshold in unselected men with coronary disease. Objective: This randomised single blind placebo controlled crossover study compared testosterone replacement therapy (Sustanon 100) with placebo in 10 men with ischaemic heart disease and hypogonadism. Results: Baseline total testosterone and bioavailable testosterone were respectively 4.2 (0.5) nmol/l and 1.7 (0.4) nmol/l. After a month of testosterone, delta value analysis between testosterone and placebo phase showed that mean (SD) trough testosterone concentrations increased significantly by 4.8 (6.6) nmol/l (total testosterone) (p = 0.05) and 3.8 (4.5) nmol/l (bioavailable testosterone) (p = 0.025), time to 1 mm ST segment depression assessed by Bruce protocol exercise treadmill testing increased by 74 (54) seconds (p = 0.002), and mood scores assessed with validated questionnaires all improved. Compared with placebo, testosterone therapy was also associated with a significant reduction of total cholesterol and serum tumour necrosis factor α with delta values of −0.41 (0.54) mmol/l (p = 0.04) and −1.8 (2.4) pg/ml (p = 0.05) respectively. Conclusion: Testosterone replacement therapy in hypogonadal men delays time to ischaemia, improves mood, and is associated with potentially beneficial reductions of total cholesterol and serum tumour necrosis factor α.
TL;DR: It is concluded that testosterone is a promising treatment for men with idiopathic osteoporosis, acting to suppress bone resorption by a mechanism that may involve estrogen.
Abstract: There is no established treatment for osteoporosis in men, a common and disabling condition the incidence of which is increasing rapidly. We conducted an open study to investigate the efficacy and mode of action of testosterone therapy in eugonadal men with osteoporotic vertebral crush fracture. Twenty-one men, aged 34–73 (mean 58), were treated with intramuscular testosterone esters (Sustanon 250®) every 2 weeks for 6 months. Bone mineral density (BMD) measurement by dual-energy X-ray absorptiometry was performed at baseline and 6 months. We also measured biochemical markers of bone turnover, testosterone, estradiol, sex hormone binding globulin (SHBG), and gonadotrophins at baseline and after 3 and 6 months of treatment. Treatment was well tolerated, and side effects were uncommon. Lumbar spine BMD increased by 5% from 0.799 to 0.839 g/cm2 (p < 0.001). All bone markers decreased, indicating that treatment suppressed bone turnover. Although serum osteocalcin levels fell only slightly, there were large reductions in urinary deoxypyridinoline and N-telopeptide (p < 0.05), which were correlated with the increase in spinal BMD. Interpretation of the findings with other markers, such as bone-specific alkaline phosphatase and pyridinoline, was confounded by the wide scatter of values. Serum testosterone increased by 55%, while SHBG decreased by 20%, leading to a rise in free androgen of 90%. Serum estradiol also increased by 45%. The change in spine BMD was significantly correlated with a change in serum estradiol but not with a change in serum testosterone. We therefore conclude that testosterone is a promising treatment for men with idiopathic osteoporosis, acting to suppress bone resorption by a mechanism that may involve estrogen.
TL;DR: It is concluded that testosterone supplementation significantly increased bone mineral density in this heterogeneous group of men with idiopathic primary osteoporosis, without an overall adverse effect on cardiovascular risk factors.
TL;DR: Echocardiographic results showed that bodybuilders who use steroids have smaller left ventricular dimension with thicker walls, impaired diastolic function, as well as higher peak systolic strain rate in steroid-using bodybuilders as compared to the other two groups.
Abstract: Anabolic androgenic steroids (AAS) are used by some athletes to enhance performance despite the health risk they may pose in some persons. This work was carried out to evaluate the possible structural and functional alterations in the heart using two-dimensional, M-mode, tissue Doppler imaging (TDI) and strain rate imaging (SRI) in athletes using supraphysiological doses of AAS. Additionally, the histological and ultrastructural changes in cardiac muscles of adult albino rats after injection of sustanon, as an example of AAS, were studied. Fifteen male bodybuilders using anabolic steroids constituted group 1, five male bodybuilders who are not using anabolic steroids constituted group 2, and five nonathletic males constituted negative control group (group 3). They were investigated by two-dimensional, M-mode, TDI and SRI. This study was performed on 30 adult albino rats. They were divided into two groups. Group I (Control group) (10) was subdivided into negative control, subgroup 1a (5), and subgroup 1b (5), which received 0.8 ml olive oil intramuscular once a week for 8 weeks. Group II (Experimental group) (20) received sustanon 10 mg/kg intramuscularly once a week for 8 weeks. The heart specimens were prepared for light microscopy and transmission electron microscopy. Echocardiographic results showed that bodybuilders who use steroids have smaller left ventricular dimension with thicker walls, impaired diastolic function, as well as higher peak systolic strain rate in steroid-using bodybuilders as compared to the other two groups. Light microscopy examination of cardiac muscle fibers showed focal areas of degeneration with loss of striations and vacuolation in the experimental group. Ultrastructural examination showed disturbance of the banding pattern of the cardiac muscle fiber with disintegration, loss of striations, dehiscent intercalated disc, and interrupted Z-bands. Administration of supraphysiological doses of AAS caused severe deleterious effects in the myocardium both in athletes and in experimental animals. The SRI shows promise in the early detection of systolic dysfunction in those athletes who use steroids.