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Men develop coronary artery disease and experience coronary events about 10 years earlier than women. Historically, this was always thought to be related to the protective effects of female sex hormones. Certainly, in animal laboratory studies oestrogen reduces the development of atherosclerosis. However, long-term studies of hormone replacement therapy in women have shown adverse effects related to excessive thrombotic events (pulmonary thromboembolism and cardiovascular events). Hormone replacement therapy in women also increases endometrial and breast cancer.1 More recently, attention has been directed at the role of testosterone in men's health.
Testosterone blood levels peak early in the morning and then fade during the day. In the blood, about 70% of the total testosterone is bound to sex hormone binding protein and the remainder is loosely bound to serum albumin with only 1–3% present as free testosterone. The biologically active component of total testosterone comprises both free testosterone and that loosely bound to albumin.
Testosterone has many functions other than its effect as a virilisation agent. It is an important anabolic hormone and has, in keeping with many other hormones, an anti-insulin effect. With age, and from the age of 50 years,2 testosterone blood levels fall; this is similar to the menopause but without obvious symptoms or signs.
Although testosterone production from the testis is under the control of pituitary hormones (luteinising hormone and follicle stimulating hormone), its degradation is influenced by the enzyme aromatase in adipose tissue cells which converts it to oestrogen. This is why many obese men appear to have some degree of feminisation and a reduction in secondary sex characteristics. More importantly, a low blood testosterone level is much more common in obese individuals. For example, men with the metabolic syndrome—comprising hypertension, dyslipidaemia and type II diabetes or insulin resistance—more commonly have low serum testosterone levels and/or …
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Competing interests The author has received honoraria for invited lectures from Bayer-Schering and Prostrakan. He is not currently in receipt of any research grants from pharmaceutical companies or national funding bodies.
Provenance and peer review Commissioned; not externally peer reviewed.
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