Andropause

Andropause, sometimes referred to as male hypogonadism or late-onset hypogonadism, describes the gradual age-related decline in testosterone and other key male hormones that typically begins in a man's late thirties or forties and progresses steadily through subsequent decades. Unlike the more abrupt hormonal transition of female menopause, andropause is a slow, incremental process, which is one reason it is so frequently unrecognised. Symptoms develop gradually, accumulate quietly, and are regularly attributed to stress, overwork, depression, or simply the inevitable effects of ageing.

Testosterone is far more than a hormone of sexual function. It plays a fundamental role in muscle mass, bone density, red blood cell production, cardiovascular health, cognitive function, mood regulation, metabolic health, and energy production. When it declines, the consequences are systemic and far-reaching, and they are not simply an unavoidable feature of growing older. They are a clinical presentation that deserves investigation and, where appropriate, intervention.

At The Schoeman Clinic, we take male hormonal health seriously and with the same rigour we apply to female hormonal medicine. We investigate the full male hormonal and metabolic picture, identify the specific drivers of decline, and develop a personalised treatment programme aimed at restoring optimal hormone levels and protecting long-term health.

Testosterone production declines at a rate of approximately one to two percent per year from the early thirties onwards in most men. This is a normal biological process, but the rate of decline is significantly influenced by a range of modifiable and non-modifiable factors.

Primary hypogonadism reflects a failure of testicular testosterone production. Secondary hypogonadism arises from disruption of the hypothalamic-pituitary-gonadal axis, the signalling pathway that instructs the testes to produce testosterone. Distinguishing between these requires careful hormonal testing, as the treatment approach differs.

Metabolic dysfunction and insulin resistance are closely associated with low testosterone. Adipose tissue, particularly visceral fat, converts testosterone to oestrogen through the aromatase enzyme, further suppressing testosterone levels and creating a self-reinforcing cycle of hormonal and metabolic decline.

Chronic stress, poor sleep, environmental toxin exposure, nutritional deficiencies, and alcohol excess all contribute to testosterone suppression and should be assessed and addressed as part of comprehensive andropause management.