Andropause Prevalence

There is no clear image of prevalence of hypogonadism, largely due to differences in study populations and diagnostic criteria. Many studies reveal consistent findings across different populations and time periods. The landmark HIM study by Mulligan et al. reported a 38.7% prevalence rate in American men aged 45 years and older visiting primary care practices, while a recent Turkish multicenter study found a remarkably similar 38.5% prevalence rate in men aged 50-75 years attending urology clinics. At the same time a comprehensive systematic literature review examining 97 studies found that chemical hypogonadism (low-T) prevalence in the general population ranged from 2.1% to 12.8% among middle-aged to older men in Europe and the USA, with higher rates observed in patients with comorbid conditions such as diabetes and obesity.

The Treatment Gap

The treatment gap represents a massive "invisible epidemic" with up to 80-92% of hypogonadal men remaining undiagnosed or untreated. The underestimation and underdiagnosis of andropause and hypogonadism result in a significant treatment gap, with many symptomatic men missing out on beneficial interventions due to inadequate screening and awareness. Based on epidemiological reviews, while reported prevalence of symptomatic hypogonadism is 2-5% in older men, the true figure may be 10-15% or higher when accounting for undiagnosed cases driven by inconsistent testing and nonspecific symptoms. See studies: Andropause in Diabetic and Non-diabetic Males, Epidemiology of Male Hypogonadism.

Underestimation is also indicated by he high prevalence of obesity and type 2 diabetes (T2D) in Western populations, which are strongly correlated with low testosterone levels and secondary hypogonadism. Obesity is estimated to affect over 20% of adults in 33 European countries, with global adult obesity at around 16-22% and T2D prevalence rising to 8-9% in many high-income nations. These conditions exacerbate testosterone decline through mechanisms like insulin resistance and inflammation, yet routine testosterone screening in obese or diabetic men remains infrequent, further contributing to underdiagnosis.

Lastly, these diagnoses are typically based on total testosterone, not free testosterone, which excludes even more cases since free testosterone can be low while total is not, potentially underestimating prevalence by an extra 10-30% in some populations.

The U-shaped Risk Hypothesis

Testosterone levels could have a U-shaped association with all-cause mortality, with optimal levels plausibly between 16–30 nmol/L (460-860 ng/dL). Below this range mortality risk appears to rise via metabolic dysfunction, including higher risks of type 2 diabetes, cardiovascular disease, and inflammatory processes. Above this range the risk through erythrocytosis (hematocrit elevation) with attendant thrombotic mechanisms and potential cardiovascular strain may increase.

While not scientifically proven and lacking formal consensus, the overall hypothesis is scientifically sound. Elevated risk at low testosterone is robust in large epidemiological cohorts, including older men and high-risk groups. At very high (supraphysiological) levels, evidence is sparser and largely mechanistic or indirect (e.g., TRT-induced erythrocytosis), but remains biologically plausible; few men naturally sustain such levels, limiting observational data. The curve pragmatically conveys an ‘optimal’ band where mortality risk is lowest.

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This image is AI generated and not based on actual data, it visualizes the hypothesis.