Low testosterone in men: signs, causes and how to test your levels

Age-related decline in testosterone production

Testosterone production is regulated by a signalling pathway running from the hypothalamus in the brain to the pituitary gland to the testes (the HPG axis). This system becomes less efficient with age. After the late 30s and into the 40s, the hypothalamus and pituitary send progressively weaker signals, and the testes' ability to respond diminishes. The resulting gradual reduction in testosterone output is sometimes described as the "male menopause," though unlike the female menopause it is a slow, continuous process rather than a distinct transition. Research from the European Male Ageing Study found that around 17% of men aged 40-79 had biochemically low testosterone levels using moderate diagnostic thresholds, and other studies suggest the proportion meeting broader definitions of testosterone deficiency may approach 25% in men over 40.

Obesity and metabolic syndrome

Excess body fat, particularly visceral fat around the abdomen, actively suppresses testosterone. Fat tissue contains an enzyme called aromatase that converts testosterone into oestrogen, reducing circulating testosterone while raising oestrogen. Simultaneously, obesity promotes insulin resistance, which further disrupts the hormonal signalling axis. Men with metabolic syndrome (the combination of central obesity, high blood pressure, elevated blood sugar, and abnormal lipid profile) have significantly higher rates of testosterone deficiency than metabolically healthy men. The relationship runs in both directions: low testosterone worsens body composition and insulin resistance, which further suppresses testosterone, creating a cycle that requires simultaneous attention to hormonal and metabolic health.

Chronic conditions and medications

Several common health conditions are associated with reduced testosterone: type 2 diabetes, chronic kidney disease, liver disease, obstructive sleep apnoea, and HIV. Certain medications significantly suppress testosterone, including long-term opioid pain medication (which can produce a pronounced and often unrecognised form of hypogonadism), some antidepressants, antipsychotics, anticonvulsants, and prolonged use of corticosteroids. Men taking any of these medications who are experiencing low-testosterone symptoms should discuss the possibility of medication-related suppression with their prescriber before attributing symptoms to age alone.

Sleep deprivation and circadian disruption

Testosterone is primarily produced during sleep, particularly during the deep slow-wave sleep stages in the first half of the night. Shift work, chronic late nights, and untreated sleep disorders including obstructive sleep apnoea (where breathing interruptions fragment the night's sleep) can meaningfully reduce testosterone output. Research has shown that even one week of sleeping 5 hours per night can reduce testosterone levels by 10-15% in young men. Addressing sleep quality is one of the most impactful non-pharmacological levers for supporting testosterone in men who are not achieving adequate sleep.

Primary versus secondary hypogonadism

Testosterone deficiency is classified by where in the HPG axis the problem originates. Primary hypogonadism involves a problem at the level of the testes themselves (from injury, infection, genetic conditions like Klinefelter syndrome, or prior chemotherapy and radiotherapy). Secondary hypogonadism involves a signalling problem at the hypothalamus or pituitary level, with the testes functioning but receiving inadequate stimulation. LH and FSH measurements in the blood distinguish between these patterns: low testosterone with low or normal LH points to a pituitary or hypothalamic problem, while low testosterone with high LH indicates that the brain is signalling normally but the testes are not responding. This distinction matters because it affects whether treatment addresses the cause directly or replaces the testosterone that is not being produced.

Stress and cortisol

Chronic psychological and physical stress elevates cortisol, which directly suppresses testosterone production. The HPA axis (stress response) and the HPG axis (reproductive hormones) compete for resources, and during sustained stress the body consistently prioritises the stress response at the expense of testosterone production. This is a biologically appropriate short-term response that becomes problematic when stress is chronic. High cortisol also promotes fat gain and insulin resistance, both of which further compound testosterone suppression.

The British Society for Sexual Medicine (BSSM) guidelines are explicit on how a diagnosis of testosterone deficiency should be made: two morning blood tests (ideally taken before 11am, when testosterone peaks) showing consistently low levels, alongside symptoms consistent with deficiency. A single borderline result is not sufficient to diagnose or rule out low testosterone, because levels fluctuate day to day and are affected by recent illness, stress, and sleep quality.

Total testosterone is the primary measure. UK clinical guidelines generally use a total testosterone below 12 nmol/L (with symptoms) as indicating possible testosterone deficiency, though the NHS typically treats below 8.6 nmol/L. Optimal rather than just "not deficient" levels are a separate consideration.

Free testosterone is the fraction that is biologically active. When total testosterone is borderline, free testosterone provides a more nuanced picture. Free testosterone is calculated from total testosterone and SHBG (it is not measured directly in most labs).

SHBG (sex hormone-binding globulin) binds to testosterone in the blood, making it biologically unavailable. Elevated SHBG (common in older men, in liver disease, and with certain medications) can make total testosterone look normal while free testosterone is low. Conversely, low SHBG (common in obesity and insulin resistance) can produce symptoms of low testosterone even at nominally adequate total testosterone levels.

LH (luteinising hormone) and FSH (follicle-stimulating hormone) identify the location of the problem within the HPG axis and are essential for directing appropriate investigation and treatment. Men with low testosterone and high LH have a primary testicular problem. Men with low testosterone and low or inappropriately normal LH have a pituitary or hypothalamic problem that needs further investigation.

Prolactin is measured because elevated prolactin (from a benign pituitary adenoma, for example) suppresses the HPG axis and is a treatable cause of secondary hypogonadism. A prolactin test is typically included in the initial workup.

Thyroid function (TSH, Free T3) matters because hypothyroidism produces fatigue, low mood, and weight changes that overlap significantly with low testosterone symptoms. Both conditions can co-exist and both need treating independently.

HbA1c and lipid profile assess metabolic health, which is both a cause and consequence of testosterone deficiency. Men with low testosterone are at higher risk of type 2 diabetes and cardiovascular disease; treating the metabolic picture alongside the hormonal one produces better outcomes.

For testosterone-specific testing (total testosterone, free testosterone, LH, FSH, SHBG, prolactin), the NHS requires both a clinical presentation consistent with testosterone deficiency and two confirmed low morning readings before treatment is initiated. Private hormone clinics and home testing providers in the UK can facilitate these tests with rapid turnaround, which may be useful for men who want to gather initial data before a GP appointment.

Resistance training and exercise

Resistance training is one of the most evidence-supported lifestyle interventions for testosterone. High-intensity and compound exercises (squats, deadlifts, bench press) produce acute testosterone spikes and over time support higher baseline levels through their effects on body composition, insulin sensitivity, and anabolic signalling. The key qualification is that excessive endurance training at high volumes without adequate recovery can have the opposite effect, suppressing testosterone through elevated cortisol and energy deficit. Moderate, consistent resistance training combined with recovery is more effective than volume extremes in either direction.

Sleep optimisation

Prioritising 7-9 hours of sleep per night, maintaining a consistent sleep schedule, and addressing untreated sleep apnoea if suspected are among the highest-impact lifestyle changes available for testosterone. Sleep apnoea in particular is significantly underdiagnosed in men and is associated with substantially reduced testosterone. A partner reporting observed apnoeas or loud snoring, combined with symptoms of daytime fatigue and low testosterone, warrants a GP discussion about sleep study referral.

Body composition and metabolic health

Because aromatase in fat tissue converts testosterone to oestrogen, and because insulin resistance suppresses testosterone production, reducing visceral fat and improving insulin sensitivity through dietary changes and exercise creates a compounding positive effect on testosterone over time. Tracking HbA1c and lipid markers alongside testosterone gives a measurable picture of whether the metabolic drivers of testosterone suppression are improving.

Nutrition, zinc, and vitamin D

Vitamin D receptors are present in the testes, and studies have found consistent positive associations between vitamin D status and testosterone levels. Men who are deficient in vitamin D and who supplement to restore optimal levels often show modest improvements in testosterone. Zinc is a co-factor in testosterone production, and deficiency (common in men with restricted diets, excessive alcohol, or gastrointestinal absorption problems) is associated with lower testosterone. Tracking vitamin D and B12 through a blood test gives a baseline to work from.