Hormone Health · Peptide Guide
Low testosterone is more common than most men realise, and more nuanced than a single blood test can capture. The clinical reality is that testosterone levels exist on a spectrum, that…
This guide covers what low testosterone is, how common it genuinely is, what causes it, how it is properly diagnosed, and what the full range of management options looks like, from lifestyle changes through to TRT.
The answer depends entirely on which definition is being used, a point of significant clinical and commercial confusion. Very different prevalence figures emerge from different methodological approaches, and this ambiguity has been exploited by direct-to-consumer marketing to overstate how many men “have low T.”
~2%
Men with symptomatic testosterone deficiency using strict criteria (low T + specific sexual symptoms)
19%
Men over 60 with low testosterone, Baltimore Longitudinal Study on Ageing
5–35%
Estimated proportion of hypogonadal men who actually receive treatment for their condition
The HIM study, which is often cited in marketing contexts, found approximately 39% of men aged 45 and older presenting to primary care offices had low testosterone on biochemical criteria alone. When the requirement for associated symptoms is added, this number falls substantially. The AUA guideline explicitly moved from “hypogonadism” to “testosterone deficiency” specifically to reinforce that the condition requires both low levels AND symptoms, not simply a lab value.[1]
The clinical challenge with testosterone deficiency symptoms is their non-specificity. Fatigue, poor concentration, low mood, and reduced exercise capacity can reflect dozens of conditions, including poor sleep, thyroid dysfunction, depression, anaemia, and metabolic syndrome, all of which are more common than testosterone deficiency. Understanding which symptoms are specific to testosterone versus which are non-specific is essential for avoiding over-diagnosis.
Specific Indicators
Most strongly linked to testosterone deficiency
The 5th ICSM 2024 specifically identified decreased spontaneous erections and low libido as the most prevalent and diagnostically specific clinical symptoms, particularly when all three sexual symptoms are present together.
Non-Specific, Many Possible Causes
Cannot reliably diagnose testosterone deficiency alone
These symptoms overlap with thyroid dysfunction, sleep apnoea, metabolic syndrome, depression, vitamin deficiencies, and simply ageing. They warrant full investigation, not assumption of testosterone deficiency as the cause.
Not all low testosterone has the same cause, and the cause determines both the likelihood of natural recovery and the most appropriate treatment. The two primary categories (primary and secondary hypogonadism) are defined by where in the HPG axis the problem originates.
Primary Hypogonadism
The testes fail to produce adequate testosterone despite normal or elevated pituitary signalling. LH and FSH are high (the pituitary is “shouting” at testes that can’t respond). This is structural, SERMs won’t restore testosterone as the problem is downstream.
TRT is typically the appropriate treatment for primary hypogonadism, the HPG axis cannot be “stimulated” because the testes are functionally limited.
Secondary Hypogonadism
The testes are capable of producing testosterone but are not receiving adequate pituitary stimulation. LH and FSH are low or inappropriately normal. The testes are functional, this is where lifestyle optimisation and SERMs can work.
Secondary hypogonadism is the most common type in clinical practice. Many cases are reversible with lifestyle change. SERMs and hCG are appropriate here when fertility is a concern.
📋 COVID-19 and Low Testosterone, A New Recognition
The 5th ICSM 2024 consensus paper added a significant new guidance point: SARS-CoV-2 infection and long-COVID have been associated with significant testosterone decline in men, alongside more severe clinical outcomes. Men with COVID-19 or long-COVID presenting with symptoms of testosterone deficiency should be considered for serum testosterone measurement as part of their clinical evaluation, a consideration that was not in previous guidelines.[2]
1
Clinical symptom assessment, identify whether sexual symptoms (the most specific indicators) are present. A symptom checklist like the ADAM questionnaire can structure this. Diagnosis requires both low levels AND symptoms.
2
First morning blood test, total testosterone must be measured between 7–10am when levels are highest. A result below 300 ng/dL (approximately 10.4 nmol/L) warrants follow-up.
3
Confirmatory second morning test, a single low result is not sufficient. A second morning testosterone must confirm low levels before a diagnosis can be made. At the same blood draw: add LH, FSH, and prolactin to begin characterising the type of hypogonadism.
4
Calculate or measure free testosterone, SHBG (sex hormone binding globulin) significantly affects how much testosterone is biologically active. Men with elevated SHBG may have low free testosterone despite normal total testosterone. Free testosterone or calculated free testosterone (using SHBG and albumin) should be assessed, particularly in men with metabolic conditions or borderline total testosterone.
5
Extended workup, based on initial results: TSH, free T4 (thyroid), vitamin D, CBC, comprehensive metabolic panel, iron and ferritin (haemochromatosis), estradiol, and PSA (in men over 40 before any treatment consideration). Pituitary MRI if prolactin is elevated or if LH/FSH are very low suggesting pituitary pathology.
6
Physical examination, testicular volume assessment, signs of gynaecomastia, body hair pattern, and signs of systemic disease. Some men with hypogonadism have a normal examination; others have specific signs (small testes, reduced body hair) that aid characterisation.
The majority of clinical complexity in testosterone management occurs not in men with clearly low testosterone (<200 ng/dL) but in men whose total testosterone sits in the low-normal range (roughly 300–450 ng/dL). These men are technically “within range” but may experience genuine symptoms of androgen deficiency.
Several factors can make a total testosterone in this range functionally low: high SHBG (binding more testosterone, leaving less free) from obesity, liver disease, ageing, or oral medications; a downward shift from that individual’s personal normal baseline that happens to land above the lab threshold; concurrent conditions that amplify the effect of suboptimal testosterone; and individual variation in androgen receptor sensitivity.
This is where free testosterone and SHBG assessment becomes clinically critical, and where reversible causes (obesity, sleep apnoea) may bring testosterone from 380 ng/dL to 520 ng/dL with weight loss alone, resolving symptoms without any hormone therapy. For men in this zone, a structured trial of lifestyle optimisation before pharmacological intervention is both clinically appropriate and often sufficient.
| Approach | Best Candidate | Mechanism | Key Consideration |
|---|---|---|---|
| Lifestyle optimisation First step for functional hypogonadism |
Men with reversible causes: obesity, OSA, opioids, glucocorticoids, chronic stress | Removes HPG axis suppressors; restores endogenous production through natural mechanisms | Most impactful and least risky option. Weight loss can raise testosterone by 100–200 ng/dL in obese men. Address before any pharmacological step. |
| Clomiphene / Enclomiphene SERMs, oral, fertility-preserving |
Secondary hypogonadism + fertility goals; men who prefer oral medication; younger men with functional hypogonadism | Blocks estrogen receptors at hypothalamus/pituitary → increases LH/FSH → stimulates endogenous testosterone production | Preserves spermatogenesis, critical advantage over TRT. Comparable testosterone increase to testosterone gel in RCTs. Off-label use. Enclomiphene available through compounding only. |
| hCG LH analogue, injectable, fertility-preserving |
Secondary hypogonadism; men desiring to preserve testicular function and fertility while treating low testosterone; adjunct to TRT | Mimics LH directly → stimulates Leydig cells to produce testosterone and maintain testicular function | Requires injection; may elevate estradiol requiring management. Brand Pregnyl available; compounding hCG restricted. Can be combined with SERMs or TRT. |
| TRT, Transdermal Gel Most common delivery |
Confirmed hypogonadism; no current fertility goals; preference for daily non-injection administration | Exogenous testosterone delivered through skin; bypasses HPG axis; suppresses spermatogenesis | Daily application required; transfer risk to partners; well-studied (used in TRAVERSE). Most convenient for many patients. Suppresses fertility. |
| TRT, Subcutaneous Injection Testosterone cypionate/enanthate |
Men who prefer weekly self-injection; lower cost than gels; desire stable levels | Same as gel, exogenous testosterone; subcutaneous preferred over intramuscular for self-administration | Weekly administration. Subcutaneous small-needle technique is well-tolerated. Produces more stable levels than biweekly dosing. |
| TRT, Oral Undecanoate Jatenzo, Tlando |
Men who strongly prefer oral administration; those unable or unwilling to inject or apply gels | Absorbed via lymphatic system (avoiding liver first-pass); delivers testosterone systemically | Must be taken with fat-containing food for absorption. Twice daily dosing. Newer and fewer long-term data than injectable/gel TRT. |
| No treatment / monitoring A legitimate clinical choice |
Men with borderline levels and mild or unclear symptoms; those with significant medical contraindications; men wanting to complete lifestyle optimisation first | N/A, active surveillance | Often overlooked as an option. For men with low-normal testosterone and non-specific symptoms, a structured lifestyle trial followed by reassessment at 3–6 months is clinically appropriate and may resolve the question. |
The Clinical Bottom Line
Low testosterone is a real condition that meaningfully affects quality of life for many men, and it is also significantly over-diagnosed and over-treated when patients present with non-specific symptoms and borderline lab values. The most important clinical step before any treatment decision is establishing that the clinical diagnosis is valid: two confirmed morning tests below threshold AND specific symptoms. The most important second step is identifying and addressing reversible causes, particularly obesity and sleep apnoea, before committing to long-term hormone therapy. For men with true, confirmed testosterone deficiency who have addressed reversible causes, the treatment options are well-developed, safe under appropriate monitoring, and genuinely effective for the right patients.
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