There is an industry built on the idea that most men over 40 have low testosterone and that a weekly injection will restore what age has taken. It is a large industry, it advertises heavily, and it is largely selling to men who do not have the condition.
Genuine hypogonadism is real, it is meaningfully underdiagnosed in some populations, and treating it properly changes lives. But it has a definition, it requires specific testing done in a specific way, and a substantial share of men who test low have a reversible cause that testosterone replacement will paper over rather than fix.
There is also a trade-off that gets mentioned far too quietly in the marketing: testosterone replacement suppresses your own production and impairs fertility, sometimes permanently. For a man in his thirties or forties who might want children, that is not a footnote. It’s the central consideration.
This article covers what testosterone does, how deficiency is actually diagnosed, the causes worth reversing before reaching for treatment, what replacement genuinely delivers, and what it costs.
What testosterone does
Produced mainly by the Leydig cells of the testes under the control of luteinising hormone from the pituitary, which is itself directed by gonadotropin-releasing hormone from the hypothalamus. This chain — the hypothalamic-pituitary-gonadal axis — is a feedback loop: rising testosterone suppresses LH and GnRH, reducing production. Remember that loop. It explains almost everything about how replacement therapy behaves.
Testosterone drives libido, spermatogenesis, muscle mass and strength, bone density, red blood cell production, body fat distribution, body hair, and contributes to mood and cognition.
Circulating testosterone is mostly bound — roughly 98% — to sex hormone binding globulin and albumin. Only the free and albumin-bound fractions are biologically available. This matters because SHBG varies considerably, and conditions that raise it (ageing, hyperthyroidism, liver disease, some anticonvulsants) or lower it (obesity, insulin resistance, hypothyroidism, corticosteroids) can make a total testosterone reading misleading in either direction.
Normal ageing versus hypogonadism
Testosterone declines gradually from around age 30 to 40, at roughly 1% per year. This is normal and it is not, on its own, a disease.
What distinguishes hypogonadism is the combination of consistently low measured testosterone and symptoms attributable to it. Neither alone is sufficient. A man with a low number and no symptoms doesn’t have a clinical problem. A man with symptoms and a normal number has something else going on that deserves investigation rather than a testosterone prescription.
Symptoms that are relatively specific
These have the strongest association with genuinely low testosterone:
- Reduced libido — the most consistent symptom
- Reduced spontaneous and morning erections
- Loss of body and facial hair, reduced shaving frequency
- Small or shrinking testes
- Gynaecomastia
- Hot flushes — uncommon but quite specific
- Infertility with low sperm count
- Low-trauma fracture or unexplained osteoporosis
Symptoms that are consistent but non-specific
Fatigue. Low mood. Reduced concentration. Increased body fat. Reduced muscle mass. Poor sleep. Irritability.
These are the symptoms every “low T” advertisement leads with, and they are shared with depression, sleep apnoea, hypothyroidism, anaemia, iron deficiency, diabetes, chronic stress and simply being under-slept. Diagnosing hypogonadism from this list alone is how large numbers of men end up on lifelong therapy for a condition they don’t have, while the thing actually making them tired goes unexamined.
Note that erectile dysfunction is not a characteristic feature of isolated hypogonadism. Low testosterone reduces desire more than mechanical function. Most ED is vascular, and treating it with testosterone when the cause is arterial disease means missing an early cardiovascular warning.
How it’s properly diagnosed
The testing protocol is specific, and shortcuts are the main reason for both false positives and false negatives.
Total testosterone, measured in the morning. Levels follow a diurnal rhythm peaking in the early morning, and an afternoon sample can read 20 to 25% lower. Samples should be taken before 10 or 11am, fasting where possible.
Confirmed on at least two separate occasions. Single measurements are unreliable — day-to-day biological variation is considerable, and a substantial proportion of men with one low reading are normal on repeat.
Not during acute illness. Any significant illness, injury, surgery or major stress suppresses testosterone temporarily. Testing during or shortly after produces a low result that means nothing. Repeat once recovered.
SHBG and free testosterone where total is borderline, or where SHBG is likely to be abnormal — obesity, diabetes, thyroid disease, older age. Calculated free testosterone is generally more useful than direct free testosterone assays, which are technically unreliable in most laboratories.
LH and FSH — this is the test that determines what kind of problem you have, and it’s frequently omitted:
- High LH/FSH with low testosterone = primary hypogonadism. The testes are failing; the pituitary is shouting at them correctly. Causes include Klinefelter syndrome, mumps orchitis, trauma, chemotherapy, radiotherapy, undescended testes.
- Low or inappropriately normal LH/FSH with low testosterone = secondary hypogonadism. The signal from above is inadequate. Causes include obesity, sleep apnoea, opioids, anabolic steroid use, pituitary tumour, hyperprolactinaemia, haemochromatosis, chronic illness.
Prolactin, particularly with secondary hypogonadism — a prolactinoma is a treatable pituitary cause, and missing one to prescribe testosterone would be a significant error.
Additional tests depending on picture: full blood count, ferritin and transferrin saturation for haemochromatosis, HbA1c, thyroid function, and pituitary MRI where secondary hypogonadism is marked or accompanied by headache or visual change.
Semen analysis if fertility matters — before any treatment decision.
Reversible causes: the part the clinics skip
A large share of low testosterone in men presenting today is secondary and reversible. Addressing the cause frequently restores levels without lifelong therapy — and lifelong is what the alternative means, because replacement suppresses whatever production remains.
Obesity. The single biggest contributor. Adipose tissue expresses aromatase, converting testosterone to oestradiol, which then suppresses the axis further — a self-reinforcing loop. Weight loss reliably raises testosterone, and substantial weight loss can raise it considerably. Bariatric surgery studies show large increases.
Obstructive sleep apnoea. Strongly associated with suppressed testosterone, and extremely common in the same men. Treatment improves levels. This one is worth actively seeking, because it also independently causes the fatigue and poor concentration being attributed to low T.
Opioids. Chronic use profoundly suppresses the axis — opioid-induced androgen deficiency is common and under-recognised in anyone on long-term opioid therapy.
Anabolic steroid use, past or present. Exogenous androgens shut down endogenous production, and recovery after cessation can take many months or fail entirely. This is an increasingly common cause of hypogonadism in men in their twenties and thirties. Anyone with a history here needs it disclosed — it changes the whole management approach.
Alcohol. Chronic heavy intake is directly toxic to Leydig cells and impairs hepatic hormone metabolism.
Poor sleep. Even short-term sleep restriction measurably lowers testosterone in healthy young men — a week of five-hour nights produces a meaningful drop.
Medications. Glucocorticoids, some antipsychotics via prolactin, spironolactone, ketoconazole, chemotherapy agents.
Uncontrolled diabetes and metabolic syndrome.
Chronic illness — renal, hepatic, HIV, inflammatory disease.
The honest sequence is: identify and address what’s reversible, retest after a genuine attempt, and then consider replacement if levels and symptoms persist. That sequence is skipped constantly, because it’s slower and less profitable than starting an injection.
What replacement actually delivers
Being precise here is worthwhile, because expectations set by advertising are consistently higher than what trials show.
Reasonably well supported:
- Libido — the most consistent benefit, and generally the clearest
- Sexual activity and satisfaction — modest but real improvement
- Bone mineral density — improves; fracture reduction less firmly established
- Lean body mass up, fat mass down — reliably, though strength gains are more modest than expected
- Anaemia — corrects testosterone-related anaemia
- Mood — modest improvement in some trials, notably in men with both hypogonadism and depressive symptoms
Weakly supported or unclear:
- Energy and vitality — the flagship marketing claim, and one of the least consistently demonstrated
- Cognition — the Testosterone Trials found no benefit on memory or cognition
- Erectile function — improvement is modest, and testosterone is not treatment for vascular ED
Not supported:
- Athletic performance enhancement in eugonadal men as a medical indication
- Reversal of normal ageing
The costs
Fertility — read this section first if you’re under 45
Exogenous testosterone suppresses LH and FSH, which shuts down spermatogenesis. Intratesticular testosterone concentration — which must be far higher than blood levels for sperm production — collapses. Testicular volume falls. Sperm counts drop substantially and frequently to zero.
Recovery after stopping is usual but takes months to years, and is not guaranteed, with poorer prospects after longer use and in older men.
Testosterone has actually been studied as a male contraceptive on exactly this basis. It is, functionally, a fertility-suppressing drug.
If fertility is or might be relevant:
- Say so explicitly before starting anything
- Get a baseline semen analysis
- Consider sperm banking
- Discuss alternatives that raise testosterone without suppressing the axis: hCG, which mimics LH and maintains intratesticular production; clomiphene or enclomiphene, which block negative feedback at the pituitary and raise endogenous output; and aromatase inhibitors in selected men with high oestradiol. These are used off-label in many countries but are standard practice in fertility-conscious management.
This conversation is not routinely initiated by direct-to-consumer providers, and a meaningful number of men discover the problem only when they start trying for a child.
Polycythaemia
Testosterone stimulates erythropoiesis. Haematocrit rises, sometimes to levels that increase blood viscosity and thrombotic risk. This is the commonest adverse effect requiring intervention, and it’s why haematocrit monitoring is mandatory rather than optional — typically at baseline, three to six months, then annually, with dose reduction, formulation change or venesection if it exceeds about 54%.
Cardiovascular risk
This has been genuinely contested. Earlier observational studies and a trial stopped early raised concerns. The TRAVERSE trial, a large randomised cardiovascular safety study published in 2023 in men with hypogonadism and elevated cardiovascular risk, found testosterone non-inferior to placebo for major adverse cardiac events — which substantially reassured the field. It did, however, note higher rates of atrial fibrillation, pulmonary embolism and acute kidney injury in the testosterone arm. The current position is that replacement in properly diagnosed hypogonadism does not appear to raise major cardiac event risk, with some residual signals warranting attention.
Prostate
Testosterone does not appear to cause prostate cancer, and the old blanket prohibition has softened considerably. But it can stimulate existing cancer, so it is contraindicated in active untreated prostate cancer, and PSA monitoring is standard — baseline, then periodically. Benign enlargement symptoms can worsen.
Other effects
Acne and oily skin. Worsening of sleep apnoea. Gynaecomastia via aromatisation. Testicular atrophy — universal and expected. Mood lability in some. Injection site reactions; skin-to-skin transfer with gels, which is a genuine risk to partners and children and requires care with application and covering.
It is generally permanent
Once the axis is suppressed for a sustained period, stopping frequently produces a symptomatic crash while endogenous production recovers — if it recovers fully. Starting replacement is a long-term commitment, and that should be understood at the outset rather than discovered later.
Monitoring, if you are on it
- Testosterone levels — timed to the formulation, aiming mid-normal range
- Haematocrit — baseline, 3–6 months, then annually
- PSA — baseline and periodically, per age and risk
- Symptom review
- Blood pressure
- Lipids and metabolic markers
- Semen analysis if fertility is relevant
Therapy without this monitoring is not treatment; it’s supply. If a provider isn’t checking haematocrit, that’s a meaningful signal about the quality of care.
Common questions
Can I just get a test online and start? You can, in various places. But a single non-morning sample without LH, FSH, prolactin or SHBG, and without excluding sleep apnoea, opioids, obesity or acute illness, isn’t a diagnosis. And starting replacement on that basis commits you to something long-term while leaving the actual cause unexamined.
My level was low but my doctor won’t treat. Why? Common reasons: it was an afternoon sample, it wasn’t repeated, it was taken during illness, SHBG explains it, or a reversible cause hasn’t been addressed. All are legitimate. Ask which applies and what the plan is — that’s a more productive conversation than seeking a second supplier.
Will it help me lose weight? Modestly, in genuine hypogonadism, mostly through body composition change. It’s not a weight-loss treatment, and given obesity causes low testosterone more often than the reverse, the causal arrow usually points the other way.
What about testosterone boosters? Supplements marketed for this have essentially no evidence of raising testosterone meaningfully. Where a deficiency exists — vitamin D, zinc — correcting it may help marginally. Otherwise this category is selling to the same anxiety as the clinics, with less to offer.
I used steroids years ago and feel terrible. Is that related? Very possibly. Post-steroid hypogonadism is common and under-recognised. It needs assessment, and management differs — restart protocols using hCG and selective oestrogen receptor modulators are often preferred over replacement, particularly in younger men. Be straightforward about the history; it changes what’s appropriate.
Is low testosterone why I have ED? Usually not on its own. Low testosterone reduces desire more than erectile capacity. Gradual-onset ED with reduced morning erections is more often vascular, and that warrants cardiovascular assessment rather than hormone therapy.
The short version
Confirm it properly before treating: morning sample, twice, not during illness, with LH, FSH, SHBG and prolactin, and free testosterone where total is borderline.
Then look hard for the reversible causes — weight, sleep apnoea, opioids, alcohol, past steroid use, poor sleep, uncontrolled diabetes. Fixing those raises testosterone without committing you to lifelong therapy, and often resolves the symptoms that prompted the question.
If replacement is genuinely indicated, understand what it delivers — libido and body composition reliably, energy and cognition much less so — and what it costs. The fertility suppression is the one to think hardest about, and the haematocrit monitoring is the one not to skip.
More in our plain-language guide to male hormones, the men’s health articles, and the men’s health range.
This article is general health information and not individual medical advice. Testosterone is a controlled substance in many countries and a prescription-only medicine everywhere; it requires proper diagnosis on repeated morning samples and ongoing monitoring of haematocrit and PSA. It suppresses fertility, often for a prolonged period and occasionally permanently. Do not start testosterone therapy without medical assessment, and discuss fertility before you do.
