What symptoms does low testosterone cause?

The symptoms of testosterone deficiency are variable in specificity — many are shared with depression, sleep disorders, obesity, and other conditions. Sexual symptoms are most specific: low libido, reduced spontaneous erections, and erectile dysfunction. Other symptoms include profound fatigue, reduction in muscle mass and strength, increased body fat particularly around the abdomen, decreased body and facial hair, gynaecomastia (breast tissue development), hot flushes in severe or sudden deficiency, mood changes and irritability, and difficulty concentrating. Bone density loss with fragility fractures can occur with longstanding deficiency. Symptoms alone do not diagnose hypogonadism — a biochemical confirmation with two morning fasting blood tests is always required.

How is low testosterone diagnosed correctly?

Testosterone has a pronounced diurnal variation — levels are highest between 8 and 10 am and can be 30–50% lower in the afternoon. This means the blood test must be taken in the morning, fasting. A single low result is not sufficient: the Endocrine Society guideline and Australian PBS criteria both require two morning fasting total testosterone measurements below the threshold, taken on separate days, away from acute illness and strenuous exercise. Where obesity or liver disease affects SHBG (sex hormone binding globulin), calculated free testosterone is also checked. LH and FSH are measured to distinguish primary (high LH/FSH, testicular failure) from secondary (low LH/FSH, pituitary or hypothalamic cause) hypogonadism.

What are the Australian PBS criteria for testosterone prescribing?

The Australian PBS has Authority Required criteria for all testosterone preparations. The clearest threshold is a total testosterone of 6 nmol/L or less on a single measurement. For testosterone between 6 and 8 nmol/L, prescribing also requires either: LH and FSH more than 1.5 times the upper limit of normal (confirming primary hypogonadism from testicular failure), or confirmed pituitary disease (structural lesion, hyperprolactinaemia treated, or specific genetic or surgical cause). Men with testosterone in the low-normal range — 8 to 12 nmol/L — typically do not meet PBS criteria. In this group, lifestyle modification, treatment of sleep apnoea, opioid review, and weight loss should be first-line.

If I want children, can I still be treated for low testosterone?

Testosterone replacement suppresses the production of LH and FSH, which directly shuts down sperm production — sometimes for many months after stopping. If you want to father children, testosterone replacement is not appropriate. Instead, HCG (human chorionic gonadotrophin), which stimulates the testes directly, or clomiphene (an off-label oral option) can raise testosterone while preserving spermatogenesis. These options require specialist management by a reproductive endocrinologist or andrologist. If testosterone replacement is started before fertility planning is complete, recovery of spermatogenesis can take 12–18 months or longer.

Is testosterone replacement safe for the heart?

Earlier observational studies raised concerns about cardiovascular events with testosterone therapy. The TRAVERSE trial (Lincoff, Nissen et al., NEJM 2023) — a large, randomised controlled trial in more than 5000 men aged 45 or older with hypogonadism and cardiovascular risk — found that testosterone was non-inferior to placebo for major adverse cardiovascular events (heart attack, stroke, death). This is reassuring for appropriately selected men. There are modest signals for atrial fibrillation and venous thromboembolism, which are not contraindications but warrant monitoring. Polycythaemia — a rise in haematocrit above 54% — is the most common significant complication of testosterone therapy and requires dose reduction or cessation.

Male hypogonadism

Low testosterone in men: diagnosis, PBS criteria, and treatment

By Dr HB Lo, FACRRM Reviewed 5 July 2026 10 min read

Male hypogonadism is the clinical and biochemical syndrome of testosterone deficiency. Diagnosis requires two morning fasting testosterone measurements below threshold — plus symptoms including low libido, erectile dysfunction, fatigue, and reduced muscle mass.

The most common cause in Australian general practice is functional hypogonadism from obesity, sleep apnoea, or opioid use. Treating the underlying cause often restores testosterone without replacement.

The PBS has strict authority criteria. Men with low-normal testosterone who don't qualify are best served by lifestyle modification, which can normalise testosterone naturally.

What male hypogonadism actually is

Male hypogonadism is the clinical and biochemical syndrome that results from testosterone deficiency. The testes produce around 95% of circulating testosterone — when testicular function fails, LH and FSH rise (primary hypogonadism). When the signal from the hypothalamus or pituitary fails or is suppressed, LH and FSH are low or inappropriately normal and testosterone falls (secondary hypogonadism).

The key word is syndrome: both clinical features and biochemical confirmation must be present before a diagnosis is made. Many men with non-specific symptoms (fatigue, reduced libido, mood change) have testosterone in the normal range for their age, and many with borderline low levels are asymptomatic. Treating testosterone level rather than the person — without confirming the syndrome — is a clinical error that the Endocrine Society 2018 guideline and Endocrine Society of Australia both explicitly caution against.

In Australian general practice, the most common form encountered is functional hypogonadism — a reversible suppression of the pituitary-gonadal axis driven by obesity, obstructive sleep apnoea, chronic opioid use, or severe systemic illness. Treating the underlying cause often restores testosterone without replacement.

A. Core clinical — the AU general practice framework

Causes

Primary hypogonadism (high LH and FSH, testicular failure):

Klinefelter syndrome (47,XXY) — the most common congenital cause, occurring in 1 in 500–1000 men. Characterised by small, firm testes, tall stature, gynaecomastia, and infertility. Significantly under-diagnosed — suspect in any tall man with small firm testes and infertility
Cryptorchidism (undescended testes), particularly bilateral
Orchitis — mumps in post-pubertal males; bacterial
Testicular torsion, trauma, or surgery
Chemotherapy and radiotherapy — gonadotoxic
Other genetic conditions — Noonan syndrome, myotonic dystrophy

Secondary hypogonadism (low or inappropriately normal LH and FSH, pituitary/hypothalamic failure):

Functional / obesity-related — the most common in clinical practice; reversible with weight loss, treating OSA, opioid reduction
Opioid-induced hypogonadism — chronic opioid therapy suppresses hypothalamic GnRH; under-recognised in chronic pain settings
Anabolic steroid use — exogenous androgens suppress LH and FSH; recovery after cessation takes 3–18 months and is sometimes incomplete
Prolactinoma or other pituitary adenoma — elevated prolactin suppresses GnRH; treat the adenoma first (cabergoline normalises testosterone in most prolactinomas within weeks)
Haemochromatosis — iron deposition in the pituitary
Kallmann syndrome — congenital GnRH deficiency combined with anosmia
Pituitary radiotherapy, surgery, or apoplexy
Glucocorticoid therapy — high-dose chronic corticosteroid use suppresses the axis

Clinical features

Sexual symptoms (most specific):

Reduced libido
Erectile dysfunction and reduced spontaneous erections
Ejaculatory dysfunction
Infertility

Physical symptoms:

Fatigue and reduced energy
Reduction in muscle mass and strength, increased visceral adiposity
Decreased body and facial hair
Gynaecomastia (true, not pseudogynaecomastia)
Vasomotor symptoms (hot flushes) — particularly with abrupt testosterone loss (post-androgen deprivation therapy)

Mood and cognitive symptoms:

Irritability, depression, reduced concentration
Sleep disturbance

Skeletal:

Osteoporosis and fragility fractures in longstanding deficiency

On examination: BMI and waist circumference; body hair distribution; testicular volume (Prader orchidometer — below 15 mL suggests hypogonadism; below 5 mL indicates primary testicular failure; above 12 mL in secondary hypogonadism); visual fields (suspect pituitary mass); anosmia (Kallmann). True gynaecomastia (glandular tissue, not adipose).

Diagnosis — the two-measurement rule

Endocrine Society 2018, ESA, and eTG align on the diagnostic standard:

Two morning (8–10 am) fasting total testosterone measurements on separate days, below the diagnostic threshold
Away from acute illness — illness transiently suppresses testosterone
Away from strenuous exercise

Where SHBG is abnormal — elevated in older age, thyroid disease, or liver disease; reduced in obesity, insulin resistance, or exogenous androgen use — the calculated free testosterone is more informative than total testosterone. A calculated free testosterone below 0.18 nmol/L suggests deficiency even when total testosterone is borderline.

LH and FSH distinguish primary from secondary hypogonadism. Their measurement also forms part of the PBS authority criteria (see section C).

Prolactin is checked in all secondary hypogonadism — prolactinoma is a common treatable cause. Thyroid function (TSH) excludes hypothyroidism mimics. Iron studies and ferritin exclude haemochromatosis. Haematocrit and haemoglobin at baseline. PSA and DRE in men aged 40 or over before initiating testosterone. DEXA bone densitometry as baseline, particularly in longstanding deficiency.

Pituitary MRI is indicated when: LH and FSH are low or inappropriately normal (secondary hypogonadism confirmed); prolactin is elevated; neurological symptoms are present; or deficiency is severe and onset unexplained. Karyotype if Klinefelter is suspected. Testicular ultrasound for primary hypogonadism or concern about a testicular mass.

Red flags — investigate before treating

Always investigate the cause before prescribing testosterone. The following require specific workup or treatment rather than testosterone replacement:

Elevated prolactin → pituitary MRI; treat with cabergoline first
Low LH and FSH → pituitary MRI; exclude structural pituitary disease
Haemochromatosis → venesection; testosterone may recover
Opioid use → consider dose reduction; hypogonadism may reverse
Obesity (BMI >30) → weight loss of 5–10% typically raises testosterone by 2–4 nmol/L per eTG
OSA → CPAP treatment raises endogenous testosterone modestly

B. Evidence — lifestyle first, TRAVERSE second

Lifestyle modification in functional hypogonadism

The Endocrine Society 2018 guideline and ESA position statement both establish weight loss as first-line for obesity-related functional hypogonadism. Adipose tissue contains aromatase, which converts testosterone to oestradiol; central adiposity also suppresses hypothalamic GnRH. Every 10% reduction in body weight raises testosterone measurably. Intensive lifestyle modification, including reduced processed food, adequate protein, resistance training (≥2 sessions per week), aerobic exercise, alcohol reduction, and sleep optimisation, can normalise testosterone in functional hypogonadism without pharmacological intervention.

The Healthy Male clinical guides support this approach explicitly.

The TRAVERSE trial — cardiovascular safety reassurance

The TRAVERSE trial (Lincoff, Nissen et al., NEJM 2023) enrolled more than 5000 men aged 45 years and older with hypogonadism and established cardiovascular disease or elevated cardiovascular risk. Random assignment to testosterone gel or placebo over a median follow-up of 33 months showed non-inferiority for major adverse cardiovascular events (heart attack, stroke, cardiovascular death). This resolves earlier observational uncertainty about cardiac harm. However, the trial did show modest increases in atrial fibrillation and pulmonary embolism — both warrant monitoring during therapy.

The T-TRIALS — symptom evidence

The Testosterone Trials (T-TRIALS, Snyder et al., NEJM 2016) — seven placebo-controlled trials in men aged 65+ with low testosterone — showed improvements in sexual function, physical performance, and bone density with testosterone, but modest and inconsistent benefits for other domains including mood and cognition. The evidence for testosterone replacement is strongest for sexual symptoms, muscle mass, and bone density in men who genuinely meet diagnostic criteria; evidence for wellbeing and cognition is less robust.

C. Testosterone replacement — Australian PBS criteria and preparations

PBS Authority criteria (2026)

Per PBS, testosterone replacement is Authority Required for:

Total testosterone ≤6 nmol/L — single measurement is sufficient at this level; Authority Streamlined
Total testosterone ≤8 nmol/L AND one of:
- LH and FSH more than 1.5 times the upper limit of normal (confirming primary hypogonadism); or
- Confirmed pituitary disease by imaging or specific genetic, surgical, or radiation cause (secondary hypogonadism)

Men with testosterone in the 8–12 nmol/L range (“low-normal”) do not meet PBS criteria in the absence of confirmed primary or structural secondary hypogonadism. Lifestyle modification is the evidence-aligned intervention for this group per eTG and AMH.

PBS-listed testosterone preparations

Preparation	Route	Dosing	Notes
Testosterone undecanoate (Reandron) 1000 mg/4 mL	IM injection	Every 10–14 weeks	Most common AU preparation; 30-min post-injection observation for POME
Testosterone enanthate (Primoteston Depot) 250 mg	IM injection	Every 2–3 weeks	More peak-trough variation
Testosterone esters (Sustanon) 250 mg	IM injection	Every 2–3 weeks	Similar to Primoteston
Androforte 5% cream	Transdermal (scrotal or non-scrotal)	Daily	PBS Authority; skin-transfer precautions with partners and children
Testogel 1% sachet 50 mg	Transdermal	Daily	Shoulder or abdomen; skin-transfer precautions
Axiron 2% solution	Axillary transdermal	Daily	Less common

Reandron is the most widely used preparation in Australia given once every 10–14 weeks by IM injection. A critical safety requirement: patients must remain in the clinic for 30 minutes after each injection due to the rare risk of pulmonary oil microembolism (POME) — presenting with cough, chest pain, or dyspnoea within minutes of injection. This is not optional monitoring.

Monitoring on testosterone replacement

Monitor at 3 months, 6 months, and annually per eTG and AMH:

Testosterone level — mid-cycle for IM preparations; trough for Reandron (2–4 weeks before next injection should be ≥10 nmol/L)
Haematocrit — stop testosterone if haematocrit exceeds 54% (polycythaemia increases thrombosis risk); venesection or dose reduction; investigate underlying cause (smoking, uncontrolled OSA)
PSA — annually; investigate any rise above 1.4 ng/mL per year or absolute PSA above 4.0
Lipids — modest LDL effects
DEXA bone density — baseline then 1–2 yearly
OSA assessment — testosterone can worsen obstructive sleep apnoea
Mood, aggression, and behavioural change — direct inquiry
Prostate examination annually

Contraindications

Active prostate cancer — absolute contraindication (testosterone is an androgen-receptor-driven tumour promoter)
Breast cancer in men — absolute
Fertility-seeking — testosterone suppresses spermatogenesis; use HCG or clomiphene instead (see below)
Haematocrit above 54% — treat polycythaemia first
Severe untreated OSA — treat OSA first; testosterone may worsen it
Severe uncontrolled heart failure — relative

D. Australian operations

Fertility-preserving alternatives

For men who want to father children, testosterone replacement is contraindicated. Options under specialist care:

HCG (human chorionic gonadotrophin) — 1500–3000 IU subcutaneously twice weekly — stimulates testicular Leydig cells to produce testosterone while maintaining spermatogenesis. This is the standard fertility-preserving alternative for secondary hypogonadism. Not PBS-listed for this indication; private cost applies
Clomiphene 25–50 mg daily or every two days — a selective oestrogen receptor modulator that raises endogenous LH and testosterone; off-label use; not PBS-listed for hypogonadism; evidence-based in specialist practice
HMG or recombinant FSH added to HCG for spermatogenesis stimulation in severe secondary hypogonadism with testicular failure

These are specialist (reproductive endocrinology, andrology) management decisions.

MBS items relevant to male hypogonadism

Standard GP consultations (23, 36, 44), complex consults (132, 133), GPCCMP (965, 967), ATSI Health Assessment (715), 75+ Health Assessment (707). Pathology: total testosterone and hormone panel (item 73807), FBC (65070), liver function (66602), PSA (65140). Imaging: DEXA bone densitometry (12306/12320), testicular ultrasound (55037/55038), ECG (11700), pituitary MRI (63056 — specialist-requested). Endocrinology consultation (132/133). Andrology consultation (specialist).

Anabolic steroid use

Approximately 0.5–3% of Australian men have used anabolic androgenic steroids for athletic or aesthetic purposes. These individuals often present with hypogonadal symptoms after stopping, because exogenous androgens suppress the hypothalamic-pituitary-gonadal axis. Recovery can take 3–18 months. A non-judgemental, confidential approach is essential. HCG and clomiphene are used off-label to support axis recovery. Healthy Male provides harm-reduction resources.

E. Special populations

Klinefelter syndrome (47,XXY). This is the most common sex chromosome abnormality in men, affecting 1 in 500–1000, and is the most common congenital cause of primary hypogonadism. It remains significantly under-diagnosed; the mean delay to diagnosis is approximately 12 years from symptom onset. Suspect Klinefelter in any tall man with small firm testes, infertility, or gynaecomastia — karyotype is confirmatory. Management involves testosterone replacement, metabolic and cardiovascular risk monitoring, bone protection, and psychological support. Fertility via microsurgical testicular sperm extraction (microTESE) and ICSI is possible in some men with Klinefelter; refer early to reproductive medicine if fertility is desired.

Adolescent hypogonadism. Delayed puberty in adolescent males requires paediatric endocrinology assessment. Pubertal induction follows specific testosterone protocols distinct from adult replacement therapy.

Older men. Testosterone declines approximately 1–2% per year from middle age — this is a physiological process, not pathological hypogonadism. The distinction between age-related decline and true hypogonadism requires careful clinical and biochemical assessment. The T-TRIALS enrolled men aged 65 and over and showed benefit in sexual function and bone density in confirmed hypogonadism.

When to escalate

Refer to an endocrinologist for:

Confirmed secondary hypogonadism (low LH and FSH) requiring pituitary MRI and cause workup
Elevated prolactin (suspected prolactinoma)
Suspected Klinefelter syndrome or other genetic hypogonadism
Complex monitoring needs (haematocrit management, bone protection)
Testosterone in the borderline range where clinical uncertainty exists about whether to treat

Refer to a reproductive endocrinologist or andrologist for:

Fertility-seeking with hypogonadism — HCG, clomiphene, microTESE planning
Infertility workup where hypogonadism is a contributing factor

Refer to a urologist for:

Testicular mass or abnormality on examination or ultrasound
PSA elevation requiring further evaluation
Complex prostate-related monitoring questions

What this article is and is not

This is general health information drawn from current Australian general practice guidelines — RACGP, Therapeutic Guidelines, the Australian Medicines Handbook, NPS MedicineWise — and the Endocrine Society of Australia position statement, Healthy Male clinical guides, and key clinical trials including TRAVERSE and T-TRIALS. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about testosterone prescribing — including whether PBS criteria are met, which preparation to use, and how to monitor — are made with your own general practitioner and treating specialists.

For Australian consumer resources: Healthy Male, HealthDirect — testosterone and men’s health, Better Health Channel — testosterone.

Sources cited

Frequently asked questions

What symptoms does low testosterone cause?

The symptoms of testosterone deficiency are variable in specificity — many are shared with depression, sleep disorders, obesity, and other conditions. Sexual symptoms are most specific: low libido, reduced spontaneous erections, and erectile dysfunction. Other symptoms include profound fatigue, reduction in muscle mass and strength, increased body fat particularly around the abdomen, decreased body and facial hair, gynaecomastia (breast tissue development), hot flushes in severe or sudden deficiency, mood changes and irritability, and difficulty concentrating. Bone density loss with fragility fractures can occur with longstanding deficiency. Symptoms alone do not diagnose hypogonadism — a biochemical confirmation with two morning fasting blood tests is always required.
How is low testosterone diagnosed correctly?

Testosterone has a pronounced diurnal variation — levels are highest between 8 and 10 am and can be 30–50% lower in the afternoon. This means the blood test must be taken in the morning, fasting. A single low result is not sufficient: the Endocrine Society guideline and Australian PBS criteria both require two morning fasting total testosterone measurements below the threshold, taken on separate days, away from acute illness and strenuous exercise. Where obesity or liver disease affects SHBG (sex hormone binding globulin), calculated free testosterone is also checked. LH and FSH are measured to distinguish primary (high LH/FSH, testicular failure) from secondary (low LH/FSH, pituitary or hypothalamic cause) hypogonadism.
What are the Australian PBS criteria for testosterone prescribing?

The Australian PBS has Authority Required criteria for all testosterone preparations. The clearest threshold is a total testosterone of 6 nmol/L or less on a single measurement. For testosterone between 6 and 8 nmol/L, prescribing also requires either: LH and FSH more than 1.5 times the upper limit of normal (confirming primary hypogonadism from testicular failure), or confirmed pituitary disease (structural lesion, hyperprolactinaemia treated, or specific genetic or surgical cause). Men with testosterone in the low-normal range — 8 to 12 nmol/L — typically do not meet PBS criteria. In this group, lifestyle modification, treatment of sleep apnoea, opioid review, and weight loss should be first-line.
If I want children, can I still be treated for low testosterone?

Testosterone replacement suppresses the production of LH and FSH, which directly shuts down sperm production — sometimes for many months after stopping. If you want to father children, testosterone replacement is not appropriate. Instead, HCG (human chorionic gonadotrophin), which stimulates the testes directly, or clomiphene (an off-label oral option) can raise testosterone while preserving spermatogenesis. These options require specialist management by a reproductive endocrinologist or andrologist. If testosterone replacement is started before fertility planning is complete, recovery of spermatogenesis can take 12–18 months or longer.
Is testosterone replacement safe for the heart?

Earlier observational studies raised concerns about cardiovascular events with testosterone therapy. The TRAVERSE trial (Lincoff, Nissen et al., NEJM 2023) — a large, randomised controlled trial in more than 5000 men aged 45 or older with hypogonadism and cardiovascular risk — found that testosterone was non-inferior to placebo for major adverse cardiovascular events (heart attack, stroke, death). This is reassuring for appropriately selected men. There are modest signals for atrial fibrillation and venous thromboembolism, which are not contraindications but warrant monitoring. Polycythaemia — a rise in haematocrit above 54% — is the most common significant complication of testosterone therapy and requires dose reduction or cessation.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.