The most common entry point into the human growth hormone conversation is a single blood test. Someone feels flat, tired, soft around the middle. They get an IGF-1 level drawn, it comes back "low-normal" or below the reference range, and the conclusion writes itself: growth hormone deficiency. That inference is the weakest link in the entire chain — and the published diagnostic literature has said so for well over a decade.

This post covers what the evidence actually says about diagnosing adult growth hormone deficiency (AGHD), why IGF-1 alone fails at it, what a 2026 real-world study found when clinicians used the newer oral stimulation test, and how Australia's PBS criteria handle the problem. For background on the molecule itself, see our HGH profile.

What is the HGH blood test, and what does it actually measure?

Growth hormone is secreted in pulses, mostly overnight. A random GH level is close to meaningless, because you might be sampling a peak or a trough. So clinicians instead measure insulin-like growth factor 1 (IGF-1), a liver-derived hormone that GH drives and which circulates at more stable levels. IGF-1 is the integrated signal; GH is the noisy one.

That logic is sound. The problem is the performance data.

Normal IGF-1 in 37–70% of deficient adults

In a 2012 review of AGHD diagnosis published in the International Journal of Endocrinology, the authors note that serum IGF-1 can be normal in patients with undisputed growth hormone deficiency, with reported rates of normal IGF-1 across studies ranging from 37% to 70% of GH-deficient adults. That is not a rounding error. On the higher end, most people with a confirmed deficiency would be missed by the test being used to screen them.

The same review highlights an age gradient: roughly 70% of GH-deficient adults under 40 had IGF-1 below the age-related 3rd centile, but only about 35% of those over 40 did. Sensitivity falls away precisely in the demographic most likely to be reading about HGH for energy and body composition.

A 2021 analysis in Scientific Reports put numbers on it directly. Using receiver operating characteristic analysis at an IGF-1 cut-off of −1.493 SD, the authors reported sensitivity of 0.685, specificity of 0.417 and an area under the curve of 0.517 — an AUC of roughly 0.5 is what you would expect from a coin toss. Their conclusion was in the title: IGF-1 level is a poor diagnostic indicator of growth hormone deficiency. This was a single-centre retrospective dataset, so it should not be treated as the last word, but it points the same direction as the earlier reviews.

The practical upshot: a low IGF-1 raises suspicion. It does not make a diagnosis. And a normal IGF-1 does not exclude one.

How AGHD is actually diagnosed: provocation testing

Because the static test underperforms, endocrinology relies on dynamic or "provocation" testing — you stress the pituitary and see whether it can mount a GH response.

Insulin tolerance test (ITT). Still described in the literature as the gold standard, because it interrogates the entire hypothalamic–pituitary–somatotroph axis. It is also labour-intensive, unpleasant, and contraindicated in older adults and in people with seizure disorders or ischaemic heart disease, because it deliberately induces hypoglycaemia.

Glucagon stimulation test (GST). Widely used as the practical alternative. Reviews note its availability, reproducibility and safety, with relatively few contraindications. Crucially, the American Association of Clinical Endocrinologists proposed BMI-adjusted cut-points: a peak GH ≤3.0 µg/L for those with BMI under 25 (and for BMI 25–29.9 with high pre-test probability), but ≤1.0 µg/L for BMI ≥30. Body fat blunts the GH response. Use a single threshold and you will diagnose deficiency in people who are simply carrying more weight.

Macimorelin. An oral ghrelin-receptor agonist approved by the US FDA in 2017 as a diagnostic agent, attractive because it is a drink rather than an infusion. Validation work published in JCEM reported an optimal GH cut-point of 2.7 ng/mL with 82% sensitivity and 92% specificity.

The 2026 real-world macimorelin data

A retrospective single-centre study published in Pituitary in 2026 (Yadav, Hamrahian and Salvatori) examined how the macimorelin test performs outside trial conditions. The authors stratified patients by pre-test probability and compared the FDA cut-off of 2.8 ng/mL against a proposed higher cut-off of 5.1 ng/mL. Among patients with low pre-test probability, BMI showed an inverse association with peak GH, and was substantially higher in discordant versus concordant cases (37.7 ± 2.7 vs 28.2 ± 4.6 kg/m²).

Same lesson as the glucagon test, from a newer agent: obesity suppresses the stimulated GH response, and a person with a high BMI and no pituitary pathology can fail a stimulation test without being growth hormone deficient. This is a single-centre retrospective series, not a prospective validation study, and it needs replication before cut-offs change.

Note the direction of travel here. Two of the most common reasons people self-diagnose "low HGH" — being over 40 and carrying extra weight — are the same two variables that most distort the tests.

HGH in Australia: the regulatory and PBS angle

If you are searching "is HGH legal in Australia", the short answer is that it is legal as a prescribed medicine and illegal otherwise. Somatropin is a Schedule 4 prescription-only medicine, TGA-approved for defined conditions, and border-controlled — importing or possessing it without a valid prescription is an offence. It is also prohibited at all times under the World Anti-Doping Code.

Australia's subsidy framework is where the diagnostic argument becomes concrete. PBS-subsidised somatropin for adults with severe GH deficiency has been available since December 2018, and the criteria published by the Endocrine Society of Australia require more than a blood test. Applicants must be 18 or over, supply biochemical evidence from provocation testing — the criteria specify thresholds including a glucagon provocation test with maximum serum GH less than 3 µg/L, or an arginine infusion test with maximum serum GH less than 0.4 µg/L — and a quality-of-life score on the QoL-AGHDA instrument of 16 or greater. The QoL-AGHDA is a 25-item questionnaire scored 0 (good) to 25 (very poor). Baseline IGF-1 and QoL scores must be no more than 12 weeks old at application.

In other words: IGF-1 is collected, but it is not the gate. The gate is a stimulation test plus documented symptom burden, and continuing subsidy depends on demonstrated improvement. Patients with childhood-onset GHD from a congenital, genetic or structural cause who previously received PBS-subsidised therapy as children are exempt from repeat provocation testing.

That architecture exists for a reason. It is the system's answer to exactly the failure mode described above — a test that, used alone, misclassifies a large share of the people it is applied to.

What this means if you're reading about HGH for ageing

None of this speaks to whether growth hormone helps healthy adults, which is a separate question with its own literature. The short version, covered in more depth on our peptides index: trials in healthy older adults have shown on the order of 2 kg of lean mass gain, alongside real and consistent adverse effects — oedema, joint pain, carpal tunnel symptoms and worsened insulin resistance. Body composition shifts; functional outcomes and hard endpoints have not followed.

What the diagnostic literature adds is a prior step. Before the risk–benefit question even arises, there is the question of whether a deficiency exists at all. A single IGF-1 result cannot answer it, in either direction, and the clinical pathway that can answer it is deliberately more demanding than one blood draw.

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FAQ

Does a low IGF-1 test mean I have growth hormone deficiency?

No. A low IGF-1 raises suspicion but cannot confirm deficiency, and a normal result does not exclude it — published reviews report normal IGF-1 in 37–70% of adults with confirmed growth hormone deficiency. Diagnosis requires dynamic stimulation testing.

How is adult growth hormone deficiency diagnosed?

Through provocation testing — most commonly the insulin tolerance test (still the reference standard), the glucagon stimulation test, or the oral macimorelin test — measuring whether the pituitary can mount a peak GH response above a defined threshold.

Is HGH legal in Australia?

Somatropin is a Schedule 4 prescription-only medicine in Australia, TGA-approved for specific conditions and border-controlled. Possessing or importing it without a valid prescription is illegal, and it is prohibited at all times in sport under WADA rules.

Does obesity affect growth hormone test results?

Yes. Higher BMI blunts the stimulated GH response, which is why guidelines use BMI-adjusted cut-points for the glucagon test, and why a 2026 real-world macimorelin study found discordant results clustered in patients with substantially higher BMI.

Sources

This article is independent information, not medical advice. Somatropin is a TGA-approved, Schedule 4 prescription-only medicine in Australia for defined conditions; retatrutide.net.au has no affiliation with any manufacturer or supplier and does not sell or source any compound.