A synthetic copy of the body's own growth hormone-releasing signal, acting through the pituitary gland so the rise stays within normal rhythm and brakes. Controlled studies in older adults confirm it raises growth hormone and its main downstream messenger, with reasonable evidence for better mental flexibility. Other claims rest on thin evidence. Safety across months is mild; decades untested. (Full Review)
| Marker | Target | Why |
|---|---|---|
| IGF-1 | 50th-75th percentile for age and sex | Primary efficacy and safety target for titration |
| IGFBP-3 | Mid to upper reference range for age | Confirms real axis activation, not assay drift |
| Fasting insulin | 2-5 mIU/L | Detects insulin resistance well before glucose moves |
| Fasting glucose | 75-90 mg/dL (4.2-5.0 mmol/L) | Tracks the consequence of insulin antagonism |
| HbA1c | Below 5.4% | Confirms glucose shifts are not accumulating |
| TSH with free T4 | TSH 0.5-2.0 mIU/L; free T4 upper half of range | Untreated hypothyroidism blunts the response |
| Fasting lipid panel with apoB | apoB below 80 mg/dL | Growth hormone alters lipid handling both ways |
| hs-CRP | Below 1.0 mg/L | Inflammation suppresses IGF-1 generation |
| PSA in men over 45 | Below 2.5 ng/mL, and stable over time | Surveillance for the mitogenic concern of IGF-1 |
| Complete blood count and comprehensive metabolic panel | Within reference range | Liver, kidney, haematological safety screen |
| Body composition by DEXA | Individual; visceral fat below the 50th percentile for age | Only objective measure of body-composition claims |
Cadence: Baseline before the first injection; IGF-1 at 4 weeks and after each dose change; full panel at 3 months, then every 6 months; body composition every 6-12 months.