Short-term testosterone supplementation relieves growth hormone autonegative feedback in men.
Veldhuis. Johannes D JD; Evans. William S WS; Iranmanesh. Ali A; Weltman. Arthur L AL; Bowers. Cyril Y CY
Key Findings
- Testosterone increased basal GH secretion by about 2‑fold and pulsatile GH by ~2.4‑fold compared with placebo.
- Testosterone reduced the negative feedback that normally suppresses GH, especially for basal secretion.
- When GHRP‑2 was given, testosterone actually blunted its ability to further stimulate GH (about 1.9‑fold less response).
- Testosterone helped GH levels recover more quickly after they were artificially suppressed with recombinant GH.
Practical Outcomes
- For biohackers using GHRP‑2 to boost GH, adding short‑term testosterone could raise baseline GH levels but may reduce the extra spike you get from the peptide. If the goal is higher overall GH exposure, a brief testosterone course (e.g., 200 mg IM weekly for 3 weeks) might be useful, but you may need to adjust GHRP‑2 timing or dose. Monitor hormone levels and watch for typical testosterone side effects, especially in older men.
Summary
In healthy men, a short 3‑week course of testosterone (200 mg IM each week) lowered the body's natural brake on growth hormone (GH) release, raising basal GH levels and helping the hormone bounce back faster after it had been suppressed. However, testosterone also dampened the extra boost you get from a GH‑releasing peptide (GHRP‑2).
Abstract
The present study tests the postulate that testosterone (Te) stimulates GH secretion, in part, by attenuating autonegative feedback. To this end, 13 healthy men (ages 43-71 yr) received three consecutive weekly im injections of placebo (Pl) (n = 7) or Te (200 mg) (n = 6) in a prospectively randomized, double-blind, parallel-cohort design. An iv pulse of saline or recombinant human (rh)GH (3 micro g/kg.6 min) was infused 2 h before bolus saline or GH-releasing peptide (GHRP)-2 (1 micro g/kg) in the fasting state. Blood was withdrawn every 10 min, GH concentrations were quantitated by chemiluminometry, secretion was determined by deconvolution analysis, and outcomes were compared by ANOVA. After Pl, rhGH suppressed basal, pulsatile, and GHRP-2-stimulated GH secretion by 2.6-, 2.4-, and 2.1-fold, respectively (each P < 0.03), and truncated GHRP-2-stimulated GH secretory bursts (P < 0.005). Compared with Pl, Te: 1) stimulated basal and pulsatile GH secretion by 1.9 and 2.4-fold (P < 0.01 and P < 0.02), respectively; 2) reduced feedback on basal GH secretion (P < 0.01); 3) blunted GHRP-2-stimulation by 1.9-fold (P < 0.01); and 4) facilitated initial recovery of rhGH-suppressed GH concentrations (P < 0.005). The foregoing actions were selective, inasmuch as Te did not relieve autoinhibition of pulsatile GH secretion. In summary, short-term Te supplementation decreases rhGH-imposed negative feedback on basal GH secretion and enhances early escape of GH from autoinhibition. In principle, such actions could potentiate the renewal of high-amplitude pulses of GH in androgen-replete individuals.
Study Information
pubmed
2004
10.1210/jc.2003-031017