GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Effects of short-term glucocorticoid deprivation on growth hormone (GH) response to GH-releasing peptide-6: studies in normal men and in patients with adrenal insufficiency.
Pinto. A C AC; Silva. M R MR; Martins. M R MR; Brunner. E E; Lengyel. A M AM
Key Findings
- Short‑term glucocorticoid (cortisol) reduction with metyrapone did not significantly alter the GH peak or overall exposure after a GHRP‑6 dose in healthy men.
- Patients with chronic hypocortisolism showed GH responses to GHRP‑6 that were modestly lower after stopping prednisone, but still comparable to controls.
- Long‑standing low cortisol may cause subtle changes in the GHRP‑6‑driven GH release pathway, though the effect is not large.
Practical Outcomes
- For most biohackers, short‑term fluctuations in cortisol (e.g., from stress or brief steroid cycles) are unlikely to impact the effectiveness of GHRP‑6 for boosting GH. However, individuals with chronic adrenal insufficiency or long‑term steroid withdrawal might experience a slightly reduced GH response, so they may need to adjust dosing or manage expectations.
Summary
The study looked at whether lowering cortisol (the stress hormone) changes how well GHRP‑6 makes the body release growth hormone. In healthy men, a short‑term drop in cortisol didn’t noticeably affect the GH boost from GHRP‑6. In people with long‑term low cortisol (adrenal insufficiency), the GH response was slightly lower, but still similar to normal levels.
Abstract
There are no data in the literature about the effects of glucocorticoid deprivation on GH-releasing peptide-6 (GHRP-6)-induced GH release. The aims of this study were to evaluate GH responsiveness to GHRP-6 1) after metyrapone administration in normal men, and 2) in patients with chronic hypocortisolism after glucocorticoid withdrawal for 72 h. In normal subjects, metyrapone ingestion did not alter significantly GH responsiveness to GHRP-6 [n = 8; peak, 39.3 +/-7.1 microg/L; area under the curve (AUC), 1958.8 +/- 445.7 microg/min x L; mean +/- SE] compared to placebo (n = 8; peak, 21.9 +/- 4.5; AUC, 1131.0 +/- 229.6). In patients with chronic hypocortisolism (n = 8), GH responses to GHRP-6 were similar both during replacement therapy (peak, 11.8 +/- 3.9; AUC, 563.2 +/- 208.7) and after withdrawal of prednisone (peak, 14.4 +/- 4.5; AUC, 695.6 +/- 272.9) and did not differ from those in controls. Interestingly, after glucocorticoid withdrawal, GH responsiveness to GHRP-6 in patients with chronic hypocortisolism was significantly lower than that in normal subjects pretreated with metyrapone. Our data suggest that short term glucocorticoid deprivation does not have a major impact on GHRP-6-dependent GH-releasing mechanisms. However, in long standing hypocortisolism, subtle changes in GHRP-6 secretory pathways may be present.
Study Information
pubmed
2000
10.1210/jcem.85.4.6536