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GHRP-6

Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2

Quick Stats
Studies 702
Trials 0
Score 3
2003 pubmed

The influence of serum cortisol levels on growth hormone responsiveness to GH-releasing hormone plus GH-releasing peptide-6 in patients with hypocortisolism.

Pekic. Sandra S; Doknic. Mirjana M; Djurovic. Marina M; Damjanovic. Svetozar S; Petakov. Milan M; Miljic. Dragana D; Dieguez. Carlos C; Casanueva. Felipe F FF; Popovic. Vera V

Key Findings

  • GH response to GHRH+GHRP‑6 is similar whether patients are on or off short‑term glucocorticoid therapy.
  • Newly diagnosed Addison’s patients (very low cortisol) have a lower GH response before starting steroids, which improves after a month of replacement.
  • Long‑standing hypocortisolism blunts the GH response but it remains above the minimal effective level (>15 µg/L).

Practical Outcomes

  • For biohackers, GHRP‑6 can still be effective without needing to manipulate cortisol levels short‑term. However, chronic low cortisol (e.g., from adrenal insufficiency or prolonged stress) might slightly reduce the GH surge, so maintaining healthy cortisol balance could optimize results. No need for short‑term steroid withdrawal to boost GHRP‑6 efficacy.

Summary

The study shows that the growth hormone boost you get from GHRP‑6 (combined with GHRH) works pretty well even if your cortisol levels are low, but if you’ve had low cortisol for a long time the GH spike may be a bit smaller, though still within normal limits.

Abstract

The aim of this study was to evaluate the influence of circulating cortisol levels on the somatotroph responsiveness to the most potent stimuli of growth hormone (GH) secretion, the GHRH+GHRP-6 test. We studied 12 patients with hypocortisolism (10 with Addison's disease and 2 with isolated ACTH deficiency) before and after glucocorticoid (GC) replacement therapy and compared them with 14 healthy subjects. In the 10 patients with Addison's disease, GH responses (GH peak, microg/L) to GHRH+GHRP-6 were similar both during GC, (68.2+/-12.8) and off GC (60.3+/-14.1) therapy and did not differ from those in controls (61.5+/-6.0). In a subgroup of 4 patients with newly diagnosed Addison's disease, GH responsiveness to GHRH+GHRP-6 prior to GC replacement (26.4+/-4.1) was significantly lower than in the 6 patients with long-standing Addison's disease after short-term GC withdrawal (82.9+/-18.2). In the newly diagnosed Addison's patients, after one month of GC replacement, mean GH peak value increased to 40.7+/-11.8. In the 2 patients with isolated ACTH deficiency, GH responses to GHRH+GHRP-6 did not differ off and on GC therapy (60.3+/-14.1 and 41.5+/-2.0, respectively). Our data suggest that short-term GC deprivation does not have a major impact on GH responsiveness to GHRH+GHRP-6. However, in patients with long-standing hypocortisolism, GH response is blunted but still within normal range (> 15 microg/L).

Study Information

Provider

pubmed

Year

2003

DOI

10.14310/horm.2002.11106