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GHRP-2

Pralmorelin, Growth Hormone Releasing Peptide-2, KP-102

Quick Stats
Studies 230
Trials 1
Score 3
2004 pubmed

Dual secretagogue drive of burst-like growth hormone secretion in postmenopausal compared with premenopausal women studied under an experimental estradiol clamp.

Erickson. Dana D; Keenan. Daniel M DM; Mielke. Kristi K; Bradford. Kandace K; Bowers. Cyril Y CY; Miles. John M JM; Veldhuis. Johannes D JD

Key Findings

  • Post‑menopausal women have lower fasting GH and IGF‑I than pre‑menopausal women under the same estradiol levels.
  • Both basal and pulsatile GH secretion are reduced in post‑menopausal women.
  • GH response to GHRP‑2 (alone or with arginine/GHRH) is blunted in post‑menopausal women, while burst frequency and waveform duration stay the same.
  • Visceral fat accounts for up to ~25% of the variation in fasting and stimulated GH levels.

Practical Outcomes

  • For biohackers using GHRP‑2, expect a weaker GH surge as you age, especially after menopause, even if you keep estrogen high. You may need higher doses, combine GHRP‑2 with other secretagogues, or focus on reducing abdominal fat to get a stronger GH response. The findings confirm that age‑related GH decline is largely independent of short‑term estrogen levels.

Summary

The study shows that older (post‑menopausal) women have lower baseline growth hormone (GH) and a weaker GH boost when given GHRP‑2 (or other GH‑releasing combos), even when estrogen levels are kept the same. The drop isn’t because they have fewer GH bursts, but because each burst is smaller, and belly fat also explains part of the difference. In short, age, not just estrogen, makes the GH‑releasing effect of GHRP‑2 weaker.

Abstract

We show that in an experimentally enforced estradiol-predominant milieu, postmenopausal compared with premenopausal women maintain 1) decreased fasting GH and IGF-I concentrations, 2) reduced basal and pulsatile GH secretion, and 3) attenuated GH secretion after maximal stimulation by the paired secretagogues l-arginine/GH-releasing peptide (GHRP)-2, l-arginine/GHRH, and GHRP-2/GHRH. These foregoing outcomes are selective, because menopausal status did not determine mean GH secretory-burst frequency or peptide-induced waveform shortening. Abdominal visceral fat mass predicted up to 25% of the variability in fasting and stimulated GH secretion in the combined cohorts under fixed systemic estradiol availability. Accordingly, as much as three-fourths of interindividual differences in burst-like GH secretion among healthy pre- and postmenopausal women arise from age-related mechanisms independently of short-term systemic estrogen availability and relative intraabdominal adiposity.

Study Information

Provider

pubmed

Year

2004

DOI

10.1210/jc.2004-0424