Subcutaneous treatment with growth hormone-releasing hormone for short stature.
Hernández. M M; Fragoso. J J; Barrio. R R; Argente. J J; Arilla. E E
Key Findings
- Six months of daily sub‑cutaneous GRF‑1‑29 (5 µg/kg) increased growth velocity in children without GH deficiency.
- 24‑hour GH secretion patterns, pulse frequency and amplitude remained unchanged during and after treatment.
- Serum IGF‑I levels showed only modest, non‑significant changes throughout the study.
Practical Outcomes
- For biohackers interested in using GRF‑1‑29 to boost growth or anabolic effects, the study suggests a modest growth‑speed benefit without major shifts in GH or IGF‑I. The dose used (5 µg/kg nightly) could serve as a starting point, but the data are limited to children and a small sample, so extrapolation to adults or anti‑aging use is uncertain. Monitoring growth metrics rather than hormone levels may be more informative when testing this peptide.
Summary
Giving the peptide GRF‑1‑29 (a short version of growth‑hormone‑releasing hormone) to 11 short‑stature kids for six months made them grow faster, even though their overall GH and IGF‑I levels didn’t change much. The treatment was well‑tolerated and didn’t alter the normal daily GH pulse pattern.
Abstract
In the present study we report the effects of therapy with growth hormone-releasing factor (1-29)NH2 (GRF) on growth rate, plasma levels of insulin growth factor I (IGF-I) and growth hormone (GH) secretion in 11 children who were selected solely on the basis of their short stature and normal GH secretion on standard provocative tests. All children received GRF for 6 months (5 micrograms/kg body weight subcutaneously) each evening. The 24-hour GH secretory profile was studied before and after 6 months of treatment. Simultaneously, GH secretory responses to single intravenous bolus GRF (1.5 micrograms/kg body weight) were also studied before, during, and 6 months off therapy with GRF(1-29)NH2. Plasma levels of IGF-I were measured before, during (1, 2 and 6 months), and after 6 months off therapy with GRF. Statural growth was measured at 3-month intervals. The peak plasma GH level in response to GRF was 56.04 +/- (SD) 24.46 ng/ml before treatment, and similar results were found after therapy. The 24-hour GH secretory profile did not show differences before, during, and after treatment. Comparably, no differences were found in GH pulse frequency, pulse amplitude, pulse height, pulse increment, pulse area and total area before, and 6 months off therapy with GRF. The increments in serum IGF-I achieved were not significantly different at all intervals studied. All patients increased growth velocities (mean +/- SD, cm/year) in response to GRF therapy. Our results demonstrate that GRF administration was effective in accelerating growth velocity in 11 children without GH deficiency.
Study Information
pubmed
1988
10.1159/000181072
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