Impairment of growth hormone responsiveness to growth hormone releasing hormone and pyridostigmine in patients affected by Prader-Labhardt-Willi syndrome.
Beccaria. L L; Benzi. F F; Sanzari. A A; Bosio. L L; Brambilla. P P; Chiumello. G G
Key Findings
- GH response to clonidine was abnormal in most patients (14/18).
- GH response to GHRH + pyridostigmine was inadequate in most patients, especially those with higher adiposity.
- GH response to GHRH + pyridostigmine decreased with increasing age and body fat.
Practical Outcomes
- For biohackers using GHRH analogs, expect reduced effectiveness if you’re older or have higher body fat. Adjusting dose or combining with agents that improve GH signaling might be needed, but the findings are specific to a rare disorder and not a proven protocol for the general population.
Summary
The study shows that people with Prader‑Labhardt‑Willi syndrome have a weak growth‑hormone (GH) response to both clonidine and a combination of GHRH plus a cholinergic drug, especially if they are older or have more body fat. This suggests that obesity and age can blunt the effectiveness of GH‑stimulating treatments like sermorelin.
Abstract
In order to evaluate the impairment of GH response in patients affected by Prader-Labhardt-Willi (PLW) syndrome, in 18 patients we studied GH response to clonidine and to GHRH + pyridostigmine, a cholinergic drug which enhances GHRH induced GH responsiveness in obese patients. After clonidine GH response was abnormal in 14/18 subjects (mean GH peak: 4.1 +/- 1.3 micrograms/l; area under curve: 208.1 +/- 74.2 micrograms/l.h) while all but 5 patients showed an inadequate GH response to GHRH + pyridostigmine (mean GH peak: 13.4 +/- 2.5 micrograms/l; area under curve: 903.4 +/- 171.0 micrograms/l.h). However, in the three patients with low adiposity index, GH response to GHRH + pyridostigmine was significantly higher than that observed in fatter subjects. In addition, GH response to GHRH + pyridostigmine was negatively correlated to age and adiposity index. In conclusion, our data are consistent with the hypothesis of the existence of a complex derangement of GH neuroendocrine regulation in these subjects.
Study Information
pubmed
1996
10.1007/bf03349040