Response to growth hormone-releasing hormone as evidence of hypothalamic defect in optic nerve hypoplasia.
Leaf. A A AA; Ross. R J RJ; Jones. R B RB; Besser. G M GM; Savage. M O MO
Key Findings
- All four children were GH‑deficient by glucagon/ITT tests but responded to a GHRH bolus, indicating a hypothalamic defect.
- A child with near‑absent pituitary tissue showed a poor response, highlighting the role of pituitary mass.
- Subcutaneous GHRH therapy gave an excellent outcome in one child, suggesting it’s the physiologically appropriate treatment.
Practical Outcomes
- For biohackers, this suggests that GHRH analogs like sermorelin may work better than direct GH shots if the GH shortfall stems from hypothalamic issues. However, the data come from a tiny pediatric study of a rare condition, so results can’t be directly extrapolated to healthy adults seeking performance or longevity benefits. Use caution and consider medical supervision before trying GHRH‑based protocols.
Summary
In four kids with optic nerve hypoplasia, standard tests showed growth‑hormone deficiency, but giving them a burst of growth‑hormone‑releasing hormone (GHRH) sparked a hormone response, proving the problem was in the hypothalamus, not the pituitary. One child with almost no pituitary tissue didn’t respond well, while another child improved a lot with daily GHRH injections, which is the most natural way to treat this defect.
Abstract
Hypothalamic-pituitary function was studied in four children with Optic Nerve Hypoplasia (ONH). All were found to be growth hormone deficient when provoked with glucagon or insulin induced hypoglycaemia (ITT), but did respond to bolus injection of GHRH. This indicates a primary hypothalamic defect. Virtual absence of pituitary tissue on high resolution CT scan explained the poor response of one child. One child has shown an excellent response to treatment with subcutaneous GHRH, which is physiologically the most appropriate treatment for this condition.
Study Information
pubmed
1989
1989-05-01T00:00:00.000Z
10.1111/j.1651-2227.1989.tb11104.x
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