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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 2
2009 pubmed 43 citations

Chronic cognitive sequelae after traumatic brain injury are not related to growth hormone deficiency in adults.

Pavlovic. D D; Pekic. S S; Stojanovic. M M; Zivkovic. V V; Djurovic. B B; Jovanovic. V V; Miljic. N N; Medic-Stojanoska. M M; Doknic. M M; Miljic. D D; Djurovic. M M; Casanueva. F F; Popovic. V V

Key Findings

  • Approximately 33% of TBI patients had GH deficiency or insufficiency years after the injury.
  • Neuropsychological test scores were similar regardless of whether patients had GH deficiency, insufficiency, or normal GH secretion.
  • There was no correlation between stimulated peak GH levels (or IGF‑I) and cognitive performance.

Practical Outcomes

  • For biohackers, using GHRP‑6 to boost GH is unlikely to improve cognition after a TBI. While monitoring GH may still be relevant for other health reasons, focusing on other pathways (e.g., neuroplasticity, sleep, nutrition) is more promising for cognitive recovery.

Summary

In adults who suffered a traumatic brain injury (TBI) at least a year ago, about one‑third still have low growth hormone (GH) levels, but this deficiency does not seem to affect their thinking abilities. The study used a GH‑releasing peptide‑6 (GHRP‑6) test to measure GH response and found no link between GH output and performance on memory or attention tests.

Abstract

The objective of the study was to asses the possible influence of hypothalamo-pituitary deficiencies, and growth hormone (GH) deficiency in particular, on cognition in adult patients with traumatic brain injury (TBI). TBI is a recently identified risk factor for cognitive deficits and hypopituitarism. Even the patients with favorable outcome after TBI may present with persistent bodily, psychosocial, and cognitive impairments, resembling patients with untreated partial or complete pituitary insufficiency. We performed retrospective and cross-sectional study of endocrine and cognitive function in TBI in 61 patients (aged 37.7 +/- 1.7 years) of both sexes (44 m,17 f), at least 1 year after TBI (3.9 +/- 0.6 years). Serum insulin-like growth factor 1 (IGF-I), thyroxin, thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone (in men), prolactin, and cortisol were measured, and GH secretion was assessed by growth hormone releasing hormone (GHRH) + growth hormone releasing peptide-6 (GHRP-6) test. Cognitive function was assessed by using a standard neuropsychological battery. GH deficiency (GHD) and GH insufficiency (GHI) were found in 20 patients (32.8%). After adjustment for confounders [age, body mass index (BMI), education level, time elapsed from TBI], there were no significant differences in results of neuropsychological tests between patients with TBI with GHD, GHI, and normal GH secretion. There were no correlations of neuropsychological variables with stimulated peak GH secretion or IGF-I level. GHD persists long after the TBI, independently of trauma severity and age at traumatic event. GH secretion is more sensitive to TBI than other pituitary hormones. No evidence is found for an association of cognitive function impairment and somatotropic axis impairment in adult patients tested more than 1 year after the TBI.

Study Information

Provider

pubmed

Year

2009

Date

2009-12-30T00:00:00.000Z

DOI

10.1111/j.1468-1331.2009.02910.x

Citations

43

References

36