Growth hormone increases and insulin-like growth factor-I decreases circulating lipoprotein(a).
Laron. Z Z; Wang. X L XL; Klinger. B B; Silbergeld. A A; Wilcken. D E DE
Key Findings
- GH or GH‑secretagogues (including hexarelin) increase circulating Lp(a) by about 100‑130% over 6‑9 months.
- Direct IGF‑I administration reduces Lp(a) by roughly two‑thirds.
- Insulin rises with GH/hexarelin treatment but falls with IGF‑I, mirroring the Lp(a) changes.
Practical Outcomes
- If you use hexarelin for muscle or anti‑aging purposes, expect a significant rise in Lp(a), which may increase cardiovascular risk. Consider monitoring Lp(a) levels or avoiding hexarelin if you have a family history of heart disease. Direct IGF‑I supplementation appears to lower Lp(a), but it has its own safety considerations.
Summary
Giving hexarelin (a growth‑hormone releasing peptide) raises IGF‑I but also boosts the blood level of lipoprotein(a), a molecule linked to higher heart‑disease risk. In contrast, giving IGF‑I directly lowers lipoprotein(a).
Abstract
Elevated serum lipoprotein(a) (Lp(a)) is a strong risk factor for coronary artery disease (CAD). Genetic factors appear to account for the major variance in Lp(a) levels but the contribution hormones make in modulating Lp(a) levels is not yet clear. In the present investigation we determined the effects of human growth hormone (hGH) and insulin-like growth factor-I (IGF-I) on circulating Lp(a). Four groups of patients were studied. Group a: adults with GH deficiency (n = 7) treated with hGH (0.05 U/kg/day, s.c.); group b: girls with Turner syndrome (n = 7) treated with hGH (0.1 U/kg/day, s.c.); group c: prepubertal boys with idiopathic short stature (n = 6) treated with the GH secretagogue (GHRP) hexarelin (60 micrograms t.i.d. intranasally); group d: Laron syndrome patients (n = 10) treated with IGF-I (100-200 micrograms/kg/day, s.c.). Following overnight fasting, serum was sampled before the initiation of treatment and during 6-9 months treatment. Serum IGF-I rose significantly in all the subjects in all four groups. In the first three groups in which IGF-I was elevated by exogenous or endogenous GH stimulation, serum Lp(a) increased significantly (119 +/- 35%, P < 0.01; 126 +/- 44%, P < 0.05; 102 +/- 29%, P < 0.01 for groups a, b, and c respectively). By contrast, serum Lp(a) levels decreased in group d to whom exogenous IGF-I was administered (-66 +/- 5%, P < 0.001). The differential effect of endogenous vs exogenous IGF-I on serum Lp(a) paralleled the behaviour of serum insulin. Insulin was significantly increased in all the subjects receiving hGH or GHRP (65.2 +/- 31%, P = 0.109; 93.7 +/- 53%, P = 0.062; 353.8 +/- 52.7%, P < 0.01 for groups a, b, and c respectively) whereas insulin levels were reduced following exogenous administration of IGF-I (-34.1 +/- 9.1%, P < 0.01). We conclude that long-term GH treatment increases and IGF-I decreases circulating levels of Lp(a). These findings may have clinical relevance in view of the increasing use of hGH in children and adults and the role of Lp(a) as a CAD risk factor.
Study Information
pubmed
1997
10.1530/eje.0.1360377