Growth hormone and the heart.
Colao. A A; Marzullo. P P; Di Somma. C C; Lombardi. G G
Key Findings
- Excess GH (acromegaly) leads to a specific cardiomyopathy with myocardial hypertrophy, fibrosis, and inflammation.
- GH deficiency causes thin cardiac walls, reduced diastolic filling, and increased vascular thickness, raising cardiovascular risk.
- Both suppressing GH in excess and replacing GH in deficiency can partially reverse cardiac abnormalities, and GH therapy shows promise for treating non‑endocrine heart failure.
Practical Outcomes
- For biohackers using GH‑releasing peptides like hexarelin, the data warn that chronic high GH levels may damage the heart, so dosing should avoid sustained supraphysiologic spikes. Moderate, intermittent GH elevation could support heart health, especially in those with low GH, but any therapeutic use for heart failure remains experimental and should be approached with medical supervision.
Summary
Growth hormone (GH) can both help and hurt the heart. Too much GH, as seen in acromegaly, can cause thickened heart walls and scar tissue, while not enough GH can make the heart walls thin and stiff, leading to poor pumping. Replacing GH in deficient people or carefully lowering it in excess can improve heart structure and function, and early studies even suggest GH might help people with chronic heart failure, though more research is needed.
Abstract
Impaired cardiovascular function has recently been demonstrated to potentially reduce life expectancy both in GH deficiency and excess. Experimental and clinical studies have supported the evidence that GH and IGF-I are implicated in cardiac development. In most patients with acromegaly a specific cardiomyopathy, characterized by myocardial hypertrophy with interstitial fibrosis, lympho-mononuclear infiltration and areas of monocyte necrosis, results in biventricular concentric hypertrophy. In contrast, patients with childhood or adulthood-onset GH deficiency (GHD) may suffer both from structural cardiac abnormalities, such as narrowing of cardiac walls, and functional impairment, that combine to reduce diastolic filling and impair left ventricular response to peak exercise. In addition, GHD patients may have an increase in vascular intima-media thickness and a higher occurrence of atheromatous plaques, that can further aggravate the haemodynamic conditions and contribute to increased cardiovascular and cerebrovascular risk. However, several lines of evidence have suggested that the cardiovascular abnormalities can be partially reversed by suppressing GH and IGF-I levels in acromegaly or after GH replacement therapy in GHD patients. Recently, much attention has been focussed on the ability of GH to increase cardiac mass suggesting its possible use in the treatment of chronic nonendocrine heart failure. In fact, GH administration can induce an improvement in haemodynamic and clinical status in some patients. Although these data need to be confirmed in more extensive studies, such promising results seem to open new perspectives for GH treatment in humans.
Study Information
pubmed
2001
10.1046/j.1365-2265.2001.01218.x