Diminished secretion of growth hormone is responsible in part for the decrease of lean body mass, the expansion of adipose-tissue mass, and the thinning of the skin that occur in old age.

Body composition changes progressively in mid and late adulthood. Lean body mass in men over 50 years old contracts at an average rate of-0.6% per year. Body weight tends to remain stable because of a reciprocal expansion of adipose mass. The shrinkage of the lean body mass reflects the atrophy of skeletal muscles, skin and visceral organs. Because growth hormone causes expansion of the lean body mass and contraction of the adipose mass, and because growth hormone secretion tends to diminish in late adulthood, it has been postulated that geriatric hyposomatotropism is a contributory cause to the body composition changes described above. The authors have tested this hypothesis by recruiting 45 independent men over 61 years old with plasma somatomedin C level below 0.35 U/ml, indicating little or no detectable growth hormone secretion. The 21-month protocol was as follows: baseline period 0–6 months, experimental period 6–18 months and post-experimental period 18–21 months. During the experimental period, 26 men (group I) received approximately 0.03 mg/kg of biosynthetic human growth hormone (hGH) subcutaneously 3 times a week, while 19 men (group II) received no treatment. Plasma somatomedin C was measured monthly. The following outcome variables were measured at 0,6, 12 and 18 months: lean body mass, adipose mass, skin thickness (dermis plus epidermis), sizes of the liver, spleen and kidneys, the cross sectional areas often muscle groups, and bone density at 9 skeletal sites. Lean body mass and adipose mass were also measured at 21 months. In group I, hGH treatment raised the plasma somatomedin C level and maintained it in the range 0.5–1.5 U/ml. Significant changes occurred in the following outcome variables, expressed as percent change at 18 months over baseline: lean body mass +6%, adipose mass -15%, skin thickness +4%, liver volume +8%, spleen volume + 23%, sum of ten muscle areas +11 %. Three months after hGH treatment stopped, about one half of the hGH-induced increment in lean body mass had disappeared and about one third of the hGH-induced decrement in adipose mass had reappeared. During hGH treatment, 9 subjects developed carpal tunnel syndrome and 4 subjects developed gynecomastia. The adverse side effects disappeared spontaneously within 3 months after cessation of hormone treatment. In group II, the somatomedin C level remained below 0.35 U/ml. At the 18-month time point, there was a significant decline in lean body mass to 96% of initial baseline and in skin thickness to 94% of initial baseline. These observations are consistent with the hypothesis that diminished growth hormone secretion in the later years of adulthood is a contributory cause to the body composition changes which occur with advancing age.

These observations show that when elderly men with low circulating IGF-I concentrations are treated continuously with hGH, elevation of plasma IGF-I above 1.0 units/ml is associated with a substantial frequency of carpal tunnel syndrome or gynaecomastia. It may be that the effects of the hormone in expanding lean body mass and reducing adipose mass can be achieved, and the side-effects avoided, by maintaining the mean IGF-I level in the range 0.5-1.0 units/ml.