Somatopause: dismetabolic and bone effects

The physiological changes that the human body undergoes during aging are similar to those observed in GH deficiency (GHD). Early changes of aging are represented by increased fat mass, increased cardiovascular risk, reduced muscle mass and strength, reduced exercise tolerance, thinned skin, decreased strength and impaired quality of life. These observations led to hypothesize that the elderly could be GH deficient and would benefit from GH treatment. However, the effects of GH treatment in healthy elderly subjects by randomized and controlled studies are less promising than initially hypothesized. The etiopathology of age-related bone loss is multifactorial including menopause, andropause, somatopause and secondary hyperparathyroidism. GH has multiple effects on bone, either direct or mediated by IGF-I, stimulating osteoblast proliferation as well as osteoclast differentiation. Consequently, decline in GH secretion reduces bone turnover that causes osteopenia in young adults, but it has been hypothesized that it could protect against fractures in elderly subjects. The increase of bone remodeling achieved by GH therapy may be helpful in elderly men and women who have severely decreased bone turnover and impaired osteoblastic function. In conclusion, the endocrine pattern of aging is distinct from the decrease of GH/IGF-I levels associated with hypopituitarism. However, GH plays a role in metabolism and bone physiology throughout the human life span, although there is insufficient evidence for a clear therapeutic role of rhGH in aging. Thus, more data are needed to define the effects of somatopause to identify who could potentially benefit from the effects of somatotropic treatment.