Because both GHD and normal aging are associated with decreases in bone density, it has been hypothesized that reduced GH secretion may account in part for age-related loss of bone mass (24). However, a causal relationship between GHD and osteoporosis has not been established. Nocturnal serum GH peaks average 20 ng/mL in 30-yr-old men, but this value declines steadily to 3 ng/mL by age 80 (24). These values are reflected in the fall of IGF-1 levels, which also occurs with aging (24). Because aging is associated with numerous physiological and hormonal changes, it has been difficult to determine definitively the degree to which the age-related decline in GH levels is responsible for bone loss. Bone density peaks at age 30, then declines progressively. In men, 25% of trabecular bone is lost by age 75 (25). One study of women with osteoporosis and vertebral compression fractures showed no difference in the GH response to insulin-induced hypoglycemia in these patients compared to nonosteoporotic controls (26). The GH response to hypoglycemia, however, may not reflect spontaneous GH secretion, and a relationship between declining GH production and osteoporosis could not be excluded. A later study showed that 141 men and women with osteoporosis and vertebral fractures had significantly reduced serum levels of IGF-1 compared to controls (27). In addition, levels of the GH-dependent protein IGF-1 were positively correlated with bone density in osteoporotic women who were not receiving estrogen replacement. No such correlation was found in other subgroups of the experimental population, nor were correlations found between IGF-1 and bone density.
To date, the evidence for a relationship between age-related declines in GH secretion and bone density is circumstantial. More investigation is required to establish this link more definitively. Even in the absence of such investigation, studies of the effects of GH administration on bone in the elderly have been conducted, and are discussed later in the chapter.
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