We studied the mechanism of impaired calcium absorption with aging in 51 healthy women whose ages ranged from 26 to 88 years. Serum concentrations of 1,25‐dihydroxyvitamin D [1,25‐(OH)2D, mean of four measurements per subject] increased with age by 22% (P < 0.05) but, by split‐point analysis, plateaued or decreased slightly after age 65. In a subset of 20 subjects, [3H]1,25‐(OH)2D3 kinetic analysis showed that this increase with age resulted from both increased production and decreased metabolic clearance of 1,25‐(OH)2D. Despite the increase in serum 1,25‐(OH)2D concentration, true calcium absorption did not change with age. The expected inverse correlation between true fractional calcium absorption and dietary calcium intake, however, was easily demonstrated (r = 0.66, P < 0.001). Serum intact parathyroid hormone (PTH) increased with age by 35% (P < 0.02) and serum bone gla protein (BGP, osteocalcin) increased by 47% (P < 0.001); the increases in serum PTH and serum BGP were directly correlated (r = 0.32, P < 0.05). The data are consistent with the following hypothetical model: (1) intestinal resistance to 1,25‐(OH)2D action accounts for the increase in serum 1,25‐(OH)2D concentrations with aging with no change in true calcium absorption; (2) this results in a compensatory increase in PTH secretion and in 1,25‐(OH)2D production that prevents true calcium absorption from decreasing; (3) the previously described defect in 25‐hydroxyvitamin D (25‐OHD) 1α‐hydroxylase activity in aging animals and humans acccounts for the leveling off in serum 1,25‐(OH)2D concentration after age 65 years; and (4) the secondary hyperparathyroidism leads to increased bone turnover and thus contributes to age‐related bone loss.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Orthopedics and Sports Medicine