Although many afflictions have been attributed to vitamin D deficiency, bone disease (i.e., osteomalacia) is the clinical entity with the strongest causal link to vitamin D deficiency.
In this study, Australian researchers sought to identify the 25-hydroxyvitamin D (25[OH]D) level below which abnormal bone physiology becomes evident. Data were obtained from a large cohort of 12,000 adults and from a smaller cohort of 150 adults who underwent more extensive testing. Patients with hypercalcemia or renal disease were excluded.
Across 25(OH)D levels ranging from 12 to 60 ng/mL (30 to 150 nmol/L), there was a weak inverse relationship between 25(OH)D and serum parathyroid hormone (PTH), and a weak positive relation between 25(OH)D and serum calcium. However, a significant break point was evident at a threshold 25(OH)D level of less than 12 ng/mL: Serum calcium levels became distinctly lower and PTH levels became distinctly higher.
The smaller cohort showed no significant correlations between 25(OH)D levels and markers of bone turnover (collagen- and procollagen-related peptides) or bone integrity (i.e., bone density, mineralization, and porosity); however, the small sample size provided limited statistical power for the latter findings.
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