Abstract

OBJECTIVE—Obesity is a well-known risk factor for vitamin D deficiency. We evaluated the interrelationship between vitamin D status, body size, and glucose homeostasis, measured by HbA_1c (A1C).

RESEARCH DESIGN AND METHODS—Data are from the survey of the 45-year-old 1958 British birth cohort (2002–2004). Information on A1C, 25-hydroxyvitamin D [25(OH)D; an indicator of vitamin D status], and BMI was collected from 7,198 Caucasian subjects.

RESULTS—25(OH)D was <75 nmol/l in 80% of the obese subjects (BMI ≥30 kg/m²) versus 68% of the other subjects (P < 0.0001). Serum 25(OH)D decreased and A1C increased by increasing BMI (P < 0.0001 for both comparisons). There was a nonlinear association between 25(OH)D and A1C: a steep linear decrease in A1C by 25(OH)D until 65 nmol/l and only smaller decreases with further increases. There was evidence for effect modification by BMI in the association between 25(OH)D and A1C (P < 0.0001), and differences appeared stronger for participants with higher compared with lower BMIs. After adjustment for sex, season, geographical location, physical activity, and social class, percent change in A1C by 10-nmol/l increase in 25(OH)D was −0.21 (95% CI −0.31 to −0.11) for BMI <25 kg/m², −0.25 (−0.37 to −0.13) for BMI 25–29.9 kg/m², −0.65 (−0.95 to −0.34) for BMI 30–34.9 kg/m², and −1.37 (−2.09 to −0.64) for BMI ≥35 kg/m².

CONCLUSIONS—Body size was a strong determinant for 25(OH)D, with concentrations being suboptimal in most obese participants. Randomized controlled trials [using dosages sufficient to improve 25(OH)D also for the obese] are required to determine whether clinically relevant improvements in glucose metabolism can be obtained by vitamin D supplementation.