Two hundred thirty-two obese and 147 nonobese subjects were enrolled (). One hundred twenty-three were Black (65% obese) and 256 were White (59% obese). Black and White subjects were not significantly different in mean age, although men were older than women overall and had lower mean body fat mass (P < 0.005). There were significant differences between Black and White subjects in socioeconomic status (P < 0.0001); therefore, socioeconomic status was included as a covariate in analyses. Black and White subjects were not significantly different in mean BMI or body fat mass. However, when examined categorically, a greater proportion of Black than White women had BMI ≥ 40 kg/m2 (P < 0.005).
Mean serum 25(OH)D (nmol/l) varied significantly by season (P = 0.006): spring 56.5 (29.7), summer 60.5 (29.7), fall 69.0 (32.7) and winter 63.3 (35.0). Neither 1,25(OH)2D (P = 0.44) nor iPTH (P = 0.31) varied significantly with season.
In obese subjects, 25(OH)D () was significantly lower than in nonobese subjects (P < 0.0001), and 25(OH)D was lower in Black than White subjects regardless of body weight (P < 0.0001). Furthermore, 25(OH)D was significantly lower in obese Black subjects than nonobese Black (P = 0.0025), or obese White (P < 0.0001) subjects. In obese White subjects, 25(OH)D was also significantly lower than in nonobese White subjects (P = 0.0008).
Calcitropic hormone serum concentrations and vitamin D intake
Hypovitaminosis D was present in 43.1% of all Black, vs 11.7% of all White, subjects (P < 0.0001, odds ratio [OR] 5.7, CI 3.4–9.6). Examined by BMI category (), 28% of overweight Black subjects had hypovitaminosis D vs 9.0% of overweight White subjects (OR 3.8, CI 1.3–11.0). Among subjects with class I obesity (OR 4.8, CI 1.5–14.7), class II obesity (OR 8.2, CI 2.6–25.7) and class III obesity (OR 4.9, CI 1.7–14.2), Black subjects had significantly higher likelihood of hypovitaminosis D (P < 0.01). For all subjects with BMI ≥ 35 kg/m2, 59% of Black participants had hypovitaminosis D, compared to 18% of White subjects (OR 6.5, CI 3.0–14.2). Both BMI (P < 0.001) and race (P < 0.001) had similarly independent effects in the prediction of 25OHD levels when a less conservative definition of vitamin D deficiency (< 80 nmol/l) was used in logistic regression.
Prevalence of hypovitaminosis D defined as serum 25(OH)D concentration less than 37.5 nmol/l (15 ng/ml). Prevalence was greater in Blacks than Whites independent of BMI (P < 0.001). The 95% confidence interval is shown as the error bar.
For the 284 subjects who completed food records (), mean daily dietary vitamin D intake was not different according to race (P > 0.1) or body mass (P > 0.9), nor was there a race by BMI interaction. There was no seasonal variation in reported dietary vitamin D intake (P > 0.6). There was no difference in mean daily supplemental vitamin D intake between Black and White subjects (P = 0.73) nor between obese and nonobese subjects (P = 0.13). In logistic regression analyses with 25(OH)D as the dependent measure and adiposity (BMI or DXA body fat), race, sex, age, season, socioeconomic status and vitamin D intake as the independent measures, adiposity expressed either as BMI (odds ratio 1.08, CI 1.04–1.13, P < 0.001) or percentage body fat (odds ratio 1.07, CI 1.02–1.12, P = 0.004) and race (odds ratio 6.8, CI 3.5–13.2, P < 0.001) were significantly and independently related to likelihood for a low 25(OH)D.
Mean iPTH () was significantly higher in obese than nonobese subjects (P < 0.0001) and in Black compared to White subjects (P < 0.0001). Mean iPTH was also significantly greater in obese vs nonobese Black subjects (P = 0.0001) and in obese vs nonobese White individuals (P < 0.005). The prevalence of secondary hyperparathyroidism, defined as iPTH > 4.2 pmol/l (40 pg/ml) when 25(OH)D was below 37.5 nmol/l (15 ng/ml), was significantly greater in all Black (21.9%) than in all White subjects (4.3%, P < 0.0001, OR 6.9, CI 3.2–14.8) and in obese Black (28.7%) than in obese White subjects (7.2%, OR 5.2, CI 2.4–11.3). The prevalence of secondary hyperparathyroidism differed in Black and White subjects according to BMI (). Among subjects with class III obesity, Black subjects had a greater likelihood of secondary hyperparathyroidism (OR 7.9, CI 2.0–31.7). For all subjects with BMI ≥ 35 kg/m2, 35.2% of Black, vs 9.7% of White subjects, had secondary hyperparathyroidism (OR 3.6, CI 1.5–98.8).
Fig. 2 Prevalence of secondary hyperparathyroidism, defined as 25(OH)D less than 37.5 nmol/l (15 ng/ml) plus iPTH greater than 4.2 pmol/l (40 pg/ml). Prevalence was greater in Blacks than Whites independent of BMI (P < 0.001). The 95% confidence interval (more ...)
Serum concentrations of iPTH and 25(OH)D were negatively associated in both Black and White subjects (, r = −0.31, P < 0.0001). Ionized calcium was negatively correlated with iPTH (r = −0.16, P = 0.0024), and ionized calcium was significantly lower in obese subjects, 1.285 (0.05), than in nonobese subjects, 1.298 (0.05) mmol/l, P < 0.01. Mean daily calcium intake including supplements was not correlated with serum iPTH concentrations (P = 0.18). Mean phosphorus was negatively correlated with iPTH (r = −0.27, P < 0.0001), whereas there was no difference in phosphorus between obese and nonobese subjects (P = 0.9). Alkaline phosphatase was significantly higher in obese subjects, 69.6 (18.5), vs 58.9 (17.0) U/l, P < 0.0001 and was positively correlated with iPTH (r = 0.16, P = 0.002) and with BMI (r = 0.34, P < 0.0001).
Association between serum concentrations of iPTH and 25(OH)D in Black and White subjects (r = −0.31, P < 0.0001).