Vitamin D status and type 2 diabetes incidence in Finnish adults—a longitudinal survey and register-based study using standardized serum 25-hydroxyvitamin D data
摘要
Improved vitamin D status (serum 25-hydroxyvitamin D; S-25(OH)D) has been recorded among Finnish adults. Whether this change lowers the risk of diabetes is unknown. Our study investigated the associations between improved vitamin D status and long-term type 2 diabetes (T2D) incidence in the Finnish adult population.
MethodsFinnish adults aged ≥ 30 years (n = 3014) in a longitudinal setting (Health 2000/2011 surveys, H2000/H2011) were followed for 8.2 years (2011–2019), and T2D cases were derived from national registers. Multivariable-adjusted Cox regression models were used to assess the associations between S-25(OH)D and incident T2D. S-25(OH)D concentration measurements were standardized according to the Vitamin D Standardization Program protocol.
ResultsDuring the follow-up, 214 T2D incident cases (7%) were recorded. Median (IQR) S-25(OH)D concentration increased from 47.6 (37.1; 57.4) nmol/L in H2000 to 67.2 (60.0; 74.8) nmol/L in H2011. Participants with new incident T2D had lower median (IQR) S-25(OH)D concentrations in H2011 than non-cases [63.97 (57.3; 73.8) vs. 67.2 (60.0; 74.8) nmol/L]. No association between S-25(OH)D concentrations in H2011 and T2D incidence in the whole study sample. Subjects with insufficient vitamin D status (< 50 nmol/L) in H2000 who were in the lowest tertile of S-25(OH)D in H2011 (< 62.8 nmol/L) had a higher T2D risk (adjusted HR 1.61 [95% CI 1.03–2.51]) than those in the highest tertile (> 71.6 nmol/L). Longitudinal changes in S-25(OH)D did not associate with T2D incidence in the whole study sample.
ConclusionThe improved vitamin D status was not associated with T2D incidence in the general follow-up sample. However, vitamin D insufficiency in 2000 (< 50 nmol/L) combined with having S-25(OH)D in the lowest tertile in 2011 (< 63 nmol/L) increased T2D risk. Maintaining an optimal vitamin D status may be protective against T2D.