Vitamin D Deficiency Tied to Diabetes in Obese Children
December 9, 2011 — Obese children who skip breakfast and drink soda are more likely to have low vitamin D levels, which may put them at greater risk for type 2 diabetes, according to a cross-sectional study published online November 9 in the Journal of Clinical Endocrinology & Metabolism.
The study, conducted by Micah L. Olson, MD, from the Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, and colleagues, also showed that obese children are more likely to be deficient in vitamin D and that low vitamin D levels were associated with insulin resistance.
Researchers measured serum 25 hydroxyvitamin D [25(OH)D] levels in 411 obese children, aged 6 through 16 years, and 87 nonoverweight children. The obese children were recruited from the Center for Obesity and its Consequences on Health at Children’s Medical Center Dallas, and were matched by age, season of data collection, and ethnicity with nonoverweight children who were recruited from the Endocrinology Center at Children’s Medical Center, Dallas, for congenital hypothyroidism, but who were otherwise healthy.
Obese children were more likely to have insufficient vitamin D levels (odds ratio [OR], 4.0; 95% confidence interval [CI], 2.3 – 6.9), after adjustment for age, ethnicity, and season of data collection. Fifty percent of the obese children and 22% of the healthy-weight children had vitamin D levels lower than 50 nmol/L (20 ng/mL), which was considered insufficient in this study.
Of the obese children, 134 (33%) reported routinely skipping breakfast, which is a strong predictor of vitamin D deficiency. “The two strongest predictors of decreased vitamin D levels were skipping breakfast (p < 0.001) and soda intake (p < 0.001.),” the authors write.
Children with low levels of vitamin D were also more likely to show signs of insulin resistance in a homeostasis model assessment of insulin resistance (HOMA-IR; r = −0.19; P = .001), as well as in 2-hour glucose testing (r = −0.12; P = .04), adjusted for body mass index and age.
“Our study found that obese children with lower vitamin D levels had higher degrees of insulin resistance,” Dr. Olson said in a press release. “Although our study cannot prove causation, it does suggest that low vitamin D levels may play a role in the development of type 2 diabetes.”
Earlier studies had uncovered the association between obesity and vitamin D deficiency in adults, adolescents, and children, and several (but not all) studies have shown that lower vitamin D levels are associated with impaired glucose tolerance or type 2 diabetes, the authors write. However, this study is one of the first to show a connection between diet and vitamin D deficiency.
“The associations in our study between decreased 25(OH)D and soda intake and skipping breakfast have not, to our knowledge, been previously reported, and they lend support to poor dietary habits playing a role in lower 25(OH)D levels seen in obese children,” the authors write.
Obese children in this study had a body mass index above the 95th percentile for age and sex, based on 1963 to 1994 norms, which now includes some 19% of US children aged 6 through 19 years.
In the obese children, investigators recorded vitamin D levels, blood pressure, dietary information, fasting glucose and insulin, 2-hour glucose from oral glucose tolerance testing, hemoglobin A1c, and HOMA-IR. Only height, weight, blood pressure, and vitamin D levels were measured in nonoverweight children.
The definitions for vitamin D deficiency in this study differ from Institute of Medicine (IOM) recommendations, which were published after the analyses for this study were completed, the authors write. Under IOM recommendations, deficiency is considered to be levels lower than 30 nmol/L (12 ng/mL), and vitamin D is judged inadequate at 30 to 50 nmol/L (12 – 20 ng/mL). Using the IOM definition, 52 of the 411 obese children (12.7%) in this study were vitamin D deficient, and 3 of the 87 nonoverweight children (3.4%) were deficient.
The study was supported by the National Institutes of Health in the form of statistical assistance. The authors have disclosed no relevant financial relationships.
J Clin Endocrinol Metabol. Published online November 9, 2011. Abstract