RESEARCH · February 13, 2013
TAKE-HOME MESSAGE
- In adolescents, the correction of poor vitamin D status through dietary supplementation may be an effective addition to the standard treatment of obesity and its associated complications.
Expert Comment
Primary Care
Peter Lin MD, CCFP
It seems that every week another vitamin D study is published. Is it really the panacea for so many medical ills?
Here, two studies look at vitamin D. The first hints at the role of vitamin D in terms of insulin resistance. Of 35 obese adolescents, half were given 4000 IU of vitamin D3 daily for 6 months. Although body mass index, glucose, and inflammatory markers did not change, fasting insulin levels were reduced. The second study measured 25(OH) vitamin D levels in over 9000 German patients and compared death rates. Investigators found that 25(OH)D concentrations < 30 nmol/L were strongly associated with all-cause, cancer, cardiovascular, and respiratory death. PubMed indexes over 1000 articles related to vitamin D deficiency and diseases linking vitamin D to bone health, immune function, cancer, asthma, and cardiovascular disease—and the list goes on and on. So how can a simple vitamin have such huge impact on multiple systems, and is it really the cure-all? Vitamin D has a role beyond that associated with bone health and calcium balance. It binds to VDRs (vitamin D receptors) that are located in the nuclei of many cells, and modulates the transcription and expression of DNA. This is why vitamin D deficiency seems to be associated with so many different organ systems and diseases. Think of it this way: vitamin D is like a caretaker in an office building, who turns on and off lights as necessary, and opens and closes windows and doors throughout the building. If the caretaker—vitamin D—stops working, various systems will operate inefficiently and various diseases will develop. It is not that vitamin D is a cure-all, but when it is deficient, systems fail. If there is not enough vitamin D for the immune system, a person is subject to more infections. Because vitamin D regulates cell growth, not enough may give way to uncontrolled cell growth, and hence the link to cancer. Unfortunately, our vitamin D levels are dropping as we move out of the sun to avoid effects of global warming and cover up to avoid skin cancer. So should we be doing more studies to see what other diseases can be linked to vitamin D deficiency, or should we be investing in ways to improve our vitamin D levels? That may be the more pertinent question to ask. And how much vitamin D do we really need? Not too much to prevent rickets, but a lot more to return to normal immune function. Or maybe we will go back to taking the awful spoonful of cod liver oil; maybe Mom and Grandma did know best. SUMMARY PracticeUpdate Editorial Team Approximately 17% of US adolescents are obese and therefore are at a greater risk of vitamin D deficiency. Poor vitamin D status has been associated with a higher prevalence of the metabolic syndrome and type 2 diabetes mellitus. Lower serum concentrations of 25(OH)D in individuals with excess adiposity are thought to be due to this fat-soluble vitamin’s preferred deposition in fat tissue, thus decreasing its bioavailability. Improving the vitamin D status of individuals with poor or marginal status may have significant benefits involving several health outcomes, including those related to obesity. Cross-sectional studies have reported inverse associations between circulating 25(OH)D concentrations and elevated fasting glucose and insulin levels. However, there is a lack of prospective randomized clinical trials of the effect of vitamin D supplementation on obesity-associated conditions in adolescents. Belenchia and colleagues assessed the efficacy and safety of 4000 IU vitamin D3/day, and examined whether increased circulating concentrations of 25(OH)D improved markers of insulin sensitivity/resistance and reduced inflammation in obese adolescents. The study enrolled 44 participants between the ages of 9 and 19 years. Participants were assigned to either of two study groups: one group received vitamin D3 (2000 IU twice daily) and the other received placebo. Body mass index (BMI) and waist circumference were routinely measured as were circulating 25(OH)D concentrations. BMI and waist circumference were not significantly different between the two groups at 3 and 6 months. Energy and nutrient intakes at baseline and at 6-month follow-up visits were also not significantly different between the groups. At baseline, the mean serum 25(OH)D concentration was 19.4 ± 7.3 ng/mL for all participants. Within 3 months of supplementation, serum 25(OH)D concentrations increased (> 20 ng/mL) such that no participants in the vitamin D group were considered to be vitamin D deficient. In the placebo group, however, 25(OH)D concentrations did not increase significantly from baseline to 3 and 6 months.
A significant reduction in fasting plasma insulin was noted between the two groups after 6 months. Fasting glucose levels remained unchanged. There was a greater decrease in fasting insulin (28.1%) than in fasting glucose (6.1%) relative to baseline. No changes were observed between the study groups regarding glycosylated hemoglobin levels from baseline at either 3 months (P = .321) or 6 months (P = .241).
This study by Belenchia and colleagues demonstrated that a supplement of 4000 IU cholecalciferol/day in obese adolescents safely increases their 25(OH)D concentrations to levels that attenuate the impaired glucose metabolism and insulin resistance associated with obesity. However, the investigators did not find evidence to support their hypothesis that increasing vitamin D status reduces the inflammation that generally accompanies the progression from obesity to impaired glucose metabolism. The investigators concluded that correcting poor vitamin D status with dietary supplements may aid in the standard treatment of obesity and its associated insulin resistance.
The American Journal of Clinical Nutrition
Correcting Vitamin D Insufficiency Improves Insulin Sensitivity in Obese Adolescents: A Randomized Controlled Trial
Am J Clin Nutr 2013 Feb 13;97(4)774-781, AM Belenchia, AK Tosh, LS Hillman, CA Peterson