The odds of getting obese for individuals who take vitamin D supplementation is lower compared to those who do not.

Studies have found an association between obesity and lower concentrations of serum 25-hydroxyvitamin D (25(OH)D). However, it is still questionable whether the relation is causal or not. If vitamin D levels in the blood are found to reduce body weight, there is a possibility that vitamin D supplementation could potentially be an inexpensive and safe treatment of obesity. On the other hand, in a meta-analysis of randomized controlled trials (RCTs), it was found that vitamin D supplementation is not effective in treating obesity, or improving cardiovascular or metabolic outcomes. As a matter of fact, in some Mendelian randomized studies, it was shown that there is no relationship between genetic variants of having low 25(OH)D status and higher BMI, or risk of type 2 diabetes or other cardiometabolic diseases. This could be explained by a reverse causation relationship with higher body weight, which results in lower serum 25(OH)D concentrations.









It has also been hypothesized that both volumetric dilution and greater sequestration of fat-soluble vitamin D by increased quantities of body fat contribute to the lower circulating vitamin D that was observed in obesity. In fact, several animal and human studies indicated that weight loss, fasting, and exercise have coexisted with an increased in serum 25(OH)D concentrations, which triggers the release of vitamin D from adipose tissue during either the change in volume of fat mass or the turnover of triglycerides for fuel.

Researchers from New Zealand conducted a systemic review and used a meta-analysis of randomized and nonrandomized controlled weight-loss trials to determine if whether weight loss or weight maintenance in humans increases serum 25(OH)D. Also, they hypothesized that if adipose tissue releases vitamin D during lipid mobilization, the amount of weight lost should be proportional to the increase in circulating 25(OH)D. The researchers also further investigated if the relationship between weight change and serum 25(OH)D exists.

They performed a systemic search for controlled weight-loss-intervention studies that were published up to March 31, 2016. One of their main inclusion criteria was that they only included studies that had participants of any age with changes in adiposity as well as 25(OH)D as primary or secondary outcomes. Moreover, the researchers identified 4 randomized controlled trials (n=2554) and 11 nonrandomized controlled trials (n=917).

The findings, published in The American Journal of Clinical Nutrition, showed that random assignment to weight loss compared with weight maintenance resulted in a higher increase in serum 25(OH)D (mean difference 3.11 nmol/L, 95% CI: 1.38, 4.84 nmol/L) between groups. A mean difference of 4.85 nmol/L (95% CI: 2.59, 7.12 nmol/L) was found in nonrandomized trials. However, there was no evidence found for the dose-response effect of weight loss on the change in serum 25(OH)D overall. The authors indicated that vitamin D status might be marginally improved with weight loss rather than in weight maintenance under similar conditions of supplemental vitamin D intake. Their results also supported that the association between obesity and lower serum 25(OH)D might be due to a reversed causation relationship with increased adiposity, which leads to suboptimal concentrations of circulating vitamin D.

Written By: Alexa Deano BSc







