Fixing A Broken Vitamin D Status
The saying goes “if it ain’t broke, don’t fix it”. In other words, don’t expect something that’s already in good shape to get better when you try to tinker with it. Common sense tells us that tightening a screw that’s already tightened won’t help matters, yet we routinely fail to follow this same logic in nutrition intervention trials. Why do we continue to measure the impact of giving vitamins to people who are already replete and then expect to see results?
Inspired by observations that both vitamin D deficiency and endothelial dysfunction are both observed among obese children, Javed and colleagues sought to determine whether supplementation with Vitamin D (100,000 IU/month for 3 months) improved flow-mediated dilation (FMD), a marker of vascular health. Unfortunately, however, no significant change in FMD was observed, yet serum vitamin D (25-hydroxyvitamin D3) increased from 55.9 to 86.9 nmol/L over the course of the study.
Wait a minute…wasn’t the whole rationale and inspiration behind this study to determine whether correcting deficient/insufficient vitamin D status would improve health? Remember that according to the Institute of Medicine, a serum 25(OH)D concentration of 50 nmol/L is considered to be an adequate status. So if participants were already sufficient at the start of the study (remember, average baseline vitamin D concentration was 55.9 nmol/L), why would we expect a benefit to occur by providing more than 160x the current RDA (600 IU)? The authors address this briefly, sharing that 6 participants had serum vitamin D concentrations below 50 nmol/L (about 1/3rd of their study population) and stating “We also acknowledge the small number of participants with 25(OH)D <50 nmol/L in our study, particularly considering that the Institute of Medicine 2011 report concluded that 25(OH)D levels of 50 nmol/L cover the requirements of at least 97.5% of the population”. (Side note: even though they acknowledge that the majority of their study population had adequate vitamin D concentrations to start in the actual manuscript, lead study investigator Dr. Seema Kumar states three times in a YouTube video discussing the study which has widely been shared by media outlets that the participants had low vitamin D concentrations to start, which was simply not the case.) Regardless, it would have been interesting to see whether a difference in FMD was observed among those six participants who actually had a low vitamin D status at baseline, however with such a small sample size that may be difficult.
I applaud Javed and colleagues for considering vitamin D status in their study design, which is certainly not always the case. Where I think they went astray, however is that they failed to base their recruitment on a nationally recognized standard for adequacy, namely the 50 nmol/L cutoff defined by the IOM. In effect, because the vitamin D status of these teens wasn’t broken, “fixing” it wasn’t going to change much. Nevertheless, this study doesn’t change what we already know: that teens and adults alike need 600 IU of vitamin D every day to support bone health, and more than 90% of Americans do not get enough vitamin D from food alone.
Javed A, Kullo IJ, Balagopal PB, Kumar S. Effect of vitamin D3 treatment on endothelial function in obese adolescents. Pediatr Obes 2015; epub ahead of print.
Fulgoni VL 3rd, Keast DR, Bailey RL, Dwyer J. Foods, fortificants, and supplements: Where do Americans get their nutrients? J Nutr 2011; 141(10): 1847-1854.