Vitamin D supplementation enhanced mitochondrial function, lessened fatigue
MONTREAL — Vitamin D supplementation in otherwise deficient patients enhances mitochondrial function and decreases symptoms such as fatigue, according to research presented at the annual meeting of the Canadian Pediatric Endocrine Group.
“We know that mitochondria is considered like the battery of the cell and makes most of the energy that our bodies use for day-to-day activities,” Akash Sinha, MBBS, MRCPCH, MD, a fellow at BC Children’s Hospital in Vancouver, Canada, said. “We wanted to see if the fatigue and myopathy that vitamin D-deficient patients report could be because of suboptimal mitochondrial function and if correction of their vitamin D deficiency would lead to a corresponding enhancement in their muscle mitochondrial function.”
The study, conducted at Newcastle University in the United Kingdom, looked at the effect of cholecalciferol therapy in 12 symptomatic patients (mean age, 34 years). The patients were significantly vitamin D deficient with serum 25-hydroxyvitamin D measuring 8.8 nmol/L. Investigators used dynamic phosphorus-31 magnetic resonance spectroscopy to measure phosphocreatine recovery kinetics, which is a surrogate for mitochondrial oxidative function, after patients engaged in moderate exercise.
Investigators observed a significant difference in phosphocreatine recovery half-time after vitamin D oral supplementation. Coupled with this suggestion of enhanced maximal oxidative phosphorylation, there were improved mean serum 25-(OH)D levels (P<.001). All 12 patients reported an improvement in fatigue after vitamin D therapy.
“This shows for the first time that vitamin D deficiency, when corrected, can lead to an improvement in mitochondrial function,” Sinha said. “There is a link between vitamin D and mitochondria of human muscle.”
The relationship may also explain the role of vitamin D in extraskeletal diseases, according to Sinha.
Although the study was not conducted in a pediatric population, Sinha said the findings can possibly be extrapolated to pediatric patients, and future research will be conducted on them. – by Louise Gagnon
For more information:
Sinha A. Oral Abstract 10. Presented at: Canadian Pediatric Endocrine Group 2014 Scientific Meeting; Feb. 20-22, 2014; Montreal.
Disclosure: Sinha reports no relevant financial disclosures.