Genetics

This blog post critically examines a landmark genetic epidemiology study that applies Mendelian randomization to determine whether low circulating levels of 25-hydroxyvitamin D play a causal role in the development of multiple sclerosis. By leveraging genetic variants associated with vitamin D metabolism across large U.S. and Swedish cohorts, the study overcomes key limitations of observational research, including confounding and reverse causation. The findings provide robust evidence that vitamin D deficiency increases susceptibility to multiple sclerosis, while having no measurable effect on disease onset or severity, thereby strengthening the biological and public health rationale for vitamin D–focused preventive strategies in at-risk populations.