The Role of Vitamin D in Nervous System Disorders

Annotation. Vitamin D is a fat-soluble prohormone that plays a critical role in calcium and phosphorus metabolism in the human body, particularly by enhancing their absorption – an essential factor in the process of osteogenesis. It has been reported that vitamin D deficiency affects more than 37% of the global population. This represents a significant threat to vulnerable groups, especially pregnant women and children, as vitamin D is a well-established anti-rachitic factor. In recent years, vitamin D has drawn considerable attention for its non-classical (pleiotropic) effects on the human body. We analyzed over 120 articles from the PubMed database, including experimental rodent models of vitamin D deficiency; meta-analyses demonstrating a direct relationship between vitamin D deficiency and neurodegenerative diseases; large systematic reviews; and original studies illustrating the molecular, genetic, and metabolic effects of the vitamin on the central nervous system (CNS). Our analysis revealed the significant role of vitamin D in CNS function. Alzheimer’s disease, multiple sclerosis, and diabetic neuropathy are the most frequently reported disorders in individuals with low serum vitamin D levels. The physiological effects of vitamin D on the brain include stimulation of neurotransmission, neurogenesis, synaptogenesis, amyloid clearance, and the prevention of neuronal death. Normal vitamin D levels support a range of essential immune functions, including the reduction of neuroinflammation – characterized by increased production of anti-inflammatory cytokines (IL-10) and decreased secretion of pro-inflammatory cytokines (IL-1β, IL-6, and tumor necrosis factor-α). Vitamin D plays an important role in the pathogenesis of multiple sclerosis and is incorporated into its treatment protocols. Both innate and adaptive immune responses require substantial energy for cellular proliferation and differentiation. Vitamin D influences the differentiation of immune cells, particularly monocytes involved in inflammation. According to the literature, low vitamin D levels have been reported in 80-85% of patients with diabetic neuropathy. Its effect on patients with diabetic neuropathic pain appears to be non-specific, primarily linked to the neuroprotective properties of the vitamin. In our opinion, the effects of vitamin D are mediated not only at the metabolic level but also at molecular and genetic levels. Further research is warranted to explore the genetic impact of vitamin D, particularly under conditions of chronic hyperglycemia.