Hypovitaminosis D is an escalating global health concern, yet high-power baseline mapping of its epidemiological burden across North Africa remains limited. Despite Libya’s abundant solar irradiance, localized studies suggest widespread vitamin D depletion. This study systematically pooled nationwide prevalence, clinical stratifications, temporal trends, and publication bias for vitamin D deficiency in Libya.A random-effects  systematic meta-analysis pooled  data  from  20  observational  studies  across  Western,  Eastern,  and Southern Libya, including 7,167 participants. Deficiency was defined as serum 25-hydroxyvitamin D [25(OH)D] <20 ng/mL. Between-study heterogeneity was explored using univariable and multivariable random-effects meta-regression. Publication bias was assessed with Egger’s regression, Begg’s rank correlation, and  trim-and-fill  analysis.The  pooled  national  prevalence  of  vitamin  D deficiency   was   71.07%   (95%   CI:   64.91%–76.81%),   with   substantial heterogeneity (I² = 96.2%; Cochran’s Q = 502.14; P < 0.0001). Pregnant women showed the highest subgroup prevalence at 80.02% (95% CI: 74.88%–84.31%), while the Southern desert region had the highest regional burden at 75.14% (95% CI: 71.05%–78.83%). Univariable meta-regression identified a significant temporal decline in prevalence (β = -0.041; P = 0.029). The multivariable model explained 24.15% ofbetween-study variance. Bias testing showed no significant funnel plot asymmetry. The findings confirm a Libyan “Mediterranean solar paradox,” where abundant sunlight does not ensure adequate vitamin D status. National prevention should prioritize food fortification, antenatal and pediatric supplementation, and standardized diagnostic assays.

Background: The failure of spontaneous remyelination represents a critical therapeutic barrier in multiple sclerosis (MS) and other demyelinating pathologies. While genetic epidemiological studies have consistently linked Vitamin D Receptor (VDR) polymorphisms to disease susceptibility and severity, the specific cellular mechanisms translating these risk haplotypes into regenerative failure have remained unresolved. Methods: To deconstruct the demyelinated lesion microenvironment, we utilized high-resolution single-nucleus transcriptomics across distinct VDR genotypic cohorts (Risk vs. Wildtype). We integrated topological intercellular communication modelling to map shifts in local cellular crosstalk and employed computational pseudo time trajectory inference to evaluate the direct developmental consequences of genetic risk on the complete oligodendrocyte lineage. Results: Our analysis revealed a profound and targeted transcriptomic collapse of the RXRA heterodimer specifically within the resident microglial compartment of the VDR-Risk cohort. This intrinsic receptor uncoupling functionally neutralized the microglial neuroprotective state, resulting in a near-total cessation of Prosaposin (PSAP) secretion. Trajectory inference demonstrated that oligodendrocyte precursor cells (OPCs) deprived of this critical microglial PSAP-GPR37 trophic signalling axis suffered a severe developmental stall, structurally preventing their terminal maturation into functional, myelin-forming oligodendrocytes. Conclusions: These findings shift the pathophysiological paradigm of VDR genetic risk from generalized neuroinflammation to a highly targeted disruption of microglial oligodendroglia crosstalk. The RXRA-mediated PSAP-GPR37 signalling cascade is identified as a pivotal mechanistic vulnerability, offering a novel, targeted therapeutic pathway to overcome remyelination arrest.

One of the main causes of non-traumatic neurological disability in young adults worldwide is multiple sclerosis (MS), a chronic immune-mediated demyelinating and neurodegenerative disorder of the central nervous system (CNS). Increasing absolute prevalences seen in recent epidemiological trends from 2021 to 2025, while age-standardized rates are stabilizing due to improved diagnostics, survival, and demographic shifts. The current narrative review's objective is to examine high-caliber studies conducted globally between 2021 and 2025 that address the epidemiology, burden, and different risk factors related to multiple sclerosis (MS), with an emphasis on the effects of age, gender, ethnicity, and other interacting factors. Key Findings: Global prevalence of~1.89 million cases in 2021 (age-standardized rate: 23.9 per 100,000), with ~62,000 new cases each year; female-to-male ratio of ~3:1. DALYs are up by 43% from 1990, but with a trend downward for age-standardized rates with advances in management. Incidence is framed by disparities with higher rates for Whites (77% of the U.S.) than Black (10%), followed by Hispanic (7%) cases, and also high levels of radiological severity, handicap, and poor outcomes for ethnic minorities of these groups. Age of peak incidence progresses to older groups for individuals aged 20-40 years. Genetic underpinnings with large effects (e.g., HLA-DRB1*15:01 for ~48% of heritability), strong susceptibility to Epstein-Barr virus infection (near ubiquity at onset; 32-fold increase for molecular mimicry), vitamin D deficiency, smoking, obesity, and altered gut microbiomes are environmental components of risk. Incidence is seen to decline modestly for age-standardized incidence rates, mortality rates, and DALYs through 2035. From this review, the emphasis on MS as a partially preventable disease falls within the context of a rising absolute prevalence and existing inequities in the field. Future complementary strategies should therefore encompass a wide range of populations as well as risk modification measures such as EBV-related therapies and smoking cessation.