Type 2 diabetes mellitus (T2DM) is an escalating public health problem in Africa with projections of large increases in affected adults. Despite abundant sunlight across the continent, studies report variable but sometimes high rates of vitamin D deficiency (VDD). Vitamin D has been implicated in glucose homeostasis through effects on immune modulation, inflammatory cytokines, insulin secretion, and insulin sensitivity. Genetic variants in the vitamin D receptor (VDR) such as FokI may modify vitamin D’s metabolic effects. The evidence on VDD prevalence and VDR genetic associations specifically among African people with T2DM was heterogeneous and limited, motivating this systematic review and meta-analysis.
The review protocol was registered in PROSPERO (CRD420251134616). The authors followed Joanna Briggs Institute (JBI) methodology for prevalence and etiologic reviews and adhered to PRISMA 2020 reporting standards. Data extraction and quality assessment procedures were applied consistently across included studies.
Comprehensive searches of PubMed, Cochrane Library, ScienceDirect, Embase, Web of Science, and Google Scholar were conducted for observational studies published up to June 11, 2025. Eligible designs included cross-sectional, case–control, and cohort studies reporting VDD prevalence, mean vitamin D levels, or data enabling calculation of mean differences (MD) or odds ratios (OR). Studies reporting genetic associations—particularly VDR variants—were also eligible. Articles without original data, small case series (<50 participants), animal or in vitro studies, and reports lacking sufficient effect-size data were excluded.
Two independent reviewers screened titles and abstracts and assessed full texts against predefined criteria; discrepancies were resolved through discussion or a third reviewer. The review reports use of JBI tools for methodological quality assessment. The selection process is summarized in a PRISMA flow diagram reported in the original article.
Primary outcome was pooled prevalence of VDD among African individuals with T2DM. Secondary outcomes included the association of VDD with glycemic control (measured as mean difference in HbA1c between deficient and sufficient groups) and the association between VDR gene variants and T2DM risk (reported as ORs). Random-effects meta-analysis was used to pool prevalence, MDs, and ORs. Analyses included heterogeneity assessment (I2), publication bias evaluation, sensitivity analyses, and meta-regression. Statistical analysis was conducted using R v4.3.1.
Twenty-two studies met eligibility criteria, comprising 3,447 participants across 11 African countries. The pooled prevalence of vitamin D deficiency among people with T2DM was 51% (95% CI: 36–65%). Heterogeneity across prevalence estimates was substantial (I2 = 95.7%). Subgroup analyses by region found the highest pooled prevalence in East Africa (56%). Details on individual study settings, assay methods, and population characteristics are provided in the source manuscript.
When comparing vitamin D–deficient to vitamin D–sufficient participants, deficient individuals had higher HbA1c: pooled mean difference = 0.89% (95% CI: 0.06–1.72; p = 0.044). This HbA1c comparison exhibited no heterogeneity (I2 = 0%). Pooled analysis of the VDR FokI polymorphism did not show a statistically significant association with T2DM risk (OR = 1.51; 95% CI: 0.23–9.73). The authors report no evidence of publication bias across the included studies.
Prevalence estimates showed very high heterogeneity, prompting subgroup and sensitivity analyses; the HbA1c comparison showed no heterogeneity. Meta-regression and other exploratory analyses were performed as reported, and no publication bias was detected using standard assessments described in the article.
The pooled estimates indicate that vitamin D deficiency is common among African adults with T2DM, and deficiency associates with worse glycemic control as reflected in higher HbA1c. However, the evidence linking the VDR FokI polymorphism to T2DM risk remains insufficient and inconclusive. High between-study heterogeneity for prevalence estimates limits the precision of pooled prevalence and suggests variability in study populations, assays, geographic factors, and study designs. The authors emphasize that while associations with glycemic control were observed, causality cannot be inferred from the available observational data.
VDD appears highly prevalent in African populations with T2DM and is associated with higher HbA1c. Current genetic evidence, specifically for the VDR FokI polymorphism, does not support a clear relationship with T2DM risk. The authors call for well-designed interventional trials to determine whether improving vitamin D status leads to better glycemic outcomes. Based on available data, the review concludes that routine screening or universal supplementation for people with T2DM in Africa is premature.