Lower serum vitamin D levels were frequently associated with higher myopia prevalence and longer axial length in pediatric, adolescent, and young adult patients, although a narrative review suggested that vitamin D may primarily reflect outdoor exposure rather than act as an independent causal factor in refractive development.
The review, published in Journal of Clinical Medicine, also found that omega-3 polyunsaturated fatty acids (PUFAs) had the strongest evidence among the nutritional factors assessed, with the researchers characterizing omega-3 PUFAs as a probable protective factor against myopia.
Researchers reviewed human studies examining vitamin D, vitamin A, zinc, selenium, omega-3 PUFAs, and refined carbohydrates in relation to myopia development and progression. The search was conducted on January 15, 2026, and focused on clinical and epidemiologic studies published between 2015 and 2026, with earlier studies included selectively for mechanistic context.
Searches of PubMed, Scopus, and Web of Science identified 142 records, of which 18 studies were included in the final qualitative synthesis. Included studies comprised cohort, cross-sectional, case-control, and Mendelian randomization analyses evaluating refractive error, axial elongation, myopia prevalence, and myopia progression.
Several observational studies found that patients with myopia had lower serum 25-hydroxyvitamin D concentrations compared with nonmyopic controls. Cross-sectional analyses also demonstrated inverse dose-response associations between vitamin D levels and myopia prevalence, and one study found that each 25 nmol/L increase in serum vitamin D level was associated with a 35% reduction in the odds of myopia.
However, the researchers emphasized that the evidence does not establish a direct causal role for vitamin D. A prospective Taiwanese birth cohort study found no association between vitamin D levels measured from birth through early childhood and subsequent myopia development or axial length. The review noted that educational intensity, near-work exposure, and limited outdoor activity may account for previously reported associations between vitamin D status and refractive outcomes.
Genetic evidence also challenged a causal interpretation. Studies of vitamin D pathway genes, including vitamin D receptor polymorphisms, have not demonstrated consistent associations with myopia. Large genome-wide association studies of refractive error have identified loci related to retinal signaling, extracellular matrix remodeling, and ocular development, but have not consistently implicated vitamin D metabolic or signaling pathways.
Evidence supporting outdoor exposure as a protective factor was more consistent. In one cross-sectional study of school-aged children born preterm, greater time spent outdoors remained associated with significantly lower odds of myopia following adjustment for near-work activity, parental myopia, and serum vitamin D levels, whereas vitamin D concentrations themselves were not associated with refractive error. Additional longitudinal data linked more time outdoors during childhood with lower myopia risk in early adulthood.
Among dietary factors, omega-3 PUFAs showed the strongest nutritional signal. One cohort study found that children with higher dietary eicosapentaenoic acid intake had lower odds of high myopia. Mendelian randomization data also suggested that genetically predicted higher omega-3 PUFA levels were associated with lower myopia risk and refractive shifts toward hyperopia. Additional observational studies linked lower omega-3 intake with longer axial length and more myopic refraction in children.
Evidence for vitamin A, zinc, selenium, and refined carbohydrates was less consistent. Some studies associated lower serum retinol, zinc, or selenium levels with high myopia, while others found no statistically significant relationship following adjustment for environmental and lifestyle variables. Studies evaluating refined carbohydrates reported associations between higher intake and greater myopia prevalence, although proposed insulin-mediated mechanisms remain hypothetical.
The researchers emphasized that most available evidence was observational, limiting causal inference. The review was narrative rather than systematic, did not include a formal risk-of-bias assessment or registered PRISMA-guided protocol, and included studies with heterogeneous exposure measurements, study designs, and outcome definitions.
Clinically, the review does not support vitamin D testing or nutrient supplementation specifically for routine myopia prevention or control. Instead, the findings support interpreting nutrition within a broader behavioral and environmental framework, particularly outdoor exposure, near-work patterns, and overall metabolic health.
“Overall, the current literature does not support specific nutritional interventions as standalone strategies for myopia control,” wrote Zuzanna Bomze, of the Medical University of Warsaw, and colleagues.
Disclosures: The researchers reported no external funding and declared no conflicts of interest.
Source: Journal of Clinical Medicine
