Asian Journal of Research and Reports in Ophthalmology

Vitamins are indispensable to ocular metabolism, yet the clinical meaning of a vitamin–eye association depends strongly on whether the individual is deficient, nutritionally replete, or receiving a pharmacological disease-specific formulation. This critical narrative review evaluates ocular effects of vitamins across that continuum, with emphasis on causal evidence, reversibility, therapeutic relevance, and methodological limitations. Literature published from 1 January 1990 to 13 June 2026 was prioritised, with earlier seminal studies included when essential to deficiency syndromes or landmark supplementation trials. Evidence was synthesised from clinical studies, randomised trials, systematic reviews and mechanistic literature. The most secure causal relationships concern vitamin A deficiency, which impairs the visual cycle and ocular-surface epithelial integrity, and selected B-vitamin deficiencies, particularly thiamine, folate and cobalamin, which can produce neuro-ophthalmic dysfunction. Severe vitamin E deficiency in fat-malabsorption disorders also provides strong, although rare-disease, evidence for retinal injury that can be modified by replacement. By contrast, observational associations involving vitamins C and D frequently exceed the certainty provided by intervention studies. Vitamin C has compelling lens biology and epidemiological signals, but randomised antioxidant trials have not established routine cataract prevention in nutritionally adequate adults. Vitamin D is associated with dry eye disease, diabetic retinopathy, myopia and other ocular outcomes, yet heterogeneity, reverse causation and confounding by outdoor exposure or systemic health complicate causal inference. The Age-Related Eye Disease Study evidence illustrates a separate category: high-dose antioxidant and mineral formulations can slow progression of established high-risk age-related macular degeneration, but this is not evidence that vitamin deficiency causes the disease or that routine supplementation prevents it in healthy populations. The evidence therefore supports correction of documented deficiency, targeted use of validated disease-specific formulations, and restraint against extrapolating physiological necessity into a presumption that additional vitamin intake improves ocular outcomes. Future research should stratify participants by baseline nutritional status, use disease-specific endpoints, report achieved biomarker concentrations and distinguish replacement from supraphysiological supplementation.