Diabetic dry eye (DDE) is a common microvascular complication of diabetes that seriously affects quality of life. This review examines the key role of nutrient supplementation and dietary patterns in the prevention and treatment of DDE. This review also focuses on pathological oxidative stress induced by hyperglycemia, which primarily activates the polyol, protein kinase C (PKC), and hexosamine pathways, leading to excessive production of reactive oxygen species (ROS). Excessive ROS, together with pro-inflammatory cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6), further initiates the NF-κB signaling cascade, upregulates intercellular adhesion molecule-1 (ICAM-1)/vascular cell adhesion molecule-1 (VCAM-1), and activates cellular apoptotic pathways and the unfolded protein response. These events damage ocular surface tissues and induce the pathogenesis of DDE. Indeed, regulating the intake of various nutrients, including macronutrients such as carbohydrates, proteins, and fatty acids; micronutrients including vitamins A, D, C, and E, as well as trace such as elements zinc and selenium; bioactive dietary components such as α-lipoic acid (ALA) and phytochemicals including anthocyanins, resveratrol, quercetin, and carotenoids, may help ameliorate metabolic disorders and inflammatory conditions in ocular surface tissues. The Mediterranean diet, which centers on core foods such as vegetables, fruits, whole grains, olive oil, fish, and nuts, is rich in polyphenols, vitamins, minerals, and unsaturated fatty acids. It is hypothesized to alleviate DDE by regulating oxidative stress, inflammatory responses, and systemic metabolism. Owing to the high antioxidant and anti-inflammatory properties of the Mediterranean diet, these food groups constitute represents an ideal dietary pattern for DDE. Although existing research supports the potential of nutritional interventions, several challenges remain. Future studies should further validate these effects through precision nutrition, interdisciplinary collaboration, and long-term clinical investigations to provide a stronger scientific basis for the prevention and treatment of DDE.
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Li et al. (2026) studied this question.
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