Vitamin D for Dry Eyes: Potential Benefits and Mechanisms

Dry eye disease is a common condition that causes discomfort, visual disturbances, and inflammation due to inadequate tear production or poor tear quality. Factors such as aging, environmental conditions, and health issues contribute to its development. While artificial tears and prescription medications are standard treatments, researchers are exploring other therapeutic options.

Vitamin D has emerged as a potential factor in maintaining ocular surface health. Studies suggest it may influence tear production, reduce inflammation, and support overall eye function. Understanding its role could provide new insights into managing dry eye symptoms.

Tear Film Composition and Ocular Surface Cells

The tear film is a multilayered structure essential for ocular surface integrity, lubrication, and clear vision. It consists of three layers: lipid, aqueous, and mucin, each produced by specialized cells and glands. Disruptions in any layer can lead to tear film instability, a hallmark of dry eye disease.

The outer lipid layer, secreted by the meibomian glands, reduces evaporation and maintains surface tension. A deficiency in lipid production accelerates tear film breakup, increasing corneal exposure. The aqueous layer, primarily from the lacrimal glands, hydrates and nourishes ocular cells while containing antimicrobial proteins that protect against infection. The innermost mucin layer, produced by conjunctival goblet cells, ensures even tear distribution by promoting adherence to the cornea.

Ocular surface cells, including corneal and conjunctival epithelial cells and goblet cells, are integral to tear film stability. Corneal epithelial cells form a protective barrier and contribute to tear film spreading. Goblet cells regulate mucin secretion, and their dysfunction is common in dry eye patients. Conjunctival epithelial cells help maintain tear film balance by modulating water and ion transport, influencing tear osmolarity.

Vitamin D Receptor Distribution in Ocular Tissues

Vitamin D exerts its effects through the vitamin D receptor (VDR), a nuclear receptor that regulates gene expression in various tissues, including the eye. The presence of VDR in ocular structures suggests a role in eye health beyond calcium homeostasis and immune function.

Studies using immunohistochemistry and molecular techniques have identified VDR in multiple eye components, particularly in tissues involved in tear production and ocular surface maintenance. The corneal epithelium, which serves as a barrier against environmental insults, expresses VDR in both basal and superficial cells, indicating a role in cell proliferation, differentiation, and wound healing. In the conjunctiva, VDR is present in epithelial cells, suggesting it helps maintain epithelial integrity and modulate responses to external stressors.

VDR is also found in the lacrimal gland, which secretes the aqueous component of tears. Research suggests VDR signaling in lacrimal gland cells may influence tear volume and composition. Additionally, the meibomian glands, responsible for lipid secretion, express VDR, implying a role in modulating lipid production and reducing tear evaporation.

Potential Mechanisms of Vitamin D in Ocular Lubrication

Vitamin D supports ocular lubrication by regulating cellular functions that influence tear stability and hydration. It enhances epithelial integrity by promoting tight junction formation, which helps prevent excessive water loss from corneal and conjunctival tissues. Strengthening these barriers may reduce tear film instability.

Vitamin D also plays a role in aqueous secretion from the lacrimal glands by influencing ion channel activity, which regulates fluid transport. Proper ion balance maintains tear osmolarity, preventing ocular irritation and inflammation. By modulating transport proteins, vitamin D may help maintain a balanced tear composition.

Additionally, vitamin D may impact lipid secretion from the meibomian glands, which produce the tear film’s outer layer. Some studies suggest it influences lipid metabolism, improving meibum quality and consistency. Optimizing lipid production may extend tear film breakup time, reducing evaporation and ocular dryness.

Interactions With Immune Cells in the Eye

Vitamin D regulates ocular immune homeostasis by influencing immune cell activity. The ocular surface is exposed to allergens, pathogens, and oxidative agents, requiring a balanced immune response to prevent excessive inflammation while maintaining tissue integrity. Immune cells such as macrophages, dendritic cells, and T lymphocytes mediate immune surveillance and repair.

Macrophages in the conjunctiva and cornea can adopt pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes. Vitamin D promotes a shift toward the M2 phenotype, associated with tissue repair and reduced inflammation. This shift may be beneficial in conditions where chronic immune activation worsens ocular surface damage.

Dendritic cells, which present antigens, express VDR and respond to vitamin D by reducing maturation and pro-inflammatory cytokine production. By tempering dendritic cell activity, vitamin D may help prevent immune responses that disrupt tear film stability.

T cells, particularly regulatory T cells (Tregs), play a key role in immune tolerance within the eye. Research suggests vitamin D enhances Treg function, promoting an immunosuppressive environment that prevents excessive tissue inflammation. This effect is particularly relevant in dry eye disease, where dysregulated T cell responses contribute to persistent irritation. By fostering immune balance, vitamin D may support tear film stability and ocular surface health.