Dry Eye Disease (DED) is a chronic condition characterized by insufficient lubrication or instability of the tear film, leading to discomfort and potential vision issues. This condition disproportionately affects women, who are nearly twice as likely as men to develop it. The disparity is pronounced in older women, especially following menopause. Biological, immunological, and external factors contribute to this difference, making the female ocular surface uniquely vulnerable.
The Central Influence of Sex Hormones
The most significant factor contributing to the sex difference in DED prevalence is the distinct role and fluctuation of sex hormones, particularly androgens and estrogen. Androgens, like testosterone, are crucial for the function of the meibomian glands, specialized sebaceous glands that secrete the oily layer of the tear film. This lipid layer prevents the rapid evaporation of the aqueous component of tears.
Women naturally have lower levels of androgens than men, and this level drops dramatically during and after menopause. This reduction in androgen signaling leads directly to Meibomian Gland Dysfunction (MGD). MGD causes the oil quality to degrade and the glands to become blocked, which is the leading cause of evaporative dry eye. Hormone receptors for androgens and estrogens are present on the lacrimal glands, meibomian glands, and the ocular surface.
The role of estrogen is more complex, as both high and low levels can be linked to tear film issues. While the post-menopausal decline in estrogen affects tear production and quality, high estrogen states (such as during pregnancy or with some oral contraceptives) can also be associated with DED symptoms. The overall hormonal environment, including the ratio of androgens to estrogens, influences the stability and composition of the tear film. This endocrine environment is a primary driver of the elevated risk for dry eye in women.
Higher Prevalence of Autoimmune Drivers
The female immune system’s predisposition to autoimmune conditions provides another explanation for the increased incidence of DED. Approximately 78% of all individuals affected by autoimmune diseases are women. This systemic inflammation frequently extends to the eyes, which are susceptible to immune-mediated damage.
The most direct link is Sjögren’s Syndrome, a chronic autoimmune disorder that targets moisture-producing glands, including the lacrimal glands. This disease results in severe aqueous-deficient dry eye and overwhelmingly affects women, who account for over 90% of all cases. Other systemic autoimmune diseases common in women, such as Lupus and Rheumatoid Arthritis, are also strongly associated with dry eye development.
These conditions cause chronic inflammation that damages the tear-secreting glands, reducing the production of the watery layer of tears and altering the tear film composition. The systemic inflammatory state contributes to chronic inflammation of the ocular surface. For many women, DED is a manifestation of a broader, underlying immune system condition.
Medications and Environmental Factors
Certain medications and lifestyle practices act as external influences on DED risk. Many drugs frequently prescribed to women have dry eye as a known side effect, including certain antidepressants and anti-anxiety medications. These drugs interfere with nerve signals that stimulate tear production, decreasing the watery component of the tear film.
Hormone-based medications, particularly hormonal replacement therapy (HRT) and oral contraceptives, are also factors. Studies suggest that HRT, especially estrogen-only formulations, can disrupt tear film stability and increase DED risk in postmenopausal women. Oral contraceptives can lower androgen levels, indirectly affecting meibomian gland function.
Cosmetic use, especially eye makeup, presents an external risk. Applying products like eyeliner and mascara near the eyelid margin can physically block the openings of the meibomian glands. This blockage leads to MGD and evaporative dry eye, as protective oils cannot be released onto the ocular surface. Makeup removers can also introduce ingredients toxic to meibomian gland cells, contributing to dysfunction.