Dry eye happens when your tears evaporate too quickly or your eyes don’t produce enough tears to stay lubricated. The evaporative type accounts for the vast majority of cases, driven by problems with the oil glands in your eyelids. But the full picture involves everything from hormones and medications to how often you blink at a screen.
Two Types of Tear Problems
Your tear film has three layers: an oily outer layer, a watery middle layer, and a mucus layer that helps tears stick to the eye’s surface. Dry eye falls into two broad categories based on which part of this system breaks down.
Evaporative dry eye is by far the more common form. It happens when tiny oil glands along your eyelid margins, called meibomian glands, stop working properly. These glands produce the oily outer layer of your tear film, which slows evaporation. When the oil is reduced or changes in quality (becoming thicker and more viscous), tears evaporate too fast, leaving the eye’s surface exposed. This triggers a cycle: the remaining tears become overly concentrated with salt, which irritates the surface, causes inflammation, and kills cells that help maintain healthy tears. Over 85% of dry eye cases involve this type of oil gland dysfunction.
Aqueous deficient dry eye is less common. Here, the lacrimal glands above each eye simply don’t produce enough of the watery component of tears. This type is often linked to autoimmune conditions that damage the glands directly.
Screen Time and Blinking
Every full blink spreads a fresh layer of tears and oils across the eye’s surface. When you stare at a screen, your blink rate drops dramatically. In a relaxed state, the average person blinks about 22 times per minute. While reading on a screen, that drops to around 7 blinks per minute. Even playing a simple computer game cuts blink rate by roughly 42% compared to resting.
It’s not just that you blink less. The blinks you do make tend to be incomplete, meaning your upper eyelid doesn’t fully close. One study found that 80% of blinks were already incomplete at baseline, but that number climbed to 92% during video game play. Incomplete blinks fail to distribute tears properly, especially across the lower portion of the eye. Over hours of daily screen use, this combination of fewer and shallower blinks accelerates tear evaporation and can kick off chronic dryness.
Reading a physical book also reduces blink rate compared to rest, but screens appear to make the problem worse. In one comparison, incomplete blinks were 7% of all blinks while reading on a computer versus about 4% while reading a printed page.
Aging and Hormones
Dry eye becomes increasingly common with age. In people over 40, prevalence reaches above 50%, and by age 71 and older it climbs to roughly 67%. Women are affected more often than men at every age, and the gap widens after menopause.
Sex hormones play a direct role in how well both the lacrimal glands and meibomian glands function. The oily tear film layer is thinner and less effective in older adults, particularly in women. Declining androgen levels appear especially important: androgens help regulate gland function and reduce inflammation. After menopause, both estrogen and androgen levels drop, and dry eye symptoms frequently increase. Women taking oral contraceptives and those who have had their ovaries removed also show higher rates of lacrimal gland problems, even though their estrogen levels vary. Estrogen itself has a complicated relationship with tear production. At low doses it may protect gland cells, while at higher levels it can actually promote inflammation.
Autoimmune and Systemic Diseases
Several conditions cause the immune system to attack the glands responsible for tear production. Sjögren’s syndrome is the most strongly associated with dry eye. In Sjögren’s, immune cells infiltrate and gradually destroy the lacrimal glands, leading to severe, persistent dryness of both the eyes and mouth.
Other autoimmune and inflammatory conditions frequently linked to dry eye include rheumatoid arthritis, lupus, scleroderma, and graft-versus-host disease (a complication of bone marrow transplants). In these conditions, lacrimal gland damage from chronic inflammation is the primary driver. Some patients have one of these conditions alongside Sjögren’s, compounding the dryness.
Diabetes also increases dry eye risk through a different mechanism. Elevated blood sugar over time can damage the small nerves that signal the lacrimal glands to produce tears, similar to how diabetes affects nerves in the hands and feet. Parkinson’s disease is another systemic condition associated with dry eye, likely due to reduced blink rate and changes in nerve signaling.
Medications That Reduce Tear Production
A number of common drug classes interfere with tear production as a side effect. Antihistamines are among the most well-known culprits. They work by blocking a chemical messenger that, among other functions, helps stimulate fluid secretion from glands, including the lacrimal glands. Antidepressants, particularly older tricyclic types, have a similar drying effect. Blood pressure medications, corticosteroids, and some anti-inflammatory drugs can also contribute. If you take any of these and notice persistent eye dryness, the medication may be a contributing factor worth discussing with your prescriber.
Environmental Triggers
Your surroundings have a measurable impact on how fast tears evaporate. Low humidity is one of the biggest environmental drivers. When humidity drops below 20%, the air pulls moisture from the tear film much faster than your glands can replace it. Wind and dust compound the effect by physically disrupting the tear layer. High temperatures also accelerate evaporation. Air conditioning and forced-air heating create the same low-humidity conditions indoors, which is why many people notice dry eye symptoms worsening in climate-controlled offices or during winter months when heaters run constantly.
Ultraviolet radiation from sun exposure can also damage the eye’s surface over time, contributing to tear film instability. People who work outdoors in hot, dry, or windy conditions face a combination of all these factors simultaneously.
Eye Surgery
LASIK is one of the most common triggers for dry eye, and virtually all patients experience some degree of dryness immediately after the procedure. The primary reason is nerve damage. Creating the corneal flap during LASIK severs a dense network of sensory nerves in the cornea. These nerves normally signal the brain to trigger tear production and blinking. When they’re cut, both reflex tearing and blink rate decrease, and the eye’s surface dries out.
Additional damage from the suction device used during surgery can destroy mucus-producing cells on the eye’s surface, and postoperative inflammation further disrupts normal tear function. The good news is that for most people, this is temporary. Corneal nerves gradually regenerate, and tear production and quality typically return to pre-surgery levels within 6 to 12 months. A small percentage of patients, however, develop chronic dry eye that persists well beyond a year.
Nutritional Deficiencies
Vitamin A plays a critical role in maintaining the health of the cells that line the eye’s surface. It supports the normal growth and specialization of these cells, including the goblet cells that produce the mucus layer of the tear film. Severe vitamin A deficiency leads to a condition called xerophthalmia, where the eye’s surface dries out, thickens, and can eventually ulcerate or scar. While this is rare in developed countries, milder deficiencies can still contribute to tear film instability. Dietary imbalances in omega-3 and omega-6 fatty acids have also been linked to dry eye, as these fats influence inflammation levels on the eye’s surface and the quality of the oil produced by meibomian glands.
Contact Lens Wear
Contact lenses sit directly on the tear film and can disrupt its structure. The lens divides the tear film into a thin layer above and below, which increases evaporation from the front surface. Lenses also reduce corneal sensitivity over time, meaning the eye becomes less responsive to dryness signals that would normally trigger more tear production and blinking. Long-term contact lens wearers frequently develop symptoms that overlap significantly with dry eye disease, particularly toward the end of the day as lens-related evaporation accumulates.