Dry eye syndrome happens when your tears can’t adequately protect and lubricate the surface of your eyes. This can mean you’re not producing enough tears, or the tears you do produce evaporate too quickly. Roughly 35% of the global population experiences dry eye, with higher rates in women (about 39%) compared to men. The causes range from hormonal shifts and medications to screen habits and autoimmune conditions, and often more than one factor is at play.
Two Types With Different Root Causes
Dry eye falls into two broad categories, and understanding which one is driving your symptoms matters because the triggers are different.
The more common form is evaporative dry eye, tied to dysfunction in the meibomian glands. These tiny glands line your eyelids and produce the oily outer layer of your tear film. That oil slows evaporation. When the glands become clogged or produce poor-quality oil, tears evaporate off the eye’s surface too fast, even if you’re making plenty of them.
The second form is aqueous tear deficiency, where the lacrimal glands simply don’t produce enough of the watery component of tears. This type is more closely associated with autoimmune conditions that gradually damage those glands. Many people have a combination of both.
The Inflammation Cycle
Whatever triggers dry eye initially, inflammation tends to make it self-sustaining. When tear volume drops or tears evaporate too fast, the remaining fluid becomes saltier (more concentrated). That increased saltiness irritates the cells on the eye’s surface, prompting them to release inflammatory signaling molecules. Key players include IL-1β and TNF-α, both of which correlate with disease severity, along with IL-6, IL-8, and IFN-γ. One of these signals actively promotes cell death and structural changes in the surface tissue of the eye.
The damage from this inflammation further reduces tear quality, which increases saltiness, which triggers more inflammation. This feedback loop is why dry eye often worsens over time if the underlying cause isn’t addressed, and why it can persist even after the original trigger is removed.
Hormones and Why Women Are More Affected
Being female is one of the strongest risk factors for dry eye. Both estrogen and androgens (like testosterone) help maintain the structure and function of the lacrimal glands. When levels of these hormones drop, the glands can begin to deteriorate. Animal research shows that removing the major source of estrogen and androgens triggers cell death in lacrimal gland tissue and even provokes an autoimmune-like inflammatory response, with immune cells infiltrating the gland. Estrogen replacement in these models prevented both the cell death and the immune infiltration.
This is why dry eye symptoms so often appear or worsen during menopause, when estrogen and androgen levels decline significantly. Pregnancy, hormonal contraceptives, and hormone replacement therapy can also shift tear production in either direction. The hormonal connection helps explain why nearly 4 in 10 women globally experience dry eye compared to lower rates in men.
Medications That Reduce Tear Production
A long list of common medications can cause or worsen dry eye. Many of them share a trait: they interfere with a signaling system your glands depend on to secrete tears, mucus, and oils. This is called anticholinergic activity, and it’s found in drugs designed for entirely different purposes.
The medication classes most commonly linked to dry eye include:
- Antihistamines (allergy medications)
- Antidepressants and antipsychotics
- Diuretics (water pills for blood pressure)
- Anti-anxiety medications (benzodiazepines)
- NSAIDs like ibuprofen
- Blood pressure medications (certain vasodilators and beta-blockers)
Some drugs cause dry eye through a completely different mechanism: they’re secreted into the tear film itself and form tiny crystals on the eye’s surface. If you’ve noticed dry eye symptoms starting shortly after beginning a new medication, that timing is worth noting.
Screen Time and Blinking
Your blink rate drops by about 50% when you’re focused on a computer screen compared to general viewing. Each blink spreads a fresh layer of tears across the eye and triggers the meibomian glands to release oil. When you blink half as often, tears evaporate faster and the oil layer thins out. Over hours of screen work, the cumulative effect is significant.
This isn’t limited to computers. Phones, tablets, and any task requiring sustained visual concentration (reading, driving, detailed handiwork) can suppress your blink rate. The difference with screens is how many hours per day most people spend on them. People who use computers heavily also show elevated levels of inflammatory markers in their tears, suggesting that screen-related dry eye isn’t just about momentary discomfort but can drive the same inflammatory cycle seen in other forms of the disease.
Autoimmune Conditions
Sjögren’s syndrome is the autoimmune condition most closely tied to dry eye. The immune system attacks the glands that produce tears and saliva, gradually destroying them. People with Sjögren’s have markedly elevated levels of inflammatory molecules in their tears and in the tissue of the eye’s surface. Diagnosis typically requires blood tests showing specific autoimmune antibodies along with a biopsy of the inner lip to confirm a characteristic pattern of gland inflammation.
Other autoimmune conditions, including rheumatoid arthritis, lupus, and thyroid disease, can also contribute to dry eye through similar inflammatory pathways. If your dry eye is severe, started relatively young, or comes with a persistently dry mouth, an autoimmune cause is worth investigating.
Contact Lenses
Wearing contact lenses disrupts the tear film in several ways. The lens physically sits within the tear layer, splitting it into a thin film above and below the lens. High-water-content lenses, somewhat counterintuitively, tend to cause more dryness because they absorb tear fluid into the lens material, thinning the remaining tear layer on both sides.
The oily layer on top of the tear film also suffers. Research shows that the lipid layer becomes thinner over contact lenses, and by about eight hours of wear, the oil spreads more slowly across the surface. Since that oil layer is what prevents your tears from evaporating, the result is faster moisture loss as the day goes on. This is why contact lens dryness typically worsens toward the end of the day rather than appearing first thing in the morning.
LASIK and Other Eye Surgeries
Dry eye after LASIK is extremely common and results from cutting corneal nerves during the procedure. The cornea is one of the most nerve-dense tissues in the body, and those nerves do more than detect pain. They regulate tear secretion, trigger the blink reflex, stabilize the tear film, and support wound healing. When the corneal flap is created and the underlying tissue is reshaped with a laser, many of these nerve fibers are severed.
Symptoms typically peak between one week and three months after surgery. The corneal nerves do partially regenerate, and most clinical signs of dry eye return to near-normal values within a year. However, some people experience persistent dryness that outlasts what standard tests can detect, likely because the nerve network doesn’t fully restore to its original density.
Vitamin A and Nutritional Gaps
Vitamin A plays a direct role in maintaining the cells on the eye’s surface. Without adequate vitamin A, the eye loses its mucus-producing goblet cells, which create the innermost layer of the tear film (the layer that helps tears stick to the eye). The surface tissue also begins to harden and become rough, a process called keratinization. This combination of lost mucus production, reduced tear output, and an irregular surface leads to severe dryness and, in advanced cases, can damage the cornea even without infection.
Vitamin A deficiency severe enough to cause eye problems is uncommon in wealthy countries but remains a significant issue globally. Even moderate deficiency, particularly in people with absorption issues, restrictive diets, or heavy alcohol use, can contribute to tear film instability. Notably, surface abnormalities from vitamin A deficiency improve quickly with supplementation, well before the goblet cells themselves regenerate.
Environmental Triggers
The environment around your eyes matters more than most people realize. Low humidity (common in air-conditioned offices, airplane cabins, and heated homes in winter) accelerates tear evaporation. Wind has the same effect. Ceiling fans and air vents that blow toward your face during sleep are a surprisingly common contributor to morning dryness.
Air pollution and cigarette smoke introduce irritants that can trigger surface inflammation directly. High altitude environments combine low humidity with increased UV exposure, both of which stress the tear film. Even the position of your screen matters: looking upward exposes more of the eye’s surface to the air than looking slightly downward, increasing the area where tears can evaporate.
Age
Tear production naturally declines with age. The lacrimal glands produce less fluid, the meibomian glands become less effective, and the composition of tears shifts. These changes begin gradually but become more noticeable after age 50, which is also when hormonal shifts in women compound the problem. Interestingly, recent data shows that dry eye is not exclusively a condition of older adults. Prevalence among people 40 and younger is around 35%, likely driven by screen time, contact lens use, and environmental factors. Still, aging remains one of the strongest independent predictors of developing dry eye, and the severity tends to increase with each decade.