Chronic dry eye happens when your tears can’t adequately protect and lubricate the surface of your eyes, either because you don’t produce enough tears or because the tears you make evaporate too quickly. About 20% of the U.S. population has been diagnosed with dry eye disease, and the causes range from gland dysfunction and hormonal shifts to medications, screen habits, and autoimmune conditions.
Two Types of Tear Problem
Your tear film has three layers: an inner mucus layer that helps tears stick to the eye, a watery middle layer that makes up most of the tear volume, and a thin outer oil layer that slows evaporation. Chronic dry eye falls into two broad categories depending on which part of this system breaks down.
The first is aqueous-deficient dry eye, where the lacrimal glands above your eyes don’t produce enough of the watery layer. This type tends to be worst when you first wake up. It can signal an underlying autoimmune condition that, over time, damages the tear-producing glands themselves.
The second, and more common, type is evaporative dry eye. Here, the oil-producing glands in your eyelids (called meibomian glands) aren’t working properly. Without a healthy oil layer on top, your tears evaporate faster than they should. This type typically worsens as the day goes on. Most people with chronic dry eye have some degree of both problems, but evaporative dry eye driven by meibomian gland dysfunction is the dominant pattern.
Meibomian Gland Dysfunction
Your eyelids contain dozens of tiny oil glands that release a thin lipid coating every time you blink. When these glands become blocked or produce thickened, waxy secretions, the oil layer deteriorates and tears break down on the eye’s surface far too quickly. A healthy tear film stays stable for at least 10 seconds between blinks. Below 5 seconds is considered diagnostic of tear film instability.
The blockages happen when the cells lining the gland ducts thicken and harden, a process that accelerates with aging. The oil itself changes in consistency, becoming more like toothpaste than the clear, free-flowing liquid it should be. Over time, chronic inflammation around blocked glands can cause permanent gland loss, creating a cycle: fewer functional glands mean less oil, which means more evaporation, more surface irritation, and more inflammation that damages remaining glands. Rosacea, a skin condition that causes facial redness, is strongly associated with this kind of gland inflammation.
Hormonal Changes
Androgens (including testosterone) play a direct role in keeping meibomian glands healthy. These glands contain androgen receptors, and the hormones help regulate both the quantity and quality of oil they produce. Animal studies show that removing androgen stimulation significantly alters the lipid profile of meibomian glands, while restoring androgens begins to normalize oil composition within weeks.
This explains why dry eye disproportionately affects women, especially after menopause, when androgen levels drop. It also helps explain why people on anti-androgen medications sometimes develop dry eye as a side effect. Interestingly, while androgens also influence the lacrimal (tear-producing) glands, androgen deficiency alone doesn’t appear to cause the watery-layer shortage in people without autoimmune disease. The primary hormonal impact is on oil production.
Screen Use and Blinking
You normally blink about 15 times per minute. During screen use, that drops to 5 to 7 times per minute. Each blink spreads a fresh coat of tears and oil across the eye, so cutting your blink rate by more than half means your tear film is breaking apart long before it gets refreshed. If you spend most of your day on a computer or phone, this reduced blinking adds up to hours of inadequate tear coverage, pushing occasional dryness into a chronic pattern.
The effect compounds in air-conditioned or heated environments, where low humidity speeds evaporation even further. Contact lens wear adds another layer of disruption by destabilizing the tear film and increasing evaporation from the lens surface itself.
Medications That Dry Your Eyes
In older adults, an estimated 62% of dry eye cases can be traced to systemic medications. Several common drug classes reduce tear production or change tear composition:
- Antihistamines, which block the chemical signals that also help stimulate tear glands
- Antidepressants and antipsychotics, which have anticholinergic effects that suppress secretions throughout the body
- Blood pressure medications, including diuretics and beta-blockers
- Anti-anxiety medications, particularly benzodiazepines
- NSAIDs (common over-the-counter pain relievers like ibuprofen)
If you take one or more of these regularly, the cumulative drying effect can be substantial. People on multiple medications are at especially high risk, which is one reason chronic dry eye becomes more common with age.
Autoimmune Conditions
Sjögren’s syndrome is the autoimmune disease most closely linked to chronic dry eye. The immune system attacks the lacrimal and salivary glands, gradually destroying them and causing severe dryness of the eyes and mouth. About 10% of people with dry eye disease have Sjögren’s syndrome, but two-thirds of those cases go undiagnosed, with a typical delay of 10 years before someone gets the correct diagnosis.
That delay matters because Sjögren’s-related dry eye tends to be more severe and progressive than other forms. It can also signal broader autoimmune activity. If your dry eye is persistent, doesn’t respond well to standard treatments, and comes with a chronically dry mouth, that combination warrants specific blood testing. Other autoimmune conditions, including rheumatoid arthritis and lupus, can also affect the tear glands, though less commonly than Sjögren’s.
Aging and Inflammation
Aging affects nearly every part of the tear system. Meibomian glands shrink and drop out over time, a process visible on specialized imaging. Lacrimal gland output gradually declines. The cells on the eye’s surface become less effective at anchoring the tear film. Androgen levels fall. And the likelihood of taking medications that worsen dryness increases with each decade.
Chronic inflammation ties these factors together. Once the eye’s surface is inadequately protected, exposed cells release inflammatory signals. Those signals damage the very glands and surface cells needed to restore a healthy tear film, creating a self-reinforcing loop. This is why chronic dry eye often worsens over time if left unmanaged, and why treatments increasingly focus on breaking the inflammatory cycle rather than simply adding moisture with artificial tears.