Age, Hormones and Dry Eye

Age is one of the established risk factors for dry-eye disease. But aging does not affect just one component of the tear system. Over time, changes can occur in multiple structures involved in maintaining the ocular surface. These can include changes in:

• •tear secretion
• •meibomian gland structure and function
• •eyelid anatomy and blinking
• •corneal sensitivity and innervation
• •ocular-surface cells
• •inflammatory regulation

At the same time, older people are more likely to use medications and have systemic diseases that can also influence the ocular surface. So when dry eye appears at 55, 65 or 75, age itself may be relevant, but age is not a mechanism. We still need to determine what has actually changed.

Medications and Dry Eye

Systemic Conditions and Dry Eye

Sex differences in dry-eye disease have been recognized for years. Part of this appears to involve sex hormones. The ocular surface is hormonally responsive tissue. Receptors for sex steroids have been identified in tissues including the lacrimal and meibomian glands and corneal and conjunctival epithelia.

But this does not mean that dry eye in women can simply be explained by estrogen. In fact, one of the most interesting things about this area of research is how complicated the hormonal effects appear to be.

Menopause involves substantial changes in the hormonal environment, including declining ovarian production of estrogen and progesterone and changes in androgen activity. At roughly the same period of life, the prevalence of dry-eye disease increases. That association is well established. But separating the effects of:

• •menopause
• •normal aging
• •sex-hormone changes
• •medications
• •and other health changes

is much more difficult. So menopause can be an important part of someone’s dry-eye history without automatically identifying the exact ocular mechanism.

This is where the simple hormonal explanation begins to fall apart. If low estrogen were simply the cause of postmenopausal dry eye, we might expect estrogen replacement to consistently improve it. But that is not what research has shown.

In the large Women’s Health Study involving more than 25,000 postmenopausal women, hormone therapy was actually associated with a greater likelihood of dry eye, particularly with estrogen-only therapy. Women using estrogen alone had an adjusted odds ratio of 1.69 for diagnosed dry eye or severe dry-eye symptoms compared with women who were not using hormone therapy. That does not prove that estrogen causes dry eye. It was an observational study, and hormone therapy users may differ from non-users in other important ways. But it clearly tells us that the following is not a reliable model:

low estrogen→dry eye→replace estrogen→dry eye improves

So is estrogen good or bad for the ocular surface? We do not have a simple answer. Estrogen receptors are present in ocular-surface tissues, and estrogen can influence epithelial cells, inflammation, tear production and meibomian gland biology.

But clinical studies of hormone therapy have produced inconsistent results. For example, a small randomized placebo-controlled trial found that estrogen treatment actually increased dryness symptoms compared with placebo, while testosterone and combined therapy produced different findings. Other studies have reported possible improvements in some tear parameters with hormone therapy. So estrogen cannot reasonably be labelled simply “good for dry eye” or “bad for dry eye.” Its effects appear to depend on a much more complicated hormonal and biological context.

Androgens are particularly interesting in dry-eye research because of their relationship with the meibomian glands. These glands are hormonally responsive. Androgen signalling appears to support meibomian gland function and lipid production, and androgen deficiency has long been investigated as a possible contributor to MGD and evaporative dry eye. This may help explain why hormonal changes later in life can influence the lipid-producing system of the eyelids.

But even here, we should avoid jumping from mechanism to diagnosis. Finding MGD in a postmenopausal woman does not prove:

“Low testosterone caused her MGD.”

MGD itself is multifactorial. Age, blinking, inflammation, eyelid disease, medications, environmental exposure and other factors can also contribute.

Meibomian Gland Dysfunction (MGD) — coming soon

Usually, a dry-eye diagnosis alone does not tell us that a systemic sex-hormone panel will identify its cause. This is an important distinction. Hormones influence the ocular surface at a biological level. But that does not mean that a single blood measurement of estrogen or testosterone can tell us why someone’s tear film is unstable.

Hormonal activity at a tissue level is influenced by much more than the serum concentration of one hormone. So normal hormone blood tests do not mean hormones have no influence on the ocular surface, and an abnormal hormone result is not automatically the explanation for the dry eye. Testing may of course be appropriate for other medical reasons, but that is a separate question.

At present, hormone replacement therapy should not be viewed as a straightforward dry-eye treatment. Research is inconsistent. Some studies have reported improvements in certain tear measurements, while others have found no meaningful benefit or an association with worse symptoms. This is particularly important because HRT is a systemic medical treatment with its own indications, benefits and risks.

The decision to use it should therefore be based on the broader medical situation, not simply on the assumption that replacing hormones will fix dry eye.

Androgen-based therapies are an interesting area of research, particularly because of the biological relationship between androgens and the meibomian glands. Small clinical studies and reviews have reported potentially beneficial effects of topical or systemic androgen approaches in some patients. But this remains an evolving area. It would be premature to conclude that MGD equals androgen deficiency, or that testosterone is an established treatment for MGD. Biological plausibility and early clinical evidence are not the same as having a well-established treatment supported by large, high-quality trials.

Pregnancy is another interesting example because it produces enormous hormonal changes without being a disease. Some women develop or notice more dry-eye symptoms during pregnancy. A 2025 review found reports of dry eye affecting approximately 20–50% of pregnant women, particularly during the second and third trimesters. Proposed mechanisms include changes in estrogen, progesterone, androgens and other metabolic and immune processes.

But there is an important caveat. The same review notes that current consensus evidence has not established pregnancy as a confirmed dry-eye risk factor, and the available evidence remains inconclusive. That is a perfect example of why hormonal dry eye should be discussed carefully. There may be a plausible mechanism. There may be an observed association. That does not automatically establish causality.

Hormonal contraceptives also alter the sex-hormone environment, so their potential relationship with dry eye has been investigated. Some studies have reported associations with ocular-surface symptoms or changes, while others have not shown a clear effect. Again, the answer cannot be reduced to:

“The pill causes dry eye.”

Different contraceptives contain different hormones and doses, and individual hormonal responses vary. If symptoms clearly began or changed after starting or changing hormonal contraception, that timeline can be useful information. But it is still only one part of the investigation.

Yes, and this is probably one of the most important connections for our dry-eye guide. Meibomian glands are not passive tubes that simply contain oil. They are living sebaceous glands whose growth, differentiation and lipid production are influenced by hormonal signalling. Androgens in particular have an important regulatory role. This means that biological changes across life could potentially alter:

• •how much meibum is produced
• •its composition
• •normal gland function

But if a patient’s meibomian glands are obstructed, the useful clinical question is still:

What are the glands actually doing?

Hormonal history may help explain the background. It does not replace examination of gland function.

Yes. The lacrimal glands are also hormonally responsive. Sex hormones can influence lacrimal gland biology, immune regulation and tear secretion. So hormonal changes are not relevant only to MGD. Potential effects can occur across different parts of the lacrimal functional unit.

This is another reason why the label “hormonal dry eye” is not very informative. Two people whose symptoms appear around menopause may have very different ocular findings. One might predominantly have MGD. Another might have reduced aqueous tears. Another might have mixed disease. And another may have dry-eye symptoms for reasons only partly related to hormonal changes.

Aqueous Deficiency

Dry Eye Is Often Mixed

This is a particularly interesting question. Perimenopause is not simply a moment when estrogen switches from “normal” to “low.” Hormone levels can fluctuate substantially during the transition. Meanwhile, other age-related changes are occurring at the same time. So someone may have tolerated:

• •screen use
• •contact lenses
• •low humidity
• •or mild MGD

for many years without symptoms. Then the biological system changes enough that the same environmental and behavioural stresses are no longer as well tolerated. In that sense, hormonal change may sometimes be one factor that shifts the balance rather than the single root cause.

Screens, Reduced Blinking & Dry Eye

Environment, Humidity, Wind and Dry Eye

No. This is one of the most important points. Saying:

“Your eyes are dry because you’re getting older.”

is not really an etiological diagnosis. Age increases risk. It does not tell us which part of the ocular-surface system has become dysfunctional. A 70-year-old patient can still have:

• •MGD
• •aqueous deficiency
• •blepharitis
• •exposure
• •medication-related dry eye
• •autoimmune disease
• •or combinations of these

Age should therefore be treated as context, not as the end of the diagnostic process.

How Dry Eye Is Diagnosed

The same principle applies. Menopause is an important biological transition associated with a higher prevalence of dry eye. But menopause is not a dry-eye mechanism. If someone develops dry eye around menopause, it still makes sense to investigate:

• •tear volume
• •tear-film stability
• •meibomian gland function
• •eyelid and blink function
• •ocular-surface damage
• •and other possible contributors

Otherwise, the word “hormonal” can become a label that stops the investigation rather than helping it.

Some women report changes in ocular comfort at different points in the menstrual cycle, and the ocular surface contains receptors capable of responding to sex hormones. However, individual symptom fluctuations are difficult to interpret because many other things also vary from day to day. Sleep, screen exposure, environment, contact-lens wear and other factors can all influence symptoms. So noticing a repeated pattern can be useful.

But symptoms changing with the cycle do not by themselves identify which hormone is responsible or prove that hormones are the primary cause.

In a broad biological sense, hormones absolutely influence the ocular surface. But “hormonal dry eye” is not a sufficiently specific explanation of what has gone wrong. Compare it with saying “My dry eye is age-related.” That gives us context. It does not give us the mechanism. A more useful chain of reasoning is:

biological or hormonal change→effect on a particular ocular-surface system→measurable dysfunction→dry-eye signs and/or symptoms

The middle part matters. That is what we need to identify.