
- March/April digital edition 2026
- Volume 18
- Issue 02
Menopause and the eye: Practical considerations for optometric care
Sex hormones play important but distinct roles in regulating the ocular surface and adnexal tissues.
The hormonal shifts that accompany menopause extend far beyond vasomotor symptoms—they affect nearly every part of the eye, from the ocular surface and cornea to the lens, optic nerve, and retina. These changes not only exacerbate dry eye disease and make contact lens wear more challenging, but there may also be an increased risk for a woman to develop glaucoma, cataracts, and age-related macular degeneration. As optometrists, we are in a unique position to guide our patients through this transition. By focusing on optimizing the ocular surface, adjusting refraction during hormonal instability, providing glaucoma screening, offering nutritional advice, and collaborating with other providers as needed, we can help women maintain comfortable, healthy vision throughout menopause and beyond using evidence-based protocols.1-3
Dry eye disease and meibomian gland dysfunction
Sex hormones play important but distinct roles in regulating the ocular surface and adnexal tissues. Estrogen and androgen receptors are expressed in the lacrimal gland, meibomian glands, conjunctiva, corneal epithelium, and retina, linking menopausal endocrine changes to ocular physiology.4,5
Androgens are the most clearly protective, exerting anti-inflammatory effects in the lacrimal and meibomian glands, supporting tear production and lipid secretion; androgen deficiency and antiandrogen therapy are strongly associated with meibomian gland dysfunction (MGD) and evaporative dry eye disease (DED), whereas androgen replacement can improve signs and symptoms. Estrogens affect the eyes in complicated ways that depend on where and how much is present. Studies in animals have yielded mixed results, and using estrogen directly on the eyes has not shown clear benefits in humans. Also, whether too little or too much estrogen is linked to DED in humans may be influenced by other factors like anxiety, depression, and sleep problems, rather than just the hormone.3-6 However, fluctuations in estrogen levels may affect tear osmolarity and corneal sensitivity.3-5 Progestins seem to help reduce eye pain and discomfort by affecting nerves, but this usually happens when the hormone is used in much higher amounts than the body normally makes and may involve several different pathways.
Clinical implication: Anticipate symptom acceleration in perimenopause; document baseline ocular surface status and refraction, then monitor closely through the transition.4,6
Patients report burning, stinging, photophobia, fluctuating vision, and contact lens intolerance. Objective findings often include reduced noninvasive tear breakup time, elevated osmolarity, lid margin telangiectasia, capped or turbid meibum, and positive ocular surface staining.3,6
Management pearls
- Foundation therapy: Lid hygiene, warm compresses, and environmental modification; initiate lipid‑supportive, preservative-free artificial tears; consider humidification and screen‑time ergonomics.3
- Anti‑inflammatory control: Topical cyclosporine or lifitegrast for inflammatory DED; short, pulse corticosteroids for flares.3
- MGD‑directed care: Thermal pulsation, radio frequency, low-level light therapy, or intense pulsed light for refractory evaporative components; in-office gland expression.3
- Systemic review: Discuss medications (anticholinergics, selective serotonin reuptake inhibitors/serotonin and norepinephrine reuptake inhibitors, antihistamines) and systemic contributors (thyroid disease, autoimmune conditions).3,6
- Contact lens strategy: Prescribe daily disposables, silicone hydrogel lenses with enhanced wettability, or scleral lenses for advanced ocular surface disease.3,6 Repeat refraction when symptoms or acuity vary; confirm stability across visits before finalizing spectacle prescriptions.
- Optimize the ocular surface before contact lens fitting or premium intraocular lens biometry; repeat keratometry/topography after DED control.3,6
Evidence supports sex steroid modulation of the meibomian and lacrimal apparatus; although some studies suggest symptom improvement with menopausal hormone therapy (MHT) in select patients, results are heterogeneous and require individualized risk-benefit assessment. 3-5
Glaucoma risk and the menopausal transition
Studies show that menopause may raise the risk of getting primary open-angle glaucoma, potentially due to lower levels of estrogen, which may affect ocular perfusion and trabecular outflow modulation.7-9
Early menopause has been linked with higher glaucoma risk in some cohorts.8,9 Although more studies need to be done on the role of estrogen and progesterone on glaucoma, estrogen exposure across the life span may confer modest neuroprotective effects on the optic nerve.7-9
Clinical actions:
- Establish a baseline comprehensive exam with IOP, central corneal thickness, gonioscopy, optic nerve/optical coherence tomography of the retinal nerve fiber layer and macular ganglion cell–inner plexiform layer, and standard automated perimetry.
- Increase surveillance frequency in women with additional risk factors (family history, African or Hispanic ancestry, thin central corneal thickness, vascular dysregulation/migraine, sleep apnea).7-9
Cataract: Earlier onset and risk modifiers
Women have a higher lifetime risk of cataract, and the decline in estrogen’s antioxidative support has been proposed as a mechanistic contributor.10 UV exposure, smoking, diabetes, and corticosteroids remain dominant modifiable risks, but menopausal status may accelerate lens opacification in susceptible individuals.10
Optometric role: Counsel UV protection, glycemic control, smoking cessation; monitor functional impact (glare disability, night driving); refer for surgery when activities of daily living are impaired—after optimizing the ocular surface to improve biometry and postoperative satisfaction.3,10
Age-related macular degeneration in postmenopausal patients
Age-related macular degeneration (AMD) becomes more common as people get older, especially in groups where women tend to live longer. Both oxidative stress and blood vessel changes are affected by hormones in complex ways.11-13
Although estrogen may support retinal and choroidal perfusion in experimental models, more studies on human data on MHT for AMD prevention are lacking.12-13
Counseling and management:
- Emphasize smoking cessation, UV/blue light protection, diet rich in leafy greens and omega‑3s; consider AREDS/AREDS2 supplementation for intermediate AMD per criteria.12,13
- Implement home monitoring (Amsler/grid or digital tools), and schedule prompt evaluations for metamorphopsia or scotomas.12,13
Patient communication and education
Explain that menopause is a normal transition with real ocular effects—chiefly on comfort and visual consistency. Set expectations: DED and MGD require ongoing care; refraction may be temporarily unstable; and regular surveillance helps prevent sight‑threatening disease. Provide written plans and reinforce adherence with brief, frequent touchpoints early in therapy.3,6
Conclusion
For optometrists, menopause is a pivotal window to protect and enhance visual function. Evidence links menopausal hormone shifts to ocular surface disease, refractive variability, and altered risk profiles for glaucoma, cataract, and AMD. A structured approach—early screening, ocular surface optimization, risk‑based surveillance, and coordinated care—translates the science into better outcomes for women in midlife.2-5,7-10,14,15
Bio
Roxanne Achong‑Coan, OD, FAAO, FIAOMC, FSLS, FBCLA, Dipl AAO CCLRT, is a nationally recognized optometrist and co‑owner of Coan Eye Care in Ocoee, Florida for 27 years. A specialist in advanced cornea and contact lens care, she completed her residency in Cornea and Contact Lens at Pacific University College of Optometry. She also serves as a clinical adjunct assistant professor at the New England College of Optometry, where she earned her Doctor of Optometry degree. Dr. Achong‑Coan is an active contributor to research and education in specialty lenses and myopia management and has been honored with numerous awards, including Vision Monday’s Contact Lens Innovator of the Year, CooperVision’s Best Practices recognition, th Best Clinical Research Poster award at the Global Specialty Lens Symposium, Contact Lens Luminary Award at the AOA Contact Lens Section, Contact Lens Visionary award, Optometric Business Innovator, and a John Asarkof OD award winner.
References:
Craig JP, Nichols KK, Akpek EK, et al. TFOS DEWS II Definition and Classification Report. Ocul Surf. 2017;15(3):276-283. doi: 10.1016/j.jtos.2017.05.008
The epidemiology of dry eye disease: report of the Epidemiology Subcommittee of the International Dry Eye Workshop (2007). Ocul Surf. 2007;5(2):93-107. doi:10.1016/s1542-0124(12)70082-4
Sullivan DA, Sullivan BD, Evans JE, et al. Androgen deficiency, meibomian gland dysfunction, and evaporative dry eye. Ann N Y Acad Sci. 2002;966:211-222. doi:10.1111/j.1749-6632.2002.tb04217.x
Sullivan DA, Rocha EM, Aragona P, et al. TFOS DEWS II Sex, Gender, and Hormones Report. Ocul Surf. 2017;15(3):284-333. doi:10.1016/j.jtos.2017.04.001
Versura P, Giannaccare G, Campos EC. Sex‑steroid imbalance in females and dry eye. Current Eye Research. 2025;40(2):162175.
Truong S, Cole N, Stapleton F, Golebiowski B. Sex hormones and the dry eye. Clin Exp Optom. 2014;97(4):324-36. doi:10.1111/cxo.12147
Vajaranant TS, Pasquale LR. Estrogen deficiency accelerates the aging of the optic nerve. Menopause. 2012;19(8):942-947. doi:10.1097/gme.0b013e3182443137
Varma R, Wang, Wang D, Wu C, et al; Los Angeles Latino Eye Study Group. Four-year incidence of Open-angle Galucoma and Ocular Hypertension: The Los Angeles Latino Eye study. Am J Ophthalmol. 2012;154(2):315–325.e1. doi:10.1016/j.ajo.2012.02.014
Hulsman CA, Westendorp IC, Ramrattan RS, et al. Is open-angle glaucoma associated with early menopause? The Rotterdam Study. Am J Epidemiol. 2001;154(2):138-144. doi:10.1093/aje/154.2.138
Hiller R, Sperduto RD, Ederer F. Epidemiologic associations with nuclear, cortical, and posterior subcapsular cataract. Am J Epidemiol. 1986;124(6):916-925. doi:10.1093/oxfordjournals.aje.a114481
Mitchell P, Wang JJ, Foran S, Smith W. Five-year incidence of age-related maculopathy lesions: the Blue Mountains Eye Study. Ophthalmology. 2002;109(6):1092-1097. doi:10.1016/s0161-6420(02)01055-2
Chew EY, Clemons TE, Sangiovanni JP, et al; AREDS2 Research Group. Secondary analyses of the effects of lutein/zeaxanthin on age-related macular degeneration progression: AREDS2 report No. 3. JAMA Ophthalmol. 2014;132(2):142-149. doi:10.1001/jamaophthalmol.2013.7376
Evans JR, Lawrenson JG. Antioxidant vitamins and mineral supplements for slowing the progression of age-related macular degeneration. Cochrane Database Syst Rev. 2017;7(7):CD000254. doi:10.1002/14651858.CD000254.pub4
Pasquale LR, Kang JH. Female reproductive factors with primary open-angle glaucoma in the Nurses’ Health Study. Eye. 2015;24(6):445-450. doi:10.1038/eye.2011.34
Younan C, Mitchell P, Cumming RG, Panchapakesan J, Rochtchina E, Hales AM. Hormone replacement therapy, reproductive factors, and the incidence of cataract and cataract surgery: the Blue Mountains Eye Study. Am J Epidemiol. 2002;155(11):997-1006. doi:10.1093/aje/155.11.997
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