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The Intersection and Interplay of Systemic Diseases and Glaucoma

Glaucoma as a multifactorial disease.

By: Derek MacDonald, OD
Optometric Management November 2, 2026 Vol 61, Issue November-December 2026 Page(s): 7-8, 10, 12

“A patient can have as many diseases as he or she pleases.” Many (if not most) of us have heard some variation on this axiom. It’s a little poetic, quite memorable, and 100% true. Moreover, those diseases are not limited to the eye. 

It’s also been said that glaucoma is “a sick eye in a sick body” because a number of conditions and treatments involving the cardiovascular, endocrine, immune, and neurologic systems can impact the incidence and progression of both primary open-angle glaucoma (POAG) and primary angle-closure glaucoma (PACG).1 This article will provide a high level (and certainly not exhaustive) review of the prevailing wisdom around systemic diseases and medications that increase or decrease the risk of glaucoma.

The cornerstone of effective glaucoma risk assessment is a comprehensive understanding of the patient’s overall health status and medication profile, and particularly in the elderly, comorbidities and polypharmacy are more often the rule than the exception. Glaucoma is increasingly being recognized as a multifactorial disease that involves far more than simply elevated intraocular pressure (IOP); it is influenced by vascular, metabolic, inflammatory, and neurologic factors.2 A thorough case history identifies relevant conditions and medications, and informs the ophthalmic investigation that follows.3

Primary Open-Angle Glaucoma

Systemic Blood Pressure and Ocular Perfusion Pressure

Although elevated blood pressure (BP) is known to lead to a modest increase in IOP, its impact on the incidence of POAG appears to be negligible.4 However, systemic hypotension, particularly iatrogenic low BP resulting from the aggressive treatment of systemic hypertension, has long been recognized as contributing to both the onset and progression of glaucomatous optic neuropathy (GON).5 An arguably overly simplified but still helpful clinical construct to inform risk assessment is diastolic ocular perfusion pressure (DOPP), the difference between diastolic BP (DBP) and IOP (DOPP=DBP-IOP).6 Note that both a decrease in DBP and an increase in IOP, a combination that occurs frequently during the nocturnal period, can compromise DOPP (Figure 1). A number of large epidemiologic and longitudinal studies have identified an association between low DOPP and the incidence, prevalence, and progression of POAG across multiple diverse populations.5,7,8 More specifically, these and other investigations have suggested that a DOPP in the low 50s in an individual treated for systemic hypertension significantly increases the risk of glaucoma onset and progression.9 The evolution of GON in the face of low in-office IOPs likely warrants 24-hour ambulatory blood pressure assessment to ascertain the contribution of DOPP.

Figure 1. A schematic representation of the interplay of a concurrent decrease in diastolic blood pressure (DBP; green curve) and increase in intraocular pressure (IOP; blue curve) resulting in a decrease in diastolic ocular perfusion pressure (DOPP; red curve), dropping below 50 mmHg during the nocturnal period (orange arrow). Many epidemiologic and longitudinal studies have suggested that a DOPP in or less than the low 50s (particularly in a patient treated for systemic hypertension) significantly increases the risk of primary open-angle glaucoma onset and progression.9 Image courtesy of Dr. MacDonald.

More recently, it has come to light that the type of antihypertensive medication also appears to matter. In prospective investigation, review of insurance data, and cross-sectional analyses, the use of systemic calcium channel blockers (CCBs) was associated with a nearly 40% greater odds of POAG (Figure 2).10 In juxtaposition to earlier hypotheses, rather than being neuroprotective (through addressing inappropriate vasospasm and faulty autoregulation in cases of primary vascular dysregulation characterized by migraine, Raynaud phenomenon, and decreased sensation of thirst), CCBs may in fact be “directly detrimental to retinal tissue.”11

Figure 2. On left: The left optic nerve of a 64-year-old woman with primary open-angle glaucoma and treated intraocular pressures (latanoprost QHS) in the mid-teens. On right: After beginning treatment for systemic hypertension with a CCB used in the evening, she presented with unchanged treated IOPs, but significant expansion of the preexisting superior temporal retinal nerve fiber layer defect and multiple disc hemorrhages (a smaller DH at the inferior margin of the RNFL defect and a much larger DH inferior temporally). Glaucoma treatment was augmented through a switch to bimatoprost QHS and the addition of brinzolamide BID (avoiding a topical BB because of the potential additive impact on systemic blood pressure) and a referral for selective laser trabeculoplasty with the goal of decreasing IOP and blunting any nocturnal spike as much as possible. At the same time, in cooperation with her PCP, the systemic antihypertensive medication was switched to an angiotensin-converting enzyme inhibitor taken in the morning in an attempt to prevent iatrogenic nocturnal BP overdipping; treated IOPs dropped to the low teens, and no further glaucoma progression was detected over the next few years of follow-up. Image courtesy of Dr. MacDonald.

In contrast, the use of diuretics, angiotensin receptor blockers, angiotensin-converting enzyme inhibitors, or systemic beta blockers (BBs) was not associated with increased risk of glaucoma.12 In fact, systemic BBs were protective due to their impact on IOP, but clinicians should also be cognizant of the fact that the impact of a topical BB may be blunted in patients who already use the medication systemically. In at-risk patients using CCBs for hypertension, angina, or arrhythmia, consulting their primary care practitioner (PCP) about the feasibility of alternate treatments could (some would argue should) be considered.

The timing of treatment for high BP may also be contributory. A marked drop in nocturnal BP, regardless of the type of drug used, exacerbates retinal nerve fiber layer and visual field loss.13,14 Again in consultation with the PCP, consideration may be given to using antihypertensive medications in the morning, with the goal of maintaining a normal nocturnal physiologic BP dip of 10% to 15%, while avoiding iatrogenic overdipping and the possibility of hypoxic end-organ damage.15

Diabetes

Diabetes mellitus has long been investigated as a risk factor for POAG. Although this was initially somewhat controversial, the contemporary understanding is that chronic hyperglycemia contributes to microvascular dysfunction, neuroretinopathy, oxidative stress, and prolonged inflammation, all of which may increase retinal ganglion cell (RGC) susceptibility.16 Interestingly, however, the treatment of diabetes appears to reduce the risk of glaucoma to a greater degree than would be expected based upon its impact on glycemic control.

A common feature of neurodegenerative diseases, including glaucoma, is dendrite retraction and synaptic disconnection following axonal injury.17 The use of insulin, both topically and systemically, promotes regeneration of dendrites, and restores synaptic connection and RGC function, which suggests that insulin may be both neuroprotective and neurogenerative.18 In fact, in light of these data, some have gone as far as to call POAG “type 4 diabetes”; others have previously termed Alzheimer disease “type 3 diabetes.”19,20

The use of metformin is associated with a dose-dependent reduction in risk of POAG that is independent of both HbA1c and IOP. In a 2015 study, individuals using a daily dose of 2 mg metformin for 2 years showed a 21% reduced risk of glaucoma, whereas the Rotterdam study suggested an even more impressive odds ratio (OR) of only 0.18 for incident POAG in patients taking metformin.21,22 Metformin possesses geroprotective (antiaging) properties that target mitochondrial dysfunction, fibrosis, inflammation, ischemia, and oxidative stress, and they reduce risk and severity of age-related disease, including glaucoma.23 This raises the fascinating, albeit somewhat outlandish, question of whether age could eventually become another modifiable risk factor in the treatment of POAG.

Finally, glucagon-like peptide 1 receptor agonists (GLP-1 RAs) potentiate glucose-dependent insulin secretion and inhibit glucagon release, appetite, and gastric emptying. These drugs also cross the blood-brain and blood-retina barriers and exhibit neuroprotective properties, enhancing mitochondrial function while decreasing neuroinflammation and glial cell activation in Alzheimer disease, Parkinson disease, stroke, and POAG.24,25 Specific to the latter, GLP-1 RAs reduce the risk of incident POAG with a robust hazard ratio of 0.08 that appears to be independent of any impact on HbA1c and IOP, but may depend upon duration of treatment greater than 3 years.26

So, which is better, metformin or GLP-1 RAs? 

In a recent retrospective comparison of 124,000 patients with type 2 diabetes, those treated with GLP-1 RAs showed a significantly decreased risk of POAG vs those treated with metformin (relative risk of 0.59 at 1 and 3 years), prompting the investigators to conclude that “although metformin’s neuroprotective effects are promising, the variability in its impact on glaucoma risk suggests that its benefits may be less consistent or potent compared with those of GLP-1 receptor agonists.”27

Although it is exciting to think that we are on the cusp of long-awaited IOP-independent neuroprotective glaucoma therapies, we must bear in mind that these data are based upon post hoc analyses of nonrandomized cardiovascular studies and must be corroborated by large, well-designed prospective randomized controlled trials with primary ophthalmic endpoints.28

Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is characterized by repeated episodes of partial or complete upper airway collapse during sleep, leading to recurrent hypoxia that increases the risk of diabetes, heart disease, and stroke.29 It is a very common condition with a prevalence as high as 4% in men that is estimated to affect 1 billion individuals worldwide.30 A relationship between OSA and POAG has long been suspected (primarily driven by chronic ischemia/reperfusion injury), but whether OSA was causative or simply a comorbidity remained in question until relatively recently. 

In contemporary meta-analyses and narrative reviews, OSA was found to confer an OR of up to 3.6 for concurrent POAG, a risk that increases to 5.5 with more severe OSA.31 Moreover, the course of glaucomatous disease is often more severe in patients with concurrent OSA. In patients with normal-tension glaucoma (NTG; arbitrarily defined as GON in the presence of statistically normal untreated IOP), the prevalence of OSA was more than triple that in controls, whereas in patients with moderate/severe OSA, the prevalence of NTG was nearly 7 times that in those with no or mild OSA.32

Although continuous positive airway pressure (CPAP) therapy does appear to help stabilize the oxygen supply to the optic nerve head, it has also been implicated as increasing nocturnal IOP via elevated intrathoracic pressure and mechanical globe compression.33 This effect has prompted some researchers to suggest that patients with comorbid OSA and POAG should opt for treatments other than CPAP; however, this conclusion remains controversial, and requires more study before a firm consensus can be reached.34

Corticosteroids

The impact of corticosteroids on IOP, whether (in order of increasing risk) systemic, periocular, topical, or intraocular, has been recognized for decades.35 With tens of millions of prescriptions written annually, the likelihood of a patient in your chair having a history of steroid use is quite high.36 Exposure to steroids increases resistance to aqueous outflow through the trabecular meshwork by suppressing phagocytosis, stiffening actin cross-linking, and increasing extracellular matrix material, potentially leading to ocular hypertension and secondary OAG.37 As many as 1 in 3 individuals are “steroid responders,” and 1 in 20 experience an IOP increase of more than 15 mmHg or to a level of greater than 31 mmHg (Figure 3).38 Individuals who have high myopia, POAG, or a family history of POAG are at increased risk.39 IOP usually normalizes within weeks of steroid discontinuation, but can become and remain quite elevated with chronic steroid use. Moreover, the ophthalmic consequences of steroid use persist, and can create diagnostic uncertainty in a patient with GON and statistically normal IOPs. In other words, is this potentially progressing NTG, or remote steroid induced glaucomatous damage that is unlikely to change over time?

Figure 3. Left: The left optic nerve head of a 62-year-old man with primary open-angle glaucoma, and intraocular pressures (IOP), treated with bimatoprost daily at bedtime, in the low teens. Right: The patient was lost to follow-up for approximately 14 months after being diagnosed with colorectal cancer that was treated with surgery, chemotherapy, and systemic dexamethasone. He presented with treated IOPs in the low 30s attributed to steroid response and progressing superior neuroretinal rim and retinal nerve fiber layer loss; glaucoma treatment was augmented through a switch to a prostaglandin analog–beta blocker fixed combination taken once daily in the morning and a referral for selective laser trabeculoplasty, resulting in treated IOPs returning to the mid-teens. Image courtesy of Dr. MacDonald.

The Importance and Challenge of Adherence

As the common adage posits, “Drugs don’t work for patients who don’t take them,” and yet 50% of patients treated for glaucoma discontinue treatment within 6 months, mirroring statistics for other chronic diseases.40 Treatment of an initially asymptomatic disease must be convenient, affordable, and tolerable. Poor adherence, whether triggered by medication burden (both topical and systemic), adverse effects, costs, or a lack of appreciation for the serious nature of a disease, sets the stage for potentially preventable progression.41 Indeed, in the Collaborative Initial Glaucoma Treatment Study, patients who reported never missing a dose of medication lost -0.62 dB mean deviation over 8 years of follow-up, while those who missed doses at two-thirds of visits lost -2.23 dB.42 An educated and engaged patient is more likely to be an adherent patient, and an adherent patient is less likely to experience unnecessary functional loss. Glaucoma, like life, is a team sport.

Primary Angle-Closure Glaucoma

As a backdrop, PACG, although less common than POAG, particularly in North America, is responsible for a disproportionate amount (~50%) of glaucoma-related vision loss worldwide.43 Multiple nonmodifiable risk factors for angle-closure disease have been identified, including East Asian ethnicity, advancing age, female sex, hyperopia, and a family history of PACG.44,45 However, the impact of systemic medications is significant, and cannot be overlooked.

Drug-Induced Acute Primary Angle Closure

Many commonly prescribed systemic medications can precipitate acute primary angle closure (APAC, a true ocular emergency) through either pharmacologic mydriasis inducing pupillary block or ciliochoroidal effusion triggering ciliary block.46 The 3 drugs with the highest OR for APAC are the antimigraine agent sumatriptan (OR 12.6), the antiepileptic topiramate (OR 5.1), and the serotonin norepinephrine reuptake inhibitor duloxetine (OR 4.0).47 The mechanism of action for the latter is felt to be mydriasis induced by anticholinergic and adrenergic effects that cause pupillary block.48 Fortunately, discontinuing duloxetine; initiating standard treatment with topical miotics, aqueous suppressants, and steroids; and performing a therapeutic laser peripheral iridotomy (LPI) are usually successful in breaking the angle closure attack.

Both sumatriptan and topiramate, however, can cause bilateral APAC through idiosyncratic ciliochoroidal effusion, which leads to anterior displacement of the lens/iris diaphragm and ciliary block.49,50 This can occur within weeks, and is accompanied by an often dramatic myopic shift.51 Unlike pupillary block, ciliary block should not be managed with oral carbonic anhydrase inhibitors, pilocarpine, or LPI, all of which can exacerbate the anterior lens/iris movement and prolong the attack.52 Rather, treatment entails immediate drug discontinuation and the use of topical steroids to quell inflammation and cycloplegic agents (both rapidly acting phenylephrine and longer acting cyclopentolate) to counter the anterior shift of the lens and iris. 

For this reason, differentiating pupillary from ciliary block is critical. The latter often presents with uniform flattening of the entire anterior chamber, significant myopic shift, and a history of contributory medication use or recent ophthalmic surgery.53

It has been estimated that 1 in every 3 cases of APAC arise at least in part due to the influence of systemic medications.54 With more than 60 drugs known to increase the risk of APAC, and more than 40 million prescriptions written in North America each year for duloxetine, sumatriptan, and topiramate alone, failure to identify susceptible individuals and precipitating medications is a missed opportunity in the prevention of APAC.

Conclusion

In many, if not most, of our patients who have or are at risk of glaucoma, systemic comorbidities and polypharmacy are the norm. An awareness of the intersection of general and ocular health, directed by a current and detailed case history for the individual in question, arms the clinician with the information needed to provide personalized care and partner with both the patient and their multidisciplinary health care team to set the stage for optimal outcomes. OM

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Derek MacDonald, OD

Derek MacDonald, OD is in full-scope private practice in Waterloo, Ontario, Canada, with special interest in ocular and systemic disease. He is a past president of the Ontario Association of Optometrists and retired council member of the College of Optometrists of Ontario, a fellow and diplomate (glaucoma) of the American Academy of Optometry, past chair of the AAO International Admittance Committee 5B, and a member of the Optometric Glaucoma and Optometric Retina Societies.