Because IOP levels may be modulated by lifestyle factors, efforts to identify activities that may lower IOP levels may be promising in developing primary prevention strategies for POAG. Most physicians will advice glaucoma patients to avoid caffeine beverages.
A study investigated the effect of caffeine on eye pressure (Ann Pharmacother 2002;36:992-5). The consumption of regular (180 mg caffeine in 200 mL beverage) and decaffeinated coffee (3.6 mg caffeine in 200 mL beverage) was compared. Regular coffee resulted in about 3 mmHg eye pressure increase in 1 hour. This magnitude of eye pressure increase is likely to be clinically important. Certainly as the study showed, glaucoma patients should not consume a 180 mg caffeine beverage.
Another study in the past had shown much lower eye pressure rise with caffeine, about 1 mm Hg pressure rise, likely not to be clinically important (Ophthalmology 1989;96:624-6). Although there was a statistically significant difference in IOP at 90 minutes between coffee and tea drinkers, the change was not clinically significant. It is important to note that the eye pressure rise will depend on how much caffeine you consume. Different beverages have differing amounts of caffeine. Beverages containing about 50 mg caffeine may be fine.
The Blue Mountains Eye Study examined the relationship between coffee and caffeine intakes and intraocular pressure (IOP). In participants with open-angle glaucoma, this study identified a positive cross-sectional association between coffee consumption/higher caffeine intakes and elevated intraocular pressure. Participants with open-angle glaucoma (OAG) who reported regular coffee drinking had significantly higher mean IOP than participants who said that they did not drink coffee. Participants consuming ≥ 200 mg caffeine per day had higher mean IOP than those consuming < 200 mg caffeine per day, after adjusting for age, sex, and systolic blood pressure, but this association did not reach statistical significance after multivariate adjustment. No association between coffee or caffeine consumption and higher IOP was found in participants with ocular hypertension (OH) and those without open-angle glaucoma (J Glaucoma 2005;14(6):504-7).
In a recent large, prospective study, overall caffeine consumption was not associated with risk of developing primary open-angle glaucoma (POAG). In one secondary analysis, this study found that greater caffeine intake was associated with increased risks of POAG characterized by elevated intraocular pressure among those with a self-reported family history of glaucoma. However, because this was the first epidemiologic investigation of the relationship between caffeine intake and glaucoma in a population-based study, these secondary results must be interpreted cautiously and confirmed in future studies (Invest Ophthalmol Vis Sci 2008;49(5):1924-1931).
The mechanism by which caffeine may influence IOP and thereby alter the risk of glaucoma is not clear, particularly because of caffeine’s varied pharmacologic effects on cellular processes. For adverse effects, there is evidence that caffeine could elevate IOP by increasing aqueous humor formation. Caffeine inhibits phosphodiesterase, which would result in maintaining high intracellular levels of cAMP of the ciliary body and possibly greater production of aqueous humor. In animals exposed to caffeine, ultrastructural changes in the nonpigmented ciliary epithelium were observed which may increase aqueous transport. In addition, acute caffeine increases blood pressure before causing elevations in IOP; increased blood pressure would increase the hydrostatic pressure for aqueous formation from plasma in the ciliary process capillary network.
The effect of caffeine in the aqueous outflow in not clear; one investigator hypothesized that caffeine may reduce outflow by decreasing the tone of smooth muscles via adenosine receptor blockade, leading to closure of trabecular pores in the aqueous outflow path. Caffeine has been shown to decrease blood flow to both the macula and the optic nerve head and choroid-retina, which may make the optic nerve more susceptible to elevated IOP. This effect was more apparent among women. Higher caffeine intake showed a dose-response trend with increasing risk of POAG with elevated IOP at diagnosis (although difference between the sexes was of borderline significance). Also, in recent data, there was some support for a possible threshold effect and acute dosage effect with average consumption of five or more cups of caffeinated coffee per day over several years, which is consistent with the mechanistic studies that show that high levels of caffeine, in doses found in approximately one to three cups of caffeinated coffee, causes transient elevations of ∼1 to 3 mmHg that lasts for ∼2 hours.
A meta-analysis quantitatively summarized the effect of caffeine on IOP in normal individuals and in patients with glaucoma or ocular hypertension (OHT). A comprehensive literature search was performed using the Cochrane Collaboration methodology to identify pertinent randomized controlled trials (RCTs). Six RCTs (two parallel-designed and four crossover-designed) evaluating 144 participants (103 were normal individuals and 41 were patients with glaucoma or OHT) fulfilled inclusion criteria. IOP at 0.5 hour (h), 1 h and 1.5 h after caffeine ingestion was the main outcome measurement. The design of each study, intervention, and general characteristics of the participants are given in the Tables.(Graefes Arch Clinical Exp Ophthalmol ;249(3):435-442).
The weighted mean difference (WMD) with 95% confidence intervals (95% CI) for each measurement point were −0.740 (–2.454, 0.974), 0.522 (–0.568, 1.613) and 0.580 (–1.524, 2.684). However, in patients with glaucoma or OHT, IOP increased at each measurement point, with the WMD and 95% CI being 0.347 (0.078, 0.616), 2.395 (1.741, 3.049) and 1.998 (1.522, 2.474) respectively. No publication bias was detected by either Begg’s or Egger’s test. The available evidence suggests that caffeine has different effects on IOP in different groups of subjects. It can elevate IOP in patients with OAG or OHT in a short period after ingestion, but not in normal individuals. The mechanisms underlying this phenomenon and the clinical significance are to be explored.
Overall caffeine consumption is not associated with increased risk of POAG. Given what we know, high amount of caffeine consumption is certainly not good for glaucoma. Whether lower amounts should also be avoided is debatable. Current evidence does not suggest a strict avoidance of caffeine, but rather a lowering of the intake. Tea (black or green – made of leaves) contains lesser caffeine and has the additional advantage of being rich in flavonoids (antioxidants good for the heart and the eye too), therefore tea may be a good alternative beverage for glaucoma patients.
Article by G.T. Georgopoulos, MD
Assoc. Professor of Ophthalmology
Athens University Medical School