Date of Award

January 2012

Document Type


Degree Name

Medical Doctor (MD)



First Advisor

James Tsai

Subject Area(s)



EFFECTS OF CAFFEINATED COFFEE ON INTRAOCULAR AND OCULAR PERFUSION PRESSURE. Aliya Z. Jiwani, Douglas Rhee, Stacey Brauner, Matthew F. Gardiner, Teresa Chen, Lucy Q. Shen, Sherleen Chen, Cynthia Grosskreutz, Kenneth K. Chang, Carolyn E. Kloek, Scott H. Greenstein, Sheila Borboli-Gerogiannis, Daniel Pasquale, Sona Chaudhry, Stephanie Loomis, Janey L. Wiggs, Louis R. Pasquale, Angela V. Turalba. Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, MA. (Sponsored by James C. Tsai, Department of Ophthalmology, Yale University School of Medicine).

This study analyzed the effects of acute caffeinated coffee intake on intraocular pressure (IOP), ocular perfusion pressure (OPP) and ocular pulse amplitude (OPA). As increased IOP and decreased OPP are risk factors for primary open-angle glaucoma (POAG) development and progression, and as OPA is a indirect measure for choroidal perfusion and low choroidal perfusion is thought to possibly play a role in the etiology of POAG, it is important to understand how acute coffee intake effects these outcomes. To the best of our understanding of the literature, there are no double-blinded randomized controlled trials examining the effects of acute caffeine intake on IOP, OPP or OPA in patients who have POAG or patients who are at risk for the condition.

This study employed a double-blinded, randomized, controlled and crossover design scheme. This trial included a total of 106 subjects, with one eye enrolled per participant. The 106 subjects included 22 with high tension POAG (glaucomatous visual field defect(s) with a history of IOP >=22 mmHg), 18 with normal tension POAG (glaucomatous visual field defect(s) with no history of IOP >=22 mmHg), 20 with ocular hypertension (history of IOP >=22 mmHg, <=0.6 cup-to-disc ratios, and no visual field defects), 21 POAG suspects (>=0.7 cup-to-disc ratios and no visual field defects), and 25 healthy subjects.

Participants were randomly assigned to consume 8 ounces of caffeinated coffee on the first visit and 8 ounces of decaffeinated coffee on the second visit or vice versa. The caffeinated coffee contained 182 mg of caffeine while the decaffeinated coffee contained 4 mg of caffeine. At each visit, the following were obtained prior to coffee consumption and 60 and 90 minutes post-coffee intake: IOP, blood pressure, heart rate and OPA. IOP, heart rate and OPA were measured using a Pascal Dynamic Contour Tonometer. IOP and blood pressure were used to calculate OPP.

Paired student t-tests were used to analyze the data between the caffeinated and decaffeinated visits. Analysis of variance tests were used to compare results among groups. Predictors of changes in IOP, OPPmean and OPA were examined using linear and logistic regression analyses.

There were no differences in baseline outcome parameters (IOP, OPPmean, OPA) prior to beverage consumption on the caffeinated versus decaffeinated visits. After caffeinated coffee ingestion (when taking into account decaffeinated coffee consumption), the average changes at 60 and 90 minutes in IOP, OPPmean and OPA were, respectively (±SD): IOP: 0.99mmHg (±1.52mmHg, p<0.0001), 1.06mmHg (±1.67mmHg, p<0.0001); OPPmean: 1.57mmHg (±6.40mmHg, p=0.0129), 1.26mmHg (±6.23mmHg, p=0.0398); and OPA: 0.23mmHg (±0.52mmHg, p<0.0001), 0.18mmHg (±0.52mmHg, p=0.0006). Linear and logistic regression analyses failed to demonstrate significant associations among changes in IOP, OPPmean and OPA and multiple covariates of interest (body mass index, gender, age, presence of hypertension, presence of diabetes mellitus, presence of POAG, IOP prior to coffee intake, caffeine intake, or the presence of glaucoma in a biological sibling or child or parent).

Ingesting 8 ounces of caffeinated coffee statistically significantly elevates, but probably does not clinically influence, IOP, OPPmean, and OPA in most of our study participants.


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