Beatríz Redondo1, Jesús Vera2, Rubén Molina1, Raimundo Jiménez1. 1. Department of Optics, Faculty of Sciences, University of Granada, Campus de la Fuentenueva 2, 18001, Granada, Spain. 2. Department of Optics, Faculty of Sciences, University of Granada, Campus de la Fuentenueva 2, 18001, Granada, Spain. veraj@ugr.es.
Abstract
BACKGROUND: Acute caffeine consumption causes a transient increase in IOP; however, the mechanisms underlying this phenomenon remain unknown. This study aims to determine the structural changes in cornea and anterior chamber associated with caffeine ingestion. METHODS:Seventeen healthy low caffeine consumers ingested acapsule of caffeine (~ 4 mg/kg) or placebo (300 mg of corn-starch) in a counterbalanced manner. We measured IOP by rebound tonometry and the anterior chamber depth (ACD), anterior chamber volume (ACV), anterior chamber angle (ACA) and central corneal thickness (CCT) with the Pentacam rotating Scheimpflug camera. Subjective feelings of arousal were also obtained. All the dependent variables were obtained before and 30, 60 and 90 min after caffeine/placebo intake. RESULTS:Caffeine intake caused an acute IOP rise (p = 0.005, η2 = 0.403) and a narrowing ACA (p = 0.028, η2 = 0.266). However, our data did not reveal any effect on CCT, ACD and ACV after caffeine ingestion (p = 0.798, p = 0.346, p = 0.175, respectively). Participants reported greater levels of activation after ingesting caffeine in comparison to placebo (p = 0.037, η2 = 0.245). CONCLUSION: The IOP rise associated with caffeine intake may be caused by an ACA reduction, which may add resistance to the outflow of aqueous humour. The current results may be of special relevance for subjects at high risk for glaucoma onset or progression and may help to understand the mechanisms underlying caffeine-induced ocular hypertension.
RCT Entities:
BACKGROUND: Acute caffeine consumption causes a transient increase in IOP; however, the mechanisms underlying this phenomenon remain unknown. This study aims to determine the structural changes in cornea and anterior chamber associated with caffeine ingestion. METHODS: Seventeen healthy low caffeine consumers ingested a capsule of caffeine (~ 4 mg/kg) or placebo (300 mg of corn-starch) in a counterbalanced manner. We measured IOP by rebound tonometry and the anterior chamber depth (ACD), anterior chamber volume (ACV), anterior chamber angle (ACA) and central corneal thickness (CCT) with the Pentacam rotating Scheimpflug camera. Subjective feelings of arousal were also obtained. All the dependent variables were obtained before and 30, 60 and 90 min after caffeine/placebo intake. RESULTS:Caffeine intake caused an acute IOP rise (p = 0.005, η2 = 0.403) and a narrowing ACA (p = 0.028, η2 = 0.266). However, our data did not reveal any effect on CCT, ACD and ACV after caffeine ingestion (p = 0.798, p = 0.346, p = 0.175, respectively). Participants reported greater levels of activation after ingesting caffeine in comparison to placebo (p = 0.037, η2 = 0.245). CONCLUSION: The IOP rise associated with caffeine intake may be caused by an ACA reduction, which may add resistance to the outflow of aqueous humour. The current results may be of special relevance for subjects at high risk for glaucoma onset or progression and may help to understand the mechanisms underlying caffeine-induced ocular hypertension.