Circadian rhythms (CR) shape almost every aspect of physiology, from metabolism and hormone release to vascular tone and mood. For eyecare professionals, understanding these daily cycles is increasingly relevant: the eye is both a detector and a regulator of circadian timing. Disrupted rhythm has been linked not only to systemic conditions, such as diabetes and hypertension, but also to ocular diseases where light, sleep and stress biology intersect. Here, I outline key circadian mechanisms and explore emerging links to glaucoma and central serous chorioretinopathy (CSCR).
Circadian rhythms are internal, self-sustaining cycles that regulate physiology over roughly 24 hours. Unlike diurnal rhythms, which respond directly to environmental change, CRs persist even in the absence of external cues. This autonomy arises from molecular clocks operating within almost all cells, coordinated by the suprachiasmatic nucleus (SCN) in the anterior hypothalamus, which synchronises peripheral clocks across organs such as the liver, heart and retina.
At the cellular level, CRs stem from transcription-translation feedback loops. CLOCK and BMAL1 proteins activate PER (period) and CRY (cryptochrome) genes, which accumulate and inhibit CLOCK/BMAL1 gene activity, completing a 24-hour cycle. Secondary loops, involving REV-ERB and ROR proteins, modulate BMAL1 expression to stabilise phase timing, while post-translational changes fine-tune precision (Fig 1).
Fig 1. CCG’s impact on cellular functions1
These cellular clocks regulate a wide range of processes – metabolism, hormone release, vascular tone, immune function – producing predictable daily rhythms. In the liver, for instance, the genes promoting glucose uptake dominate during the day, while those driving gluconeogenesis take over at night, maintaining energy balance during fasting.
