Patricia L. Turner

Circadian photoreception: ageing and the eye’s important role in systemic health

Aim: To analyse how age-related losses in crystalline lens transmittance and pupillary area affect circadian photoreception and compare the circadian performance of phakic and pseudophakic individuals of the same age. Methods: The spectral sensitivity of circadian photoreception peaks in the blue part of the spectrum at approximately 460 nm. Photosensitive retinal ganglion cells send unconscious information about environmental illumination to non-visual brain centres including the human body’s master biological clock in the suprachiasmatic nuclei. This information permits human physiology to be optimised and aligned with geophysical day–night cycles using neural and hormonal messengers including melatonin. Age-related transmittance spectra of crystalline lenses and photopic pupil diameter are used with the spectral sensitivity of melatonin suppression and the transmittance spectra of intraocular lenses (IOLs) to analyse how ageing and IOL chromophores affect circadian photoreception. Results: Ageing increases crystalline lens light absorption and decreases pupil area resulting in progressive loss of circadian photoreception. A 10-year-old child has circadian photoreception 10-fold greater than a 95-year-old phakic adult. A 45-year-old adult retains only half the circadian photoreception of early youth. Pseudophakia improves circadian photoreception at all ages, particularly with UV-only blocking IOLs which transmit blue wavelengths optimal for non-visual photoreception. Conclusions: Non-visual retinal ganglion photoreceptor responses to bright, properly timed light exposures help assure effective circadian photoentrainment and optimal diurnal physiological processes. Circadian photoreception can persist in visually blind individuals if retinal ganglion cell photoreceptors and their suprachiasmatic connections are intact. Retinal illumination decreases with ageing due to pupillary miosis and reduced crystalline lens light transmission especially of short wavelengths. Inadequate environmental light and/or ganglion photoreception can cause circadian disruption, increasing the risk of insomnia, depression, numerous systemic disorders and possibly early mortality. Artificial lighting is dimmer and less blue-weighted than natural daylight, contributing to age-related losses in unconscious circadian photoreception. Optimal intraocular lens design should consider the spectral requirements of both conscious and unconscious retinal photoreception.

Blue-Blocking IOLs vs. Short-Wavelength Visible Light: Hypothesis-Based vs. Evidence-Based Medical Practice

In this issue, Artigas et al reexamine the persistently controversial issue of intraocular lens (IOL) chromophores that decrease visible light. Contemporary blue-blocking, yellowtinted IOLs absorb roughly half the light in the third of the visible spectrum between 400 and 500 nm (violet is 400– 440 nm and blue is 440–500 nm). Violet and blue light provide 45% of scotopic, 83% of circadian, and 94% of S-cone photoreception (isoilluminance source). The IOL chromophore story began in 1978 with recognition that early polymethylmethacrylate IOLs transmitted ultraviolet (UV) radiation to the retina and speculation that repetitive acute retinal phototoxicity (photic retinopathy) might be a risk factor for age-related macular degeneration (AMD). Ultraviolet radiation is not required for human photoreception, so UV-absorbing chromophores had no visual downside when they were introduced in the early 1980s. Blue-blocking IOLs were introduced clinically in 1991 following a 1986 suggestion that blocking some violet (not blue) light in addition to UV-radiation might improve photoprotection without significantly compromising scotopic vision. Blue light sensitive retinal ganglion photoreceptors were discovered in 2002. They play a critical role in nonvisual photoreception essential for optimal physical and mental health. The phototoxicity-AMD hypothesis has stimulated useful retinal research over the past 3 decades but languished clinically. Epidemiological studies on this subject have limitations, but 10 of 12 major evaluations of this conjecture failed to support it. Furthermore, compelling epidemiological evidence now demonstrates that cataract surgery does not accelerate development or progression of AMD, as it should if light were a significant risk factor for AMD. Nevertheless, the phototoxicity-AMD hypothesis endures as the rationale for blue-blocking IOLs. After almost 20 years of use, however, these IOLs have no scientifically proven clinical justification and reports of their benefits warrant further scrutiny. A small study concluded that blue-blocking IOLs decrease disability glare. It compared pseudophakes 56 months after surgery with colorless, spherical injectionmolded IOLs to those 11 months after surgery with blueblocking, aspheric injection-molded IOLs. If there were clinically significant differences in the glare sensitivity between these dissimilar groups, the colorless IOL group’s performance was disadvantaged by spherical aberration and 4 more years to develop capsular abnormalities and glistenings that produce straylight (the cause of disability glare). Moreover, the study’s nonclinical testing protocol favored yellow filters. Blue-blocking IOL chromophores can not reduce clinical disability glare because they decrease target luminance in the same proportion as veiling straylight. They do not improve contrast sensitivity significantly because contrast transfer at mid-to-high spatial frequencies depends on wavelengths between 500 and 600 nm which are essentially unaffected by yellow chromophores.