Drs Mainster and Sparrow have provided an excellent perspective on the relative merits and difficulties of extending intraocular lens (IOL) absorption into the blue portion of the spectrum.1
However, they have not considered an unintentional consequence of blockage of the blue portion of the spectrum—reducing the activity of intrinsically photosensitive retinal ganglion cells.2,3 These cells subserve several non-visual ocular photoreceptive tasks, most prominently the entrainment of the circadian clock to external light-dark cycles.4 Pupillary light responses in mice are also at least partially controlled by this system, which appears to use a novel opsin (melanopsin)5,6 and possibly also a flavoprotein (cryptochrome)7,8 as photopigments.
Experiments in mice have suggested that the action spectrum for these photopigments peak in the blue, at approximately 480 nm, but with substantial sensitivity to blue light to 430 nm.9 This system appears to be functional in humans as documented by the action spectrum for light suppression of the pineal hormone, melatonin.10,11
The clinical importance of these photoreceptors is presently unknown, although it appears that loss of retinal ganglion cells predisposes children and young adults to disorders of sleep timing that outer retinal disease does not.12 While, as the authors note, there may be substantial benefit in blocking blue light phototoxicity, particularly for patients with pre-existing outer retinal degeneration, these lenses may have unintended consequences with respect to the timing of sleep and wakefulness or levels of certain neurohormones.
References
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