On Macular Degeneration….Again…..
February 28th, 2006 | No Comments »Reading the New York Times this morning prompts me to write again about the MD condition and its connection with my explanation of light interaction in the eye. It is my premise that the fundamental cause of the MD condition is the entrance of ultraviolet radiation into the eye with the eventual result, after perhaps many years of insult, being irreversible biological damage to the macula/retina. The only thing new in this statement is my emphasis on the term fundamental. Public statements go on to parse the condition defining various medical states of degradation (wet or dry MD?) and pointing to regimens of vitamins and minerals that probably have the effect of rendering the retina healthier and staving off eventual degradation. But I would claim that the fundamental issue involves UV radiation.
I have found (discussed in other parts of this page, with references) that the wavelength of light is associated with constriction of the pupil of the eye. This connection seems not to be well understood it being generally assumed that light intensity is the sole controlling factor in pupillary constriction. The size, or diameter, of rod receptors determines, through the dimension of rod-to-rod apposition length, the (probably) exact short wavelength limit of visual response. The 400nm wavelength generally quoted as the limiting wavelength was undoubtedly evolutionarily selected as it is just at the point of a biologically-damaging UV threshold. I have proposed that the rod array of the peripheral retina acts jointly as the “light meter” of the eye controlling, through pupillary constriction, light – and particularly short wavelengths – entrance into the eye. I would therefore propose that if one wants to look for a genetic basis for the MD condition it will be found in the factors controlling the diameter of rod receptors on the retina.
I add what I had written on this subject on April 14th, 2003
On Blue Light And Age Related Macular Degeneration (AMD)
One proposal of this model is that the peripheral retina, i.e., the predominantly rod-containing area beyond approximately twenty degrees, is integrated (rod receptors connected in parallel) to generate the signal that controls pupillary constriction and light entrance into the eye. The peripheral retina then becomes, in effect, a “light meter” functioning to control the amount of light to levels that preclude damage to sensitive eye structures. It seems widely held that light intensity alone (i.e., luminance) controls pupillary constriction. A less obvious question asks what effect wavelength might have on constriction and, if so, what is the most effective wavelength or wavelengths?
This question seems not to have been intensively investigated but one paper by Drew et al (”Pupillary Response to Chromatic Flicker”, Exp. Brain Res., (2001) 136, pp256-262) found that hue (color) modulated flicker has a much greater effect on constriction than a luminance modulated signal. Their words: “red-blue color-paired flicker consistently produced the strongest constrictions. These responses occurred even when the flicker was of a lower luminance, both physically and perceptually, than a preceding non-flickering color, indicating that chromatic rather than luminance-sensitive mechanisms are involved in this response” (my italics).
George Wald in his Nobel lecture reported that the peripheral retina was monochromatic but he did not go on to specify wavelength. This result is in consonance with this model but we go on to find and predict that the rod-rod appositions of this portion of the retina will render it solely sensitive to short wavelength (blue) light. Moreover, we propose that this provides a fundamental basis for the fact that 400 nm forms the short wavelength limit of visual response. But important here: we propose that blue light controls pupillary constriction.
It would seem that nature would have so designed the system using this highest energy radiation to control light entrance into the eye abutting as it does the damaging UVA region (320-400 nm).
It has been asserted that the yellow carotenoid pigment lutein present in the eye has the function of absorbing UV radiation preventing damage to ocular structures. We would propose that this pigment does so function but provides a “second line of defense” against UV in individuals exposed to excessive sunlight where pupillary constriction alone cannot provide sufficient protection. I would like to see a study of the lutein concentration in the eyes of individuals as a function of sun exposure in their occupation etc. Has such a study been made?
The onset of age related macular degeneration (AMD) may be related to a loss of the ability to constrict the pupil of the eye as one ages. Is there a quantitative measure or test of pupillary constrictive ability - quantifying the “strongest constrictions” seemingly measured in the above cited paper by Drew et al? Has such a study been made?
Thus I propose that there are grounds for the proposal that there is a connection between higher energy, i.e., blue radiation, and the onset of AMD. Reinforcement should be given to the advice to wear blue-blocking sunglasses etc to minimize this specific wavelength into the eye.
The fundamental rule of this hypothesis is that the geometric rod-to-rod distance (mediated by the diameter of the inner segments of these recep;ors) in the peripheral retina sets the discrete short wavelength limit of visual response - not “almost” but the exact limit. I have assumed this to be 400 nm as this is the oft quoted value. But…there are probably genetic differences in the size of rod receptors among individuals. Supposing that rods were slightly smaller… this would shift the short wavlength limit towards, or into, the damaging UVA region. Might it be found that rod size varies in this manner in individuals suseptble to AMD?
GCH
