Why are contacts a real problem for humans?
- April 30, 2016
Contacts often block UVA light. Neuropsin is a UVA opsin that fine tunes the SCN in the visual system. It is the ultimate metronome for the eye.
- Neuropsin is one of seven related “opsin” proteins in mammals. Four enable the rod and cone cells of the retina to absorb light of different wavelengths and transmit that information to the brain so that the eye can see images. Another opsin, melanopsin (UBI 24), also absorbs light but uses it to guide processes like pupil constriction and circadian rhythms. It is found in nerve cells that connect the retina to the body’s master clock, the suprachiasmatic nuclei of the brain. On its own, this master SCN clock tends to run slower than 24 hours in humans (day dwellers), and faster than 24 hours in mice (nocturnal), so it needs to be constantly reset to the light/dark environment by signals from the retina. Nearly every tissue in the body also has a local molecular “clock” for regulating patterns of activity, but most of them cannot be reset by incident light on their own as the retinal clocks can. This makes the eye very special. Instead, all but one of these molecular clocks are synchronized by the master clock within the brain (SCN)—the exception being the retina, which maintains its own rhythms while sending the master clock the signals it needs to set the light-dark activity synch for the rest of the body.
- Russell van Gelder, M.D., Ph.D., a professor of ophthalmology at the University of Washington, studied the circadian rhythms of genetically tweaked mice that were missing rod and cone cells and melanopsin. As expected, the circadian rhythms of these mice continued cycling but could no longer adapt to changes in light exposure. Surprisingly, though, the activity patterns of their retina’s were still responsive to light changes, suggesting that there was another pigment in play in the eye and skin. That pigment was neuropsin.
- The retina is the only tissue known to ignore the master clock based in the SCN, but it does keep itself on a schedule, based upon all the data we have. That made me ask the question, how does this occur?
- I looked at articles where opsin were removed from animals (see above). It turned out the retinas of the mice without neuropsin lost their ability to adapt to new patterns of light and darkness. I found out that neuropsin and melatonin function must be coupled because melatonin is the hormone of darkness that is regenerated by daytime later morning UV light (9-11AM). Was neuropsin key in this recycling of melatonin? Does neuropsin also work with UV light in some way during the day?
Jack Kruse, Today at 8:40 AM
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The scientists working with these mice began by repeating their experiments with different wavelengths of light, the they found that neuropsin responds to UV-A and violet light up to 400 nm. This implied that the retina uses separate light signals based upon frequency to set its own clock and that of the body’s master clock in the SCN. The central retinal pathways controlled by melanopsin are exquisitely sensitive to light in 435nm-465nm light which is based in the blue/green part of the spectrum. 400-430 nm light is present in early AM sunlight, before UVA shows up, and it becomes very prominent at dusk when the sun slowly sets. These frequencies of light are ideally absorbed by melanopsin over several hours at dusk. Melanopsin can be thought of as an opsin that pays attention to light as it dims. Regarding neuropsin, we still don’t know precisely what kind of signals, either photonic, chemical or electrical, that neuropsin uses to set the retina’s clock. My current bet it will be found to be photoelectric because of another clue the eye has given us. Neuropsin is found in the cornea and the skin and this makes it very unique. Why would we have a UV-A light sensor fro bright mid day light frequencies in a transparent cornea. Since neuropsin works via UV-A light this is a tell that our modern beliefs that the cornea and lens block UV light is a pure fallacy. It also tells us that sunlight is important to melatonin recycling.
- How did we find out neuropsin was in the cornea? Researchers used a specialized “locator gene,” called a reporter gene, to figure out where neuropsin does its work. They found that, like melanopsin, it is located in neural cells that connect the retina to the brain via the central retinal pathways. From there though, we do not know precisely yet today where these particular cells go within the human brain. Using this technique they did mysteriously confirm it is present it in the cornea. This shocked many, including the eye doctors. The cornea was not thought to contain any UV photo pigments by ophthalmologists, since its job is to let light through to the rest of the eye. We now know this data needs updating.
- It also maybe an indictment of cataract surgery and of lasix