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BLUE LIGHT ON YOUR SKIN IS A PROBLEM...........

Discussion in 'Redox Rx' started by Jack Kruse, Aug 18, 2019.

  1. Jack Kruse

    Jack Kruse Administrator

    It’s not just in the Eyes, it is the skin too!
    Until 2017 we thought that melanopsin only existed in the eyes of humans. A study published in Nature showed that subcutaneous white adipocytes express a light sensitive signalling pathway mediated via a melanopsin/TRPC channel axis. It is now evident that melanopsin was present in the skin and fat cells and can translate light signals even if we block blue light from entering our eyes.
    When TRPC receptors are exposed to blue light after dark it is very common that inflammation occurs. This is probably one of the reasons why night shift workers are the highest users of prescription pain relief medication and why we have a major dependence on pain medication in the developed world. Personally, if I have my skin exposed to blue light after dark I get very twitchy and itchy and this is sure fire proof that blue light is irritating my skin via the TRPC channels via melanopsin activation.
    In humans the bond between melanopsin to retinol is a very weak covalent bond. The bond is easily broken by short wavelength blue light. What do human’s live and work under 24/7? You guessed it, BLUE LIGHT. When you look at rodent models you still find melanopsin in the skin, but how they differ from human’s is they have fur covering the skin, which weakens the influence of blue light on melanopsin. That is why ancestrally speaking when we were covered in hair the main receptors for blue light would be found in the eye. However, we have evolved not to need our body hair and as such have exposed our melanopsin to the outside world. This is now a much larger surface area for melanopsin to be affected by artificial blue and green light after dark.

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    WHAT IS THE BLUE LIGHT HAZARD = melanopsin dissociates from retinal and free retinal destroys photoreceptors = destroys optical signaling. The lower your redox is the more retinal is released. Certain stimuli are more apt to release retinal in this way. Blue light is the one that is now best identified. Now that we know the human bond between melanopsin is a weak covalent bond we know that 1G-5G waveforms can also separate them. We’ve believed that melanopsin was only present in the eye since its discovery in humans since 1998. We then discovered it in human blood vessels in 2014. Then, in December 2017 we got the shock data it was also in our skin and subcutaneous fat helping explain why nature put leptin, another photoreceptor molecule, in our subcutaneous fat. Leptin is designed to take optical data from the skin and skin arteriole surface about day and night and couple that with energy balance information and deliver it to the hypothalamus under the cover of darkness. Free retinol from surface light at the wrong time of the day is what ruins this hormones behavior optically. Once leptin signaling is disrupted by circadian mechanisms, the hypothalamus loses control of all growth and metabolism inputs. This leads to many chronic human maladies such as obesity, diabetes, and metabolic syndrome. They are all defects in optical signaling caused by Vitamin A’s ability to destroy photoreceptors. This is why the the authors in the article make this statement, about blue light, ”It's toxic. If you shine blue light on retina, the retinal kills photoreceptor cells as the signaling molecule on the membrane dissolves.”
    That is a definitive unequivocal statement.https://www.ncbi.nlm.nih.gov/m/pubmed/31418890/
     
  2. Jack Kruse

    Jack Kruse Administrator

    mrc likes this.
  3. Jack Kruse

    Jack Kruse Administrator

    Why is the pupillary response the most critical part of the cranial nerve exam diagnosing TBI
    The ipRGCs are known to connect to many brain regions that regulate very different tasks. The cells tell one part of the brain how bright it is outside so that our pupil can rapidly close—in less than a second. When this does not happen with a TBI patient it alerts us there is a problem with the catecholamines like dopamine or with melanopsin damage in the retina due to the liberation of Vitamin A from this opsin. The same ipRGCs also connect to the master clock in the brain that regulates our sleep-wake cycle. However, it takes several minutes of bright light (blue) to make us fully awake. How the same ipRGCs do these very different tasks with different time scales was not clear until now based upon this study. Some clinicians have realized this for a long time and been using the pupillary light test with blue light and red light to see the damage in the eye clock in TBI cases for years.
    The investigators found that the difference has to do with the way that light detected by the retina reaches the brain. By delivering the mini-SOG to the eyes of the mice, they were able to trace the signal to the part of the brain that constricts the pupil in response to light to identify the pathways.
    It turned out these connections were much stronger—similar to water pouring out of a garden hose. Whereas the connection between the ipRGCs and the master clocks in the SCN in the retina were much weaker—more like drip irrigation. This is because the ipRGCs deliver the light signal to the circadian center in the eye clock phenomena through this slower drip system, it takes longer for any meaningful information to reach and reset the brain clock. It also implies since this system works slower in the retina in TBI’s the use of light has to be altered to reduce the symptoms of photophobia and post-concussive effects.
    CITES:
    https://www.cell.com/cell-reports/fulltext/S2211-1247(19)31183-0
     

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