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Dry Eyes

Discussion in 'Ask Jack' started by Dickran, Feb 12, 2019.

  1. Dickran

    Dickran Silver

    Hello Dr. Kruse,

    Having problem with dry eyes. Not enough oily tears for eyes causing inflammation of eye surfaces.

    Using eye drops with no preservatives until I can hack the problem.

    Suggestions on how to fix?

    - I'm 71 year old healthy male.
    - "skin in the game" in So.California- AM sun ~30 minutes (UV 1 2) 3-4 times a week and day sun UV 4-5 right now
    3-4 times per week.
    - eating epi-paleo with seafood as much a possible.
    - wear blue light day and night blockers.
    - nnEMF low with WiFi off at night.
    - drink non-fluoride water and San Pelllegrino.
    - blood tests in normal ranges with Vit D at 70.
    - sleep 7.5 to 8 hours a night.

    Best Regards,
    Dickran
     
  2. Jack Kruse

    Jack Kruse Administrator

    One of the earliest signs of neurodegeneration process in the eye and brain is developing is the famous dry eye. When I hear somebody is complaining of a new onset dry eye I no longer think about the autoimmune conditions that usually cause it, I always ask questions about indoor existence and the use of technology gadgets and then begin to look for other symptoms that maybe so mild they are ignored by the patient. Then I ask about the city and state they live in. Then I ask about how they use the AM sunrise every day prior to them asking me about their dry eyes. Their answers usually contain the clue why their eyes are dry. It is always tied to a choice about their light environment. Dry is a blue light hazard problem usually linked to a dopamine deficit in the retina afferent arrays into the brainstem and back via the efferents to the lacrimal glands. It is a quantum clue that danger lurks in the future of that brain if that environment does not change. Blue light hazard causes most cases of the dry eye these days.

    Where have you heard this before? Melanopsin dysfunction. Protect your eyes and skin, avoid screens and blue light, wear blue blockers and use blue light filter apps on your phone.
    https://www.dailymail.co.uk/health/article-6693223/How-phones-blue-light-harm-skin-sight.html

    Based on your answer above......your city and state contain serious nnEMF risks, add in the blue light cocktail of modern life........Voila.

    [​IMG]


    Is nature living inside of you? If not, what kind of life have you built or settled for?

    The irony of life is we have little control over the world around us because we cannot harness nature, but full control over the world within us that we rent from nature for a short period of time.

    The acceptance of mediocrity is a slippery slope. The price of excellence is discipline. The price of mediocrity is disappointment. Always ask yourself “how far away from perfect was I with these dry eyes? Then your next thought should be how do I close that gap?”

    Leadership isn’t a position or title. It’s a way of living your life because you think more deeply than most even try too. Some people lead, some manage and others follow. Me, I lead people to the sun and I follow her like a lemming so that their eyes can once again tear in the Eastern sun at every sunrise.

    [​IMG]
     
  3. Jack Kruse

    Jack Kruse Administrator

    Can early eye symptoms help people avoid Parkinson's disease? Is a lack of dopamine there a predictor of future brain disease from a poorly lighted environment? The paper linked below is from 1963. It was the first time PD and the retina were linked in the literature. Since then a lot more has been learned about neurodegeneration but not too much about how light and the retina are fundamental to the disease. Observations from Malmfors in 1963 first highlighted the role catecholamines might play in rat retinal function. It was noted that rats (nocturnal but it was 1963!!), pharmacologically depleted of catecholamines using reserpine, showed marked photosensitivity despite their small pupil size. The principal dopaminergic (DA) cell in the retina is an amacrine subtype called A18 although a second, less well-defined DA cell has also been identified in primate and rodent retinas. The density of A18 neurons is low but their widespread dendritic arborization and long fine axons ensure overlap with neighboring DA cells as well as other amacrine cells and bipolar cells. From a functional physiologic standpoint, it is now clear that DA neurons are depolarized by the light onset and this occurs under both scotopic and photopic conditions, implying input from depolarizing bipolar of both rod and cone varieties (Zhang et al., 2007). DA neurons contact two other types of the amacrine cell belonging to the rod pathway—the AII and the A17 amacrine cell. The A(II) amacrine cells receive input from the rod and cone bipolar cells and pass this information forward to ON and OFF RGCs (Famiglietti and Kolb, 1975; Dacheux and Raviola, 1986). AII cells are coupled to cone ON bipolar by gap junctions allowing rod signals to flow into the ON cone pathway (Xia and Mills, 2004). They also make glycinergic synapses onto OFF RGCs, inhibiting them under scotopic (rat) conditions. Thus, not only are the A(II) amacrine cells involved in the so-called ‘horizontal’ processing of retinal signaling but also play a pivotal role in channeling visual information ‘vertically’ through the retina in low light states. AII cells express D1-subtype dopamine receptors and gamma-aminobutyric acid type-A (GABA-A) receptors, activation of the former leading to ‘excitation’. Given that DA cells also contain GABA, this suggests that both neurotransmitters are involved in modulating amacrine function in the retina and maybe where PD begins when too much blue light is illuminating the retina to destroy dopamine signaling in the eye before symptoms commence in the brain. I point this out because one of the earliest signs of PD is the famous dry eye. When I hear somebody is complaining of a new onset dry eye I no longer think about the autoimmune conditions that cause it, I always ask questions about indoor existence and the use of technology gadgets and then begin to look for other symptoms that may be so mild they are ignored by the patient. It is a quantum clue that danger lurks in the future of that brain if that environment does not change. http://onlinelibrary.wiley.com/doi/10.1111/j.1748-1716.1963.tb02632.x/full
     
    Richelle Jones and CjHedberg like this.
  4. Jack Kruse

    Jack Kruse Administrator

  5. Jack Kruse

    Jack Kruse Administrator

    The pupillary light reflex allows the eye to adjust the amount of light reaching the retina and protects the photoreceptors from bright lights. The iris contains two sets of smooth muscles that control the size of the pupil. These muscles are under autonomic control and they cannot be conditioned by behavior. They respond to characteristics of light. The interesting aspect of the retina surface is that it projects to the central grey matter where the PVN rules the sympathetic system and parasympathetic and sympathetic control of the cranial nerves are housed segmentally in the brainstem. This is where dry eyes begin as I laid out in the Time 1 blog.

    The lacrimal gland is the major contributor to the aqueous layer of the tear film which consists of water, electrolytes and proteins. The amount and composition of this layer is critical for the health, maintenance, and protection of the cells of the cornea and conjunctiva (the ocular surface). Small changes in the concentration of tear electrolytes have been correlated with dry eye syndrome. While the mechanisms of secretion of water, electrolytes and proteins from the lacrimal gland differ, all three are under tight neural control. This allows for a rapid response to meet the needs of the cells of the ocular surface in response to environmental conditions. The neural response consists of the activation of the afferent sensory nerves in the cornea and conjunctiva to stimulate efferent parasympathetic and sympathetic nerves that innervate the lacrimal gland. Neurotransmitters are released from the stimulated parasympathetic and sympathetic nerves that cause secretion of water, electrolytes, and proteins from the lacrimal gland and onto the ocular surface.

    Your environment is sensed via your cornea. This is why eye signs are key. IT IS THE MAIN topologic effect Uncle Jack looks for. The first segment of the lacrimal gland functional unit that regulates lacrimal gland secretion is the activation of sensory nerves in the corneal and conjunctival epithelia. The ocular surface epithelia are richly endowed with sensory nerve endings that respond to changes in the environment causing a rapid secretion of lacrimal gland fluid to wash away and chemically neutralize foreign substances that have entered the tear film (Mutch 1944; Ruskell 1971; Ruskell 2004). Stimulation of corneal sensory nerves causes both fluid secretion from and vasodilation in the lacrimal gland. Lacrimal gland fluid secretion is dependent upon vasodilation with increased blood flow augmenting secretion and decreasing blood flow inhibiting stimulated-secretion (Botelho, Martinez et al. 1976).

    The stimulation of corneal sensory nerves stimulate the lacrimal gland by a trigeminal-parasympathetic reflex (Yasui, Karita et al. 1997). This reflex was mediated by the facial nerve, but not glossopharyngeal nerve. Activation of the facial nerve stimulated lacrimal gland blood flow and increased tear volume (an indirect measurement of lacrimal gland secretion) with similar intensity and duration of stimulation, but the efferent mediators of the two functions differed substantially. Secretion was blocked by muscarinic antagonists, but vasodilation was not blocked by muscarinic, VIP, or sympathetic antagonists. The mechanism responsible for the coupling between lacrimal gland vasodilation and fluid secretion is unknown in books but I believe it is light and melanopsin in the vessels around the eye.

    Although the lacrimal gland is innervated by both the parasympathetic and sympathetic nerves, the parasympathetic system predominates, both anatomically and functionally.

    Ding et al (Ding, Walcott et al. 2003) reviewed the extent of sympathetic innervation and found it is not only species dependent, but also the object of discrepancy in the literature. For rat, mouse, guinea pig, and monkey lacrimal gland, some reports show dense and some show sparse sympathetic innervation. Ding et al (Ding, Walcott et al. 2003) found different densities of sympathetic innervation in distinct areas of the gland. THIS IS A BIG CLUE for the black swan how light operated between scoptopic and photoptic retinas. Careful re-evaluation of the density of sympathetic nerves with multiple markers of sympathetic nerves including tyrosine hydroxylase, dopamine beta hydroxylase, and phenylethanolamine-N-methyltransferase is warranted because of the effect on DOPAMINE.

    Blue light exposure causes low dopamine effects and this will affect tearing.

    The story is complete.
     
    Richelle Jones and CjHedberg like this.
  6. Jack Kruse

    Jack Kruse Administrator

    Ubiquitination 24 should be re read too.

    [​IMG]
     
    Richelle Jones and CjHedberg like this.
  7. Dickran

    Dickran Silver

    WOW! Working on dry eye recovery will be my mission for optimal health. What I am wondering is how I identify the blue light that is causing this problem.
    I am wearing day blue light blockers and night time blue light blockers as much as I can. Suggestions on what else to do? Suggestions on how to treat dry eyes until this resolves?

    Thanks,
    Dickran
     
  8. Jack Kruse

    Jack Kruse Administrator

    Meters and a spectroscope is how I do it.
     
    CjHedberg likes this.
  9. caroline

    caroline Moderator

    this is a must read everyone ........
     
    CjHedberg, Lahelada and Karl Sapp like this.
  10. Dickran

    Dickran Silver

    Got it... thanks...
     

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