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Eye flotators outdoor only.

Discussion in 'Beginners Area' started by BrunoB, May 27, 2018.

  1. BrunoB

    BrunoB New Member

    Hi good day. Does anyone know why I only see eye flotators outdoors? But not inside the houses. Thanks in advance.
  2. AstralJam8

    AstralJam8 New Member

    I only notice mine when looking at blue sky or illuminated white walls. however, you'll see ALL of your floaters if you look into a microscope at high magnification. looks like pearl bead curtains
    BrunoB likes this.
  3. shannoncorrin

    shannoncorrin New Member

    Floaters are much more noticeable with bright illumination and against a bright background. that’s why you see them better outside.
    BrunoB likes this.
  4. Jack Kruse

    Jack Kruse Administrator

    I'd be concerned about geo-engineering in your area if that was happening to me.
    BrunoB likes this.
  5. KellyR

    KellyR New Member

    I experienced floaters for the first time in my life at age 55 this past summer under same conditions as yourself .
    Two things ....both sides of my property was aerial sprayed 4 times by a GMO farmer and secondly
    I found three ticks on me this early spring .
    I’ve also started experiencing terrible symptoms reflecting Lyme disease about the same time as the floaters .
    Floaters are gone but other symptoms that appears to be Lyme still remains. I live in Ohio..... not much sun here so I am outside just about everyday almost all day spring, summer and fall. Currently working on a Lyme protocol .... heading to Fl soon for some sun .
  6. KellyR

    KellyR New Member

  7. Jack Kruse

    Jack Kruse Administrator

    Eye floaters = problem with Muller's cells = vitreous shrinking due to dehydrating effects of EMF = globe flattening = low dopamine = myopia = poor AM solar exposure to the eye = poor electric charge from environment = geoengineering is possible = or a Maunder minimum/high latitude issue = more high energy radiation coming in from lowerheliopause. This hints that you might have a lot of issues with Muller cells in the retina and often this is related to the flicker effect of light. Outdoor light only flickers when geoengineering particles are above = vitreous.

    1989 David K. Berler did a study on monkey eyes with fluorescent lights. Studies of Müller cell biology using tissue culture and animal models provide evidence of the remarkable capacity of this cell type for graded responses to environmental insult, the capacity to proliferate, translocate from the retina and alter phenotype and thus, functional characteristics of the eye. There is now evidence that Müller cells function as an effector cell type in traction retinal detachment associated with proliferative vitreoretinopathy (PVR) and proliferative diabetic retinopathy (PDR) which leads to blindness. The first step in this process is that flickering leads to bubbles forming inside the Muller cells and I think the scattering of light from the bubbles might be the cause of floaters. I think flicker (LED) is the major cause of floaters. Only one light does not flicker.......SUNLIGHT -------> real terrestrial sunlight.
  8. "Outdoor light only flickers when geoengineering particles are above."

    That's an interesting new insight.

  9. BrunoB

    BrunoB New Member

    You've been "lucky" I think...I started to see them when I was about 8 years old!!
    Actually I should have died as a baby...they killed me with antibiotics! = adnm destroyed= methylation +dq2=etc etc= artificial blue light= chronic disease
  10. Jack Kruse

    Jack Kruse Administrator

    Seeing a floater early = a shit environment or a germ line problem from mom and/or dad.

    A floater is a tiny cluster of cells or fleck of protein lodged in the vitreous humor. This is made from a very special type of collagen with unique piezoelectric and flexoelectric properties which interact with the photoelectric effect of the environment around the globe.

    This clear, stable gel, which looks like a raw egg white, supports and fills the rear two-thirds of the eyeball (see pic below). The vitreous provides another accessory pathway for light coming into the eye through the lens. Muller cells are another.

    The vitreous connects to the retina, the patch of light-sensitive cells along the back of the eye that captures images and sends them to the brain via the optic nerve.

    What you see isn’t actually the floater itself, but the shadow cast it casts onto the retina. Floaters move as your eyes move. Their motion is tied to redox state of the environment around your and in the anterior chamber. They appear to zoom away when you try to look directly at them and drift slowly when your eyes stop moving.

    The vitreous slowly shrinks with age as heteroplasmy rises, causing it to become a bit stringy with time. The strands cast shadows on the retina, causing floaters. About one-quarter of people have some vitreous shrinkage with floaters by their 60s; that rises to about two-thirds of 80-year-olds. Floaters also appear more often in people who are nearsighted/myopic, those who have had cataract surgery or a previous eye injury, and those with diabetes. All these people are low redox patients. Although most people tolerate floaters just fine, others feel that floaters affect their vision and disrupt their ability to read.[​IMG]

    Flashes occur when the vitreous gel bumps, rubs, or tugs against the retina. Like floaters, flashes are generally harmless and require no treatment.


    Sometimes floaters and flashes signal a condition that can lead to vision loss.

    The shrinking vitreous can tug on the retina and pull away from it. The same thing happens in the brain with age. The brain shrinks and atrophies and pulls away from the dura and you become prone to a bleeding subdural with minimal trauma. I call the shrinking vitreous the subdural phenomena of the eye because the retina is not part of the eye. It is part of the brain.

    This event, called a posterior vitreous detachment, is common, and usually doesn’t threaten vision. In about one in six people, a posterior vitreous detachment causes the retina to tear. Fluid from inside the eye can then seep through the tear and separate the retina from the tissues that nourish it. This separation, called retinal detachment, can lead to permanent vision loss. It is becoming more common now in 5G cities in younger people. This is why the geoengineering shows up above. 5G and geoengineering tend to walk hand in hand.

    Retinal tears and detachments are painless. Key warning signs include:

    • new onset of floaters and flashes of light in the eye
    • gradual shading of vision from one side (like a curtain being drawn)
    • the rapid decline in sharp, central vision. This occurs when the macula — the area of the retina responsible for central vision — detaches.
    Retinal tears can be treated in several ways. We can use cold and lasers. Cold as in CT and lasers = light with large OAM and no flicker. Pinpoints of laser light can be used to fuse the retina to the back wall of the eye via photoablation = Laser photocoagulation. Extreme cold is also used in this condition via a procedure called cryopexy. Cold and lasers really act in the same way. This is a clue to the Black swan how cold and OAM are interrelated in quantum biology!!!

    Cold and laser light can also be COMBINED with the injection of a gas bubble into the eye in a procedure called pneumatic retinopexy to repair a detached retina. There are two older operations also used for this called scleral buckling and vitrectomy to reattach a retina. Non-native EMF has a variety of interesting effects to the eye.
    JanSz and Brent Patrick like this.
  11. Katie Durham

    Katie Durham New Member

    Large floaters, and my first need for reading glasses, appeared within a month of developing lyme disease 10 years ago. On a lyme forum I joined these were common complaints. Myopia is a little worse since then. Floaters unchanged and my major vision complaint (they're in the way!). It's well worth it to me to have skin in the game to see if I can make progress on these and other eye issues.
  12. Jack Kruse

    Jack Kruse Administrator

    Lyme is all about the nnEMF environment.

    It is a sign of a defect in your environment and not inside of you. I expect many infections to show up in humans who inhabit environments loaded with nnEMF of all types.
    Functional medicine and alternative docs are abusing thousands into believing a treatment is needed because they have no idea how solar light programs your adaptive immune system. Save your money on drugs and tests. Change your light hygiene first.
    WHY? What is the science telegraphing those who think well?
    ⚕️Does immune response vary by time of day?
    Of course, yet researchers/food gurus continue to be "surprised" by the role of circadian rhythm in everything. Light controls the process and not food.
    A 1974 study found that whether a mouse administered E. coli lives or dies depended on the time of day of the injection.
    Is this why so many people with Lyme and Bartonella and Viral particles in their blood get confused? When these diseases show up in the blood is the infection real or is it the result of a circadian mismatch in the adaptive immune system which is controlled by lymphocytes activated by solar light?
    Can blue light or nnEMF lead to a false positive diagnosis of Lyme, Bartonella or any other viral infection? Yes, it can. This is why all astronauts and cosmonauts come home with these things in their blood.
    So if you have these symptoms in your blood do not be fooled in thinking the defect is in you and floating in your blood. It means your environment is loaded with nnEMF and blue light and the non-toxic pathogens once housed in you are looking to escape an environment that is damaging to your mitochondria.
    THAT IS WHAT IT MEANS to the BLACK SWAN in training.

    The rapidity and power cause massive shifts in heteroplasmy of our mitochondria. I’d strongly suggest that you listen to this video carefully. Heteroplasmy can be described as mitochondrial DNA damage that alter the respiratory proteins in the inner mitochondrial membrane. This radicals changes their ability, and the tissues ability, to tunnel electrons, reduce oxygen, and to make the proper free radical signals in mitochondria. As heteroplasmy percentage increases, NAD+ drops, pseudohypoxia develops, ROS/RNS profiles change = changes in quantum spin and OAM of light, and the amount of ELF-UV increases in a cell. These are the fingerprints of a rising mitochondrial heteroplasmy and FALLING SOLAR redox state
    recoen likes this.
  13. Jack Kruse

    Jack Kruse Administrator

    Also why MS first signs are eye signs too.
    recoen likes this.
  14. Jack Kruse

    Jack Kruse Administrator

    Diseases that have massive acute shifts in mitochondrial heteroplasmy, however, cannot engage regeneration programs (mitophagy); an example of this is Kawasaki’s disease (KD) and sepsis. I covered this disease in recent member webinars.

    In KD, the incident non native electromagnetic light source is very powerful because its frequency is higher powered than the visible UV spectrum, and this disease can kill a healthy child in 24 hours over a large swath of a hemisphere. Sepsis operates in the same way but the mechanism is different.

    The same is true of many prion diseases in the brain too (PD/AD/ALS), except its timescales are in weeks and months as the colony fails. In recent months, I showed members how electromagnetic hypersensitivity syndrome (EHS) can come on more slowly than KD or a prion disease, but just slow enough, that most clinicians do not and would not be able to attribute these patients symptoms to the true etiology of the syndrome driving this increased heteroplasmic % in the respiratory proteins. Everybody bottom in these diseases vary because of the geometry change in their mtDNA. It is tied to their haplotype and SNP profile. This is why no two cases are the same in these diseases and this is why the butterfly effect blocks docs from understanding what is really going on at the quantum level in the cytochromes. This same process is behind other misunderstood diseases like fibromyalgia, Lyme disease, and mycotoxin illnesses like Sick Building Syndrome, sepsis.
  15. Jack Kruse

    Jack Kruse Administrator

    This relates to skin diseases like psoriasis too. It is another disease that comes on over even slower times scales than EHS does due to colony failure, because of alterations of the photoelectric interactions at the surface of our skin, eye, and gut happens at varying rates due to Fermat's law. This leads to variable clinical scenarios.

    This disease is really a gateway disease to many other diseases of neuroectoderm also firmly linked to heteroplasmic amplification of badly performing mitochondrial DNA.

    Psoriasis is a gateway illness to epi-oncogenesis because of its tie to an altered light spectrum and its lack of interaction of light at the surface of the skin.

    The light that hits our surfaces has to be solar derived and not artificially driven by blue color temperature light. blue light alters melanopsin and this liberates the Vitamin A to transition to destroy photoreceptors in the surface of the skin that alters its OPTICAL DENSITY. Once this happens the circadian biology of RBC is also altered. This leads to more collateral effects in the gut and eye of these patients.

    Our skin is specifically evolved to slow specific frequencies at its surfaces in a very sensitive and specific fashion (quantized) by the atomic lattice on our surfaces. This process is quantized by both photochemical and photoelectric interactions. Light has to be slowed down by atoms in specific layers of our skin to be used properly to control cellular growth in that level of the epidermis. When it is not......blue light stimulates the basal dermis to grow like mad and you get plaque psoriasis.
    recoen likes this.
  16. Jack Kruse

    Jack Kruse Administrator

    No one can stop a ticking atomic clock designed to pulse with electromagnetic signals……..but the best of us can figure out how to slow its mechanism down. This allows us to recapture timing and reverse the process. Your skin and eye layers are designed to do just that; slow light to create more time to live the life your choices allow. When the skin/eye is altered with “an emergent autoimmune condition” or "an emergent infectious disease" you cannot do this well because your immune system becomes misprogrammed to fight this battle.

    It also needs solar programming to work properly.
  17. Jack Kruse

    Jack Kruse Administrator

    People forget when sunlight hits the retina/skin 40-60% of our circulation increases in these capillary beds. They react the same way to sunlight. Their reaction to bright chronic blue light devoid of purple UV or red IR light is a different story.

    What does full spectrum sunlight destroy naturally if your skin and eye are in the game of nature?

    UVA and B light naturally lowers adrenalin (the stress hormone of the sympathetic nervous system) while its photons re-zip collagen that cortisol release causes at 4 AM that wakes us up by allowing water flows to occur between glial cells and neurons via the aquaporin 4 gates in the brain. AM sunrise light has no UVA or UVB present initially. It has blue, green, and red present. It has more blue than any other part of the spectrum and this is stimulatory to waking us up. Naturally, UVA light shows up later in the AM, depending upon your location in latitude, and this frequency of UVA light acts to begin to re-zip the collagen in our skin and eyes. That initial blue light stimulus from the sun’s rise is used to unwind our collagen to increase water flows to stretch the interspaces in neurons to wake our body and mind up at dawn from sleep. The aquaporin 4 gates are what is destroyed in Multiple sclerosis, which controls the flow of DDW from astrocytes to neurons, which is another photoelectric autoimmune condition. (Vitamin C is in that water transaction too)

    When we are missing UV and/or IR light for any reason, these photoelectric and photochemical are not made. When full spectrum sunlight is absent in someone who is chronically stressed for any reason, sleep cannot be induced because the ocular melatonin cycle requires that these two frequencies of light be present to stimulate the regeneration processes in the eye during the daytime. If you think about your childhood, when you spent the day at the park of the beach, you might remember how easy it was to fall asleep after good solar exposure. If you had a lot AM light exposure you built your solar callus and this would mitigate a sunburn. If you did not you got burned early and had to take refuge, but either way, your sleep improved. The reason is simple, sunlight induces sleep because this light creates melatonin because the regeneration pathways that use melanopsin need daylight to regenerate.

    When you did fall asleep, the redness of your skin did not come from the thermal burn, but it was from the increased blood flow due to the release of nitric oxide that acted to bring the arterioles of the dermis layers to the surface. This is a photochemical change induced by sunlight to allow the skin to absorb the UVA and UVB light at the surface. UVA and UVB light does not penetrate deep.

    To absorb the UV light we need the circulatory system to come from the dermis and engorged the arterioles with RBC’s. This assumes there is no PEROXIREDOXIN damage in RBC's. (see my circadian RBC redox thread in the Redox forum)

    The RBC’s are filled with hemoglobin and porphyrins that absorb both UV and IR frequencies. The sunburn is really an absorption of too much thermal IR energy. Deep sunburns can result from several factors: excessive sun, or thin skin, thick skin, or a poor adaptation to seasonal light due to chronic use of UV blocking makeup, clothing, or sunblock use in strong light cycles.

    In fact, falling asleep in the strong daytime sun, is a key clinical sign to the astute clinician your normal daily light environment really is. UV and IR sunlight normally lowers endocrine steroids naturally(CT 7 blog) and lowers the nucleic acids in the surface keratinocytes without any liberation of heat on the skin’s surface = AUGER effect This last photochemical change shows you how UV and IR sun working together helps dissipate surface photonic power by exposing more nucleic acids to the incident rays of the sun.
  18. Jack Kruse

    Jack Kruse Administrator

    This photoelectric action helps to prevent aberrant optical scattering at deeper levels in the skin allowing for proper cell signaling in deeper skin levels. This is broken and lost in a disease like psoriasis because the surface nonlinear optics are broken by a serious deficiency in surface sunlight exposure. Many people fail to realize that the epidermis has no nuclear DNA because as skin layers rise to the surface, DNA is exposed to a cell's interior naturally as the cell sloughs away and dies a natural death. This exposure of the nucleic acids to incident sunlight allows the degenerating keratinocytes DNA to absorb all the extra UV light frequencies that the RBC’s cannot tolerate. This photochemical and photoelectric dispersion of energy acts as a free chemical within the epidermis. The irony is, it acts as a natural sun protectant or sun blocker without altering the vitamin D3 cycle at deeper levels. The more photo-degradation our skin senses, the more skin cells show up in the epidermis and the skin thickens in summer months. This gives us an acute skin callus to sunlight.
    Karen & Glen C. likes this.
  19. Jack Kruse

    Jack Kruse Administrator

    This also acts to lower our hemoglobin and hematocrit to lower UV assimilation. If sunlight is a chronic stimulus, melanin production will be stimulated in the skin to protect the skin. Melanin also absorbs all UV frequencies and acts to serve as a storage protein for the power of UV light. It offloads these frequencies of light at night and not during the day. This provides photoelectric protection of other atoms in our skin lattice to protect deeper molecules in the skin from excessive growth. In this way, your skin acts as a time crystal. In psoriasis, this protection system is broken in your crystalline surfaces.

    As a skin cell rises to our surfaces epidermis, our DNA/RNasts like a natural sunscreen for the absorption of surface UV light. What happens to if that DNA is not degenerated enough to perform this vital surface function? More powerful blue and violet light energies get through to deeper levels to drive the growth of the basal levels of the skin.

    This is why many people nnEMF diseases have floaters skin and eye problems linked and few of them know it.......
    Karen & Glen C. likes this.
  20. Jack Kruse

    Jack Kruse Administrator

    If you want to make floaters worse = blindness or a cancer........listen to your eye doctor or your vanity by wearing a contact or sunglasses.

    An important photochemical mechanism that occurs using the photoelectric effect in proteins involves reduction of disulfide bridges (SS) upon UV excitation of Tryptophan and Tyrosine side chains (Kerwin & Rammele, 2007, Neves-Petersen et al., 2002 & 2009a).

    UV-excitation of tryptophan or tyrosine can result in their photoionization and to the generation of solvated electrons. The generated solvated electrons can subsequently undergo fast geminate recombination with their parent molecule, or they can be captured by electrophilic species like molecular oxygen (02).

    Molecular oxygen decreases the chance of pseudohypoxia and this make formation of an exclusion zone (EZ) in water in skin cells. This leads to coherent domains of H3O2+ (EZ), (at a lower pH than normal) that allows photo molecular interactions to occur between cysteine and cystines (EE 12 blog on cysteine/cystine).

    In the eye, the surface cornea gets its oxygen directly from the air in front of it so if you wear sunglasses or contacts and have psoriasis you really are creating a massive mismatch for the mitochondria to deal with and this is why I believe psoriasis is a considered a premalignant AI.

    This will spur massive heteroplastic growth in the deeper layers of the retina and skin altering the central retinal pathways and the arterioles in the skin governing melanopsin dysfunction and alterations of ocular/dermal melatonin regeneration cycles.

    Simple biophysics.

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