CAN THE LIGHT USED IN EYE SURGERY SET THE STAGE FOR ALZHEIMER'S DISEASE ???

Pharmacological treatments for Alzheimer’s disease (AD) have not resulted in desirable clinical efficacy over 100 years. Hydrogen peroxide (H2O2), a reactive and the most stable compound of reactive oxygen species, contributes to oxidative stress in AD patients.  What does elevated H2O2 do to neurons?

IN AD in human more glutamate is released when the environment is loaded with blue light and/or nnEMF.  This in turn cascades to deplete Vitamin C.  
Where did this concern come from?  Brain and eye surgery where light illumination is used.  
Concerns have been raised about whether operating microscopes and endo-illumination used during ophthalmic surgeries contribute to retinal damage. Despite the recognition that ascorbic acid (vitamin C) helps to protect the eye from light and the abundance of vitamin C in the retina, artificial aqueous humors used during surgery USUALLY only contain the antioxidant glutathione (GSH below).

Light-induced retinal damage is irreversible and results in permanent visual loss, especially when damage involves the macular area. Ocular tissues are more sensitive and vulnerable to MAN-MADE light than other organs (Sliney, 2002). Although light-induced photoreceptor damage has been well described (Noell et al., 1966; Kuwabara and Gorn, 1968), illumination of the ocular fundus by man-made light is inevitable in clinical settings during ocular examinations and surgeries. As a large number of intraocular surgeries, such as corneal and cataract surgeries and vitrectomies, require direct microscopic illumination of ocular tissue, acute retinal damage has been increasingly observed. The damage is thought to result, at least in part, from the effects of this illumination (Arafat et al., 1994; Kuhn et al., 1991; Michels et al., 1992; Kleinmann et al., 2002). What most eye docs fail to realize is this light does not have any UV light in it, yet they continue to blame UV light for damage.  If they used a spectroscope they would see that blue light is the most dominant light in artificial light and is behind the cause of eye damage during surgeries.  Most experiments studying light-induced injury show retinal damage with continuous illumination over several days (Grignolo et al., 1969; Malik et al., 1986; Edward et al., 1993; Organisciak et al., 2003).
Very little UV light penetrates the surface of the globe but all of the blue light from the bulbs we use do penetrate the globe to affect the retina.

Photooxidation of light, in turn then depletes the patient's eyes of endogenous Vitamin C and it H2O2 directly inhibits formaldehyde dehydrogenase (FDH) in neurons. FDH inactivity and semicarbazide-sensitive amine oxidase (SSAO) disorder resulted in endogenous formaldehyde (FA) accumulation. Unexpectedly, excess FA, in turn, caused acetylcholine (Ach) deficiency by inhibiting choline acetyltransferase (ChAT) activity in vitro and in vivo.  

Acetylcholine (ACh) has a crucial role in the peripheral and central nervous systems. The enzyme choline acetyltransferase (ChAT) is responsible for synthesizing ACh from acetyl-CoA and choline in the cytoplasm and the vesicular acetylcholine transporter (VAChT) uptakes the neurotransmitter into synaptic vesicles. Following depolarization, ACh undergoes exocytosis reaching the synaptic cleft, where it can bind its receptors, including muscarinic and nicotinic receptors. ACh present at the synaptic cleft is promptly hydrolyzed by the enzyme acetylcholinesterase (AChE), forming acetate and choline, which is recycled into the presynaptic nerve terminal by the high-affinity choline transporter (CHT1). Cholinergic neurons located in the basal forebrain, including the neurons that form the nucleus basalis of Meynert, are severely lost in Alzheimer’s disease (AD). AD is the most ordinary cause of dementia affecting millions of people worldwide. The hallmarks of the disease are the accumulation of neurofibrillary tangles and amyloid plaques. However, there is no real correlation between levels of cortical plaques and AD-related cognitive impairment.  The plaques correlate with the disease process because a falling mitochondrial redox state links to protein misfolding.  Nevertheless, synaptic loss is the principal correlate of disease progression in AD and loss of cholinergic neurons contributes to memory and attention deficits.

This is why AD brains have low voltage on EEG.  Levels of ACH are linked to voltages on EEG studies.

  
What else do the eye docs forget to account for during their surgeries?

 
Free radical scavengers such as glutathione (Winkler and Giblin, 1983), α-tocopherol (vitamin E) (Penn et al., 1987) and ascorbic acid (vitamin C) (Woodford et al., 1983) are thought to serve as components of an endogenous defense system that helps to limit light-induced retinal damage. Vitamin C is also abundant in the human retina, where its concentration in guinea pigs and rats is about 1.6 mM (Heath et al., 1961; Woodford et al., 1983). However, intraocular irrigating solutions currently employed during ocular surgery in humans only contain oxidized glutathione as a corneal protectant (Edelhauser et al., 1975, Araie, 1986). Importantly, these surgical solutions USUALLY do not contain vitamin C, even though human aqueous humor contains high concentrations of the vitamin.

Does this make any sense?  Could this be why anterior chamber surgery has the side effect profile it does today?

  
The public does not know these answers because researchers rarely ask these questions in their experiments and never control for the light spectra used in surgery.  How can we learn when we ask the wrong questions in our studies? 

 
How could we measure this if we wanted too? 

 
LDH = Lactate dehydrogenase = lactate biochemistry = the link to Vitamin C physiology of the light stress response.

 
LDH activity can be measured spectrophotometrically from samples of blood taken every hour during surgery. The activity of LDH can be determined by the rate at which its substrate, pyruvate, is reduced to lactate, as monitored by diminished absorbance of the reduced form of nicotinamide adenine dinucleotide (NADH) at 340 nm at cytochrome 1.   If I can figure it out, why can't they?  

Remember the reduction of lactate implies the additions of electrons to lactate.  Guess where the electrons come from in the human retina?

  
Vitamin C is an electron donor in human biochemistry.  This implies that Vitamin C presence or absence allows a stressed cell to choose to use lactate over glucose in metabolism.  

The protective effects of vitamin C are not mimicked by glutathione, an agent routinely included in surgical solutions used in eye surgery, because glutathione does not donate electrons as well in the retina (below) in biochemical reactions as Vitamin C does. 

It means that ocular surgery using solutions devoid of antioxidants normally found in the retina may be driving diabetic changes in eyes and brains below our perception as surgeons.

  
How is that for an unintended consequence? 

 
Following extensive light exposure in surgery, it has been found that the level of vitamin C in the retina is diminished (Woodford et al., 1983). Moreover, the fact that diurnal mammals have a normally high concentration of vitamin C in their aqueous humor but nocturnal mammals do not (Koskela et al., 1989) suggests a significant role for vitamin C in protecting diurnal animals from sunlight.  Most eye research is done on nocturnal mammals so this effect magnifies the problem for humans.  It should be clear now that Vitamin C does have a solar component  of action (diunal actions) most never account for in their studies. Interestingly, light-induced retinal damage may be more pronounced in scorbutic than control monkeys (Tso, 1987), again suggesting the importance of vitamin C as a retinal protectant in humans and primates is reenforced.

FACTOID:  What does this imply for 5G and the IoT...........needs that RFID eye chip below to control you. The bar code for the eye is terrestrial sunlight not man made parts of the electromagnetic spectrum used for telecommunications and back lit tech screens all cause these problems in your eyes.

  
This all points out why blue light and nnEMF are LIKELY causative in the etiology of Alzheimer's Disease in our modern world. 

 
2G-5G networks create the Fenton free radical in our mitochondria as the pictures in this blog show. 

 
What does this imply for eye surgery and for AD risks longer term?

You've got to ask the right questions if you're going to find the right answers.  On your transition to a Black Swan, you need to ask great questions.  Questions are how you uncover real truths in Nature to learn what you should and unlearn what you must.

  
Considering the risk of phototoxicity of manmade blue lights via the blue light hazard (above)-, van den Biesen et al. (2000) warned that the safe exposure time of commercial endo-illumination is less than 11 minutes, a time frame that is unrealistic in today's vitreoretinal surgery. Complicating this is the fact that the detached retina is even more sensitive to light (Zilis et al., 1991). Could this be why these surgeries seem to have a high failure rate and lead to more eye surgery? 

 
These observations, coupled with the results of the present study, suggest that supplying effective free radical scavengers other than glutathione in surgical solutions may be beneficial for preventing light-induced retinal damage during intraocular surgery, especially vitrectomy, and for maintaining the physiological integrity of the retina for an extended period following surgery. The importance of carefully considering the content of surgical solutions is magnified by the fact that the following vitrectomy the retina is exposed to the ophthalmic solution for 24 hours or more, given the time it takes to replenish the 4.0 ml vitreous cavity with endogenous aqueous humor that is produced at a rate of 3.04 μl/min (Tsukamoto and Larsson, 2004). 

Exogenous Vitamin C itself is not appropriate for use in surgical solutions. In the presence of ferrous ions released during bleeding, exogenous vitamin C participates in the Fenton reaction with iron liberated from bleeding (Fisher and Naughton, 2004) and this results in the production of toxic hydroxyl radicals with blue light hazard (435-465nm light).

This thread should be eye opening to any skeptic that blue light or nnEMF can cause disease in man.

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