Check out my latest article: WHY ARE ALS AND ATRIAL FIBRILLATION LINKED? linkedin.com/pulse/why-als-…

The oculomotor nerve (CNIII) is responsible for controlling the pupillary size.  It contains several parasympathetic functions related to the eye. The oculomotor PNS fibers originate in the Edinger-Westphal nucleus in the central nervous system and travel through the superior orbital fissure at the base of the orbit to synapse in the ciliary ganglion located just behind the orbit (eye). From the ciliary ganglion, the postganglionic parasympathetic fibers leave via short ciliary nerve fibers, a continuation of the nasociliary nerve (a branch of the ophthalmic division of the trigeminal nerve). The trigeminal nerve is critical in the mammalian dive reflex.  This is why the astute quantum clinician can use cold water on the face to help people.  The short ciliary nerves innervate the orbit to control the ciliary muscle (responsible for accommodation) and the iris sphincter muscle, responsible for miosis or constriction of the pupil (in response to light or accommodation).  

As bright light enters the pupil, the carotid circulatory system must provide blood flow, and the superior cervical ganglion optimizes this coordination.  This is often not appropriately yoked with circadian mismatches in heme proteins Rev Erb Alpha and beta.  This is especially true in diabetics and children with cyanotic heart disease.  This means this ganglion controls blood flow to the CNS due to a light-activated mechanism.  Since the brain gets 20% of cardiac output, this has a massive effect on the quantum abilities of the eye. It also means that when bright light does not increase cerebral blood flow, we know we have a patient with a serious circadian mismatch in the local environment.
2. Why don't I listen to people who wear sunglasses or contacts? BECAUSE THEY CANNOT THINK WELL.

How does a brain surgeon know this and prove it to the public?

DECENTRALIZED SCIENCE. Image
3. Normally, bright light from the sun increases metabolic demand in the retina and visual cortex, triggering SCG-mediated vasodilation to increase CBF. This is part of neurovascular coupling, where neural activity drives blood flow (e.g., via nitric oxide release, as discussed in my blogs at length). Sunlight also stimulates PER clock genes. This is important for cardiac function.

Circadian Mismatch Indicator: If CBF does not increase with bright light, it suggests:
SCN Dysfunction: Inadequate light exposure (e.g., UV blockage) impairs circadian entrainment.Image
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4. Sympathetic Dysregulation: The SCG fails to adjust blood flow, possibly due to circadian misalignment of Rev-Erb-alpha/beta/beta or CCO dysfunction. Mitochondrial Stress: Low NAD+ and pseudohypoxia impair vascular responsiveness, as mitochondria in endothelial cells (e.g., in the carotid system) rely on CCO for energy and signaling.

Note the bottom line of the slide.Image
5. Clinical Relevance: This mismatch should manifest as visual symptoms (e.g., poor adaptation to light), neurological symptoms (e.g., fatigue, cognitive impairment), or systemic issues (e.g., arrhythmias in Afib).
It’s a diagnostic clue for clinicians to assess light exposure, circadian health, and mitochondrial function.

Relevance to My Thesis: This aligns with my focus on light as a critical environmental input for mitochondrial and autonomic health. It also supports my earlier point about UV light’s role in nitric oxide release and vascular tone, which directly influences CBF.Image
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6. Without proper cerebral blood flow, one cannot think well, so when your profile pic shows you wearing them, I ignore you and your opinion. Why? Because I know I am wiser than you. Image
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More from @DrJackKruse

Apr 30
The main finding of this study is that levels of 5-AVAB and cLP are higher in newborns who later develop autism compared to neurotypical controls.

They blame diet but miss the real cause: transgenerational epigenetics of the parent germ line to light programming is a critical miss in this paper. Why are they blaming it on diet?

We already know that the TCA cycle cannot be used without proper solar signaling, which fully explains this volcano graph.

They found additional putative associations between metabolites previously linked to autism in cross-sectional studies, indicating that these alterations are likely to be present at birth. If this is the case, it cannot be diet, but it could be transgenerational UPEs in the parents' germline, as I told Nicole in the Quantum Engineering #45 blog I wrote for her daughter, Echo. @MitoPsychoBio @NicoleShanahan

Highlighting alanine as a robust biomarker for primary mitochondrial dysfunction in children with autism, with a high odds ratio and statistical significance (-log(p) > 4), suggests that since alanine metabolism is disrupted, it has to be due to impaired mitochondrial function, which affects energy production and amino acid handling.

Blue light, with its high-energy, short wavelength (around 450-495 nm), penetrates tissues and can influence mitochondrial activity. Blue light via melanopsin signal disrupts NAD+/NADH. Mitochondria contain chromophores like cytochrome c oxidase, which absorb blue light. This absorption can alter the electron transport chain, potentially increasing the production of reactive oxygen species (ROS).

Excessive ROS can impair mitochondrial function, leading to metabolic shifts, like elevated alanine, since alanine is a byproduct of pyruvate metabolism when the TCA cycle is disrupted. Blue light exposure, especially at non-optimal times (e.g., evening screen time), should dysregulate circadian rhythms of the parents prenatally via melanopsin in the retina, further stressing mitochondrial function through hormonal imbalances (e.g., melatonin suppression). This would be passed on to the child. A sign that it has happened is a child with jaundice. Jaundice is also associated with autism risk in children.

nnEMF, such as from Wi-Fi or cell phones, operates at frequencies (e.g., 2.4 GHz for Wi-Fi) that can interact with biological systems. nnEMF may disrupt mitochondrial membrane potential by affecting voltage-gated calcium channels, leading to calcium influx and oxidative stress. This stress can impair mitochondrial energy production, pushing cells toward glycolysis and increasing alanine production as a compensatory mechanism. The slide’s focus on mitochondrial dysfunction aligns with this, as nnEMF-induced stress should exacerbate the metabolic imbalances seen in autism.

In my decentralized photo-bioelectric thesis, blue light and nnEMF act as environmental levers that disrupt the biochemical "boxcars" (metabolic pathways) by derailing mitochondrial function. Blue light directly affects mitochondrial energy production and circadian signaling, while nnEMF adds a layer of electromagnetic stress. Both converge on oxidative stress and metabolic dysfunction, reflected in the slide’s alanine elevation. This suggests that controlling light and nnEMF exposure could be key to managing mitochondrial health in autism.Image
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2. Altered products of gut bacterial tryptophan metabolism have previously been reported in children with autism, but no one has linked this to my work in the slide. It is the light dummy. Image
3. Why the Study Misses This Connection
The study attributes metabolic differences partly to maternal diet. Still, as I pointed out earlier, these alterations at birth suggest a pre-conception or prenatal origin, likely transgenerational UPE program of the parental germline.

While the study acknowledges the role of gut bacterial tryptophan metabolism in autism, it doesn’t explore how environmental factors like light exposure could influence this pathway via melatonin.

Researchers are unaware of my work on light programming via UPEs because they are biochemists at heart, or they may lack the framework to connect light-induced melatonin changes to microbial metabolism and transgenerational effects due to scientific myopia.

Autism research often focuses on more tangible factors like diet or nuclear genetics. At the same time, light’s role in epigenetics and mtDNA metabolism is less studied, despite growing evidence of its impact on circadian and mitochondrial health.Image
Read 7 tweets
Apr 27
1. A child born with jaundice exhibits an atavistic state, reflecting GOE-era stressors where porphyrins (and bilirubin) acted as oxygen sensors, generating ROS/UPEs under light stress. Parents and pediatricians do not understand what jaundice really means. It is a child born under mtDNA duress. They need more sun and less centralized doctoring, otherwise they become more injury prone to any mtDNA toxin. These are things MAHA won't find by September.Image
2. Neonatal Jaundice: Blue Light Therapy is a Human Disease Incubator
Neonatal jaundice treatment shifted from full-spectrum light to blue light (425–475 nm) in the last 35 years, ignoring quantum biology. Centralized medicine, blind to neuropsin (UVA receptor) and melanopsin (435–465 nm), assumed blue light was safe for bilirubin photoisomerization (Oláh et al., 2013). Infants, with translucent skin and underdeveloped skeletons, allow deep blue light penetration, reflecting off bone to stimulate melanocytes. Long-term studies reveal increased dysplastic nevi in these children, a melanoma risk factor (Oláh et al., 2013). Never assume that the optical window of children with jaundice is normal, because they are not.Image
3. Blue light’s mitotic effect mirrors uveal melanoma (UM) studies: human UM cells exposed to blue light (475 nm) show increased proliferation, an effect blocked by blue-light filters (Hu et al., 2014). In neonates, blue light decouples POMC signaling, overstimulating alpha-MSH and melanogenesis without UV’s protective feedback.

This drives mitochondrial heteroplasmy in melanocytes, as blue light suppresses cytochrome c oxidase, increasing ROS and mtDNA mutations (Godley et al., 2005). Mothers with circadian mismatches often from blue light exposure pass higher heteroplasmy rates to infants, amplifying the risk (Wallace, 2010).Image
Read 18 tweets
Apr 24
Interesting talk. I wonder if Friston talks to Nick Lane. If not he should.

Friston’s surprise (F(s,μ) = -ln p(s|m)) mirrors Shannon’s entropy (H = -Σ p(x) log p(x)), where minimizing surprise (prediction error) reduces uncertainty, akin to maximizing information content. This connection is crucial for my photoe-bioelectric thesis, as it ties bioenergetic processes (light-driven UPE) to information processing. Obviously this is a core theme in my decentralized narrative fo rmedicine.
2. Markov Blankets and Edges as Quantum Computers: My concept of the edges of biology (skin, gut, eyes) as quantum computers making bioelectric bets aligns with Friston’s view on Markov blankets. The skin (with VDR), eyes (with rhodopsin, melanopsin), and gut (with bacterial UPE) form statistical boundaries, separating internal states (e.g., mitochondrial matrix, neural networks) from external states (light, environment). Sensory states (e.g., light detection by melanopsin) and active states (e.g., H+/D fractionation, melatonin synthesis) mediate this boundary, minimizing free energy by predicting and adapting to light signals. This supports my idea that these edges process information via UPE and bioelectric signals, acting as decentralized nodes rather than centralized bots. This is why I disagree with Levin path on biology right now. Too myopic.Image
3. Free Energy Minimization and Bio-Photonic Coherence: Friston’s FEP states that systems minimize surprise (free energy) to maintain homeostasis, which echoes Fritz-Albert Popp’s bio-photonic coherence (previous addition). Popp argued that coherent bio-photons (200–800 nm) maintain health, while entropy (rogue frequencies) drives disease.

In my thesis, sunlight (via VDR, CCO) stabilizes mtDNA and cellular function by reducing ROS/RNS, aligning with Popp’s coherence and Friston’s free energy minimization. Modern light stress (nnEMF, blue light) increases surprise (prediction error) by spiking UPE and ROS, driving entropy in diseases like ALS, cancer, and autoimmune disorders.Image
Read 8 tweets
Apr 21
1. What do your photoreceptors have in common with your red blood cells? The outersegments of photoreceptors have no mitochondria. Neither do adult RBCs. Why? What does it mean? Shannon's theory on information transfer tells us for a message to high fidelity, the message has to be unusually. The message built into certain cells in our biology is whispering some of Nature secrets to us. Are we listening?Image
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2. When a cell does not have mitochondria it means that the TCA metabolic efficiency is very low. It means that these tissue are starved of oxygen. It means their physiologic ability is atsavistic. It reverts to older evolutionary pathways to exist than the more modern TCA cycle that high efficiency organs require. Remember the human brain gets 20% of the cardiac output. That is a lot of oxygen. That tell us the brain like the TCA cycle.Image
3. Many of the biochemist food gurus like Seyfried will tell you the Warburg metabolism is pathologic. Very few of them will tell you that humans have tissues that only use it to operate in adult human life. They are impotent to tell you why it is useful in one place and cancerous in another. The teleological explanation for the presence of the Warburg effect in the mammalian retina is simple to understand once you have a basic idea of what Krebs bicycle really is. This is where the TCA cycle and urea cycle overlap.  

When proteins synthesis is massively upregulated by ubiquitin, the cell cannot rely on the steady removal of anions from the TCA or urea cycle to fuel biosynthesis because of slowed down metabolic kinetics of either cycle. These cycles slow down because OXYGEN is absent. These cycle mimic what life ws like during the GOE.Image
Read 23 tweets
Apr 20
Since today is resurrection day what would tell a guy standing outside a cave with healed wounds? I know must of you would say get some sun. But I am thinking about his future longevity?

I would tell them the truth about the biggest scam in the longevity world. Everyone knows that exercise is good. Do you know that exercise has a dose-response curve?

Did you know weight lifting is beneficial in lowering all-cause of mortality in CVD and cancer until you hit approximately 140 minutes a week...So exercise/weight training has a context. Did your doctor tell you this?

More than 140 minutes a week, then your risk of death actually increases. So if you do not want to revisit the cave and the shrouds you had on you might want to take a look at those slides because the food guru biochemists won't tell you this. Their knowledge is all from the DoD, DoE and DARPA.

Do you believe the phrase, "Praise be to Orwell because he gave humanity the antidote to the mind poison of tyranny."

Big Harma money produces the centralized science it wants. Yes or no?

The hallmark feature of Deep State scientific programs linked to DoD and DARPA is to refuse to cite anything that runs against their agendas. The whole truth and nothing but the fucking truth even it offends your ancestors. That is what we tell guys who just came back from death.Image
2. My second thing to tell him.......avoid creatine by opting for your Daddy's light every AM. Key part of staying out of the cave. Mammals who see sunrise always default to a TCA cycle that spins with the clock........those who break the rule go spinning counter to the clock and they are always running around looking to buy creatine from GNCs. Do not be them.Image
3. And if you need a CITE here is something I wroite before you got nailed to the wood structure. And never wear sunglasses or contact either. Or you will become a Bugle Boy too on your way back to the cave. jackkruse.com/emf-4-why-migh…
Read 6 tweets
Apr 19
1. To address how a dose of LSD, known for its effects on absorption and emission spectra and the release of massive ultraweak photon emission (UPE), impacts myelin, we need to consider the biophysics of LSD’s interaction with neural tissues, the role of myelin in neuronal function, and the potential effects of UPE on cellular structures. This response will integrate insights from neurobiology, biophysics, and photobiology, while aligning with the photo-bioelectronic framework of my decentralized medicine thesis. So if you have not read my work or the book below, you'll be shit out of luck. But I have the goods. Given the complexity of LSD’s effects and the link of UPE’s impact on myelin biology decentralized medicine can explain this picture of LSD retinal toxicity.Image
2. LSD’s Effects: Lysergic acid diethylamide (LSD) is a psychedelic that primarily acts on serotonin receptors (5-HT2A), altering neural signaling, perception, and consciousness. These receptors all respond to UPE in the ultraweak UV range. Its molecular structure, with conjugated π-electron systems, suggests it can absorb and emit photons, increasing UPE (biophoton emission from cellular processes). A large dose (e.g., >200–300 µg) amplifies these effects, potentially overwhelming neural and cellular homeostasis. So you need to read the book to understand the rest.......Music teacher is fucked. But you could put TOOL on and keep reading.Image
Read 16 tweets

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