QUANTUM ENGINEERING #45: AUTISM & MELANIN/MELANOPSIN: A MIGRATION PROBLEM
Added 2023-06-07 05:34:38 +0000 UTCMORE ON THE ipRGCs of the retina and SCN. Someday if someone funds my research, autism might be the first topic I'd suggest we study. Why?
Melanin seems to be important for migration of neurons in all mammals. I told you that in the recent blogs around melanin and metastasis. And this idea clued me long ago in that I might be able to explain autism because of my unique perspective on melanocyte migration and how it links to melanopsin regeneration.
Implications of a lack melanin pigment in mothers and fathers and what this might mean to their germ lines that become a child? Here is one of my kids above.
Today's lesson is going to come from kitty. Most of you know I love cats. My favorite cat has always been the Siamese cat. My first cat was one and my current cat (above) is a Siamese. You might not know why I am fond of Siamese cats but you will soon. They taught me a lot about melanin when I was a boy in New York City.
CATS & HUMANS WHO ARE ALBINOS HAVE A MELANOPSIN LESSON TO TEACH
Most albino human beings and albino cats lacking retinal pigment in the RPE have observable nystagmus and many exhibit strabismus. The optic chiasm (pic above) of albino mammals including human beings and cats shows that almost all their retinal ganglion cells cross at the optic chiasm with few uncrossed optic fibers. This shows you there is a problem with morphology in mammals neurulation patterns. Something has to be behind this misrouting behavior. My bet is a lack of melanin allows the stickier deuterium isotope to affect cell migration during neurulation of the mammalin brain due to the kinetic isotope effect of deuterium on hydrogen in cells. One D controls 96 atoms of H+ (pic below). I think the massive increase of atomic weight and the kinetic isotope effect are critical in the misrouting behavior of neurons and this has dramatic effects on organization of the visual system of mammals. There are details about mammalian embryology that have lead me to this conclusion. I think it might be behind what causes autism, as well. A lack of melanin in the parents and their germ line cells maybe the precipatating event that begins this cascade of events on. I believe this idea is tied to autism because the effect is quite heterogenous in presentation, hence why they call autism a spectrum of disorders.
In 1965, C.L. Sheridan noticed that retinal ganglion cells originating in temporal retina of albino rats did not function well, hypothesizing that albino rats have fewer uncrossed, non-decussating optic fibers. R.D. Lund anatomically verified that albino rats have fewer non-decussating optic fibers compared to pigmented rats. For several years the abnormality of reduced non-decussating optic fibers at the optic chiasm in albinos was thought to be limited to rats and rabbits. Guillery reported atypical visual system organization in Siamese cats, but the association with albinism was not identified.
CIRCADIAN BIOLOGY ENTERS THE FRAY OF MY KITTY STORY
The mammalian SCN is controlled by light and temperature and by the ipRGC of melanopsin. I told you that a long time ago in the Cold Thermogenesis #6 blog. What else didn't I mention back then?
In 1971, Creel initially published the connection between Siamese cats and albinism, and hypothesis that reduced non-decussating optic fibers likely is a “highly general transspecies phenomenon in albino mammals”. Siamese cats all have blue eyes and blue eyes = less melanin in the iris. Siamese cats, Himalayan mice, rats, and rabbits all express a mutation that is a temperature-sensitive pigmentation defect, that is, allowing pigment to show up only on the cold parts of the body.
This is why their coats are so grey and white (my kitty above). Moreover, their retinae lack pigment too. Many human infants are born with blue eyes because their brains are devoid of melanin because humans brains are born into life in an immature state. That is the case for human blue eyes, but what about the cats? Why do Siamese cats have blue eyes almost all time? It is not just their iris that has reduced melanin. Here we see the interplay of UV light and cold and begin to understand why this link is present from an evolutionary standpoint. Wide band gapped semiconductors can make the same light endogenously from atoms doped to proteins or via cooling environmental temperatures. I believe this is the basis of where the mammalian dive reflex comes from. Most humans who live at high latitudes where it is colder also tend to have blue eyes and blonde hair. The link is unmistakable when you realize it.
Cooling is usually occurs at surfaces in mammals (eccrine sweat glands) and most of their surface has arterioles loaded with higher levels of deuterium that act a Bose Einstein condensate because of deuterium unique nuclear spin. This makes their surface something important. It is called a topological insulator. Mammals interiors are filled with fermions = electrons and H+ ions. They follow Dirac fermion statistics. Here we see a physical difference manifesting in mammals for some reason.
Is there a trade off for mammals who live in colder environments? Yes there is. what is it?
They have less visual and non visual photoreceptors in their sensory organs.
Is this true in human mammals too, Uncle Jack? YEP.
Note when humans have normal pigmentation in the eye (RPE) tend to have optimized neuro-opthalmological migration in their visual system as well. It appears melanin is a beacon for proper migration of neurons in the eye to deeper brain structures in humans. This is critical in the eye because of the location of the SCN to the RPE. The SCN controls the eye clock, circadian rhythms, and the pupillary response in mammals to bright light. It also affects their behavior. This is markedly changed in autistic kids.
In humans with pigmented retinae, retinal blood vessels spare the foveal area. In albino human retinae, blood vessels intrude into foveal area. Pigmented human retina exhibit an avascular zone surrounding the fovea. Albinos do not exhibit this arrangement. They have blood vessel encroach into their fovea. Humans with destroyed RPE from diseases like diabetes get the very same neovascularization of the fovea. This ruins their central vision over time.
This is a big clue for what decentralized clinicians should be looking for in human's with autism. If a lack of melanin is part of the pathophysiology of this disorder than we should see some subtle changes in OCT and their arteriole beds in the diencephalic derivative of the brain if we look for it, if I am correct. I think a lack of melanin pigment initiates atavistic expression in autistic kids of the central and peripheral nervous system. This lack of POMC or POMC translation leads to alterations in the melanopsin system that ruins normal neural migration.
The phenomenon is called atavism—this is the reappearance of a trait that had been lost during evolution before in the same species. In autism many of these kids cannot talk or interact with their species. We know our nearest cousins cannot speak either. We also know that early primates were loners and that social networking became a big trait later on in evolutionary history of the primate. This is another throw back behavior seen in autism that would have been seen in transitional chimps on their way to us. This change would not be found in our DNA either. Our genes do not determine who we are, but with atavism, they can sometimes serve as reminders of our evolutionary past. Functionally this is what autism in humans looks like to me from my current perspective. Another big clue for my hypothesis is found in the embryology of the visual and auditory systems of mammals.
MELANIN IS ALSO A TIME CRYSTAL FOR EMBRYOGENESIS IN MAMMALS
Embryonic progression in albino mammals’ visual and auditory systems seem to also take a step back in evolutionary time and it seems this program is initiated by lack of melanin pigment. Non albino animals do not exhibit this altered migratory pattern. Abnormalities of optic chiasmic misrouting in albino mammals is a developmental field defect that is seen normally in preceding phylogeny. Complete crossing of optic neurons at the chiasm is a normal developmental event in vertebrates prior to mammals. This reinforces my beliefs that atavism is a central problem in understanding modern autism.
The presence of melanin pigment in the embryonic retina is the signal that initiates retinal ganglion cell pathway routing from the eye to the SCN and from the SCN deep into the brain. Insufficient coding for retinal pigment launches an earlier, more stable genetic package directing a different targeting of optic neurons and this results in autism.
Genetic makeup includes preserved earlier evolutionary features. Charles Darwin popularized atavism in the 1860s as the term for reappearance of ancestral characteristics in future generations.
Today we know that vision and hearing evolved together dating back to the PaxB gene, which is a single gene controlling eye and precursors to hearing (mechanoreceptors) in box jellyfish. This occurred before independent Pax 2 and Pax 6 genes showed up in primates much later. There are evolutionary connections between eyes and mechanoreceptors of the inner ear to the extent that during evolution are linked to melanin generation in those sense organs. I told you earlier in the series melanin was the favored semiconductor of all mammals post KT event. This story fits this narrative as well. If POMC/melanin is absent for any reason, it appears human neuroplastiticty allows sensory cells to shift their sensory modalities to an older phylogeny experienced in evolutionary history. Why is this a big deal? The melanopsin phylogeny predates even primate evolution in time.
I think this happens in modern humans because of a loss of information and energy transformation in the embryo due to a lack of POMC or POMC translation in the parents cells and their germ lines that create their child. I think this is what autism is at its core. It is lack of POMC that has huge implications for the neurulation of the diencephalon in humans and its really old relationship to melanopsin biology.
BACK TO THE CATS
What happens when cats lack melanin in their eyes? Do they exhibit traits that mimic human autism? They exhibit fewer photoreceptors, they have foveal/area centralis hypoplasia, & exhibit misrouting of the temporal retinal ganglion cells, while having a variation of geniculate terminations, and most importantly they develop vascular intrusion into foveal area. They also exhibit abnormal cortical projections, and fewer cones in macular area. Lacking pigment in the cat leads to some major migration problems in the adult form. It seems albino kitties and Siamese cats have a lot in common with autism.
The animal model closest to organization of primate visual system studied the most is the albino cat. Albino cats have observable nystagmus, and many have strabismus. Figure 1 above pictures the optic chiasm of an OCA1 albino cat shows almost all retinal ganglion cells (RGCs) cross at the chiasm.
Not all of them do and the ones that do not cross tend to innervate areas they should not be in. The non visual photoreceptor associated with these RGCs is melanopsin. The number of binocular cells was found to be reduced in visual cortical areas of Brodman numbered 17, 18, and 19 in Siamese cats and albino cats. This impairs their stereovision. So these cats do not have great vision, but this is because they are adapted to colder environments with more blue light and less UV light. Their SCN periodicity can be retuned by cold weather. The trade off for their lack of melanin is altered neural migration in their brains.
This surface temperature thing is a big deal in mammals because our SCN changes its periodicity to temperature and light. I believe this explains why autistic kids do not like temperature changes or being touched. (another sensory processing delay). I have a sense why this happens in autistic kids because these changes are seen in cats as well who lack pigment. Autistic kids have a broken topological insulator in their skin, eyes, and circulatory system. I think they are exquisitely sensitive to the chiral pinch of deuterium in their blood and this creates a lot of endogenous light that overwhelms their system because they have poor melanin sheets within the basal levels of their skin. This allows too much deuterium to leach out of the circulatory system and into the substance of their subcutaneous tissues. These leaching of deuterium than alters non visual photoreceptors in that location.
There is some rather unique things to know about this situation. Evolution seems very fond of the SCN melanopsin connections I mentioned in QE #44. Why? Melanopsin retinal ganglion cells are always completely crossed or bilaterally projected into suprachiasmatic nuclei above the optic chiasm and these projections are not affected by albinism in any mammals. Interesting don't you think?
I think this goes back to where melanopsin came from phylogenetically. It came from our fish amphibian origins 380 million years ago. Phylogenetically older connections are less abnormal in albino mammals by exhibiting a bilateral suprachiasmatic projection pathway to the SCN. These tracts appear to be unaffected in albinos. This tells me this system is highly protected by evolution because of how important it is to be able to simulate the physics of your environment to be highly adaptable. This also explains another peculiarity about the melanopsin system.
Melanopsin regeneratiion acts largely independently of the visual cycle. This tells me the melanopsin system has old roots in evolution and evolution has specifically made sure it did not co evolve similar mechanisms with the rod and cone system of the eye. Melanopsin neurons also control pupillary size with the autonomic nervous fibers of the third cranial nerve.
When this system is disrupted we get mammals that are not adaptable at all. This defines modern humans who are on the autism spectrum. Most children with autism have trouble sleeping, which may exacerbate other challenges associated with the condition. Sleep problems hint at disruptions in the circadian clock, a cellular timer that keeps cells in sync with the day-night cycle. Vitamin A disruption causes sleep disorders.
I have a sense that we will find out in the future that autistic children have wiring defects in their chiasms and in their sensory relay pathways because of a broken Vitamin A cycle in the melanopsin system along with a lack of melanin and POMC activity in the germ cells. This Vitamin A problem will lead to science realizing these kids all have altered melanopsin regeneration pathways compared to humans that do not have this deficit. I believe the melanopsin system has its own regeneration system because it is VITAL to accurate time crystal managment of the circadian mechanism you saw in the last blog. The SCN simulates the physics of our environment to program our metabolism from these light signals. This is broken in autism.
LACK OF POMC/MELANIN = ALTER MELANOPSIN REGENERATION = VITAMIN A PROBLEM
Vitamin A is necessary for normal embryonic development in humans, but its role in the adult brain is poorly understood by centralized science in 2023. Vitamin A derivatives, called retinoids, are involved in a complex signaling pathway that regulates gene expression and, in the central nervous system, controls neuronal differentiation and neural tube patterning.
There is another reason why I think this Vitamin A, melanin, melanopsin story is linked to autism. Most people know that the majority of melanin in the eye is in the RPE. What many however do not know is that the photosensitivity melanopsin requires a steady supply of cis-retinaldehyde, a type of retinoid. The primary source of this vitamin chromophore (328nm) in the vertebrate eye comes from a complex multistep enzymatic pathway, known as the retinoid or visual cycle (above). In this cycle by 11-cis retinaldehyde is regenerated from bleached all-trans originating in photoreceptor outer segments of rods. The critical elements of this pathway occur in the retinal pigment epithelium (RPE). Here is the problem. Since melanopsin is found in the more superficial layers of the retina, quite distant from the RPE, it would seem poorly placed to obtain cis-retinaldehyde from this RPE source. So how does melanopsin do it? Why does it have its own regeneration pathway separate from rods and cones?
Chromophore regeneration in rod photoreceptors relies solely on a tissue adjacent to the rod and cone layer of the retinal pigment epithelium. Cone photoreceptors rely both on the RPE and Müller glia, which traverse the entire depth of the retina to regenerate. Melanopsin doesn't use either system.
In the mammalian photoptic retina light activates melanopsin to trigger a G protein cascade that causes membrane depolarization. The ipRGCs/melanopsin response is opposite to that seen in our rods and cones, which hyperpolarize, but resembles the actions of photoreceptors found in invertebrates like fruit flies and horseshoe crabs. This system exhibits atavism mentioned above. In humans, ipRGCs fire spikes. They are understood to use glutamate as their primary neurotransmitter; uniquely among RGCs, they also express a peptide neurotransmitter called PACAP (pituitary adenylate cyclase activating peptide).
Known influences of ipRGCs extend well beyond their direct targets. Examples are regulation of melatonin synthesis in the pineal gland and the development of synaptic plasticity in the hippocampus. I believe they drive synaptic plasticity in all of our brain's circuits and this is why melanopsin is the most numerous opsin in humans.
Why do I mention this detail? Most people forgot human embryology of the brain and skin. They have forgotten that Vitamin A/retinoic acid have massive effects in the morphogenesis and growth of the neural tube. Not only will deuterium affect neural migration from the notochord, but the chemical signal governing it is likely also awry. Most of which can be explained by defective notochord signalling. This would cause neurulation defects from the thalamus to the adult hemispheres. This process is how humans create their hemispheres in the last trimester and postnatally. This set of circumstances fits the modern phenotype of autism based upon my knowledge of human brain embryology. I think the key problem in the autistic embryo is a problem of Vitamin A signaling being comingled in the eye, optic chiasm, hypothalamus, thalamus and eventually the neocortex in humans. This would create a wide spectrum phenotype in the adult human.
Modern humans are new phylogenetic creatures in evolution and we know that optic projections near chiasm projecting into hypothalamus antecede vertebrates evolution because they occurred in early chordates. Chordates first appeared on Earth 590 million years ago. Those are the animals that innovated melanopsin originally.
It appears that fact surprised Dr. Huberman and Dr. Berson based on what Huberman said in the Rubin podcast. It did not shock me because I knew mammals came from early chordates because of my time in the Museum of Natural History in New York. This is why it made sense to me why we had melanopsin in our brains. I was shocked to learn in 2014-2017 that we also have it all our blood vessels, skin, fat, and our outer inferior retina. Nature does not make mistakes.
This is my kitty today as I write this blog. She likes IR-A and UV-A light now. I have a sense all parents with autism need to learn a lot more about full spectrum sunlight and the key frequencies of IR-A light and the 380 nm light that controls the photorepair mechanisms in mammals. When they do, they will realize how to help fix the problem they created by their abuse of blue light and tech screens.
SUMMARY
When I was 8 was the first time I got a Siamese cat. I asked the lady at the museum why my cats eyes were different colors than other cats and she did not know the answer. She told me she'd find out and few weeks later I found out about melanin as an 8 year old kid. She told me all chordates had retinal pigments matching vertebrates. Humans were the latest version of vertebrates. That lesson would come in big later in my life. I never forgot about my kitty's eyes. And that is why it never surprised me that the melanopsin chromophore showed up in human brain. My childhood was prepping me for a later discovery around this amazing protein. People with autism one day may thank Siamese cats for solving this enigma disorder for centralized science.
CITES
1. Sheridan CL. Interocular transfer of brightness and pattern discriminations in normal and corpus callosum sectioned rats. Journal of Comparative and Physiological Psychology. 1965;59:292-294
2. Lund RC. Uncrossed visual pathways of hooded and albino rats. Science. 1965;149:1505-1507
3. Giolli RA, Guthrie MD. The primary optic projections in the rabbit: An experimental degeneration study. The Journal of Comparative Neurology. 1969;136:99-126
4. Guillery RW. An abnormal retinogeniculate projection in Siamese cats. Brain Research. 1969;14:739-741
5. Creel DJ. Visual system anomaly associated with albinism in the cat. Nature. 1971;231:465-466
6. Creel DJ. Differences of ipsilateral and contralateral visually evoked responses in cats: Strains compared. Journal of Comparative and Physiological Psychology. 1971;77:161-165
7. Creel D, Witkop CJ Jr, King RA. Asymmetric visually evoked potentials in human albinos: Evidence for visual system anomalies. Investigative Ophthalmology & Visual Science. 1974;13(6):430-440
8. Sanderson KJ. Retinogeniculate projections in the rabbits of the albino allelomorphic series1. The Journal of Comparative Neurology. 1975;159:15-27
9. Creel DJ, Giolli RA. Retinogeniculate projections in albino and ocularly hypopigmented rats. The Journal of Comparative Neurology. 1976;166:445-455
10. Guillery RW, Oberdorfer MD, Murphy EH. Abnormal retino-geniculate and geniculo-cortical pathways in several genetically distinct color phases of the mink (Mustela vison). The Journal of Comparative Neurology. 1979;185:623-655
11. Piatigorsky J, Kozmik Z. Cubozoan jellyfish: An Evo/Devo model for eyes and other sensory systems. The International Journal of Developmental Biology. 2004;48(8-9):719-729
12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1571178/
13. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6601915/
14. https://www.cell.com/cell-reports/pdf/S2211-1247(18)31754-6.pdf
Comments
Does this include folate acid?
Josie
2024-10-11 02:50:11 +0000 UTCAmazing article this stimulates my unusual brain so much ! Thank you 🙏 ✨💓
Solreta Antaria
2024-10-02 07:18:11 +0000 UTCAnything you do by habit begin to do another way.
Dr. Jack Kruse
2024-09-27 20:36:33 +0000 UTCDr. Kruse, you stated above that "stimulus" could be applied to "rewire the bad first design" [resulting in autism]. Specifically, what are some examples of things that can be done to "rewire the brain?" I've read that if you're right-handed, then brushing one's teeth with the left hand increases neuroplasticity--this may not be the type of "stimuli" you're referring to. Any and all hacks/suggestions are appreciated.
Lashawn Hill
2024-09-27 17:48:26 +0000 UTCThe same way light environment can impact scientific results, so can things like race and gender. Western medicine has traditionally been focused on males so, of course, this also explains why boys/men have been the predominant faces of autism and ADHD. Meanwhile, there's been an explosion of girls and adult women (the "Lost Generation") who are finally receiving a proper diagnosis. The sad part is you finally figure out what's wrong with you, only to be told there is no cure.
Lashawn Hill
2024-09-27 17:12:15 +0000 UTCWhen I first discovered Dr. Ben Lynch's work, I jumped on the methylated vitamins bandwagon--big mistake. I proceeded to test my methylation status with a Walsh-trained practitioner, and it was determinated that I'm an Undermethylator. I don't need any folic acid, active form or otherwise. I used to blame my not feeling well 100% on being in perimenopause, but as it turned out, some of my "brain foggy" feeling was actually the histamines being released in my body (MCAS) as a result of eating folic acid-laden foods. My poor sister had really bad asthma as a child, and she also has a bad allergic response to folates. I took Vitamin C amongst other supplements to clear up my pathways.
Lashawn Hill
2024-09-27 16:46:12 +0000 UTCThis comment is not to be missed if you have AS or autism: https://x.com/DrJackKruse/status/1837895852809244987
Dr. Jack Kruse
2024-09-23 01:33:36 +0000 UTCGot that covered. Concerned about winter in NE USA.
Ron Petrosky
2024-09-13 12:19:14 +0000 UTCThe sun is where you start not with a magnetico.
Dr. Jack Kruse
2024-09-13 11:56:04 +0000 UTCHi - we tried it all. Red light therapy, diet per JK’s epi paleo RX, and mineral rebalancing have been the most beneficial. Getting enough sunlight and grounding as much as possible.
Ron Petrosky
2024-08-20 16:02:31 +0000 UTCHi Ron, what exactly do you do to help your son? I just found out my nephew is autistic and would like to know where to start to be able to help my brother and nephew out. Thanks :)
Christina Gior
2024-08-20 15:51:59 +0000 UTCUncle Jack, how does the Magnetico sleep pad fit into this story? Could it benefit by 2.5 year old son who was diagnosed with Autism? We have him on a good path now, thanks to you, and he’s showing improvement but I want to keep up the momentum and am considering a Magnetico. Truly grateful for your work, god speed!
Ron Petrosky
2024-07-07 19:38:53 +0000 UTCThere has been some recent news out about folate levels, sunlight and artificial light. Many people do not know folate is a photosynthetic chemical and it links dark skin (melanin) for natural folate protection. Vitamin B9 (Folate) was first extracted from spinach leaves in 1941. The term folate comes from the same root as foliage: green and leafy. Folates are vital: they accept carbon atoms and pass them on as needed as the fundamental basis for proper methylation. This implies that during summer months folate levels should be expected to be at their lowest levels NATURALLY. Folate biology has a specific and tight seasonal control mechanism linked to light. This is not a food story at all What if there is no seasonal or light controls in place? Folate is often given to pregnant women to prevent spinal dysraphisms today. This is something pediatric neurosurgeons deal with and why I know a lot about them. The incidence of these conditions has dropped but it is has done at a COST. Why? but too much folate/folic acid causes cognitive haze and sleep difficulty and may cause neural migration problems in artificially lit environments. This should awaken you. In North America, (CAN/USA) folic acid was added to all grains in 1996. This is only a few decades ago and we are seeing the transgenerational effects of this right now. In general, it does not appear that even large amounts of folic acid taken orally are acutely toxic in adults. However, given the fundamental role of folate levels in synthesizing nucleotides (including RNA and DNA) and in methylation reactions as a methyl donor, high levels may have inadvertent implications for proper methylation of DNA during times of rapid cell division, such as in prenatal development. You'd think the idea that adding folic acid to the food supply might have caused centralized medicine to expect unintended consequences. Few thought about, much less studied it. I have always been worried about this effect since I learned that B12 was a photoreceptor in humans. This idea has been speculated in research circles as early as 2005, and specifically speculated to be relevant for the increase in autism in 2011. An early review of potential problems with mass folic acid supplementation of the food supply was undertaken by Lucock and Yates. Here, they noted that a drastic increase in folates could lead to a selection for the previously rare MTHFR genetic substitution of T for C at area 677 (MTHFR C677T), and that if folic acid is supplemented at doses above 400 mcg that unmetabolized folic acid will circulate in the blood supply at a level largely consistent with the excess dose. In 2005, Lucock and Yates noted that high levels of folic acid in the blood does not generally occur as a result of ingesting natural folates and that “no work has been done so far to evaluate the biological and genetic consequences of excess long term exposure” to these circulating folic acids on DNA/RNA biology. After that review, there were two separate findings of unexpected increases in asthma and breathing problems associated with folic acid use. It now appears that we have clear data that excessive methyl donor transfer has significant epigenetic effects in humans. This work dovetailed with another review questioning the wisdom of mass folic acid supplementation published in 1996. Smith et al. pointed out that by supplementing the food supply; several hundred thousands of persons are exposed to greatly increased levels of folic acid. These authors noted that prior research had shown that expectant mothers with low vitamin B-12 (most vegans/vegetarians) AND high levels of folic acid were associated with offspring having an unexpected increased risk for insulin resistance and disease associated with this condition. This is worrisome when you know that blue light exposure does the same thing. Troen et al. found that some women past childbearing age subjected to high folic acid supplementation may be at risk for reduced immune system functioning causing inflammatory autoimmune conditions to spike. This problem has gotten worse since I first looked into it in 2005. SUNLIGHT reduces all these risks, while modern lighting exacerbates it. Moreover, it appears nature is trying to tell us that the sun raises melanin and melanin is protective. Strong solar cycles in photosynthesis seem to simultaneously lower folate in foods in the summertime for a deep reason. That reason is epigenetic hypermethylation which can lead to sleep apnea and cancer formations later in life due to altered DNA methyl marking. This process also alters how RBC (ferrodoxin) can work within their circadian cycles with the innate immune system and TOLL receptors. Folate is destroyed by strong sunlight with both UVA and UVC light. Darkened skin protects the stores we have, but there is now proof that folate levels are designed to be low when the solar radiation is strong in the local environment. These days most people are eating food humans have been engineered and/or genetically altered in some way. Then add in the effect of Artifiical light day and night. This throws off the normal variation of the natural folate cycle during seasons. Today, people in developed countries are getting MASSIVE amounts of folates in the form of folic acid. This is the real reason to avoid grains. Folates are now being ingested in three ways: as natural folates from food, as synthetic folic acid added to processed grains and synthetic from vitamin supplements. All of these idea are counter evolutionary to Nature's laws. As a result of the supplementation, the circulating level of unmetabolized folic acid, as well as total folates, has greatly increased over the past generation, probably to levels largely unprecedented in human history. Folic acid has been shown to be able to epigenetically alter the functioning of the genome and to have long term effects on gene expression as I mentioned above. The Centers for Disease Control Vaccine Safety Datalink data set compared children with autism to control children on several variables. Many people who think the link of vaccines to autism might be shocked to find out that folic acid supplementation during gestation is associated with a serious increased risk for autism. I believe the combination of artificial light and folic acid supplementation are causing neural migration problems. This is why parental melanin levels are important clues. This effect remains even when health-seeking behaviors and other variables are controlled. This is information parents of kids with AUTISM need to know. Autism, asthma, allergy, ectopy, eczema, diabetes T1D, T2D, and MODY, auto-immunity, and spinal abnormalities have their lowest incidence is lowest in equatorial environments and it appears now we know why this is the case. This is decentralized medicine 101. CITES Valencia-Vera E, Aguilera J, Cobos A, Bernabó JL, Pérez-Valero V, Herrera-Ceballos E.. 'Association between seasonal serum folate levels and ultraviolet radiation'. 'J Photochem Photobiol B'. 2019 Jan;190:66-71
Dr. Jack Kruse
2024-06-09 17:45:07 +0000 UTCAutophagy is critical in growing and maintaining the neocortex size of humans. This is especially true in cases of neurodegeneration and autism when you are trying to repair defects from Vitamin A liberation. This turns Vitamin A into an aldehyde that acts to destroy all visual and non-visual photoreceptors that impede tissue regeneration in humans. The quality of their sleep (also linked to the Vitamin A cycle) is also critical because it maximizes autophagy and does not deplete our stem cells in the recycling process. The more efficient autophagy is the more you protect your stem cell supply and the longer you can live or regenerate. Autophagic efficiency is linked directly to energy-mass equivalence (Einstein). The more electrons you have in your brain the more autographic efficiency you will have to absorb exogenous or endogenous light production. All cells created in the young human's brain are newly minted post-mitotic cells (think Autism). Autophagy augments longevity in all post-mitotic cells in 5 ways: The 5 cytoprotective effects of autophagy: 1. Reduced accumulation of toxic protein aggregates or misfolded proteins via Vitamin A damage 2. Destroying bad mitochondria via mitophagy and sensed via size and shape changes in mitochondria 3. Reduced apoptosis to prevent stem cell depletion = organ failure 4. Reduced necrosis to stop organ failure. 5. Improved hormesis by increasing the redox stickiness of semiconductors made of carbon and water like melanin & collagen. This is why children sleep more than adults and why it is why autophagic efficiency is higher in younger mammals with better redox potential. In Autism this is often lost due to the Vitamin A issue (QE #45 blog) Many people report poor sleep with ketosis and this is tied to the type of ketosis they employ. This was covered in the blog OSF #8 on my website. Contrary to modern centralized belief, not all ketotic templates are equivalent thermodynamically. It also points out how fasting, sleep, ketosis, and autophagy all couple together to add to healthy development and exceptional longevity in the human neocortex. DHA content in your cell membranes increases your ability to engage in autophagy. Vitamin A destruction impedes this effect by lowering resolvins and elovanoids in the photoreception repair process in humans. https://www.sciencedirect.com/science/article/abs/pii/S0531556514000722
Dr. Jack Kruse
2023-07-16 19:28:58 +0000 UTCI’m not a doctor, just a mum trying to get my head around this and heal my son diagnosed with RE. From what I’ve been told by many neurologists, there is no cure or way of stopping the seizures besides the hemispherectomy :( With this much appreciated information that you have provided, is there anything I can do about it to help him?
Tracy Goldin
2023-07-02 21:34:08 +0000 UTCThere are various mechanisms related to Rasmussean's Encephalitis (RE) but the big one is POMC by way of adaptive immunity and likely melanopsin/retinol damage. I think this is a transgenerational epigenetic disease like autism. Why do I say this? Brain innate immunity is regulated by hypothalamic arcuate neuronal activity that is dominated by POMC neurons. POMC neurons are believed to change innate immune function. Adaptive immunity, innate immunity, and/or a stresful light stimulus/viral infection are all involved in the development of RE. Immunopathological studies have shown that cytotoxic CD8+ T lymphocytes are the most common T lymphocyte subgroup in the brains of patients with RE (Pardo et al., 2014). The intensity of peripheral CD8+ T cell expansion is related to the severity of the disease (Schneider-Hohendorf et al., 2016). Although the adaptive immune response is an important effector of central nervous system damage, the innate immune response mediated by the activation of microglia and astrocytes is also the core of the pathogenesis of RE. The degree of microglial activation follows the progression pattern of RE, parallels the degree of T lymphocyte infiltration, and is observed in the early stages of cortical involvement (Pardo et al., 2004; Troscher et al., 2019).
Dr. Jack Kruse
2023-07-02 20:35:49 +0000 UTCp53 is the protector of the genome. It seems Penelope never googled this Uncle Jack quote before.
Dr. Jack Kruse
2023-06-16 14:22:23 +0000 UTCYup:-)
Penelope Pappas
2023-06-15 17:12:57 +0000 UTCIn work published last year, the Dana-Farber group found that alpha-MSH, needed to induce melanin production, does not come from melanocytes (melanin-producing cells in the skin). They believe the hormone, instead, is produced in keratinocytes, the most common type of skin cells. The reason: they found broken alpha-MSH receptors on the surface of melanocytes in subjects with an inability to tan. Other lab work had shown that p53 activates during tanning. And, sure enough, when the Dana-Farber team probed the protein pro-opiomelanocortin (POMC)—which splits to make several hormones including alpha-MSH—it discovered "a perfect p53 binding element there," Fisher says. When testing both mouse and human keratinocytes in vitro, the team observed that after six hours of exposure to UV radiation, p53, POMC and alpha-MSH levels had all jumped dramatically, with the latter's rising 30 times higher than normal. The finding was confirmed in knockout mice missing the gene that codes for p53: Without the protein, POMC was never activated, the mice did not tan (on their hairless ears and tails), and eventually they all developed melanomas.
Penelope Pappas
2023-06-15 17:12:31 +0000 UTChttps://www.scientificamerican.com/article/protein-p53-fixes-dna-damage-promotes-tanning/ So does that mean if you can tan, you have a perfectly fine P53 gene? :-) Naturally, they are trying to replace this process with a pill... :-)
Penelope Pappas
2023-06-15 16:58:11 +0000 UTCLast burning question - nail polish - just another tarp on our bodies?
Laura Kissmann
2023-06-15 14:14:30 +0000 UTCDr Kruse - just wondering the background on the top photo of the man holding the others face. Feel like its from a movie I cant place. Is the message meant to try to get someone to open their eyes and "see" the truth instead of half-truths?
Laura Kissmann
2023-06-15 14:13:35 +0000 UTCI have been wondering something similar of late - those with more grey (and whiter) at the front of the head (me included) - could that be pulling all the melanin from the hair there from facing blue lit screens (PCs and TVs especially)?
Laura Kissmann
2023-06-15 13:54:01 +0000 UTChttps://optimalklubs.com/kruse-for-dummies-general/
Dr. Jack Kruse
2023-06-14 11:46:55 +0000 UTCnot all of them are.
Dr. Jack Kruse
2023-06-14 11:45:37 +0000 UTCtrue relationship
Dr. Jack Kruse
2023-06-14 11:45:15 +0000 UTCWhere can I purchase it at?
Abdullah BenSaeed
2023-06-14 10:45:51 +0000 UTCOther interesting side note…. I’ve noticed The patients over the last 3 years or so, that have the DARKEST SUNGLASSES tend to have the WHITEST HAIR. Im sure this is secondary to lack of retinohypothalamic signaling to the SCN. That lack of UV retinal signaling either is pulling all the melanin from the hair/skin OR the LACK of signaling is setting the body up to absorb as much UV for vitamin D and neurotransmitter production. Hopefully absorb EVERY LAST DROP. Also those patients tend to have polycythemia. Probably secondary to lack of melanin causing mitochondrial hypoxemia, hence signaling the system to produce more RBCs. Just a couple observations.
Brian G
2023-06-14 01:31:06 +0000 UTCThis seems like an elementary question concerning melanin migration, depending on the systems needs…. Given the fact that neuromelanin is produced by the dopaminergic and noradrenergic cells in the substantia nigra and locus coerulleus (breakdown product of dopamine) and if we think that melanin is being PULLED from the deep system (like Parkinsons), if you biopsied a melanoma lesion, would it consist of neuro melanin?
Brian G
2023-06-14 01:21:11 +0000 UTCI have.
Dr. Jack Kruse
2023-06-13 21:51:09 +0000 UTCEveryone should begin with sunlight. But you need to understand how water and magnetism fit into your specific issues. Most human diseases link back to the binary code of biology which was the subject of the first Kruse for Dummies lecture. That lecture can still be heard if purchased.
Dr. Jack Kruse
2023-06-13 21:50:53 +0000 UTCHave you seen this one? https://www.sciencedirect.com/science/article/abs/pii/S0306987707005373 . Autism is associated with less UVB penetration, higher latitudes, urban areas, more airpollution, more preciptation (i.e. being indoor > https://www.nber.org/system/files/working_papers/w12632/w12632.pdf). Last one is done with a natural experiment approach allowing for causal inference.
Snorre Ralund
2023-06-12 09:35:06 +0000 UTCMy muscle and bones have been annihilated my nerves are shot I can feel degeneration all over my body, I believe God made all of this happen for a reason, I have been brought to the absolute lowest I have ever felt and I am now stumbling upon your work, I am not asking for a free hand out im just curious with my condition being very severe, where do you recommend that I start from on your literature. God bless you Dr. Jack Kruse 🙏 I will reverse all of this damage done in ignorance through love and intelligence and once I have completed this I will let my light shine into the world…. The truth will set us free ☀️ 💧 🧲 💛
Abdullah BenSaeed
2023-06-11 18:58:49 +0000 UTCNot sure I have released it yet for public consumption
Dr. Jack Kruse
2023-06-11 17:11:33 +0000 UTCGood day Dr. Kruse. I'm from the Caribbean...High school teacher in Maths and physics. Read both pf J. Otts books, listened to Dr. Wunstch lectures...found you in 2021. Brother...yuh time series is it...Im just now on time series 11...33 factorial...like 8.628 x 10^36 solar frequencies...Jack...I'm trying to make a link between you and Hilton Hotema and George W. Carey's work on regeneration and physiology... Thanks bro...Im starting to wake my students up...tek hell with the adults...Consider St. Maarten/St. Martin Dr. JK. Will be starting the Quantum Engineering blogs next week...POMc my God..., semiconduction, Woooooiiiiiii...Jack, we really don'tunderstand light...I thing Dr. Peter L. Ward retired geophysicist is correct...its ALLL aboit resonance. Finally...Im catching hell from the higher ups about me questioning the new LED lighting system in my school...I need to calculate the resonant frequencey of the rods and cones to see if there are hormonics with blie light... Thanks Uncle...🤝
Alberick Arrendell
2023-06-10 23:52:09 +0000 UTCWhere can I get access to your Epcot Rx Protocol Webinar (September 2012)? The link on the site is 404'd. I tried paying for access and that didn't work either.
Scott Barrett
2023-06-10 15:32:56 +0000 UTCyou will learn about photorepair as the series goes on.
Dr. Jack Kruse
2023-06-10 15:11:57 +0000 UTCJack, in one of your recent podcasts with Dr. Ed you mentioned exposing people with chronic fatigue syndrome to UV and IR light to help them to photo-adapt and heal. You also use these lights in pretty much every podcast I've seen you do. Obviously sunlight is the best source of these lights. After reading literature on IR light and how most artificial lights are massively more irradiant than sunlight and are often pulsed which doesn't happen naturally in sunlight, do you have a list of acceptable devices / lights that you can safely use to help photo-adaptation when indoors?
David Mc Gettigan
2023-06-10 11:52:29 +0000 UTCMy nephew’s mom was a vegetarian for about 8 years 😫😢😫 ooff! She only started eating meat right before trying to conceive. Thank you for this info!
Michelle Helen
2023-06-09 14:08:16 +0000 UTCThere are lessons to learn about Vitamin A and neurons found in the eye. People forget the retina is a diencephalic derivative so it is a great proxy for understanding the thalamic neurulation that goes awry in autism. In the eye, with exposure to light, during rhodopsin photolysis, toxic retinoid side products (Vitamin A) can be produced in photoreceptor cells. Biogenesis of these products occurs when two molecules of all-trans retinal condense with one molecule of phosphatidylethanolamine in the photoreceptor membrane. Evolution has developed a powerful mechanism that prevents the accumulation of retinoid breakdown products in terminally differentiated photoreceptor cells. It has to clear them to avoid problems. I believe the same thing is true in the autistic brain. Throughout life, the debris of the photoreceptor outer segment (POS) apical part is phagocytized and digested by RPE cells, while new photoreceptor discs with rhodopsin molecules are synthesized by the photoreceptor inner segments. This process is protected by Bazan's short loop by recycling DHA chronically which is acting like aspirin to stop inflammation to get us to wound healing via 380nm light with docosanoids & elovanoids. If Vitamin A is unleashed here photorepair never happens in neurons and tissue intergrity and optics is destroyed. However in the eye, the lysosomal enzyme system of the RPE cell is not effective in the degrading of POS debris, because the latter is supposed to contain modified retinoid side products of rhodopsin photolysis, as well as modified lipids and proteins. In other words, the lysosomal enzyme system of the RPE cell cannot recognize such modified molecules and do not digest them. As a consequence, lipofuscin granules (LGs), containing retinoid derivatives, are formed and accumulated in RPE cells with age. Photorepair however helps limit this process. Retinoid derivates and lipofuscin have been long believed to be just a cell metabolism by-product. However, it has been established that LGs are one of the sources of reactive oxygen species (ROS) in RPE cells. This explains why melanin is the most prominent protein in the RPE because it handles the ROS/RNS from the LG's with ease. If melanin and DHA is not present together or degraded then lipofuscin becomes a problem. DHA degrades into docansoids and elovanoids to clean up this mess without side effects. It is the only PUFA on Earth that can do this. This why DHA has never been replaced once by evolution in 600 million years. It is the most remarkable chemical in biology in my opinion. Visible light exposure induces ROS formation in LGs, initiating oxidative stress in RPE cells. Oxidative stress is believed to be central to the development of AMD. The quantum biologic reality is quite different. If melanin/DHA is not present then and only then is ROS/RNS/ and lipofuscin a problem. It absence is characterized by increased level of ROS resulting in damage or modification of cellular proteins, lipids, and DNA, impairing their physiological functions in the tissue. This impacts the colony of mitochondria in that tissue. Therefore, the development of AMD is associated with the progressive accumulation of lipofuscin and retinoids. Ya' might want to rethink your choices. Watch my Vermont 2017 video on youtube to fill in the blanks. As dissolved O2 in a cell rises ROS/RNS becomes more problematic for the structures deeper in the eye lacking melanin/DHA protection. This changes the optical relays in the visual system which innervates the pituitary and the hypothalamus to cause leptin resistance. Anything that changes the topology of the surface affects the biochemistry of the deeper layers because the biophoton creation is highly dependent on the optics of the tissue. This is Quantum Biology 101. This is why atrophic skin in parents is a precondition for autism. It also explains why vegans have experienced massive increases in autistic offspring in the last 30 yrs. DHA is part of this story and vegan sources of DHA not in the SN-2 position just do not set up photorepair. This sets the stage for autism to explode.
Dr. Jack Kruse
2023-06-09 02:49:03 +0000 UTChttps://www.linkedin.com/pulse/contact-lenses-statins-unintended-consequences-jack-kruse/
Dr. Jack Kruse
2023-06-09 00:41:59 +0000 UTCViolet light = UV light. Myopia has exploded worldwide in the past 50 years. What has changed at the same time? Screen time under blue light has massively increased, and we spend less and less time outdoors blocking 360-400nm light. This is a recipe for ocular disaster. Light with shorter UV wavelengths than 360 nm cannot penetrate the cornea and lens. Thus, violet light, 360 nm to 400 nm, is the most ideal light for myopia control not only from the point of efficacy but also safety. More violet light exposure in society and personally may stop, at least to some extent, the pandemic of myopia in Asia and other parts of the world. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5233810/
Dr. Jack Kruse
2023-06-09 00:11:11 +0000 UTChttps://jackkruse.com/ubiquitination-24-are-myopia-light-and-aging-linked/
Dr. Jack Kruse
2023-06-09 00:09:02 +0000 UTC100% …. Where as my father in law, also born 2 months early in a rural ocean town in Newfoundland Canada was born at home by midwife , no hospital or nicu visits. He was expected to pass. He lived out his preemie days being held by his 10 older siblings, sleeping in a shoe box next to a wood stove (no electricity in town) . Thankfully he was born end of June so he likely got what little sunlight the northern peninsula provided. Zero medical intervention & went on to live a prosperous life as a fisherman. No autism. ..really makes you think 🤔
Michelle Helen
2023-06-08 17:15:28 +0000 UTCDear Jack, I would like to learn everything about myopia and ways to offset it. Where would you point me to? Thanks in advance!
Luciano
2023-06-08 13:16:12 +0000 UTCThis was my next question, thank you Michelle and Jack for providing both question and answer.
David Mc Gettigan
2023-06-08 13:16:11 +0000 UTCSadly the poor kid left Chernobyl in his mom and was welcomed to another nuclear reactor in centralized medicine we call the NICU. Not a good way for a kid to start a life.
Dr. Jack Kruse
2023-06-08 12:47:39 +0000 UTCMy bet is there is something to this idea. Nature does not make errors. Expelling a baby early is a sign to decentralized uncle Jack that the child needs the light more than it needs its toxic mother's womb. Harsh, but that is how Nature operates. It is always a decision based on probability of survival. In QED that Nature uses, certainty was replaced by probability, which rises and falls like a wave. surfers love waves but centralized biology hates guesses, and is not a big fan of wave surfing because it limits their beliefs of truth. Our species often claims to hunger for truth, but seldom like the taste when it's served up. Humans are a plethora of stolen viruses and a stolen bacteria depleted of its genes. Evolution creates each new species so that it carries with it a plethora of opportunities to make it in this brave new world to surf Nature's waves. Man has pushed nature's limits because we are the only creature who refuses to be what we are. We are a creature who needs sunlight all the time. The Earth only plays music for those who listen to her tune. Those who don't listen are forced to changed or they become extinguished. That baby is trying to survive.
Dr. Jack Kruse
2023-06-08 12:44:52 +0000 UTCFascinating. My nephew has autism & was born 2.5 months early. I always wondered if the “autism” caused him to be born premature or if the after effects of being in the NICU (bright lights / not in the comfort of mom anymore, trauma, extra medication/ shots etc.) played into his autism. Thank you for providing some important pieces I was missing in my understanding.
Michelle Helen
2023-06-08 12:31:25 +0000 UTCGreat question and also answered by embryogenesis and Vitamin A via timing. In vitamin A-deficient (VAD) female mammals, reproduction usually fails prior to implantation so female births never make it early on. The same is not true about males because embryogenesis is different in the sexes. Studies show that vitamin A participates in a signaling mechanism to initiate meiosis in the female gonad during embryogenesis, and in the male gonad postnatally. This is why more males are born with autism. Female meiosis begins in the embryo and it doesn't in males. This means male embryos will get to term more often with Vitamin A issues during pregnancy.
Dr. Jack Kruse
2023-06-08 01:33:37 +0000 UTCMales are far more likely to be diagnosed with autism than females. Chromosomal differences? How does light play into the equation?
Michelle Helen
2023-06-08 01:19:04 +0000 UTCNope.....the vaccine has toxins melanin clears causing a lack of melanin and matrix redox power in its wake.
Dr. Jack Kruse
2023-06-08 00:10:14 +0000 UTCMany parents tell similar stories regarding a dramatic shift that occurred in their infants health following vaccination leading to loss of language and an eventual diagnosis of autism. Could hyperstimulation of the immature immune system with vaccines be the straw that breaks the camels back?
Robert Koagedal
2023-06-07 21:38:21 +0000 UTCThe human brain remains neuroplastic its entire existence. The key is will enough stimulus be applied to rewire the bad first design created by the parents choices around light use.
Dr. Jack Kruse
2023-06-07 21:10:23 +0000 UTCA lot to digest there. As a thought experiment, if one was able to get an autistic child/adult to be properly regulated with good circadian rhythm and regular exposure to full spectrum sunlight, how much change do you think is possible over time for them? Fascinated to know what you might predict is possible.
David Mc Gettigan
2023-06-07 20:10:38 +0000 UTC
