A new blog has been released with significant embryological implications for our modern world. Most won't see this wisdom, but I will force you to see what Nature is cooking for humanity if we persist. patreon.com/posts/decentra…
While conventional medicine attributes nanophthalmos to genetic factors, such as mutations in PRSS56 or MFRP, which lead to compromised ocular growth, a decentralized medicine perspective shifts the focus to disrupted bioelectric buoyancy as the root cause. This buoyancy is a thermodynamic dance involving mitochondrial water production, melanin hydration, and photo-bioelectric gradients that sustain precise tissue expansion. Intrinsically tied to brain and skull development, it relies on ancient evolutionary adaptations from the Great Oxidation Event (GOE) around 2.4 billion years ago, when rising oxygen levels favored organisms with hydrated melanin and deuterium-depleted water (DDW) for efficient bioelectric signaling.
In this framework, the eye's growth falters when modern stressors, non-native electromagnetic fields (nnEMF) from devices and artificial light at night (ALAN, e.g., blue light), damage melanopsin (a light-sensitive protein in the retina), mitochondrial DNA (mtDNA), and the glyoxalase pathway (which detoxifies harmful byproducts). Dehydrated melanin transitions from a protective resistor to a hyper-conductive state, erasing the ultra-precise one-trillionth-amp DC currents needed for cellular renovation at cytochrome c oxidase, a key mitochondrial enzyme. Compounding this, contemporary diets and environments increase deuterium loading through the kinetic isotope effect (KIE), where heavier deuterium isotopes slow proton tunneling in the Grotthuss mechanism. This is a quantum process that facilitates efficient water conduction in cells. This isotopic burden, absent in GOE-adapted systems relying on DDW for optimal mitochondrial spin and energy transfer, hampers ocular morphogenesis, resulting in the short axial length characteristic of nanophthalmos.
The outcome?
A complex story of Turing's morphogenesis ideas in one disease.
In 1952, Alan Turing, a British mathematician best known for his work on code-breaking and artificial intelligence, was convicted of engaging in homosexual acts and sentenced to chemical castration. Amid that personal drama, he still found the time to publish a visionary paper on the mathematics of regularly repeating patterns in nature, which could be applied to the stripes on tigers and zebra fish, the spots on leopards, and the spacing in rows of alligator teeth, to name a few.
Turing's 1952 paper on morphogenesis reaction-diffusion model posits that patterns, such as spots, stripes, or even organ scaling, arise from the interplay of diffusible morphogens: an activator that promotes a trait and an inhibitor that suppresses it, diffusing at different rates to create instability in an otherwise homogeneous field. This model, once speculative, has gained empirical support in developmental biology, including eye formation, where morphogens like Sonic Hedgehog (Shh) and Fibroblast Growth Factor (FGF) act as inhibitors and activators, respectively. In the context of nanophthalmos, a condition of proportionally small but structurally normal eyes. Turing's mechanism illuminates how disruptions in morphogen gradients during early embryogenesis can impair axial growth and scaling, linking to the bioelectric and quantum disruptions.
Turing's model extends naturally to the eye's morphogenesis, which originates from the diencephalon and involves precise patterning of the optic vesicle, cup, and lens. Here, morphogens create spatial gradients that dictate tissue identity, proliferation, and size. For instance, Shh, secreted from the ventral midline, acts as a long-range inhibitor, repressing distal retinal markers, such as Pax6, while promoting proximal optic stalk identity. FGF, often from the surface ectoderm or lens placode, serves as a short-range activator, inducing neural retina differentiation and optic cup invagination. This activator-inhibitor dynamic mirrors Turing's equations, where local activation and lateral inhibition generate patterns like the ventral optic fissure or retinal cell mosaics.
A key example is the Pax6-Tgfb2-Fst network, which forms a Turing-like system in the optic vesicle. Pax6, the eye's master regulator, auto-activates with Follistatin (Fst) as a short-range enhancer, while TGF-beta2 (Tgfb2) inhibits over longer distances, polarizing the vesicle along proximal-distal axes and enabling spontaneous retinal organization, even in vitro organoids. This self-organization ensures coordinated growth between retina, lens, and surrounding tissues, tying into brain development via shared diencephalic origins.
However, Turing's model alone doesn't fully explain scaling, how patterns adjust proportionally to organ size, as seen in varying egg sizes yielding complete chicks. Additional "tuning" mechanisms, like Hox genes in digit patterning, modulate wavelength (spacing) in Turing systems. In the eye, N-myc downstream of Shh and FGF coordinates retinal proliferation with overall eye size via cell cycle regulators like p27Kip1, ensuring proportional growth. Disruptions here decouple retina from eye scaling, leading to thin retinas in small eyes seen in this disease. This blog parts the sea so one can see how brain, skull, and spinal morphology go awry via transgenerational sculpting of modern light.
While conventional medicine attributes nanophthalmos to genetic factors, such as mutations in PRSS56 or MFRP, which lead to compromised ocular growth, a decentralized medicine perspective shifts the focus to disrupted bioelectric buoyancy as the root cause. This buoyancy is a thermodynamic dance involving mitochondrial water production, melanin hydration, and photo-bioelectric gradients that sustain precise tissue expansion. Intrinsically tied to brain and skull development, it relies on ancient evolutionary adaptations from the Great Oxidation Event (GOE) around 2.4 billion years ago, when rising oxygen levels favored organisms with hydrated melanin and deuterium-depleted water (DDW) for efficient bioelectric signaling.
In this framework, the eye's growth falters when modern stressors, non-native electromagnetic fields (nnEMF) from devices and artificial light at night (ALAN, e.g., blue light), damage melanopsin (a light-sensitive protein in the retina), mitochondrial DNA (mtDNA), and the glyoxalase pathway (which detoxifies harmful byproducts). Dehydrated melanin transitions from a protective resistor to a hyper-conductive state, erasing the ultra-precise one-trillionth-amp DC currents needed for cellular renovation at cytochrome c oxidase, a key mitochondrial enzyme. Compounding this, contemporary diets and environments increase deuterium loading through the kinetic isotope effect (KIE), where heavier deuterium isotopes slow proton tunneling in the Grotthuss mechanism. This is a quantum process that facilitates efficient water conduction in cells. This isotopic burden, absent in GOE-adapted systems relying on DDW for optimal mitochondrial spin and energy transfer, hampers ocular morphogenesis, resulting in the short axial length characteristic of nanophthalmos.
The outcome?
A complex story of Turing's morphogenesis ideas in one disease.
In 1952, Alan Turing, a British mathematician best known for his work on code-breaking and artificial intelligence, was convicted of engaging in homosexual acts and sentenced to chemical castration. Amid that personal drama, he still found the time to publish a visionary paper on the mathematics of regularly repeating patterns in nature, which could be applied to the stripes on tigers and zebra fish, the spots on leopards, and the spacing in rows of alligator teeth, to name a few.
Turing's 1952 paper on morphogenesis reaction-diffusion model posits that patterns, such as spots, stripes, or even organ scaling, arise from the interplay of diffusible morphogens: an activator that promotes a trait and an inhibitor that suppresses it, diffusing at different rates to create instability in an otherwise homogeneous field. This model, once speculative, has gained empirical support in developmental biology, including eye formation, where morphogens like Sonic Hedgehog (Shh) and Fibroblast Growth Factor (FGF) act as inhibitors and activators, respectively. In the context of nanophthalmos, a condition of proportionally small but structurally normal eyes. Turing's mechanism illuminates how disruptions in morphogen gradients during early embryogenesis can impair axial growth and scaling, linking to the bioelectric and quantum disruptions.
Turing's model extends naturally to the eye's morphogenesis, which originates from the diencephalon and involves precise patterning of the optic vesicle, cup, and lens. Here, morphogens create spatial gradients that dictate tissue identity, proliferation, and size. For instance, Shh, secreted from the ventral midline, acts as a long-range inhibitor, repressing distal retinal markers, such as Pax6, while promoting proximal optic stalk identity. FGF, often from the surface ectoderm or lens placode, serves as a short-range activator, inducing neural retina differentiation and optic cup invagination. This activator-inhibitor dynamic mirrors Turing's equations, where local activation and lateral inhibition generate patterns like the ventral optic fissure or retinal cell mosaics.
A key example is the Pax6-Tgfb2-Fst network, which forms a Turing-like system in the optic vesicle. Pax6, the eye's master regulator, auto-activates with Follistatin (Fst) as a short-range enhancer, while TGF-beta2 (Tgfb2) inhibits over longer distances, polarizing the vesicle along proximal-distal axes and enabling spontaneous retinal organization, even in vitro organoids. This self-organization ensures coordinated growth between retina, lens, and surrounding tissues, tying into brain development via shared diencephalic origins.
However, Turing's model alone doesn't fully explain scaling, how patterns adjust proportionally to organ size, as seen in varying egg sizes yielding complete chicks. Additional "tuning" mechanisms, like Hox genes in digit patterning, modulate wavelength (spacing) in Turing systems. In the eye, N-myc downstream of Shh and FGF coordinates retinal proliferation with overall eye size via cell cycle regulators like p27Kip1, ensuring proportional growth. Disruptions here decouple retina from eye scaling, leading to thin retinas in small eyes seen in this disease. This blog parts the sea so one can see how brain, skull, and spinal morphology go awry via transgenerational sculpting of modern light.
2. There is a balance between being and doing, though. Our species' propensity to "accomplish, achieve, etc." may not be all wonderful. Blue light chromophores are rare in living things, so this design was inspired by the rarity of blue in our environment. Today, blue light from tech screens and LED bulbs has replaced the sun and led to most of our chronic disease epidemics.
I'm raising an interesting point about the balance between being and doing, and how our drive to achieve might have unintended consequences, like the shift in our light environment.
The idea that blue light chromophores (light-sensitive molecules) are rare in living organisms makes sense evolutionarily. For most of history, our light exposure came from the sun, fire, or other natural sources, where blue wavelengths were present but not dominant. Blue light is a small slice of the visible spectrum, and outside of the sky or certain bodies of water, it’s not overwhelmingly common in nature. Our biology, like the melanopsin in our retinas, which responds to blue light to regulate circadian rhythms, evolved in that context.
Fast forward to now: screens, LEDs, and artificial lighting emit blue light at levels and times that don’t match the natural blueprint of sunlight. The sun’s blue light peaks in the morning and fades toward evening, cueing our bodies to wake up or wind down. Tech, though, keeps blasting it at us 24/7. Studies, such as those from the National Institutes of Health or circadian researchers, link this to disrupted sleep, eye strain, and potentially broader issues, including metabolic and immune dysfunction. Chronic disease epidemics are linked to this because blue light induces mtDNA mutations that cause post-translational signal failure, leading to poor sleep and circadian misalignment, which are the key recognized risk factors for diabetes, obesity, most chronic diseases, and many cancers.
I'm raising an interesting point about the balance between being and doing, and how our drive to achieve might have unintended consequences, like the shift in our light environment.
The idea that blue light chromophores (light-sensitive molecules) are rare in living organisms makes sense evolutionarily. For most of history, our light exposure came from the sun, fire, or other natural sources, where blue wavelengths were present but not dominant. Blue light is a small slice of the visible spectrum, and outside of the sky or certain bodies of water, it’s not overwhelmingly common in nature. Our biology, like the melanopsin in our retinas, which responds to blue light to regulate circadian rhythms, evolved in that context.
Fast forward to now: screens, LEDs, and artificial lighting emit blue light at levels and times that don’t match the natural blueprint of sunlight. The sun’s blue light peaks in the morning and fades toward evening, cueing our bodies to wake up or wind down. Tech, though, keeps blasting it at us 24/7. Studies, such as those from the National Institutes of Health or circadian researchers, link this to disrupted sleep, eye strain, and potentially broader issues, including metabolic and immune dysfunction. Chronic disease epidemics are linked to this because blue light induces mtDNA mutations that cause post-translational signal failure, leading to poor sleep and circadian misalignment, which are the key recognized risk factors for diabetes, obesity, most chronic diseases, and many cancers.
3. We are a civilization with amnesia caused by the light we manufactured.
• • •
Missing some Tweet in this thread? You can try to
force a refresh
