CertifiedGoy
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Light and Circadian Biology
Light is the most fundamental environmental input. Every photon that strikes the retina or skin changes molecular machinery inside the body. The circadian system is built around photoreception. Specialized melanopsin-containing photosensitive retinal ganglion cells (ipRGCs) respond to ~480 nm blue light, sending signals through the retinohypothalamic tract into the suprachiasmatic nucleus (SCN).
The SCN is the master clock. Its molecular gears are the transcriptional–translational feedback loops: CLOCK and BMAL1 proteins bind DNA to promote transcription of PER and CRY genes. As PER and CRY proteins accumulate, they inhibit CLOCK/BMAL1, creating an oscillation around 24 hours. REV-ERBα and RORα stabilize this loop by tuning BMAL1 expression.
These clocks regulate metabolism directly. CLOCK/BMAL1 upregulate enzymes for glucose uptake and oxidation, while PER/CRY feedback ties metabolism to the light–dark cycle. SIRT1, AMPK, and mTOR integrate energy status: AMPK phosphorylates CRY, advancing the clock in low energy states, while SIRT1 deacetylates BMAL1 and PER2, linking NAD+ to circadian amplitude.
Light also acts directly on mitochondria. Cytochrome c oxidase (complex IV) absorbs red and near-infrared photons (600–1000 nm). Photons displace inhibitory nitric oxide, accelerating electron transport, restoring mitochondrial membrane potential, and boosting ATP production. The burst of electron flux generates controlled ROS, which act as signals: activating Nrf2 to drive antioxidant enzyme expression, FOXO3a to trigger autophagy, and SIRT3 to deacetylate mitochondrial enzymes for efficiency.
In the skin, UVB photons convert 7-dehydrocholesterol to vitamin D3, which binds the vitamin D receptor to regulate over a thousand genes, many tied to mitochondrial function and immunity. UVA liberates nitric oxide, lowering blood pressure and tuning complex IV. Morning sunlight stimulates serotonin synthesis, which provides substrate for melatonin production at night. Melatonin itself enters mitochondria, scavenging hydroxyl radicals and stabilizing ETC complexes, protecting mitochondrial DNA from oxidative attack.
When light input is distorted, the system collapses. Artificial blue light at night keeps melanopsin firing, suppressing AANAT activity in the pineal, blocking melatonin synthesis. Mitochondria lose their nighttime antioxidant shield, leaving ROS unchecked. Cortisol rhythms flatten, disrupting AMPK/mTOR balance and impairing tissue repair. On the molecular level, SIRT3 activity falls, electron transport slows, and ROS activate NF-κB, driving pro-inflammatory cytokine release. DNA repair enzymes falter, mtDNA mutates, and cellular aging accelerates.
Peripheral clocks also depend on light entrainment through the SCN. In the liver, circadian genes regulate gluconeogenesis and lipid oxidation; disruption pushes SREBP-1c–driven lipogenesis and fatty liver. In the pancreas, CLOCK/BMAL1 tunes β-cell insulin secretion; disruption creates postprandial hyperglycemia. In the gut, microbiome communities oscillate; circadian misalignment promotes dysbiosis, LPS leakage, and TLR4→NF-κB inflammation.
Blue Light, the Pineal Gland, and Hormonal Collapse
Blue light at night is destructive. Melanopsin is hyper-excited in a spectral range devoid of balancing infrared and UV. This suppresses melatonin output from the pineal gland, dismantling nighttime repair.
Melatonin normally enters mitochondria to activate antioxidant defenses and stabilize complexes I and III. Without it, ROS accumulate, lipid membranes oxidize, and mtDNA mutations accelerate. SIRT3 activity plummets because NAD+ recycling falters in the absence of melatonin-driven repair.
The pineal is the key hormone switchboard. Disrupted melatonin rhythm breaks hypothalamic–pituitary–gonadal signaling. GnRH release falters, lowering LH and FSH, collapsing testosterone, estrogen, and progesterone production. The HPA axis also drifts: cortisol loses its morning peak, flattening energy cycles and impairing autophagy. Growth hormone secretion becomes blunted, impairing tissue regeneration.
This means CLOCK/BMAL1 lose amplitude, REV-ERBα control over BMAL1 weakens, and PER/CRY feedback destabilizes. Downstream, AMPK/mTOR cycles desynchronize. Cells switch into a pseudo-constant growth mode, driven by mTOR, but without proper repair signals. The result is insulin resistance, leptin resistance, and eventual metabolic collapse.
Non-Native EMFs and Calcium Overload
Electromagnetic fields from wireless technologies act on cell membranes and mitochondria through voltage-gated calcium channels (VGCCs). Oscillating EMFs trigger excessive calcium influx into the cytoplasm.
The elevated calcium activates nitric oxide synthase, producing high NO. Under oxidative stress, NO combines with superoxide to form peroxynitrite (ONOO−), a highly reactive species that nitrates tyrosine residues, damages mitochondrial complexes, and fragments mtDNA. This ONOO− cycle sustains itself, keeping NF-κB chronically active and driving inflammatory cytokine release.
At the mitochondrial level, excess calcium opens the mitochondrial permeability transition pore (mPTP). This collapses membrane potential, halts ATP production, and releases cytochrome c into the cytosol, triggering caspase-driven apoptosis. Chronic low-level activation creates a steady leak of ROS and mtDNA fragments, priming the immune system for autoimmunity.
VGCC-mediated calcium influx also disrupts circadian function. Calcium-calmodulin pathways normally stabilize CLOCK/BMAL1 transcriptional activity; overload scrambles these signals. Pineal melatonin output falls even further under EMF exposure, compounding the damage of blue light.
Mitochondrial Water, EZ, and Deuterium
Mitochondria do not only produce ATP — they structure water. The proton gradient across the inner membrane drives ATP synthase, but the same proton tunneling through cytochrome c oxidase generates exclusion zone (EZ) water, a coherent phase of structured water first described by Pollack.
EZ water lines mitochondrial membranes, supporting proton tunneling and maintaining dielectric properties critical for electron transport. Its formation depends on infrared light and tight mitochondrial geometry.
Deuterium is the hidden disruptor. Deuterium is hydrogen with an extra neutron; its heavier mass disrupts proton tunneling in ATP synthase and NADH dehydrogenase. High deuterium intake clogs the nanoscopic turbines of ATP synthase, reducing efficiency and generating excess ROS.
Mitochondria evolved deuterium depletion systems. Beta-oxidation of fats preferentially removes deuterium, delivering low-deuterium hydrogen to the ETC. When diets shift toward carbohydrates and processed foods, deuterium floods the matrix, sabotaging ATP production. Water from mitochondrial respiration — metabolic water — is naturally low in deuterium, but this requires robust fat oxidation and intact mitochondrial structure.
Deterium overload impairs NADH/NAD+ recycling, lowers SIRT1 and SIRT3 activity, destabilizes FOXO3a-mediated stress responses, and accelerates HIF-1α activation, mimicking pseudohypoxia.
DHA, Electron Tunneling, and Photoelectric Coupling
Docosahexaenoic acid (DHA) is unique among fatty acids. Its six double bonds create an electron cloud that is highly responsive to photons. DHA integrates photons from light into electron flow across membranes, essentially acting as a photonic-to-electronic converter.
In neuronal membranes, DHA maintains ultra-fast electron tunneling between respiratory complexes. It couples with cardiolipin in mitochondrial membranes to optimize electron resonance. Without DHA, electrons leak, generating excess ROS.
Photons captured by DHA in retinal membranes directly support the photoelectric effect that drives circadian entrainment. Inadequate DHA intake breaks this quantum link. Neural signaling slows, mitochondrial efficiency drops, and circadian cycles fragment.
On the molecular side, DHA stabilizes the function of complex I, reduces reverse electron transport, and optimizes CoQ10 redox cycling. It also modulates membrane fluidity, ensuring insulin receptor mobility and TLR4 signaling balance. Loss of DHA-rich membranes stiffens cells, driving insulin resistance and chronic inflammation.
Cold Thermogenesis and Hypoxia Pathways
Cold exposure is a mitochondrial signal. Exposure to cold activates the sympathetic nervous system, releasing norepinephrine. This upregulates uncoupling protein 1 (UCP1) in brown fat, allowing protons to leak across the inner mitochondrial membrane without generating ATP, instead producing heat.
This deliberate uncoupling lowers mitochondrial ROS production by preventing high membrane potential buildup. It increases mitochondrial biogenesis through PGC-1α activation and SIRT1/SIRT3 signaling. FOXO3a is triggered, promoting autophagy and longevity pathways.
Cold also activates AMPK, shifting metabolism toward fat oxidation, and stabilizes HIF-1α under mild hypoxia, driving angiogenesis and metabolic flexibility. These pathways overlap with hormetic stress responses that keep mitochondria youthful.
Cold exposure increases adiponectin, improves leptin sensitivity, and resets insulin receptor signaling. It also restructures water in and around mitochondria, since infrared release during uncoupling expands exclusion zones.
Magnetism, Grounding, and Electron Spin
The Earth’s magnetic field provides a steady background signal for mitochondrial electron transport. Cryptochromes are magnetosensitive proteins. Their radical pairs are influenced by geomagnetic fields, meaning circadian timing is tied directly to Earth’s magnetism.
Non-native EMFs form electronic devices disrupt this mechanism, scrambling cryptochrome spin states and desynchronizing circadian feedback loops. Grounding, by reconnecting the body to the Earth’s surface electrons, replenishes redox potential. Free electrons from the ground neutralize ROS, reducing NF-κB activation and inflammation.
Mitochondrial electron transport is itself dependent on electron spin coherence. Disturbances from EMFs, loss of DHA, or deuterium overload break spin alignment, leading to electron leakage, ROS, and loss of ATP efficiency.
This is all jack kruses work btw
Light is the most fundamental environmental input. Every photon that strikes the retina or skin changes molecular machinery inside the body. The circadian system is built around photoreception. Specialized melanopsin-containing photosensitive retinal ganglion cells (ipRGCs) respond to ~480 nm blue light, sending signals through the retinohypothalamic tract into the suprachiasmatic nucleus (SCN).
The SCN is the master clock. Its molecular gears are the transcriptional–translational feedback loops: CLOCK and BMAL1 proteins bind DNA to promote transcription of PER and CRY genes. As PER and CRY proteins accumulate, they inhibit CLOCK/BMAL1, creating an oscillation around 24 hours. REV-ERBα and RORα stabilize this loop by tuning BMAL1 expression.
These clocks regulate metabolism directly. CLOCK/BMAL1 upregulate enzymes for glucose uptake and oxidation, while PER/CRY feedback ties metabolism to the light–dark cycle. SIRT1, AMPK, and mTOR integrate energy status: AMPK phosphorylates CRY, advancing the clock in low energy states, while SIRT1 deacetylates BMAL1 and PER2, linking NAD+ to circadian amplitude.
Light also acts directly on mitochondria. Cytochrome c oxidase (complex IV) absorbs red and near-infrared photons (600–1000 nm). Photons displace inhibitory nitric oxide, accelerating electron transport, restoring mitochondrial membrane potential, and boosting ATP production. The burst of electron flux generates controlled ROS, which act as signals: activating Nrf2 to drive antioxidant enzyme expression, FOXO3a to trigger autophagy, and SIRT3 to deacetylate mitochondrial enzymes for efficiency.
In the skin, UVB photons convert 7-dehydrocholesterol to vitamin D3, which binds the vitamin D receptor to regulate over a thousand genes, many tied to mitochondrial function and immunity. UVA liberates nitric oxide, lowering blood pressure and tuning complex IV. Morning sunlight stimulates serotonin synthesis, which provides substrate for melatonin production at night. Melatonin itself enters mitochondria, scavenging hydroxyl radicals and stabilizing ETC complexes, protecting mitochondrial DNA from oxidative attack.
When light input is distorted, the system collapses. Artificial blue light at night keeps melanopsin firing, suppressing AANAT activity in the pineal, blocking melatonin synthesis. Mitochondria lose their nighttime antioxidant shield, leaving ROS unchecked. Cortisol rhythms flatten, disrupting AMPK/mTOR balance and impairing tissue repair. On the molecular level, SIRT3 activity falls, electron transport slows, and ROS activate NF-κB, driving pro-inflammatory cytokine release. DNA repair enzymes falter, mtDNA mutates, and cellular aging accelerates.
Peripheral clocks also depend on light entrainment through the SCN. In the liver, circadian genes regulate gluconeogenesis and lipid oxidation; disruption pushes SREBP-1c–driven lipogenesis and fatty liver. In the pancreas, CLOCK/BMAL1 tunes β-cell insulin secretion; disruption creates postprandial hyperglycemia. In the gut, microbiome communities oscillate; circadian misalignment promotes dysbiosis, LPS leakage, and TLR4→NF-κB inflammation.
Blue Light, the Pineal Gland, and Hormonal Collapse
Blue light at night is destructive. Melanopsin is hyper-excited in a spectral range devoid of balancing infrared and UV. This suppresses melatonin output from the pineal gland, dismantling nighttime repair.
Melatonin normally enters mitochondria to activate antioxidant defenses and stabilize complexes I and III. Without it, ROS accumulate, lipid membranes oxidize, and mtDNA mutations accelerate. SIRT3 activity plummets because NAD+ recycling falters in the absence of melatonin-driven repair.
The pineal is the key hormone switchboard. Disrupted melatonin rhythm breaks hypothalamic–pituitary–gonadal signaling. GnRH release falters, lowering LH and FSH, collapsing testosterone, estrogen, and progesterone production. The HPA axis also drifts: cortisol loses its morning peak, flattening energy cycles and impairing autophagy. Growth hormone secretion becomes blunted, impairing tissue regeneration.
This means CLOCK/BMAL1 lose amplitude, REV-ERBα control over BMAL1 weakens, and PER/CRY feedback destabilizes. Downstream, AMPK/mTOR cycles desynchronize. Cells switch into a pseudo-constant growth mode, driven by mTOR, but without proper repair signals. The result is insulin resistance, leptin resistance, and eventual metabolic collapse.
Non-Native EMFs and Calcium Overload
Electromagnetic fields from wireless technologies act on cell membranes and mitochondria through voltage-gated calcium channels (VGCCs). Oscillating EMFs trigger excessive calcium influx into the cytoplasm.
The elevated calcium activates nitric oxide synthase, producing high NO. Under oxidative stress, NO combines with superoxide to form peroxynitrite (ONOO−), a highly reactive species that nitrates tyrosine residues, damages mitochondrial complexes, and fragments mtDNA. This ONOO− cycle sustains itself, keeping NF-κB chronically active and driving inflammatory cytokine release.
At the mitochondrial level, excess calcium opens the mitochondrial permeability transition pore (mPTP). This collapses membrane potential, halts ATP production, and releases cytochrome c into the cytosol, triggering caspase-driven apoptosis. Chronic low-level activation creates a steady leak of ROS and mtDNA fragments, priming the immune system for autoimmunity.
VGCC-mediated calcium influx also disrupts circadian function. Calcium-calmodulin pathways normally stabilize CLOCK/BMAL1 transcriptional activity; overload scrambles these signals. Pineal melatonin output falls even further under EMF exposure, compounding the damage of blue light.
Mitochondrial Water, EZ, and Deuterium
Mitochondria do not only produce ATP — they structure water. The proton gradient across the inner membrane drives ATP synthase, but the same proton tunneling through cytochrome c oxidase generates exclusion zone (EZ) water, a coherent phase of structured water first described by Pollack.
EZ water lines mitochondrial membranes, supporting proton tunneling and maintaining dielectric properties critical for electron transport. Its formation depends on infrared light and tight mitochondrial geometry.
Deuterium is the hidden disruptor. Deuterium is hydrogen with an extra neutron; its heavier mass disrupts proton tunneling in ATP synthase and NADH dehydrogenase. High deuterium intake clogs the nanoscopic turbines of ATP synthase, reducing efficiency and generating excess ROS.
Mitochondria evolved deuterium depletion systems. Beta-oxidation of fats preferentially removes deuterium, delivering low-deuterium hydrogen to the ETC. When diets shift toward carbohydrates and processed foods, deuterium floods the matrix, sabotaging ATP production. Water from mitochondrial respiration — metabolic water — is naturally low in deuterium, but this requires robust fat oxidation and intact mitochondrial structure.
Deterium overload impairs NADH/NAD+ recycling, lowers SIRT1 and SIRT3 activity, destabilizes FOXO3a-mediated stress responses, and accelerates HIF-1α activation, mimicking pseudohypoxia.
DHA, Electron Tunneling, and Photoelectric Coupling
Docosahexaenoic acid (DHA) is unique among fatty acids. Its six double bonds create an electron cloud that is highly responsive to photons. DHA integrates photons from light into electron flow across membranes, essentially acting as a photonic-to-electronic converter.
In neuronal membranes, DHA maintains ultra-fast electron tunneling between respiratory complexes. It couples with cardiolipin in mitochondrial membranes to optimize electron resonance. Without DHA, electrons leak, generating excess ROS.
Photons captured by DHA in retinal membranes directly support the photoelectric effect that drives circadian entrainment. Inadequate DHA intake breaks this quantum link. Neural signaling slows, mitochondrial efficiency drops, and circadian cycles fragment.
On the molecular side, DHA stabilizes the function of complex I, reduces reverse electron transport, and optimizes CoQ10 redox cycling. It also modulates membrane fluidity, ensuring insulin receptor mobility and TLR4 signaling balance. Loss of DHA-rich membranes stiffens cells, driving insulin resistance and chronic inflammation.
Cold Thermogenesis and Hypoxia Pathways
Cold exposure is a mitochondrial signal. Exposure to cold activates the sympathetic nervous system, releasing norepinephrine. This upregulates uncoupling protein 1 (UCP1) in brown fat, allowing protons to leak across the inner mitochondrial membrane without generating ATP, instead producing heat.
This deliberate uncoupling lowers mitochondrial ROS production by preventing high membrane potential buildup. It increases mitochondrial biogenesis through PGC-1α activation and SIRT1/SIRT3 signaling. FOXO3a is triggered, promoting autophagy and longevity pathways.
Cold also activates AMPK, shifting metabolism toward fat oxidation, and stabilizes HIF-1α under mild hypoxia, driving angiogenesis and metabolic flexibility. These pathways overlap with hormetic stress responses that keep mitochondria youthful.
Cold exposure increases adiponectin, improves leptin sensitivity, and resets insulin receptor signaling. It also restructures water in and around mitochondria, since infrared release during uncoupling expands exclusion zones.
Magnetism, Grounding, and Electron Spin
The Earth’s magnetic field provides a steady background signal for mitochondrial electron transport. Cryptochromes are magnetosensitive proteins. Their radical pairs are influenced by geomagnetic fields, meaning circadian timing is tied directly to Earth’s magnetism.
Non-native EMFs form electronic devices disrupt this mechanism, scrambling cryptochrome spin states and desynchronizing circadian feedback loops. Grounding, by reconnecting the body to the Earth’s surface electrons, replenishes redox potential. Free electrons from the ground neutralize ROS, reducing NF-κB activation and inflammation.
Mitochondrial electron transport is itself dependent on electron spin coherence. Disturbances from EMFs, loss of DHA, or deuterium overload break spin alignment, leading to electron leakage, ROS, and loss of ATP efficiency.
This is all jack kruses work btw
