If you have or had breast cancer, you better not miss this lesson. It could save your life. forum.jackkruse.com/threads/new-me…
2. Vitamin D 3 has 44 hydrogens in its chemical formula of C27 H44 O. The chemical formula for 25-hydroxyvitamin D3 (the form your body makes) is C27 H44 O2.
We know ONE DEUTERIUM ATOM AFFECTS 96 ATOMS of H+. So this means that one misplaced D in Vitamin D3 or 25D(OH) can knock out two entire molecules of Vitamin D3/25 D(OH). That is an asymmetic destruction and explains fully why human breast cancer cases appear so heteropgenous. Centralized oncologist kill many breast cancer patients by not knowing the following: vitamin D status is particularly important for survival of women with triple negative breast cancer, an aggressive form of the disease with few effective treatment options.
Vitamin D resistance in any breast cancer emerges during tumor progression through mechanisms such as VDR methylation or CYP24A1 amplification. Also please remember, CYP24A1 is a heme protein that needs renovation with AM sunlight (red); CYP24A1 specifically is a mitochondrial inner-membrane cytochrome P450 enzyme. It possesses a canonical P450 fold with a heme prosthetic group that is essential for its monooxygenase activity. If a women gets a triple negative breast cancer by definition the oncologist should know this woman never sees AM sunlight and is afflicted with a tons of light post sunset. This is the main reason why chemo drugs and XRT are worthless in these cases. It also points out why DDW is one of the better ideas for this cancer that oncologists never tell women.
We know ONE DEUTERIUM ATOM AFFECTS 96 ATOMS of H+. So this means that one misplaced D in Vitamin D3 or 25D(OH) can knock out two entire molecules of Vitamin D3/25 D(OH). That is an asymmetic destruction and explains fully why human breast cancer cases appear so heteropgenous. Centralized oncologist kill many breast cancer patients by not knowing the following: vitamin D status is particularly important for survival of women with triple negative breast cancer, an aggressive form of the disease with few effective treatment options.
Vitamin D resistance in any breast cancer emerges during tumor progression through mechanisms such as VDR methylation or CYP24A1 amplification. Also please remember, CYP24A1 is a heme protein that needs renovation with AM sunlight (red); CYP24A1 specifically is a mitochondrial inner-membrane cytochrome P450 enzyme. It possesses a canonical P450 fold with a heme prosthetic group that is essential for its monooxygenase activity. If a women gets a triple negative breast cancer by definition the oncologist should know this woman never sees AM sunlight and is afflicted with a tons of light post sunset. This is the main reason why chemo drugs and XRT are worthless in these cases. It also points out why DDW is one of the better ideas for this cancer that oncologists never tell women.
3. Plato’s cave manifests by living detached from natural light, while worshipping screens in your pocket, desk, and on you wall that dances and twirls to allow you to collect deuterium in your eccrine glands, apocrine glands, exocrine glands, and your mitochondrial matrix.
Hundreds of observational and clinical studies have addressed the possibility that vitamin D status alters development or progression of breast cancer. Studies have examined the presence of VDR, CYP27B1 and CYP24A1 (heme proteins) in tumors in relation to progression and the impact of vitamin D status (as reflected by serum 25D and 1,25D, UVR exposure, dietary intakes of processed foods loaded with deuterium, use of supplemental vitamin D loaded with deuterium laced seed oils, SNPs/SAPS in vitamin D pathway genes, (etc) on both development and progression of breast cancer.
Hundreds of observational and clinical studies have addressed the possibility that vitamin D status alters development or progression of breast cancer. Studies have examined the presence of VDR, CYP27B1 and CYP24A1 (heme proteins) in tumors in relation to progression and the impact of vitamin D status (as reflected by serum 25D and 1,25D, UVR exposure, dietary intakes of processed foods loaded with deuterium, use of supplemental vitamin D loaded with deuterium laced seed oils, SNPs/SAPS in vitamin D pathway genes, (etc) on both development and progression of breast cancer.
4. Vitamin D signaling in normal breast and in breast cancer is highly heterogeneous and incompletely understood by centralized oncologists because none of them have a clue about how the biophysics of deuterium alters 96 hydrogen atoms in all the pathways of biochemistry.
When someone has an idiosyncratic response to the standard chemo regimen of drigs used in these cancers it is a screaming signal that deuterium is the reason why it is happening due to a bad relationship with light. That is why the Tulane study exists below.
When someone has an idiosyncratic response to the standard chemo regimen of drigs used in these cancers it is a screaming signal that deuterium is the reason why it is happening due to a bad relationship with light. That is why the Tulane study exists below.
5. Ecological studies have found decreasing breast cancer incidence with increasing proximity to the Equator (Gorham et al., 1990, Mandal et al., 2009, Mohr et al., 2008). Since latitude is an influential determinant of cutaneous vitamin D production, these ecologic findings supported the hypothesis that exposure to vitamin D reduces breast cancer risk. However, other epidemiological studies of circulating vitamin D and breast cancer risk have been inconsistent and preliminary results from a recent large pooled analysis suggest no association with breast cancer risk (Visvanathan et al., 2015). Do you know why this finding occured? If a woman's body and breast glands are loaded with deuterium and studied this way, and no deuterium controls are done what would you expect this methodology to show?
This is how BigHarma and Centralized oncology keep their casino running wide open. Now you know why the truth stays hidden, why many oncolgist get paid for chemo drugs, and why no one talks about the biophysics of deuterium in quantum biology.
This is how BigHarma and Centralized oncology keep their casino running wide open. Now you know why the truth stays hidden, why many oncolgist get paid for chemo drugs, and why no one talks about the biophysics of deuterium in quantum biology.
6. All the pieces fit in decentralized medicine.
7. Hydration status is related to solar exposure via CCO function which links directly to heme and melanin biology. Proper solar exposure determines DDW production at CCO which is ALSO a HEME protein. All heme proteins on the IMM are loaded with red light chromophores. CCO has 4 of them embedded in it.
Heme influences POMC via circadian regulators Rev-Erb-alpha/beta (also heme proteins), integrating oxygen metabolism with light-driven rhythms that are all destroyed in women with breast cancer.
The GOE introduced a new player to Earth’s environment: molecular oxygen. For early anaerobic life forms, oxygen was a toxic electrical stressor. Oxygen, with its high electronegativity, changes the electrical resistance of biological membranes, disrupting the delicate balance of charge that early cells relied on for survival. Back then there was no heme or melanin proteins to protect cells from oxygen and this is why cancer exists today. When melanin and heme proteins go MIA for any reason in any organ cancer become more probable.
Membranes, which are essentially lipid bilayers, act as capacitors, storing and managing electrical gradients critical for cellular function. The sudden presence of oxygen would have altered these gradients, creating an existential crisis for early life. Today's modern environments with fake lights, a lack of sun, technocracy abuse, and a lack of grounding in Nature is what makes cancer more probable. It mimics the GOE environments.
Heme influences POMC via circadian regulators Rev-Erb-alpha/beta (also heme proteins), integrating oxygen metabolism with light-driven rhythms that are all destroyed in women with breast cancer.
The GOE introduced a new player to Earth’s environment: molecular oxygen. For early anaerobic life forms, oxygen was a toxic electrical stressor. Oxygen, with its high electronegativity, changes the electrical resistance of biological membranes, disrupting the delicate balance of charge that early cells relied on for survival. Back then there was no heme or melanin proteins to protect cells from oxygen and this is why cancer exists today. When melanin and heme proteins go MIA for any reason in any organ cancer become more probable.
Membranes, which are essentially lipid bilayers, act as capacitors, storing and managing electrical gradients critical for cellular function. The sudden presence of oxygen would have altered these gradients, creating an existential crisis for early life. Today's modern environments with fake lights, a lack of sun, technocracy abuse, and a lack of grounding in Nature is what makes cancer more probable. It mimics the GOE environments.
8. Decentralized wisdom emerges not from centralized attempts to hoard knowledge, but from the collective understanding distributed across networks and individuals. Only fools chase exhaustive facts in isolation, for the essence of life lies in grasping interconnections. While knowledge can spotlight isolated ideas through data and algorithms, true decentralized wisdom flourishes in the shadows of uncertainty, where the vast, interconnected scale of the universe, or a blockchain ecosystem, reveals itself beyond any single node's grasp. Knowledge delivers factual inputs from structured sources, yet it misses the emergent observation of wisdom born from crowdsourced insights. In this framework, knowledge equips you with awareness of potential actions, like executing smart contracts or aggregating data, but decentralized wisdom teaches restraint, knowing when to withhold, allowing the crowd's collective judgment to guide outcomes without overreach.
Consider how I apply this idea to modern cancer therapeutics.
Evolutionary Context and Szent-Györgyi’s Lens
Szent-Györgyi argued in 1968 that electronic states in biomolecules, like proteins, could mediate energy transfer and cellular function, potentially via light. Pre-GOE prokaryotes relied on glycolysis and fermentation, releasing broader-spectrum light (200-1100 nm) via metabolic byproducts and ROS, think of luciferase-like bioluminescence or chemiluminescence. Post-GOE, with oxygen and mitochondria, the TCA cycle and oxidative phosphorylation (OXPHOS) became dominant, producing more UV biophotons (200-400 nm) from ROS and excited carbonyls, as seen in modern eukaryotes.
Apoptosis likely evolved near the Cambrian (~541 Mya), post-GOE, when UV light increased due to oxygen forming ozone, yet still penetrated shallow oceans. My hypothesis is that anti-apoptotic proteins (e.g., Bcl-2) might avoid UV spectra to mimic pre-GOE “wide-spectrum” conditions, favoring survival, while pro-apoptotic proteins (e.g., Bax) align with UV-rich post-GOE signaling for cell death. However, Bcl-2’s UV-centric Trp/Tyr profile challenges this directly—its spectra match the “unusual” UV range, not a pre-GOE broad spectrum. We see here evidence of a change in solar spectra changing the proteins that control apoptosis. Loss of apoptosis is the key step in developing cancer of any type.
Plausible Alternative Interpretation: Perhaps anti-apoptotic Bcl-2 doesn’t emit UV to “signal” death but absorbs it to stabilize mitochondria, quenching pro-apoptotic UV biophotons. Pro-apoptotic Bax/Bak, by releasing cytochrome c and ROS, could amplify UV emission, triggering apoptosis. This fits Szent-Györgyi’s idea of electronic control, with ultraweak UV biophotons as a mtDNA death signal, getting rid of mtDNA that might easily produce an atavistic primative cell in the face of normoxia. This is what cancer is, and its presence would need to be tightly controlled in more complex life with organ systems if one was to battle entropy for time. This is how light modulates protein interactions to make cancer less probable.
Consider how I apply this idea to modern cancer therapeutics.
Evolutionary Context and Szent-Györgyi’s Lens
Szent-Györgyi argued in 1968 that electronic states in biomolecules, like proteins, could mediate energy transfer and cellular function, potentially via light. Pre-GOE prokaryotes relied on glycolysis and fermentation, releasing broader-spectrum light (200-1100 nm) via metabolic byproducts and ROS, think of luciferase-like bioluminescence or chemiluminescence. Post-GOE, with oxygen and mitochondria, the TCA cycle and oxidative phosphorylation (OXPHOS) became dominant, producing more UV biophotons (200-400 nm) from ROS and excited carbonyls, as seen in modern eukaryotes.
Apoptosis likely evolved near the Cambrian (~541 Mya), post-GOE, when UV light increased due to oxygen forming ozone, yet still penetrated shallow oceans. My hypothesis is that anti-apoptotic proteins (e.g., Bcl-2) might avoid UV spectra to mimic pre-GOE “wide-spectrum” conditions, favoring survival, while pro-apoptotic proteins (e.g., Bax) align with UV-rich post-GOE signaling for cell death. However, Bcl-2’s UV-centric Trp/Tyr profile challenges this directly—its spectra match the “unusual” UV range, not a pre-GOE broad spectrum. We see here evidence of a change in solar spectra changing the proteins that control apoptosis. Loss of apoptosis is the key step in developing cancer of any type.
Plausible Alternative Interpretation: Perhaps anti-apoptotic Bcl-2 doesn’t emit UV to “signal” death but absorbs it to stabilize mitochondria, quenching pro-apoptotic UV biophotons. Pro-apoptotic Bax/Bak, by releasing cytochrome c and ROS, could amplify UV emission, triggering apoptosis. This fits Szent-Györgyi’s idea of electronic control, with ultraweak UV biophotons as a mtDNA death signal, getting rid of mtDNA that might easily produce an atavistic primative cell in the face of normoxia. This is what cancer is, and its presence would need to be tightly controlled in more complex life with organ systems if one was to battle entropy for time. This is how light modulates protein interactions to make cancer less probable.
9. @threadreaderapp make me a roll
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