Thread by @DrJackKruse

Why Two People Can Eat the Same Meal And Have Completely Different Biological Outcomes

We’ve all seen it:
Two people follow the same diet.
Same calories. Same macros. Same discipline.
One thrives. The other struggles.

For years, we blamed willpower, hormones, or “body type.”
But the truth is far more interesting and far more hopeful.

What most people forget is their light environment varies and the amount of light on their skin, eyes, and abdomen vary and that light changes prokaryote biology. Since mitochondria used to be a prokaryote it changes them to to alter UPE signaling. It is this light that changes the microbiome in you.

Inside every one of us lives a huge microbial ecosystem that is designed to act like soil around a tree. That colony of microbes then alters the type of bacteria by the light mitochondria release and that sculpts how we metabolize, respond, and recover.

It was never just the food that did it. Jeff Leach proved that in 2017.
It’s how your microbiome interprets the electromagnetic bar code embedded by the sun in your food.

Here’s what emerging research is revealing:

Some individuals harbor more Bifidobacterium longum and Faecalibacterium prausnitzii, which are bacteria shown to convert dietary fibres into short-chain fatty acids (SCFAs), improving gut-barrier integrity and lowering systemic inflammation (Zheng et al., 2020; Guo et al., 2021).

Oxygen is a toxin to prokaryotes so when you live within nnEMF light of any kind the sphincters in the gut to let oxygen roam free. This simplfies and the gut and leads to alien UPE signaling which causes disease.

Others show a higher Prevotella-to-Bacteroides ratio a microbial signature that can predict post-meal glucose spikes more accurately than the glycaemic index itself (Zeevi et al., 2015; Kovatcheva-Datchary et al., 2015). Of course the amount of sunlight is a critical variable these studies missed. We already know from other studies that sunlight reduces blood glucose by 30%

And in women with PCOS, increasing levels of Akkermansia muciniphila correlate with stronger gut-barrier function, lower endotoxin leakage, and improved insulin sensitivity (Depommier et al., 2019; Liu et al., 2023). Solar power increases gut barrier strength (Reverse Frey Effect while lowering endotoxin loads and improving insulin because it is a solar hormone.

This isn’t old-school nutrition.
This is quantum biology explaining the nuance food gurus miss.

We are entering the era of precision nutrition, where we move beyond calories and start decoding microbial fingerprints.

Where 16S rRNA sequencing, metagenomics, and metabolomics help us design diets that work with the gut ecosystem rather than against it.

The future of nutrition isn’t about restriction.
It’s about interpretation.
Intrepration of the UPEs the microbiome makes is key.

Same meal.
Different microbiome.
Different biology.
Different outcome.
UPEs are the kinetic force carrier of this change.
Light is how we sculpt our outcomes.

Stop Feeding Your Gut Bacteria, Start Feeding Your Gut Environment

Humans don’t have a bacteria problem in their guts; you have an ecosystem problem related to the light you imbibe that changes the prokaryotes in your gut.
Most probiotics fail because we’re feeding the wrong thing. The microbiome needs light from the sun.

What most need to learn now is how we reshape the approach to these topics to sculpt humans
• metabolic health
• mental health
• PCOS and women’s health
• autoimmune disorders
• and even biological ageing

The gut isn’t just a passenger.
It’s a conductor for light.

And it’s time we started listening to this reality.

2. Biophoton Emission in the Colon and My Decentralized Thesis

My thesis posits that bacteria in more hypoxic environments (like the colon) emit more light, particularly in the ultraweak UV range, and that this light interacts with the gut wall, potentially explaining the high VDR expression in the gut. The colon, with its dense microbial population (10¹¹ bacteria/mL, as per my slide), is a strictly anaerobic environment where bacteria like Bifidobacteria and Bacteroides ferment complex carbohydrates. I previously estimated their biophoton emissions to peak in the visible range (500–600 nm) due to fermentation-based metabolism producing fewer reactive oxygen species (ROS) compared to oxidative metabolism. However, if we assume a shift toward the near-UV range (300–400 nm) in the colon, perhaps due to specific light stress responses, metabolic byproducts, or unique redox reactions in anaerobes, this would have distinct implications for colonic processes. Blue light and nnEMF can do this.

3. Why Near-UV Biophotons (300–400 nm) in the Colon?
Near-UV biophotons typically arise from oxidative processes, as they have higher energy and are often linked to ROS production or excited states of molecules like flavins or porphyrins. In the colon, strict anaerobes dominate, so oxidative stress is minimal under normal conditions. However, several scenarios could lead to near-UV emissions:
Oxidative Stress from Immune Activity: Immune cells (e.g., macrophages) in the colon produce ROS during inflammation (e.g., in response to dysbiosis or pathogens), potentially exciting bacterial or host molecules to emit near-UV biophotons.
Metabolic Byproducts: Anaerobic metabolism in Bacteroides or Bifidobacteria involves redox reactions with cofactors like flavins (e.g., FAD) or porphyrins, which can emit near-UV light when excited, even in low-oxygen conditions.
Stress Responses: Brief oxygen exposure (e.g., during transient breaches in the gut barrier) or other stressors (e.g., bile acids, antimicrobial peptides, alien ) might induce low-level ROS production in anaerobes, shifting their biophoton emissions toward the near-UV range.

4. Given my thesis that posits hypoxic bacteria emit more light, a shift to 300–400-800 nm could occur if these anaerobes upregulate certain pathways under stress, producing excited states that emit at higher frequencies than expected.
Processes in the Colon Enhanced by Near-UV Biophotons (300–400 nm)
Near-UV biophotons have enough energy to interact with biological molecules (e.g., DNA, proteins, lipids) and could influence several processes in the colon. Below are the likely processes enhanced, with a focus on my thesis about VDR and hypoxia:

5. 1. VDR Activation and Immune Regulation
Mechanism: The VDR, highly expressed in the colon, regulates immune responses, barrier function, and microbial homeostasis. Near-UV biophotons (300–400 nm) overlap with the UVB range (280–315 nm) that activates vitamin D synthesis in the skin. These biophotons, emitted by dense populations of Bifidobacteria and Bacteroides, should mimic UV light exposure, interacting with VDR in colonic epithelial cells or immune cells (e.g., dendritic cells, T cells).
Enhanced Process: Near-UV biophotons could enhance VDR-mediated antimicrobial peptide production, such as defensins and cathelicidins, would shape the microbiome by selectively killing pathogens while sparing commensals. This aligns with the colon’s role in fermentation, as a balanced microbiome is crucial for efficient carbohydrate breakdown. Additionally, VDR activation would act to reduce inflammation by downregulating pro-inflammatory cytokines (e.g., TNF-α), supporting a stable microbial ecosystem. It would also slow down electron chain transport. This means we would need less food to operate on = My Leptin Rx. Red light emitted from the UPE of the micorbiome would also help offset the need for food in this case because UPE at the nanolevel are stronger and would act upon the ATPase to spin it with 100% efficieny as the 2004 paper in NAture has shown.

Tie to My Thesis: My hypothesis that biophotons in hypoxic environments interact with VDR is directly supported here. The colon’s hypoxia favors anaerobes, and if they emit near-UV biophotons (as you propose), this could amplify VDR signaling, explaining its high expression in the gut. This process would enhance microbial homeostasis, ensuring the colon remains a fermentation hub.

6. 2. Gut Barrier Integrity and Epithelial Cell Repair
Mechanism: Near-UV biophotons can interact with chromophores in colonic epithelial cells, such as flavins, melanocytes, or DNA, triggering redox signaling pathways. For example, they might activate nuclear factor erythroid 2-related factor 2 (Nrf2), which upregulates antioxidant enzymes (e.g., glutathione peroxidase) to protect against oxidative damage. Nrf2 is a story about the GOE as well when certain metals were selected to be used inside of mitochondria and not iron.

Why?

Enhanced Process: This would enhance the colon’s barrier function, protecting epithelial cells from damage caused by microbial metabolites (e.g., SCFAs, bile acids) or inflammation. Near-UV biophotons might also stimulate DNA repair mechanisms (e.g., via photolyase activation), repairing damage from low-level oxidative stress or microbial toxins, thus maintaining the integrity of the gut wall.

Tie to My Thesis: The hypoxic colon, rich in bacteria, would produce a cumulative “light field” of near-UV biophotons, as I have suggested. The microbiome is the movie projector and the enterocytes is the screen. This is the kinetic lever for the GALT This light signals to epithelial cells, enhancing repair and barrier function, via my photorepair blog, which is critical in the colon where fermentation produces potentially damaging byproducts.

7. 3. Microbial Communication and Community Dynamics
Mechanism: Near-UV biophotons might facilitate non-chemical communication between bacteria, as seen in studies where E. coli cultures exposed to stress altered the biophoton emissions of nearby cultures. In the colon, dense populations of Bifidobacteria and Bacteroides could use biophotons for quorum sensing or to coordinate metabolic activity.

Enhanced Process: This would enhance microbial community dynamics, ensuring efficient fermentation of complex carbohydrates. For example, near-UV biophotons might signal to bacteria to upregulate genes for SCFA production (e.g., butyrate), which benefits both the microbiome and the host by providing energy to colonocytes and reducing inflammation.

Tie to My Thesis: My idea of increased light emission in hypoxic environments fits here. The colon’s dense microbial population could create a significant near-UV biophoton field, enhancing bacterial communication and supporting the fermentation process, which is central to colonic function.

8. 4. Modulation of Inflammation and Immune Surveillance
Mechanism: Near-UV biophotons might interact with immune cells in the colon (e.g., macrophages, T cells), triggering redox or calcium signaling pathways that modulate inflammation. UV light is known to affect immune responses via the VDR, often by inducing anti-inflammatory pathways (e.g., via IL-10 production).
Enhanced Process: This would enhance immune surveillance in the colon, maintaining a balance between tolerance to commensals and defense against pathogens. Near-UV biophotons should dampen excessive inflammation (e.g., by reducing NF-κB signaling), preventing conditions like colitis while supporting the colon’s fermentation environment.
Tie to My Thesis: The hypoxic colon, with its high bacterial density, could emit enough near-UV biophotons to influence immune cells, as my thesis proposes. This would support immune homeostasis, ensuring the colon remains a stable environment for fermentation.

9. 5. Stimulation of Colonocyte Metabolism
Mechanism: Near-UV biophotons might interact with mitochondria in colonocytes, exciting molecules like cytochrome c oxidase, which absorbs light around 300–400 nm. This could enhance mitochondrial respiration and ATP production.
Enhanced Process: This would enhance colonocyte metabolism, particularly their use of SCFAs (e.g., butyrate) produced by bacterial fermentation. Butyrate is the primary energy source for colonocytes, and increased ATP production would support their role in maintaining the gut barrier and absorbing water and electrolytes. Sunlight and or UPEs from the microbiome alters this via NO because it inhibits ATP function.
Tie to My Thesis: The hypoxic colon’s microbial population, emitting near-UV biophotons, could directly support host cell metabolism, aligning with my idea that bacterial light emissions benefit the gut wall, potentially via VDR-mediated pathways that also regulate metabolism.

10. Why Near-UV Biophotons in the Colon Matter
If the colon’s bacteria shift their biophoton emissions to the near-UV range (300–400 nm), as I am proposing, this would enhance processes critical to the colon’s function:
Immune Regulation: Via VDR activation, maintaining microbial balance.
Barrier Function: Protecting epithelial cells from fermentation byproducts.
Microbial Dynamics: Coordinating fermentation through bacterial communication.
Anti-Inflammation: Supporting immune homeostasis.
Host Metabolism: Boosting colonocyte energy production.
These enhancements align with the colon’s role in fermenting complex carbohydrates, and support my thesis that hypoxic bacteria emit light that interacts with the gut wall, potentially explaining the high VDR expression in the gut. No centralized gastroenterologist can explain its anatomy based on ideas in their texts. I can.

11. UPE and Free Radical Signaling Changes in chronic hypoxic states at the mtDNA level in other organs can cause massive problems for bad guts:
UPE reflects mitochondrial redox activity (~10–100 photons/s/cm² in healthy cells). Hypoxia reduces TCA/ETC-derived ROS, decreasing UPE, but nnEMF/blue light-induced ROS cause an initial UPE spike, later suppressed by NO binding to heme. This points out why use of Vitamin C via IV push is dangerous in a Warbug shifted state = it drives Fenton reactions further with no protection.
Free radical signaling is dysregulated as increased membrane resistance traps ROS, enhancing mtDNA damage while impairing signaling (e.g., Nrf2). High lactate exacerbates this via excitotoxicity. Adding oxygen when you cannot use it = more ROS = more UPEs = more gut dysfunction.
GOE Relevance: The GOE favored the new evolution of Cu/Zn/Mn-SODs, reducing UPE from Fe-driven Fenton reactions, as Cu/Zn/Mn systems produce less OH·. Modern nnEMF/blue light exposure mimics these mtDNA effects, but metHb (Fe³⁺) increases Fenton chemistry, amplifying UPE and damage in the gut, reversing evolutionary protections. This is the essence of the mdoern problem going undiagnosed in modern hospitals.