Tumors divert vitamin B3 (niacinamide) away from normal energy production into a pathway that supports their survival, revealing a metabolic weakness that can be targeted.
As Dr. Mercola reports, current research strongly supports the idea that cancer has a fundamental metabolic dimension. The most widely accepted model integrates genetics, metabolism, epigenetics, and the tumor microenvironment. Tumor metabolism has gone from being considered a secondary consequence of cancer to being seen as a central component of its biology.
Warburg effect: Many tumor cells dramatically increase glucose uptake and utilize glycolysis and lactate production even when oxygen is available. This provides not only energy but also materials for building new cells. Current reviews continue to consider this a fundamental metabolic feature.
In 2025, a review titled “The Warburg hypothesis and the emergence of the mitochondrial metabolic theory of cancer” was even published, which analyzes precisely the growing role of mitochondrial dysfunction/reprogramming in tumor origin and evolution. Therefore, the current view is more like: Metabolic alteration ↔ mitochondria ↔ cell signaling ↔ genetics/epigenetics → cancer
The modern view is much more interesting: tumor cells can switch between glucose, glutamine, fatty acids, and other nutrients, depending on the tumor type and the environment. A 2026 review describes precisely this metabolic flexibility and how glycolysis, glutaminolysis, lipid metabolism, and redox control systems are involved.
Metabolism can modify gene expression: some metabolites function as signals that epigenetically modify which genes are active. Therefore, metabolism and genetics are not two independent explanations: they reinforce each other. The 2024 review on Warburg analyzes precisely the connection between metabolic reprogramming, epigenetic remodeling, and cellular dedifferentiation.
A 2025 review specifically dedicated to colorectal cancer describes metabolic reprogramming as an important component of its biology, including the Warburg effect and the switch between oxidative phosphorylation and glycolysis.
As reported by Dr. Mercola, iron also appears as a metabolic vulnerability. A 2025 review analyzes how iron metabolism is involved in tumor growth and the tumor microenvironment, and how it could become a therapeutic pathway.
A review and meta-analysis of patients with colorectal cancer found that those with metabolic syndrome had:
• A 34% higher risk of all-cause mortality (HR 1.342).
• More than double the colorectal cancer-specific mortality rate in the available studies (HR 2.122).
• A 57% higher risk of poorer disease-free survival (HR 1.574).
This is very interesting for metabolic theory, because metabolic syndrome encompasses precisely alterations such as insulin resistance, hyperinsulinemia, obesity, hypertension, and lipid abnormalities.
Furthermore, a 2025 systematic review and meta-analysis found that exercise in patients with colorectal cancer significantly reduced CRP, a marker of systemic inflammation.
And another meta-analysis from 2025, this time in patients with metastatic colorectal cancer, found an association between physical activity and a 36% lower mortality rate (HR 0.64), although here the evidence comes from cohorts and does not allow for establishing causality.
It is more beneficial to achieve a metabolically healthy body: physical activity implies better insulin sensitivity, less hyperinsulinemia, better AMPK/mTOR regulation, better mitochondrial function, less inflammation, and better immunosurveillance. Simultaneously, exercise helps preserve muscle mass, which is essential, especially in older adults: we do not want to achieve a cancer-prone metabolism by losing muscle and weight.
The research from 2025–2026 is painting a rather sophisticated picture: Colon cancer circulating tumor cells involve liver preparation (“pre-metastatic niche”) with interaction between immunity, microbiota, and hepatic metabolism, metabolic adaptation of the tumor cell, and implantation and growth.
And here again, cancer emerges as a metabolic disease: metabolism is not a secondary detail, but one of the mechanisms that allow colorectal cells to adapt to the liver.
Current evidence allows us to construct a fairly robust hypothesis: energy metabolism + insulin/IGF-1 + mTOR + mitochondria + inflammation + Microbiota + tumor microenvironment + epigenetics.
Modern research is converging toward something like this:
Genetic mutation → signaling alteration → metabolic reprogramming → growth → new genetic/epigenetic alterations. But it can also occur in the opposite direction: Metabolic alteration → epigenetic changes → changes in gene expression → tumor behavior.
THIS IS WHY THE IDEA THAT “CANCER IS ALSO A DISEASE OF CELLULAR METABOLISM” CURRENTLY HAS STRONG SCIENTIFIC SUPPORT.
"This suggests cancer is not just about genes; it's about how your cells process fuel."
More to support Dinkov's research suggesting start from the beginning of our bodies ability to provide the energy to make it possible for all the various systems, teams to work in concert so if or when Cancers appear, the body can restore or repair the cells back to normal or allow the disrupted cell to die. Start from the beginning with what feeds the mitochondria to feed everything else downstream. Also, consider starting with the Foundations of what feeds Life, proper Sun exposure, Quality Air, Quality Water and Quality Foods in their proper percentages in the range feeding, supporting foundational Body Health.
Great reference, JUST, Georgi Dinkov, whom you mention, and it's also interesting because it connects with a real and quite active part of modern research on metabolism, mitochondria, and cancer.
Dinkov argues that before asking ourselves how to destroy a cancer cell, we should ask ourselves why a normal cell lost the ability to maintain its metabolism, repair damage, and correctly decide between surviving and dying. His most recent interview on this topic is from February 2026.
The process he proposes is roughly: Adequate cellular energy → functioning mitochondria → repair/homeostasis → normal cell. If damage occurs: cell damage → repair → recovery, or if the damage is irreparable: damage → apoptosis → cell elimination.
The problem arises when the cell is in a metabolically impaired state and lacks sufficient bioenergetic capacity to maintain these control systems. It can then survive in an abnormal state and proliferate.
Mitochondria are not just ATP factories. They also participate directly in cell life/death decisions. The release of cytochrome c from mitochondria, for example, can activate apoptosis. Recent reviews continue to consider mitochondria as centers of integration between energy, metabolism, signaling, and apoptosis.
Autophagy and apoptosis are two critical processes that determine whether a cell lives or dies in response to cellular stress. Both play an important role in cancer formation, growth, and treatment response, as well as in patient survival. Autophagy and apoptosis are two evolutionarily conserved catabolic processes that play an important role in maintaining cellular homeostasis and determining cell fate when cells are exposed to various types of stress in vivo. The interaction between autophagy and apoptosis has been extensively studied in cancer research and has been shown to affect cancer initiation and tumor formation, disease progression, therapeutic resistance, and overall survival.
And here Dinkov meets modern science: A 2025 review The mitochondrial theory of cancer analyzes precisely the hypothesis that the deterioration of mitochondrial function and oxidative phosphorylation may be much closer to the origin of cancer than traditionally thought.
An important clarification: this does not mean that it has been proven that all cancer is simply reversible by providing more energy. Tumors are metabolically very plastic and can utilize both glycolysis and oxidative phosphorylation; in fact, there are cancers in which mitochondrial respiration remains considerable.
What is truly fascinating is that current research is beginning to study precisely how to metabolically exploit the vulnerabilities of cancer cells to induce their death. A 2016 review in Nature Reviews Cancer describes pathways such as ferroptosis, cupoptosis, and disulfideptosis as forms of cell death related to metabolic alterations.
That is why your formulation is particularly apt: "we must recover the bioenergetic and metabolic terrain that allows the organism to maintain homeostasis, repair what can be repaired, and eliminate through apoptosis what can no longer be repaired."
Metabolic prevention makes sense even before a detectable tumor exists. We don't need to wait for a tumor mass to appear to worry about mitochondria, energy metabolism, inflammation, oxidative stress, DNA repair, autophagy, immunity, and apoptosis.
Dinkov's research is making significant inroads into mainstream biomedical research: how to ensure cells maintain sufficient bioenergetics to preserve their identity and, when a cell becomes irretrievable, how to ensure the proper functioning of cell death mechanisms.
In this vein, cancer cells often undergo metabolic reprogramming to maintain their rapid growth and proliferation, as well as to meet their energy and biosynthetic needs. Meanwhile, immune cells carry out their immune response functions through specific metabolic pathways, either to recognize, attack, and eliminate cancer cells or to promote their growth or metastasis. Altering cancerous microenvironments impacts the metabolism of both cancer and immune cells, modulating the survival and proliferation of cancer cells, as well as the activation and effectiveness of immune cells.
As Dr. Mercola reports, current research strongly supports the idea that cancer has a fundamental metabolic dimension. The most widely accepted model integrates genetics, metabolism, epigenetics, and the tumor microenvironment. Tumor metabolism has gone from being considered a secondary consequence of cancer to being seen as a central component of its biology.
Warburg effect: Many tumor cells dramatically increase glucose uptake and utilize glycolysis and lactate production even when oxygen is available. This provides not only energy but also materials for building new cells. Current reviews continue to consider this a fundamental metabolic feature.
https://pmc.ncbi.nlm.nih.gov/articles/PMC12118702/ (2024)
In 2025, a review titled “The Warburg hypothesis and the emergence of the mitochondrial metabolic theory of cancer” was even published, which analyzes precisely the growing role of mitochondrial dysfunction/reprogramming in tumor origin and evolution. Therefore, the current view is more like: Metabolic alteration ↔ mitochondria ↔ cell signaling ↔ genetics/epigenetics → cancer
https://link.springer.com/article/10.1007/s10863-025-10059-w (2025)
The modern view is much more interesting: tumor cells can switch between glucose, glutamine, fatty acids, and other nutrients, depending on the tumor type and the environment. A 2026 review describes precisely this metabolic flexibility and how glycolysis, glutaminolysis, lipid metabolism, and redox control systems are involved.
https://www.nature.com/articles/s12276-026-01697-0 (2026)
Metabolism can modify gene expression: some metabolites function as signals that epigenetically modify which genes are active. Therefore, metabolism and genetics are not two independent explanations: they reinforce each other. The 2024 review on Warburg analyzes precisely the connection between metabolic reprogramming, epigenetic remodeling, and cellular dedifferentiation.
https://www.annualreviews.org/content/journals/10.1146/annurev-cancerbio-062822-120857 (2024)
In colorectal cancer, it is especially relevant.
A 2025 review specifically dedicated to colorectal cancer describes metabolic reprogramming as an important component of its biology, including the Warburg effect and the switch between oxidative phosphorylation and glycolysis.
https://www.nature.com/articles/s41420-025-02623-5 (2025)
As reported by Dr. Mercola, iron also appears as a metabolic vulnerability. A 2025 review analyzes how iron metabolism is involved in tumor growth and the tumor microenvironment, and how it could become a therapeutic pathway.
https://pubmed.ncbi.nlm.nih.gov/39749705/ (2025)
A review and meta-analysis of patients with colorectal cancer found that those with metabolic syndrome had:
• A 34% higher risk of all-cause mortality (HR 1.342).
• More than double the colorectal cancer-specific mortality rate in the available studies (HR 2.122).
• A 57% higher risk of poorer disease-free survival (HR 1.574).
This is very interesting for metabolic theory, because metabolic syndrome encompasses precisely alterations such as insulin resistance, hyperinsulinemia, obesity, hypertension, and lipid abnormalities.
https://pubmed.ncbi.nlm.nih.gov/36287138/ (2023)
Furthermore, a 2025 systematic review and meta-analysis found that exercise in patients with colorectal cancer significantly reduced CRP, a marker of systemic inflammation.
https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2025.1612674/full (2025)
And another meta-analysis from 2025, this time in patients with metastatic colorectal cancer, found an association between physical activity and a 36% lower mortality rate (HR 0.64), although here the evidence comes from cohorts and does not allow for establishing causality.
https://pubmed.ncbi.nlm.nih.gov/41450420/ (2025)
It is more beneficial to achieve a metabolically healthy body: physical activity implies better insulin sensitivity, less hyperinsulinemia, better AMPK/mTOR regulation, better mitochondrial function, less inflammation, and better immunosurveillance. Simultaneously, exercise helps preserve muscle mass, which is essential, especially in older adults: we do not want to achieve a cancer-prone metabolism by losing muscle and weight.
The research from 2025–2026 is painting a rather sophisticated picture: Colon cancer circulating tumor cells involve liver preparation (“pre-metastatic niche”) with interaction between immunity, microbiota, and hepatic metabolism, metabolic adaptation of the tumor cell, and implantation and growth.
And here again, cancer emerges as a metabolic disease: metabolism is not a secondary detail, but one of the mechanisms that allow colorectal cells to adapt to the liver.
https://www.sciencedirect.com/science/article/abs/pii/S1040842825003348 (2025)
https://link.springer.com/collections/fhhgeefadi?gad_source=1&gad_campaignid=21675443969&gbraid=0AAAAADu685NPnriE7MBKbvoQNLE1ii8AV&gclid=CjwKCAjwyabTBhBFEiwAM3mNUKp8iVWDJF3FbL4dO91G5oV3Owit5AKaZC25w7Ng6f2KG4YtU8PBlRoCngAQAvD_BwE (2025-26)
CONCLUSION
Current evidence allows us to construct a fairly robust hypothesis: energy metabolism + insulin/IGF-1 + mTOR + mitochondria + inflammation + Microbiota + tumor microenvironment + epigenetics.
Modern research is converging toward something like this:
Genetic mutation → signaling alteration → metabolic reprogramming → growth → new genetic/epigenetic alterations. But it can also occur in the opposite direction: Metabolic alteration → epigenetic changes → changes in gene expression → tumor behavior.
THIS IS WHY THE IDEA THAT “CANCER IS ALSO A DISEASE OF CELLULAR METABOLISM” CURRENTLY HAS STRONG SCIENTIFIC SUPPORT.
"This suggests cancer is not just about genes; it's about how your cells process fuel."
More to support Dinkov's research suggesting start from the beginning of our bodies ability to provide the energy to make it possible for all the various systems, teams to work in concert so if or when Cancers appear, the body can restore or repair the cells back to normal or allow the disrupted cell to die. Start from the beginning with what feeds the mitochondria to feed everything else downstream. Also, consider starting with the Foundations of what feeds Life, proper Sun exposure, Quality Air, Quality Water and Quality Foods in their proper percentages in the range feeding, supporting foundational Body Health.
Great reference, JUST, Georgi Dinkov, whom you mention, and it's also interesting because it connects with a real and quite active part of modern research on metabolism, mitochondria, and cancer.
Dinkov argues that before asking ourselves how to destroy a cancer cell, we should ask ourselves why a normal cell lost the ability to maintain its metabolism, repair damage, and correctly decide between surviving and dying. His most recent interview on this topic is from February 2026.
https://media.mercola.com/ImageServer/Public/2026/March/PDF/cancer-cellular-energy-metabolism-pdf.pdf
https://www.youtube.com/watch?v=L-ZlBl891q0
https://www.iheart.com/podcast/269-rooted-in-resilience-106807317/episode/rethinking-cancer-through-cellular-energy-321205547/----------------------------------
The process he proposes is roughly: Adequate cellular energy → functioning mitochondria → repair/homeostasis → normal cell. If damage occurs: cell damage → repair → recovery, or if the damage is irreparable: damage → apoptosis → cell elimination.
The problem arises when the cell is in a metabolically impaired state and lacks sufficient bioenergetic capacity to maintain these control systems. It can then survive in an abnormal state and proliferate.
Mitochondria are not just ATP factories. They also participate directly in cell life/death decisions. The release of cytochrome c from mitochondria, for example, can activate apoptosis. Recent reviews continue to consider mitochondria as centers of integration between energy, metabolism, signaling, and apoptosis.
Autophagy and apoptosis are two critical processes that determine whether a cell lives or dies in response to cellular stress. Both play an important role in cancer formation, growth, and treatment response, as well as in patient survival. Autophagy and apoptosis are two evolutionarily conserved catabolic processes that play an important role in maintaining cellular homeostasis and determining cell fate when cells are exposed to various types of stress in vivo. The interaction between autophagy and apoptosis has been extensively studied in cancer research and has been shown to affect cancer initiation and tumor formation, disease progression, therapeutic resistance, and overall survival.
https://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2025.1720652/full (2026)
https://openurl.ebsco.com/EPDB%3Agcd%3A15%3A1602319/detailv2?sid=ebsco%3Aplink%3Acrawler-gcd&id=ebsco%3Agcd%3A194129242&crl=c&jrnl=20726694&link_origin=scholar.google.com (2026)----------------------------
And here Dinkov meets modern science: A 2025 review The mitochondrial theory of cancer analyzes precisely the hypothesis that the deterioration of mitochondrial function and oxidative phosphorylation may be much closer to the origin of cancer than traditionally thought.
An important clarification: this does not mean that it has been proven that all cancer is simply reversible by providing more energy. Tumors are metabolically very plastic and can utilize both glycolysis and oxidative phosphorylation; in fact, there are cancers in which mitochondrial respiration remains considerable.
What is truly fascinating is that current research is beginning to study precisely how to metabolically exploit the vulnerabilities of cancer cells to induce their death. A 2016 review in Nature Reviews Cancer describes pathways such as ferroptosis, cupoptosis, and disulfideptosis as forms of cell death related to metabolic alterations.
That is why your formulation is particularly apt: "we must recover the bioenergetic and metabolic terrain that allows the organism to maintain homeostasis, repair what can be repaired, and eliminate through apoptosis what can no longer be repaired."
Metabolic prevention makes sense even before a detectable tumor exists. We don't need to wait for a tumor mass to appear to worry about mitochondria, energy metabolism, inflammation, oxidative stress, DNA repair, autophagy, immunity, and apoptosis.
Dinkov's research is making significant inroads into mainstream biomedical research: how to ensure cells maintain sufficient bioenergetics to preserve their identity and, when a cell becomes irretrievable, how to ensure the proper functioning of cell death mechanisms.
In this vein, cancer cells often undergo metabolic reprogramming to maintain their rapid growth and proliferation, as well as to meet their energy and biosynthetic needs. Meanwhile, immune cells carry out their immune response functions through specific metabolic pathways, either to recognize, attack, and eliminate cancer cells or to promote their growth or metastasis. Altering cancerous microenvironments impacts the metabolism of both cancer and immune cells, modulating the survival and proliferation of cancer cells, as well as the activation and effectiveness of immune cells.
https://pubmed.ncbi.nlm.nih.gov/24513530/ (2014)
https://pubs.rsc.org/cs/article-abstract/53/24/12014/845078/A-new-era-of-cancer-phototherapy-mechanisms-and (2024)
https://link.springer.com/article/10.1007/s10863-025-10059-w (2025)
https://www.nature.com/articles/s41392-025-02311-x (2025)
https://www.nature.com/articles/s41392-025-02141-x (2025)
https://pmc.ncbi.nlm.nih.gov/articles/PMC11667227/ (2025)