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The Warburg Effect: Cancer Prevention & Understanding How We Can Starve Cancer Cells Naturally

  • Writer: David S. Klein, MD FACA FACPM
    David S. Klein, MD FACA FACPM
  • Sep 15
  • 5 min read

The Warburg effect, decoded


The Warburg Effect is an important concept to understand, if you intend to reduce your risk of cancer
Whatis the Warburg Effect?

Nearly a century ago, Otto Warburg observed that many tumors avidly ferment glucose to lactate even when oxygen is plentiful—so-called aerobic glycolysis. Rather than fully oxidizing glucose in mitochondria to squeeze out maximal ATP, cancer cells divert a large fraction of glucose carbon toward rapid ATP generation and biosynthesis (nucleotides, amino acids, lipids) needed for proliferation. Warburg originally argued this reflected “injured respiration”; modern work shows the reality is more nuanced: oncogenic signaling and the tumor microenvironment reprogram metabolism to favor glycolysis while mitochondria remain functional and essential for anabolism and redox balance. Understanding this principal is key to cancer prevention. refp.cohlife.orgPMCScience


In contemporary cancer biology, metabolic reprogramming is recognized as a hallmark of malignancy. This reprogramming is not simply about energy; it’s a control system that tunes redox state, epigenetic marks, and immune evasion. As Hanahan’s updated “Hallmarks of Cancer: New Dimensions” emphasizes, altered metabolism is intertwined with genomic instability, inflammation, and immune escape—features that collectively enable tumor progression. PubMed


Why glycolysis becomes an advantage

The Warburg Effect is the background phenomenon that provides the ability to kill cancer cells, selectively.
How understanding the Warburg Effect may improvie your longevity

Glycolysis is fast. When coupled to high glucose uptake and lactate export (via monocarboxylate transporters), it enables cells to grow under fluctuating oxygen and to sustain the pentose phosphate pathway and one-carbon metabolism. The acidified microenvironment created by lactate (pH ~6.3–6.9) promotes invasion, angiogenesis, and immune suppression. Lactate is not merely “waste”; it’s a signaling metabolite that shapes gene expression (including histone lactylation) and alters the behavior of stromal and immune cells. Clinically, our exploitation of this phenotype underpins FDG-PET, which images tumors because they often take up far more 18F-fluorodeoxyglucose than surrounding tissues. PMC+1Nature


Prevention: what the Warburg effect teaches us


It is crucial to avoid over-claiming: no diet or supplement “shuts off” the Warburg effect across cancers. That said, the phenotype highlights upstream levers—adiposity, insulin/IGF-1 signaling, and physical inactivity—that create a metabolic milieu favorable to glycolysis-dependent growth. Observational and mechanistic data connect chronic hyperinsulinemia and insulin resistance to higher risks of several cancers; insulin acts as a growth factor and can increase glucose uptake and glycolytic flux in susceptible tissues. PMC+1

Body weight and body composition. Excess adiposity fosters hyperinsulinemia, chronic inflammation, and altered adipokines—all of which tilt cells toward glycolytic programs and anabolic growth. Global consensus statements from the World Cancer Research Fund/AICR estimate that maintaining a healthy weight and limiting weight gain across adulthood lowers risk for multiple cancers. World Cancer Research Fund

Physical activity. Regular activity improves insulin sensitivity, reduces chronic inflammation, and enhances mitochondrial oxidative capacity—physiologic counterweights to the Warburg phenotype. Evidence syntheses and guidelines recommend 150–300 minutes/week of moderate or 75–150 minutes/week of vigorous activity, with more generally better; adherence is associated with lower incidence and mortality across several cancers. American Cancer SocietyPMC+1

Dietary pattern and carbohydrate quality. The Warburg frame sometimes inspires extreme carbohydrate restriction; evidence for universal cancer-prevention benefit of very low-carb or ketogenic diets remains limited. More solid is the signal that dietary patterns emphasizing fiber-rich, minimally processed foods (vegetables, fruits, legumes, whole grains) and minimizing refined starches and added sugars improve metabolic health and may lower risk of several cancers, notably colorectal. Meta-analytic and cohort data link higher glycemic load or poor carbohydrate quality to elevated colorectal cancer risk in some populations. PMC+1ScienceDirect


How clinicians already leverage the phenotype


The Warburg effect is not just a laboratory curiosity; it has diagnostic and therapeutic implications. FDG-PET/CT uses tumor glycolysis to localize disease and monitor response; in parallel, a wave of investigational strategies attempts to target metabolic nodes (glycolysis, lactate transport, redox recycling) or to recondition the microenvironment. While these approaches are still maturing clinically, they reflect a central point: tumor metabolism is plastic and intertwined with signaling, epigenetics, and immunity. Journal of Nuclear MedicineNature


Practical, evidence-anchored takeaways


  1. Manage insulin exposure. Maintain a healthy waist circumference; prioritize dietary patterns that blunt post-prandial spikes (fiber-rich, minimally processed foods) and distribute carbohydrates with protein and healthy fats. For people with diabetes or prediabetes, evidence-based management (diet, exercise, medications as indicated) matters for cancer prevention as well as cardiometabolic health. PMC

  2. Move more, most days. Accumulate at least the ACS-recommended activity minutes weekly, and reduce sedentary time. Even small increments improve insulin sensitivity and mitochondrial function, pushing cellular metabolism away from glycolysis-dominant states. American Cancer Society

  3. Think in patterns, not magic bullets. No single food or supplement reliably “starves” cancer. Focus on patterns—weight control, fitness, high-quality carbohydrate, limited alcohol, and smoking cessation—that harmonize metabolism and reduce inflammatory tone long-term. World Cancer Research Fund


Bottom line


The Warburg effect captures a fundamental reprogramming that makes growth possible under stress; it also offers a lens for prevention. By improving insulin sensitivity, reducing chronic inflammation, and reinforcing mitochondrial health through diet and physical activity, we make it harder for premalignant cells to inhabit a glycolysis-favored niche. That’s not a guarantee—but it is a principled, evidence-based way to shift risk in our favor.


References (publication format with links)

  1. Warburg O. On the Origin of Cancer Cells. Science. 1956;123(3191):309–314. https://www.science.org/doi/10.1126/science.123.3191.309 Science

  2. DeBerardinis RJ, Chandel NS. Fundamentals of cancer metabolism. Sci Adv. 2016;2(5):e1600200. https://www.science.org/doi/10.1126/sciadv.1600200 Science

  3. DeBerardinis RJ, Chandel NS. Fundamentals of cancer metabolism. Sci Adv. 2016;2(5):e1600200. (Open-access version) https://pmc.ncbi.nlm.nih.gov/articles/PMC4928883/ PMC

  4. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646–674. https://pubmed.ncbi.nlm.nih.gov/21376230/ PubMed

  5. Hanahan D. Hallmarks of Cancer: New Dimensions. Cancer Discov. 2022;12(1):31–46. https://pubmed.ncbi.nlm.nih.gov/35022204/ PubMed

  6. Faubert B, Solmonson A, DeBerardinis RJ. Metabolic reprogramming and cancer progression. Science. 2020;368(6487):eaaw5473. https://www.science.org/doi/10.1126/science.aaw5473 Science

  7. Ippolito L, et al. Lactate: A Metabolic Driver in the Tumour Landscape. Trends Cell Biol. 2019;29(10):748–762. https://www.sciencedirect.com/science/article/abs/pii/S0968000418302275 ScienceDirect

  8. Pérez-Tomás R, Pérez-Guillén I. Lactate in the Tumor Microenvironment: An Essential Molecule in Cancer Progression and Treatment Resistance. Cancers (Basel). 2020;12(11):3244. https://pmc.ncbi.nlm.nih.gov/articles/PMC7693872/ PMC

  9. Chen J, et al. Lactate and lactylation in cancer. Signal Transduct Target Ther. 2025;10:??? (online). https://www.nature.com/articles/s41392-024-02082-x Nature

  10. Kawada K, et al. Mechanisms underlying 18F-fluorodeoxyglucose accumulation in colorectal cancer. Int J Clin Oncol. 2016;21(5):898–906. https://pmc.ncbi.nlm.nih.gov/articles/PMC5120247/ PMC

  11. Salas JR, et al. Signaling Pathways That Drive 18F-FDG Accumulation in Cancer. J Nucl Med. 2022;63(5):659–666. https://jnm.snmjournals.org/content/63/5/659 Journal of Nuclear Medicine

  12. Perry RJ, et al. Mechanistic Links between Obesity, Insulin, and Cancer. Trends Endocrinol Metab. 2020;31(10):684–695. https://pmc.ncbi.nlm.nih.gov/articles/PMC7214048/ PMC

  13. Jee SH, et al. Obesity, Insulin Resistance and Cancer Risk. Yonsei Med J. 2005;46(3):449–455. https://pmc.ncbi.nlm.nih.gov/articles/PMC2815827/ PMC

  14. American Cancer Society. Guideline for Diet and Physical Activity for Cancer Prevention. Updated May 5, 2025. https://www.cancer.org/cancer/risk-prevention/diet-physical-activity/acs-guidelines-nutrition-physical-activity-cancer-prevention/guidelines.html American Cancer Society

  15. World Cancer Research Fund/AICR. Diet, Nutrition, Physical Activity and Cancer: A Global Perspective (Third Expert Report). 2018. https://www.wcrf.org/wp-content/uploads/2024/11/Summary-of-Third-Expert-Report-2018.pdf World Cancer Research Fund



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