From Mutation to Metabolism: A Broader View of Cancer Development
Posted: August 18, 2026 Filed under: behavior, cancer, Evolutionary perspective, healing, health, lifestyle, self-healing | Tags: cancer, environmental toxins, genetics, glucose, health, Metabolic Theory, metabolism, mitochondria, nutrition, Somatic Mutation Theory, Warburg effect, wellness 2 CommentsErik Peper, PhD, BCB1 and Richard Harvey, PhD2
1 Biofeedback Health, Berkeley, CA and 2 Institute for Holistic Health, San Francisco State University
My aunt died of breast cancer and my mother was an identical twin. She and her sister resembled each other so closely that family members often couldn’t tell them apart. For the first 26 years of their lives, they both lived in Amsterdam. After they married, they moved to different cities. At the age of 82, my mother’s twin was diagnosed with breast cancer with metastasis to the brain and died that year. For my mother, this was one of the most devastating experiences of her life. It was as if half of her had died. Even with this loss, my mother never developed cancer and lived to the age of 95. The situation became even more complicated when my cousin (the daughter of my mother’s twin) also died of breast cancer at the age of 53, while my mother’s two daughters remained cancer-free. -Erik Peper, PhD. Reproduced by permission from Peper, Gorter and Faass (2026).
Cancer, with a capital ‘C’ along with each of the many kinds of malignant cellular processes is often understood primarily in terms of a disease driven by genetic mutations. This blog begins with observations from twin studies along with ongoing and emerging research suggests that genetics may represent susceptibility rather than destiny. In the case of identical twins, the experience of developing different cancer outcomes illustrates the importance of environmental exposures, lifestyle choices, specific metabolism interactions, immune functions, and particular cellular physiology.
The blog examines prevalent hypotheses about cancer processes which acknowledge interactions and functions such as immune, metabolic and evolutionary pressures. In particular, the paper argues in favor of revisiting the Warburg effect and the role of mitochondrial dysfunction in cancer development. The Warburg metabolic theory proposes that impaired mitochondrial energy production may drive cells toward an ancient survival pathway characterized by increased glucose fermentation, loss of specialized cellular function, and uncontrolled or unregulated proliferation. This perspective does not reject the strong role of genetics in cancer processes but rather places DNA and RNA within a broader biological context influenced by metabolism, epigenetics, and the environment. Understanding cancer as a systemic metabolic disorder may expand prevention strategies and complement existing treatments by emphasizing lifestyle, environmental, and metabolic interventions.
Twin Studies: Genetics as Predisposition, Not Destiny
For decades, research on cancer causes and treatments has been dominated by the Somatic Mutation Theory (SMT), which proposes that cancers arise through the accumulation of DNA mutations (Weinberg, 2023; Huang et al., 2025). This SMT framework has guided the “War on Cancer” and has led to remarkable advances in targeted therapies, chemotherapy, immunotherapy, and radiation treatments. These strategies have saved countless lives, yet they primarily focus on eliminating malignant cells rather than understanding why normal cells become malignant in the first place. While a variety of mutation-focused approaches has yielded remarkable therapeutic successes, one could expect that genetically identical individuals would develop the same or similar cancers.
Decades of twin research suggests otherwise. In the landmark Nordic Twin Study of Cancer, Lichtenstein and colleagues (2000) analyzed nearly 45,000 pairs of monozygotic (identical) and dizygotic (fraternal) twins from Sweden, Denmark, and Finland. If one identical twin developed cancer, the co-twin’s probability of developing the same cancer was about 10% which is much lower than expected if inherited genes alone determined cancer risk. Heritable factors accounted for only a portion of susceptibility (approximately 27% for breast cancer, 35% for colorectal cancer, and 42% for prostate cancer). The remaining risk was attributed largely to environmental influences, lifestyle, aging, and biological processes that occur during life (Lichtenstein et al., 2000; Mucci et al., 2016; Harris et al., 2019).
Both specific cancer investigations along with epidemiological findings across many places, people, and types of cancers suggest that genes create a predisposition, but they do not inevitably determine whether cancer develops. Instead, the cellular environment, metabolic health, environmental exposures, and epigenetic regulation strongly influence whether that predisposition is expressed. Simplistically stated, Genetics loads the gun and lifestyle and environment pulls the trigger (Peper et al., 2026).
The success of cancer treatments based on current oncology theories means that the Somatic Mutation Theory (SMT) provides a partial explanation of cancer processes. Extending the SMT of carcinogenesis to include Warburg-like theories has led to increasing evidence which suggests that metabolic dysfunction, mitochondrial injury, chronic inflammation, immune dysregulation, and environmental exposures all contribute to carcinogenesis. A useful framing of cancer risk related to inherent or heritable factors in comparison to non-intrinsic or non-genetic factors has been described by others (Brennan & Davey-Smith, 2022; Karras et al., 2024; Rahman et al., 2018; Wu et al., 2018).
For example, Wu et al., (2018) suggest that it is not possible to modify ‘random errors in DNA replication’ as an intrinsic risk factor, it is possible to partially modify endogenous risk factors related to inflammation or hormone production or fully mediate or modify directly and indirectly moderate non-genetic exogenous risk factors associated with toxic carcinogenic exposures that include exposures to some products from carcinogenic interactions with bacterial, viral, fungal and parasitic products, tobacco products, ultra-processed food and beverage products and chemicals (e.g., preservatives, pesticides, contaminants, dyes, non-nutritive chemicals such as sweeteners), industrial pollutant and chemical products (e.g. endocrine disrupting ‘forever’ chemicals such as in plastics), and lifestyle moderators such as lack of sleep, exercise, relaxation from mental ruminations and strain. A simplified model pathway would be: Risk of cancer is based on intrinsic genetic factors plus non-intrinsic endogenous and exogenous ‘epigenetic’ factors moderated by individual adaptive capacity to reduce endogenous or mitigate exogenous non-intrinsic factors.
Rather than competing explanations, mechanisms of cancerous disease processes may interact to determine whether genetically susceptible cells remain healthy or progress toward malignancy. These factors may explain that the overall cancer mortality has declined substantially over the past several decades and is predominantly due to the decreased tobacco use, earlier detection, and improvements in treatment. At the same time, the incidence of several cancers, including colorectal and breast cancer, has increased among younger adults (Siegel et al., 2025; American Cancer Society, 2024; Ugai et al., 2022; Lee, 2026). These trends suggest that additional biological and environmental factors deserve closer examination. Beyond regulating exposure to lifestyle factors such as tobacco products as a mediator of reduced cancer mortality, theories by Warburg and colleagues have pointed to metabolic regulation, including regulation of sugars, as a mediator in cancer mortality.
The Metabolic Origin: Revisiting the Warburg Effect
An alternative framework proposes that cancer is fundamentally a disorder of cellular metabolism. This concept dates back to Otto Warburg, who received the 1931 Nobel Prize in Physiology or Medicine for discovering that cancer cells exhibit a distinctive pattern of energy metabolism (Bononi et al., 2022; Otto, 2016; Nobel Prize Outreach, 2026). He showed that cancer cells rely predominantly on glucose fermentation, an anerobic process for making energy without oxygen (e.g. glucose splits into pyruvate and makes two adenosine triphosphate molecules) which is much less efficient than making energy through oxidative phosphorylation, even when oxygen is abundant in a cancer cell. The vast majority of cancerous cell growth depends on a less efficient glucose metabolism form of energy (Kim, 2017; Warburg, Negelein & Posener, 1924). The Warburg effect has been recognized as a hallmark of cancer for nearly a century (Seyfried & Chinopoulos, 2021).
Non-cancerous healthy cells mainly generate energy by producing ATP through oxidative phosphorylation within the mitochondria. Healthy cells are metabolically flexible and can generate energy from both glucose and free fatty acid oxidation (FAO). During periods of fasting, exercise, or carbohydrate restriction, triglycerides stored in adipose tissue are broken down into free fatty acids and glycerol (Eberle, 2013). The liver also converts free fatty acids into ketone bodies, which provide an efficient alternative fuel for the brain and many other tissues when glucose availability is reduced (Wakil & Abu-Elheiga, 2009; Edwards & Mohiuddin, 2023).
When mitochondrial respiration is chronically impaired by environmental toxins, oxidative stress, metabolic dysfunction, or other factors associated with carcinogenesis, cells may shift from efficient oxidative phosphorylation to a more primitive, glycolytic mode of energy production that can generate ATP in the absence of oxygen. Mitochondrial function can decline as people age when accumulation of reactive oxygen species which can directly harm mitochondrial DNA (Bondy, 2024; Cui et al., 2012; Madamanchi & Runge, 2007). In addition, mitochondrial function can also decline due to the indirect moderating effects of lifestyle choices (Caturano et al., 2025; Lemos et al., 2023; San-Millán, 2023).
As described by Miwa et al., (2022), when mitochondrial function declines, mitochondrial dysfunction can contribute to cellular senescence which is the hallmarks of aging. As a response healthy cells can progressively relinquishes their specialized role within the tissue and adopts characteristics of a more ancestral, less differentiated state (Zhang et al., 2025).
Zhang et al. (2025) suggests a few mechanisms which explain the shift of healthy cells away from specialized states towards a less differentiated state, such as shifts in the tricarboxylic acid cycle (TCA) which rely on healthy mitochondria to produce cofactors such as acetyl-CoA and positively charged Nicotinamide Adenine Dinucleotide (NAD+), along with drops in chromatin, inhibiting DNA and histone demthylases (locking chromatin in a hyper-methylated state, and an upregulation of glycolysis. Additionally, cells ‘sense’ when mitochondria have low energy production such as a high ratio of adenosine mono-phosphate or di-phosphate (AMP/ADP) to adenosine tri-phosphate (ATP), which then leads to the AMP-activated protein kinase (AMP-K) pathway (Mihaylova & Shaw, 2011). Finally, hypoxia-inducing factor (HIF) signaling is how cells ‘sense’ and adapt to changes in available oxygen, and HIF binds to DNA, activating specific genes (Huang et al., 2023). The Warburg theory suggests that when mitochondrial dysfunction directly or indirectly reduces oxidative phosphorylation, the cells shift energy production from the mitochondria to cytoplasmic glycolysis which is a hallmark of unicellular ‘ancestral’ organisms or more embryonic or stem-like cellular activity (Suomalainen, & Nunnari, 2024; Zong et al., 2024).
It is as if your cells suddenly forget they’re part of a team. Instead of working together like citizens in a well-organized society, they revert to their most primitive programming; the “me first” mentality of our single-celled ancestors. This is what happens in cancer where sophisticated multicellular cooperation gets hijacked by an ancient survival script buried deep in our biological software. Sonnenschein and Soto (1999) describe this process in their book The Society of Cells (1999), “the default state of cells is proliferation.” In other words, multiplication isn’t some aberrant behavior; it’s actually the factory setting when single cells began. Every cell carries this “go forth and multiply” command like prehistoric programming code.
In healthy tissue, cells have learned to override this ancient impulse. They’ve evolved sophisticated “stop” signals, quality control mechanisms, and cooperative protocols that keep the peace. Cancer occurs when these civilized controls break down, and cells revert to their evolutionary factory settings—endless growth, damn the consequences.
It’s as if your cells suddenly decide to ignore millions of years of evolutionary teamwork and go back to playing by the rules that worked when life was just lone microbes floating in primordial soup.
Under Survival Threat, Organisms Revert to Their Oldest Survival Mechanisms
The same regression process can be observed in human beings. When children experience overwhelming stress, they often revert to earlier developmental behaviors, such as becoming incontinent or seeking protection by hiding behind a parent. Similarly, when adults perceive an immediate threat to survival, the stress response is not always fight or flight. Instead, the body may enter a freeze response characterized by profound immobilization.
This freeze response represents an ancient survival strategy that is activated when the nervous system perceives extreme, life-threatening danger. In this state, heart rate slows, metabolism is reduced, and movement is inhibited through activation of the dorsal vagal complex which is the evolutionarily older branch of the vagus nerve according to polyvagal theory, (Porges, 2023). For reptiles and other primitive vertebrates, this physiological strategy can increase the likelihood of survival until the danger has passed.
Metabolic Theory in Context
A ‘metabolic perspective’ related to carcinogenicity, or related to reversion to more primitive types of behaviors, does not dismiss the importance of genetics. Rather, a metabolic perspective places genetic mutations within a broader biological framework in which metabolism, mitochondrial integrity, immune surveillance, environmental exposures, and epigenetic regulation interact to determine whether a cell remains healthy, or progresses toward malignancy. From this perspective, cancer represents more than the accumulation of genetic mutations. It reflects a regression to an ancient cellular survival program in which energy production and reproduction, rather than specialized function and cooperation with neighboring cells, becomes the overriding priority. Genetic mutations may therefore be viewed not only as the initiating a set of complex interactions that reflect causes of cancer but also as downstream consequences of chronic metabolic dysfunction and mitochondrial damage.
If cancer represents the activation of an evolutionarily ancient cellular survival program triggered by metabolic dysfunction, then interventions that improve metabolic health can reduce risk associated with carcinogenesis which complement conventional treatment. As Dang (2012) points out, “excessive caloric intake is associated with an increased risk for cancers, while caloric restriction is protective, perhaps through clearance of mitochondria or mitophagy, thereby reducing oxidative stress.”
One practical implication is for people to follow often repeated advice: decrease the availability of rapidly absorbed carbohydrates by minimizing the consumption of sugar-sweetened beverages, refined starches, and ultra-processed foods while emphasizing whole, nutrient-dense foods. Broadly stated, such dietary changes in sugar intake can improve metabolic resilience, reduce chronic inflammation, and create a physiological environment that is less favorable for the metabolic adaptations observed in many cancers. Although additional clinical research continues to provide evidence supporting the effectiveness of ‘lifestyle’ and epigenetic strategies across different cancer types, the metabolic perspective offers a compelling framework for prevention and adjunctive therapy.
The metabolic theory of cancer based upon the Warburg effect offers hope in treatment by reducing glucose availability may help slow the growth of some cancers. The process is described clearly by Professor Thomas Seyfried of Boston College (Seyfried et al., 2014; Seyfried et al., 2021). His metabolic theory remains an active area of research, however is not the current consensus view on cancer biology. Consider watching the compelling overview of this metabolic theory presented by Professor Thomas Seyfried’s in his YouTube lecture, Cancer as a Metabolic Disease,
What can you do to reduce cancer risk and support healing
The metabolic theory of cancer presented in this paper suggests behavioral and lifestyle strategies to reduce cancer risk and slow or prevent cancer growth. Simply stated, reduce excessive glucose availability which becomes the main energy source for cancer cells. Clinical improvement may be possible if cancer cells are put on a diet (Stetka, 2016). Changing diet is one component to optimize what you can do to reduce cancer risk, support our immune system to promote healing and optimize health although the outcome is not totally in our hands. Implement the following environmental and lifestyle behaviors promote health and healing.
Reduce and eliminate ultra-processed foods, simple carbohydrates and sugar. These increase the risk of cancers by 20 to 50 percent. Sadly, many patients undergoing chemo and radiation therapy and have difficulty with swallowing, are recommended to drink oral caloric rich supplements (such as Ensure Plus or Boost Very High Calorie) that are specially formulated to provide dense calories and protein in a small volume. They contain between 15 to 22 grams of sugar (1 to 2 tablespoons of sugar) in an 8 ounce serving– the sugar which paradoxically encourages cancer growth.
Reduce and eliminate exposure to endocrine disruptors. These are chemicals that can mimic, block, or interfere with the body’s hormones, due to higher estrogen levels (in milk and beef, for example) and pesticides (some of which act as estrogen mimics). This means eliminating as much as possible all plastics and eat mainly organic foods that do not contain herbicides or pesticides. If possible, eat organic foods.
Reduce air and water pollution that are known factors to cause cancers. This means use air and water filters at home since more than 50% of drinking water in the United States contain cariogenic substances and air pollution from car or fires are harmful.
Increase physical activity. Movement/exercise is important because that reduces lymphatic circulation and blood flow, impacting the immune system in the long term.
For detailed information and recommendations what you can use to reduce cancer risk and optimize health, see our book, Cancer Reconsidered-Why Environment, Lifestyle and Immunity Matter more than we thought.
Additional relevant blogs
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Edited with the help of ChatGPT
Managing Blood Sugar: Lifestyle Changes for Better Health
Posted: May 25, 2026 Filed under: ADHD, attention, behavior, cancer, Evolutionary perspective, healing, health, lifestyle, Nutrition/diet, self-healing, Uncategorized | Tags: AIC, carbohydrate, continous glucose monitoring, diet, exhaustion, glucose, insulin, metabolic disease, obesity, sugar, ultra-processed foods Leave a comment
It was 4:45 p.m., and I was looking forward to swimming. I briskly walked the eight blocks from my house to the heated outdoor city pool. The pool is unusual—100 feet long instead of the standard 25 yards—and I enjoy the rhythm of swimming lap after lap.
I arrived just as the sign flipped from Closed to Open. I quickly changed into my bathing suit, locked my clothes in a metal locker, took a short shower, and jumped into the lane. The sun was still out, and only one other swimmer shared my lane. I felt energized and expected to complete my usual forty laps.
However, after about eighteen laps, my energy suddenly disappeared. There was nothing left in the tank. I swam to the side, pulled myself slowly onto the pool deck, and even slowly and unsteadily walked to the men’s locker room. I sat down on the bench feeling shaky, weak, and exhausted. This was not ordinary fatigue. After resting for several minutes, I slowly showered, dressed, and walked home with heavy, almost uncoordinated legs.
As I reflected on the experience, I remembered something similar that had happened two weeks earlier. Around 5 p.m, I had taken my son’s dog for a brisk walk. Again, I began energized, walking quickly, and then suddenly felt drained and sweaty. When I returned home, all I could do was sit down and recover.
What happened
Reflecting back, I realized that both cases I had eaten sweets—cake one time and a large chocolate chip cookie the other about two hours earlier Most likely, the rapidly absorbed sugars and refined carbohydrates caused a sharp increase in blood glucose, followed by a significant insulin response (Ludwig & Ebbeling, 2018). During exercise, my muscles then demanded additional glucose, and my blood sugar may have dropped rapidly enough to trigger symptoms of reactive hypoglycemia: shakiness, sweating, weakness, and fatigue (Morales-Brown, 2025, June 12).
The process is more complex than simply “sugar highs” and “crashes.” Carbohydrates are broken .break down into glucose during digestion, which begins in the mouth. Chewing breaks down food physically, while the enzyme amylase in saliva starts the chemical breakdown by splitting starches into sugars (Peyrot des Gachons & Breslin, 2016). This raises blood glucose levels, which stimulates insulin release from the pancreas. Insulin helps move glucose from the bloodstream into cells. In some people—especially those developing insulin resistance or prediabetes—the insulin response may overshoot, leading to a later drop in blood glucose. Exercise can amplify this effect because active muscles rapidly consume glucose for energy (American Diabetes Association, 2024).
This experience was a wake-up call for me because my hemoglobin A1C is 5.7%, the lower threshold for prediabetes. Hemoglobin A1C reflects average blood glucose levels over approximately the previous three months (American Diabetes Association, 2026).
Like many people, I enjoy and am even addicted to bread, potatoes, pastries, and sweets. Looking back, the subtle changes began during COVID. Before the pandemic, I spent much of the day teaching in person, walking across campus, moving, and interacting with students. During lockdown, I sat for hours teaching online. My physical activity during the day dramatically decreased while my eating habits did not significantly change.
When we are inactive, excess sugars and refined carbohydrates are less likely to be immediately used by muscles for fuel. Instead, repeated spikes in blood glucose and insulin can contribute over time to insulin resistance, weight gain, metabolic dysfunction, and increased inflammation (Ludwig & Ebbeling, 2018).
Although my episodes were minor, they reminded me that lifestyle patterns especially eating ultra-processed foods can increase the risk for chronic diseases such as type 2 diabetes, cardiovascular disease, obesity, and some cancers and dementia (Lane et al., 2024; Menegassi & Vinciguerra, 2025). The scientific literature strongly links obesity, insulin resistance, and type 2 diabetes with increased risk for several cancers, including colorectal and postmenopausal breast cancer (Peper et al., 2026; Scully et al., 2021: Lauby-Secretan et al., 2016). Ultra-processed foods and sugar-sweetened beverages are also associated with increased risk for obesity and metabolic disease; moreover, cancer survivors who consume higher amounts of ultra processed foods face a significantly increased risk of both all-cause and cancer-specific mortality (Hall et al., 2019; Bonaccio et al., 2026). However, cancer is multifactorial, and no single food alone “causes” cancer. Rather, long-term dietary patterns, inactivity, obesity, chronic inflammation, genetics, environmental exposures, sleep, and stress all interact together ( Marino et al., 2024; Dalamaga et al., 2026; Peper et al., 2026).
What to do
The encouraging news is that these processes are often reversible.
Weight, hunger, blood sugar fluctuations, and even A1C are not fixed. They can improve significantly through lifestyle changes. Research consistently shows that reducing ultra-processed foods, lowering intake of refined carbohydrates and sugary beverages, increasing fiber-rich vegetables, improving sleep, reducing stress, and exercising regularly can improve insulin sensitivity and metabolic health (Bird & Hawley, 2017; Vaezi et al., 2025; American Diabetes Association, 2024; Peper et al., 2026).
For many people, continuous glucose monitors (CGMs) can provide powerful real-time feedback (Ehrhardt & Zaghal, 2020). Seeing how specific foods affect your glucose levels can increase awareness and motivate healthier choices. Often, we do not realize how dramatically a muffin, fruit juice, or bowl of white rice may affect blood sugar until we see the data on the screen.
The goal is not perfection or rigid dieting. Instead, it is learning to observe how your body responds and gradually shifting toward foods that support stable energy, satiety, and long-term health.
Before making major dietary changes, watch the superb interview with Dr. David Unwin, a British physician known for his work using lower-carbohydrate dietary approaches to help patients improve type 2 diabetes and metabolic health. His clinical work demonstrates that many patients can significantly improve blood sugar control and sometimes reduce medications through lifestyle changes (Unwin et al., 2020). The video, The Sugar Doctor’s Warning: The “Healthy” Foods Quietly Destroying Your Body! – Dr. David Unwin, is from the podcast, The Diary of a CEO with Steven Bartlett.
The Link Between Diet, Lifestyle, and Cancer Risk: Steps You Can Take
Read the new book, Cancer Reconsidered: Why Environment, Lifestyle, and Immunity Matter More than We Thought, by Erik Peper, Robert Gorter, and Nancy Faass. It explore the many of the lifestyle factors that can increase cancer risk—or help protect against it. The book brings together an extraordinary range of scientific research to illuminate how everyday habits and modern lifestyles influence cancer risk and healing. Drawing from both conventional medicine and integrative approaches, the authors thoughtfully examine the many factors involved in cancer causation while offering hopeful, evidence-based strategies for supporting recovery and restoring health.
What makes this book especially compelling is that it goes far beyond reviewing the science. It translates research into practical, everyday actions people can use to support healing and improve quality of life. At its heart is lifestyle medicine—the recognition that stress management, hope, physical activity, nourishing foods, supportive relationships, community, and resilience during times of crisis profoundly affect health and well-being. The book also offers a detailed and highly practical discussion of sugar metabolism and explains how continuous glucose monitoring sensors (CGMS) with the smartphone app can help people directly observe how specific foods and daily habits influence their blood sugar levels. Instead of relying on abstract nutrition advice, readers learn how to become active investigators of their own health.
Throughout the book, the message is empowering: our daily habits, social connections, attitudes, and environment may influence health as much as—if not more than—genetics alone. The book is available from Amazon: https://www.amazon.com/Cancer-Reconsidered-Environment-Lifestyle-Immunity/dp/1587907402
Listen to the in-depth discussion of this blog created with Google NotebookLM
Addition relevant blogs
References
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