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.
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“We can invest in preventing illness now by reducing our exposure to environmental toxins — or we can pay a far higher price later trying to treat the resulting chronic and often debilitating diseases.”
Ever since the 1962 publication of Rachel Carson’s groundbreaking book, Silent Spring, which documented the harm environmental pollution caused, government has, often reluctantly, set limits intended to protect Americans from exposure to harmful chemicals in our food, air and water (Carson, 1964). These regulations did not emerge easily. As the governmental regulations were being proposed and implemented, they were consistently challenged by the very large corporations that manufactured and profited from these chemicals.
History reminds us how slowly public health protections can unfold. Consider how long it took for smoking to be prohibited in public spaces even though the harmful effects had been documented since the 1950s (Doll and Hill, 1954; Doll & Hill, 1964; Wynder & Graham,1985). For decades, the science was clear, yet policy and governmental actions were delayed. Only in the early 2000s did many states began banning smoking in workplaces, restaurants, and bars. The shift in public policy saved many lives and the reduction in smoking has been the major reason for the decrease in cancer mortality over the last twenty-five years.
We are going backwards
The Trump administration has rescinded the 2009 U.S. Environmental Protection Agency endangerment finding on greenhouse gases, loosening vehicle emission standards, and weakening pollution controls on power plants and oil and gas operations (Tabuchi, 2026). The health consequences may not appear immediately; however, they are predictable. The increased exposure today will again contribute to increased rates of cancer, respiratory illness, cardiovascular disease, and developmental disorders tomorrow.
To understand how the government regulations have been revised so that once again Americans will be more exposed to toxins in their food, air, and water, read the superb investigative report published by U.S. Right to Know whose mission is to pursuing truth and transparency for public health.
Their most recent report, Tracing Bayer’s ties to power in Trump’s Washington, describes in detail the hidden social connections, lobbying and political donations that lead “The White House to invokes the Defense Production Act to guarantee supplies of elemental phosphorus and glyphosate-based herbicides. Regulators reapprove dicamba, a Bayer herbicide twice blocked by federal courts, and clear the way for new pesticides containing toxic, persistent PFAS “forever” chemicals (Malkan, 2026).“
When regulatory safeguards weaken, corporations can once again function as disease vectors-not through infection, but through environmental exposure. By loosening the pollution standards, federal policy will negatively affect the health of both present and future generations.
I encourage you to explore many superb investigative reports and practical suggestions how to avoid these toxins exposure that are available on U.S. Right to Know website:
Doll, R., & Hill, A. B. (1954). The mortality of doctors in relation to their smoking habits: A preliminary report. British Medical Journal, 1(4877), 1451–1455. https://doi.org/10.1136/bmj.1.4877.1451
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Albert Schweitzer began working in equatorial lowlands of West Africa in 1913. He was astonished to encounter no cases of cancer among the thousands of native patients he saw each year. However, as the natives [took to] living more and more after the manner of the whites, cancer in his patient population became ever more frequent (Taubes, 2016, pp 257).
Wise elders, grand parents or statesmen have been traditional roles for aging adults. Wisdom transforming into Alzheimer’s disease does not compute (Peper, 2014).
In 1960’s Surgeon Captain T. L. Cleave proposed that common western diseases (diabetes, colon cancer, ischemic heart disease, gallstones, obesity, diverticulosis, and dental carries), to which I would add Alzheimer’s disease, autoimmune diseases and allergies, could not be due primarily to genetic factors but to new factors in the environment to which man had not yet had time to adapt (Cleaves et al, 1969). As he states, “One such factor was the processing of food which resulted in the consumption of large quantities of pure sugar and starch. This led to disease because man was evolutionary adjusted to eating smaller amounts of carbohydrates intimately mixed with fiber and protein.”
Clinicians and epidemiologist have consistently reported that none western cultures, whether the Masai in Africa, the Inuit in Northern Canada, the Japanese in Japan, or the Native American, had very low incidences of these western diseases. Yet, when these people adapted a western diet of highly refined carbohydrates and sugar the prevalence of these diseases increased and approached the incidence in western cultures (Burkitt & Trowell, 1975; Taubes, 2016).
Historically these illness were initially observed in the ruling class. The affluent class was privileged and tended to eat more refined carbohydrates and sugars (white bread, cakes, pastries and sugar in coffee and tea). It is only recently that this class effect is reversed. Lower economic classes tend have a higher prevalence of these western diseases. Affluent people can afford and often eat low processed organic foods while economically disadvantaged people cannot afford low processed foods and instead eat predominantly highly processed carbohydrate and refined foods.
Highly refined processed foods and sugar–not fats–are significant risk factors for the development diabetes and cardiovascular disease and mortality (Imamura et al, 2015; Taubes, 2016; Yang et al, 2014) . What is not as well known is that some cancers and Alzheimer’s disease also correlates with the increase intake of refined carbohydrates and sugar (Das, 2015; Kandimalla et al, 2016; Peper, 2014).
It is highly likely that the increase in beta-amyloid protein plagues in the brain is not the cause of the Alzheimer’s but the brain’s defense mechanism to protect it from the fluctuating high insulin and glucose levels. A high sugar and simple carbohydrate diet are risk factors for inflammatory diseases such as diabetes, heart disease and metabolic syndrome. These inflammatory diseases are recognized as a precursor for Alzheimer’s. Alzheimer’s is sometimes described as Type 3 diabetes (Kandimalla et al, 2016; Steen et al, 2005).
Taking the perspective that foods are significant risk factors for the development of these western diseases, the focus should be on prevention and less on treatment. The research to develop drugs to treat Alzheimer’s have up till now been unsuccessful despite that the billions spent on attempting to develop new drugs. For example, the pharmaceutical company Eli Lilly has spent 3.7 billion dollars over the last decade while the National Institutes of Health spends more than half a billion dollars a year on pursuit of treatment (Coghlan, 2017).
The treatments cost of these western diseases, which at best ameliorate the disorders, is overwhelming. In the USA, we spent $147 billion to treat obesity and $116 billion to treat diabetes. While the medical costs to treat diabetes for a single patient is about $6000/year or $400,000/lifetime (Pollan, 2009).
As a refined carbohydrates and high sugar diet is a risk factor for western diseases, the focus should be on prevention. Thus, reduce sugar and refined carbohydrates intake and increase high fiber vegetable. To implement such a simple preventative measure means:
Educate the public about the harm of sugars and refined carbohydrate foods.
Ban advertising of foods that are high in sugar and refined carbohydrates.
Reward companies to produce foods low in sugar and refined carbohydrates.
Tax food products high in sugar and refined carbohydrates just as tobacco has been taxed.
I am positive that in the future when we look back at the 20th and early 21st century, we will be appalled that the government allowed people to poison themselves with sugar and highly refined carbohydrates. Just as we now warn against the harm of tobacco, limit the sales to minors, and have ongoing public health stop smoking campaigns.
We are the first generation that is covertly and chronically exposed to radio frequency radiatio (RFR). The long term effects are still partially unknown. Who knows what the future effects will be for children whose brains and bodies are still developing while being exposed the cellphone/tablet radio frequency radiation for hours a day. Remember,the RFR is similar to the radar beam–albeit at a lower intensity–used to cook your food in your microwave oven.
National Toxicology Program Finds Cell Phone Radiation Causes Cancer
SPIN vs FACT: National Toxicology Program report on cancer risk from cellphone radiation
The National Toxicology Program (NTP) of the National Institutes of Health reported partial findings from their $25 million study of the cancer risk from cellphone radiofrequency radiation (RFR). Controlled studies of rats showed that RFR caused two types of tumors, glioma and schwannoma. The results “…could have broad implications for public health.”
A factsheet on the NTP study that summarizes some biased statements, or “Spin,” about the study that tend to create doubt about data quality and implications, as well as “Facts” from decades of previous research is available at http://bit.ly/NTPspinfacts.
According to the NTP report:
“Given the widespread global usage of mobile communications among users of all ages, even a very small increase in the incidence of disease resulting from exposure to RFR [radiofrequency radiation] could have broad implications for public health.”
Overall, thirty of 540 (5.5%), or one in 18 male rats exposed to cell phone radiation developed cancer. In addition,16 pre-cancerous hyperplasias were diagnosed. Thus, 46 of 540, or one in 12 male rats exposed to cell phone radiation developed cancer or a pre-cancerous lesion as compared to none of the 90 unexposed male rats. The two types of cancer examined in the exposed rats were glioma and schwannoma. Both types have been found in human studies of cell phone use.
In the group exposed to the lowest intensity of cell phone radiation (1.5 watts/kilogram or W/kg), 12 of 180, or one in 15 male rats developed cancer or a pre-cancerous lesion.
This latter finding has policy implications for the FCC’s current cell phone regulations which allow cell phones to emit up to 1.6 W/kg at the head or near the body (partial body Specific Absorption Rate or SAR).
The NTP study is likely a “game-changer” as it proves that non-ionizing, radiofrequency radiation can cause cancer without heating tissue.
The results of the study reinforce the need for more stringent regulation of radiofrequency radiation and better disclosure of the health risks associated with wireless technologies — two demands made by the International EMF Scientist Appeal — a petition signed by 220 scientists who have published research on the effects of electromagnetic radiation.
Along with other recently published studies on the biologic and health effects of cell phone radiation, the International Agency for Research on Cancer of the World Health Organization should now have sufficient data to reclassify radiofrequency radiation from “possibly carcingogenic” to “probably carcinogenic in humans.”
The risk of cancer increased with the intensity of the cell phone radiation whereas no cancer was found in the sham controls—rats kept in the same apparatus but without any exposure to cell phone radiation.
In contrast to the male rats, the incidence of cancer in female rats among those exposed to cell phone radiation was not statistically significant. Overall, sixteen of 540 (3.0%), or one in 33 female rats exposed to cell phone radiation developed cancer or a pre-cancerous lesion as compared to none of the 90 unexposed females. The NTP has no explanation for the sex difference. The researchers pointed out that none of the human epidemiology studies has analysed the data by sex.
The researchers believe that the cancers found in this experimental study were caused by the exposure to cell phone radiation as none of the control animals developed cancer. The researchers controlled the temperature of the animals to prevent heating effects so the cancers were caused by a non-thermal mechanism.
One of two types of second-generation (2G) cell phone technology, GSM and CDMA, were employed in this study. The frequency of the signals was 900 MHz. The rats were exposed to cell phone radiation every 10 minutes followed by a 10-minute break for 18 hours, resulting in nine hours a day of exposure over a two-year period. Both forms of cell phone radiation were found to increase cancer risk in the male rats.
For each type of cell phone radiation, the study employed four groups of 90 rats — a sham control group that was not exposed to radiation, and three exposed groups. The lowest exposure group had a SAR of 1.5 W/kg which is within the FCC’s legal limit for partial body SAR exposure (e.g., at the head) from cell phones. The other exposure groups had SARs of 3 and 6 W/kg.
Glioma is a common type of brain cancer in humans. It affects about 25,000 people per year in the U.S. and is the most common cause of cancer death in adults 15-39 years of age. Several major studies have found increased risk of glioma in humans associated with long-term, heavy cell phone use.
In humans, schwannoma is a nonmalignant tumor that grows in Schwann cells that cover a nerve which connects to the brain. Numerous studies have found an increased risk of this rare tumor in heavy cell phone users. In the rat study, malignant schwannoma was found in Schwann cells in the heart.
For references to the research that found increased risk of malignant and nonmalignant tumors among long-term cell phone users see http://bit.ly/WSJsaferemr.
When Breath Becomesa remarkable first-person memoir by neurosurgeon Paul Kalanithi that follows his transformation from being an outstanding neurosurgeon and scientist to being a patient diagnosed with stage lV lung cancer. It shares in detail the challenges of the patient doctor relationship and the eventuality of facing death. It is a must book to read to understand the intense training that physicians undergo to reach the top of their profession. It also explores in detail the challenges facing patients and all of us when death stares us in the face.
Dr. Kalanithi’s drive was to be the preeminent neurosurgeon and scientist. When diagnosed with stage IV cancer, he receives the best scientific treatment at Stanford University Medical Center. His stellar treatment also illustrates medicine’s disregard of the healing process and how the patient may contribute to his own healing process. Even though the initial diagnosis appeared hopeless; nevertheless, he responded well to the cancer treatment. It is at this point the superb scientific Western medical approach failed him. The failure was the medical culture of the hospital, his oncologists, and most importantly his own lack of somatic awareness. He did not listen to his own body crying out: “I am exhausted.”
When reading the book, I was shocked to realize how little he appeared to appreciate factors that suppressed the immune system. He continued to be stressed to the extreme through working, working and working. After the initial recovery, he went back to the same pattern which had preceded the initial illness instead of respecting the biological regeneration process so that he could support the recovery of his immune system. He totally focused on performing surgery without listen to the needs of his own body.
When he initially recovered from the cancer after the disease had regressed, he decided, “I would push myself to return to the OR (operating room). Why? Because I could.” After a month, he was again operating at nearly a full load. As he stated almost every evening he ended his days “exhausted beyond measure, muscle on fire, Coming home each night, I would scarf down a handful of pain pills, then crawl into bed.”
He was dedicated to his career and patient care. However, he did not listen to his own exhaustion. When reading this part in the book, I sadly predicted that his cancer would return with vengeance and that he would die. Although there are many causes of cancer and many treatments, in the end one component that may facilitate surviving cancer is the patient supporting his own functional immune system
Why was this brilliant neurosurgeon, his colleagues, and his physicians, so disconnected from common sense? After trauma ,the body needs time to regenerate and recover. Having meaningful work and relationships is important; however, pushing yourself to exhaustion in pursuit of professional is a prescription for illness.
Whatever happened to the well documented knowledge that ongoing excessive stress without time to regenerate is a predictable risk factor for illness and even death? High stress is associated with poorer survival in patients with cancer. (Chida et al, 2008; Denaro et, 2014). How come the medical staff was unaware of the concept of “Karoshi” a Japanese word invented in 1978 which means death from overwork (International Labor Organization, 2013).
Possibly, this disconnect from common sense is embedded in medical training in which residents and interns work 24 hours or longer shifts. With the drive and pride to perform at any time, medical staff are trained to disregard the signals of their own body. One cannot burn the midnight oil indefinitely with incurring consequences. Do we really want our doctors, those to whom we entrust our very lives, living and working on the knife-edge of exhaustion?
Possible medicine need to encourage and support common sense such as a regular life style, exercise, healthy diet, and social support (see the book Fighting Cancerby Robert Gorter and Erik Peper, 2011). I hope that by reading Dr. Kalanithi’s remarkable book, it will encourage you to listen to yourself and nurture the self-healing potential of the body. Hopefully, the future medical prescription, instead of offering high technology and pharmaceutical solutions, will also respect and support the intrinsic self-healing processes of the body. Possibly the future prescription will read: have 8 hours sleep, take time to regenerate, learn relaxation skills, have regular meals, and nurture social connections.
My previous blog, Are herbicides a cause for allergies, immune incompetence and ADHD? focused on the health risks associated with the herbicide Roundup® (glyphosate) as a possible contributing factor for allergies, immune incompetence and ADHD. The danger of using glyphosate may even be worse!
The IARC defines the category Group 2A as follows: The agent is probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. Limited evidence means that a positive association has been observed between exposure to the agent and cancer but that other explanations for the observations (called chance, bias, or confounding) could not be ruled out. This category is also used when there is limited evidence of carcinogenicity in humans and strong data on how the agent causes cancer.
One Computerized tomography (CT) scan of the abdomen and pelvis will expose you to more radiation than the residents of Fukushima, Japan absorbed after the Fukushima Daiichi nuclear power plant accident in 2011. –Consumer Reports, March 2015, Vol.80 No.3, 39.
High-risk patients with heart failure and cardiac arrest hospitalized in teaching hospitals had a significantly lower 30-day mortality when admitted during dates of national cardiology meetings (70% survival when doctors attended meeting as compared to 60% survival when doctors did not attend the meetings). –-Jena et al, 2014.
There are so many questions
I feel healthy but worry that cancer could be lurking in the background, should I do a preventative body scan?
I sometimes have slightly higher blood pressure especially when the doctor measures it. It is probably borderline, should I go on medication?
Should I have my PSA tested?
I am a healthy fifty year old, should I have a mammogram?
Should I have an annual physical?
In the quest to stay healthy or prevent disease, we are bombarded by information that preventative testing would save lives and improve health. Only in the United States and New Zealand allow direct to consumer medical advertising which tends to increase excessive drug use and medical testing (Liang & Mackey, 2011). The messages imply that medical screening and testing (e.g., body scan or stress tests) can identify early stages of a disease and implying that earlier treatment will improve quality of life and survival. Similar messages encourage basically healthy people to take drugs for borderline conditions (e.g., borderline hypertension, osteopenia, increased cholesterol levels. What is not shared is the possible risk of unnecessary medical interventions or the harm caused by drug or treatment side effects especially when they are used for a long time period. When unbiased research such as the Cochran Reviews are done, even the annual physical exam appears to offer no benefits (Krogsbøll et al, 2013). Similarly, mammograms and PSA testing for a healthy population appears to offer no benefits and may increase risks. It is truly difficult to accept that an annual health check up is worthless or that a routine mammogram or PSA test may do more harm than good since for many years the public message has been the opposite: to get more screening and testing. There are many reasons for this approach such as:
Genuine belief, although not evidence based, that an early intervention and more testing would reduce suffering.
Financial incentives for the parties that perform testing and preventative screening or encourage increased drugs sales for borderline conditions for which the risk and benefits are not well documented.
Fear of lawsuits by medical providers. If a patient develops an illness which possibly could have been diagnosed by screening, even though the screening may not have affected the actual outcome, the health professional could be sued.
Become an informed consumer
When you have a symptom and do not feel well, see your doctor and get diagnosed, it may safe your life. At the same time be an educated consumer and when unexpected findings are discovered and not related to your specific symptom/complaint, ask questions before agreeing to have more tests or treatments. Ask your provider some of the following questions which were initially outlined by Dr. Eugene Robins (1984):
Why are you doing this test or procedure?
What are the risks and what are the benefits?
What are the risks of treatment and what are the benefits of treatment?
How accurate is the test?
How will the test results change the treatment strategy?
Are there less invasive strategies that could be used? Be very careful of exposing yourself and especially children to CT scans. It is estimated that for every 1000 children who have an abdominal CT scan, one will develop cancer as a result (2015, Consumer Report, March 16).
Dr. Erik Peper is interviewed by Dr. Larry Berkelhammer about the research he did in the late 60s and early 70s on EEG alpha training. He describes how he learned to turn off alpha brain rhythms in one hemisphere and turn them on in the other.
Neurofeedback equipment allows researchers and clinicians to get extremely useful feedback, allowing people who are hooked up to get very good at identifying their own brain rhythms and to alter them at will. This can potentially allow us to re-train our brains. Dr. Peper talks about how the real gift of science is about being open to explore rather than to assume our beliefs are factual. Science is about curiosity, experimentation, and exploration. In studying people with cancer and other diseases it is vital that we study more than just pathology–we need to study those individuals who are the outliers, that is, those who recovered against all odds–let’s see what they did to mobilize their health.
Hi, I'm Erik Peper, Professor of Holistic Health of San Francisco State University, President of the Biofeedback Federation of Europe, and I also maintain a private practice (www.biofeedbackhealth.org) I love exploring new ways of empowering people to optimize health and wellness. I am inspired by seeing people heal and a good cappuccino.