One in two people in the UK is expected to develop cancer during their lifetime. Discover the science linking metabolism, insulin resistance, inflammation and lifestyle with cancer risk, alongside evidence-based ways to support conventional medical treatment.
The suggestion that one in two people in the UK may develop cancer during their lifetime is understandably alarming. However, this statistic needs context. It describes estimated lifetime risk, rather than suggesting that half the population has cancer at any one time. It also reflects the fact that we are living longer, detecting more cancers and surviving diseases that previously caused earlier death.
Cancer is not one disease. It is a collection of hundreds of diseases in which abnormal cells acquire the ability to survive, multiply, invade neighbouring tissue and sometimes spread to distant organs.
Is cancer a metabolic disease?
Cancer is often described primarily as a genetic disease, as genetic mutations alter cancer cells’ growth, DNA repair and cell death programming. However, abnormal metabolism is also a recognised feature of cancer.
Many cancer cells increase their use of glucose and convert much of it to lactate even when oxygen is available. This is commonly called the Warburg effect. It can help rapidly dividing cells obtain both energy and the molecular building blocks required to manufacture new cells.
This does not mean that defective metabolism is always the original cause of cancer. Genetic changes can reprogramme cellular metabolism, while metabolic disturbances can alter gene regulation, inflammation and the cellular environment. A more accurate description is that cancer is a genetic, evolutionary, metabolic and immune disease.
Metabolic reprogramming is therefore an important therapeutic target, but it is one component of a complex biological process.
Insulin resistance and cancer
Insulin allows cells to take up and use nutrients. In insulin resistance, muscle, liver and other tissues respond less effectively to insulin. The pancreas compensates by producing more, creating persistent hyperinsulinaemia in many people.
Insulin is not merely a glucose-lowering hormone. It also provides growth signals. High insulin concentrations may activate insulin receptors and related pathways like insulin-like growth factor IGF-1 and mTOR, which encourage cancer cells to rapidly divide and resist chemotherapy. Insulin resistance is also frequently accompanied by excess visceral fat, fatty liver, altered sex hormones and chronic low-grade inflammation.
These mechanisms may help explain why obesity and type 2 diabetes are associated with higher risks of several cancers, including endometrial, postmenopausal breast, bowel, liver, kidney and pancreatic cancers. Nevertheless, the strength and nature of the association vary considerably between cancer types. Insulin resistance should therefore be considered an important contributing risk factor, not a single universal cause.
Oxidative stress: both harmful and complicated
Reactive oxygen species are produced during normal metabolism and immune activity. In controlled quantities, they act as useful signalling molecules. Oxidative stress occurs when their production exceeds the body’s ability to control or repair the resulting damage.
Long-standing oxidative stress can damage DNA, proteins and cell membranes. It may contribute to mutations, inflammation, tissue ageing and an environment that permits abnormal cells to survive.
However, the story is not simply that all oxidation is harmful and all antioxidants are beneficial. Radiotherapy and several chemotherapy drugs deliberately generate oxidative damage to kill cancer cells. Large doses of antioxidant supplements could theoretically interfere with some treatments, although this depends on the treatment and supplement.
Patients should tell their oncology team about every vitamin, antioxidant and herbal preparation they use rather than assuming that “natural” products are harmless.
Does sugar feed cancer?
All cells use glucose, including the brain, muscles, immune cells and cancer cells. Many tumours consume more glucose than surrounding tissue, which is one reason glucose-based PET scans can help identify some cancers.
But it does not follow that removing dietary sugar selectively starves a tumour. The body can maintain blood glucose by breaking down stored glycogen and manufacturing glucose from protein and fat. The National Cancer Institute states that studies have not demonstrated that eating sugar directly makes cancer worsen or that stopping sugar causes cancer to disappear.
This does not give unlimited added sugar a clean bill of health. Sugary drinks and highly processed, energy-dense foods can promote weight gain, fatty liver, dental disease and metabolic dysfunction. Reducing them is sensible.
The practical message is:
- Limit sugary drinks, sweets and heavily refined foods.
- Prefer vegetables, pulses, fruit, nuts, seeds and minimally processed foods.
- Choose fibre-rich carbohydrate sources such as beans and whole grains when tolerated.
- Match carbohydrate intake to activity, glucose control, nutritional needs and treatment side effects.
A low-carbohydrate diet may help certain people manage diabetes or weight, but evidence does not support presenting complete carbohydrate avoidance as a general cancer treatment. During active treatment, excessive restriction may cause weight loss, muscle loss and nutrient deficiency.
Should patients fast before chemotherapy or radiotherapy?
Short-term fasting and fasting-mimicking diets are being investigated as additions to cancer treatment. The proposed mechanism is called differential stress resistance: healthy cells may enter a protective maintenance state during temporary nutrient restriction, while cancer cells may remain committed to uncontrolled growth and become more vulnerable to treatment.
Animal studies are interesting, and small human studies suggest that carefully supervised fasting may be feasible for selected, well-nourished patients. Some have reported possible reductions in fatigue or treatment toxicity. However, the clinical evidence remains limited, and there is not yet sufficient proof that fasting improves survival or routinely enhances chemotherapy or radiotherapy outcomes. Reviews conclude that larger, properly controlled trials are required.
Fasting can be particularly dangerous for people who are underweight, frail, diabetic, pregnant, losing weight unintentionally or experiencing vomiting, swallowing problems or poor appetite. Cancer-associated malnutrition and muscle loss can reduce treatment tolerance and worsen recovery.
No patient should fast around cancer treatment without agreement from their oncologist and a specialist oncology dietitian. Treatment-specific evidence is essential: chemotherapy and radiotherapy are not interchangeable, and recommendations cannot be generalised from one cancer or drug to another.
Why are more cancers being diagnosed?
The largest reason for the rising number of UK cancer diagnoses is population growth and ageing. Cancer is predominantly a disease of accumulated cellular damage, so an older population will experience more cases.
Detection has also improved. Screening, imaging, endoscopy, pathology and public awareness identify cancers that previously might have remained undiagnosed.
Lifestyle and environmental factors contribute as well. Tobacco remains a major preventable cause. Excess body weight, alcohol, inactivity, ultraviolet radiation, occupational exposures, air pollution and certain infections also play roles. The rising incidence of obesity and metabolic disease is likely to influence some cancers, but it cannot explain every trend.
Cancer Research UK reported in April 2026 that annual UK cases had exceeded 400,000. It identified the growing and ageing population as the principal reason, while also noting improved diagnosis, persistent tobacco exposure and increasing obesity.
Some cancers are increasing among younger adults, particularly bowel cancer in several countries. Possible contributors include obesity, dietary patterns, inactivity, microbiome changes, environmental exposures, improved detection and other factors. This remains an active research question rather than a settled metabolic explanation.
Why does cancer occur predominantly in older people?
Cancer usually requires several biological changes to accumulate in the same cell lineage. With age:
- Cells undergo more divisions, creating more opportunities for copying errors;
- DNA has had longer exposure to tobacco smoke, ultraviolet radiation, infections and other carcinogens;
- DNA-repair and immune-surveillance mechanisms become less efficient;
- Senescent cells and chronic inflammation alter the tissue environment;
- Mitochondrial and metabolic regulation may deteriorate;
- Epigenetic control becomes less stable.
Age therefore provides both more time for harmful changes to accumulate and a tissue environment in which abnormal cells may be more likely to survive.
What genuinely helps prevent cancer?
No lifestyle can guarantee prevention, and cancer is never a moral failure. Nevertheless, a substantial proportion of cases can be prevented or detected earlier.
The highest-priority measures are to avoid tobacco, maintain a healthy weight, remain physically active, minimise alcohol, protect the skin from excessive ultraviolet exposure, receive recommended HPV and hepatitis B vaccination, address cancer-causing infections when appropriate, limit processed meat and participate in NHS screening when invited.
Dietary patterns should emphasise vegetables, fruit, pulses and other fibre-rich plant foods. Exercise improves insulin sensitivity, reduces visceral fat, preserves muscle, supports immune and cardiovascular health, and may help regulate sex hormones and inflammation.
These measures are more strongly supported than any supplement, detoxification programme or extreme dietary regimen.
Lifestyle during conventional treatment
Lifestyle care should support—not replace—surgery, radiotherapy, chemotherapy, hormonal treatment, targeted treatment or immunotherapy.
Priorities during treatment include:
- Preventing malnutrition and maintaining muscle.
- Taking appropriate physical activity, adapted to symptoms and blood counts.
- Obtaining adequate protein, energy and fluids.
- Managing diabetes and other cardiovascular risks.
- Protecting sleep and mental health.
- Avoiding smoking and keeping alcohol low.
- Checking supplements and dietary restrictions with the treatment team.
Exercise is generally safe when individually adapted and can reduce treatment-related fatigue, anxiety and loss of physical function.
Promising developments in treatment
Modern cancer care is increasingly based on the biological characteristics of an individual tumour rather than its location alone.
Important developments include immune-checkpoint inhibitors, CAR-T and other engineered immune-cell treatments, precision drugs targeting specific mutations, antibody–drug conjugates, bispecific antibodies and radiopharmaceuticals that deliver radiation to selected tumour cells. Researchers are also investigating cancer vaccines, personalised neoantigen approaches and treatments exploiting specific metabolic vulnerabilities.
These are not universal cures. Their effectiveness depends on the tumour type, biomarkers, stage, previous treatment and the patient’s overall health. Metabolic treatments are most likely to succeed when they target a clearly demonstrated tumour dependency rather than applying a single diet to every cancer.
Can cancer patients regain vitality and longevity?
Yes. Many people are cured, and many others live for years or decades with cancer controlled as a chronic condition. Recovery depends on the cancer type and stage, treatment response, age, other illnesses and treatment-related effects.
Vitality can often improve through rehabilitation, gradual aerobic and strength exercise, adequate nutrition, sleep, psychological support and careful management of pain, hormonal changes, neuropathy, heart health and metabolic conditions.
Survivorship does not always mean returning immediately to one’s previous self. It may involve constructing a sustainable “new normal”. Regular follow-up, healthy eating and exercise can help manage late effects, while physical activity has been associated with better outcomes in some groups of survivors.
The balanced conclusion
Metabolism matters enormously in cancer. Insulin resistance, obesity, inflammation and oxidative stress can influence cancer risk and tumour biology, and metabolic pathways offer exciting treatment targets.
But metabolism is not the entire story. Avoiding sugar cannot starve away a tumour; fasting is not yet a standard cancer treatment, and lifestyle interventions must not be presented as alternatives to oncology care.
The most responsible approach is to reduce preventable risks, protect metabolic health, use exercise and nutrition to maintain resilience, participate in screening, seek prompt assessment of symptoms and combine supportive lifestyle care with evidence-based medical treatment.
Key Take-Home Messages
- Cancer is not simply a genetic disease—it also has important metabolic characteristics.
- Good metabolic health may reduce the risk of several common cancers, although it cannot eliminate risk.
- Exercise remains one of the most powerful lifestyle interventions for reducing cancer risk and supporting recovery.
- Nutrition should support evidence-based cancer treatment, not replace it.
- Healthy longevity is built on metabolic resilience long before cancer ever develops.
If you found this discussion useful, you may be interested in my recently published book, “Your Metabolic Shift”, which explores these concepts in greater depth.
Frequently Asked Questions
Does eating sugar cause cancer?
No. Sugar itself does not directly cause cancer. However, diets high in refined sugars can contribute to obesity, insulin resistance and chronic inflammation, all of which are associated with increased risks for several cancers.
Can stopping sugar cure cancer?
No. There is currently no scientific evidence that removing sugar from the diet cures cancer. Cancer cells use glucose, but so do healthy cells. The body can also manufacture glucose from protein and fat.
Is cancer really a metabolic disease?
Cancer is increasingly recognised as having important metabolic features. Most experts now describe cancer as involving genetic, metabolic, immune and environmental processes rather than a single cause.
Does insulin resistance increase cancer risk?
Growing evidence suggests yes. Insulin resistance and elevated insulin levels are associated with higher risks of several cancers, including breast, bowel, liver, pancreatic and endometrial cancers.
Should cancer patients follow a ketogenic diet?
Research is ongoing. Some early studies are promising in selected cancers, but ketogenic diets should never replace conventional treatment and should only be undertaken with professional supervision.
Should patients fast before chemotherapy?
Some early clinical trials suggest fasting or fasting-mimicking diets may reduce treatment side effects in selected patients, but there is currently insufficient evidence for routine clinical practice. Patients should never fast during cancer treatment without advice from their oncology team.
Why does cancer mainly affect older people?
Age allows genetic damage to accumulate while the immune system becomes less effective at identifying abnormal cells. Mitochondrial function, inflammation and metabolic regulation also change with ageing.
Can people live a long, healthy life after cancer?
Yes. Millions of cancer survivors go on to enjoy many years of healthy life. Regular exercise, maintaining muscle mass, healthy nutrition, good sleep and controlling metabolic health all contribute to improved quality of life and long-term wellbeing.
This article is intended for educational purposes only and should not replace personalised medical advice. Readers with existing medical conditions should consult their healthcare professional before making significant dietary or lifestyle changes.
References
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- Seyfried TN. Cancer as a Metabolic Disease. Wiley; 2012.
- World Cancer Research Fund/American Institute for Cancer Research. Diet, Nutrition, Physical Activity and Cancer: A Global Perspective.
- National Cancer Institute. Cancer Prevention Overview.
- Cancer Research UK. Cancer Statistics for the UK.
- Sung H, et al. Global Cancer Statistics 2024. CA: A Cancer Journal for Clinicians.
- Vander Heiden MG, Cantley LC, Thompson CB. Understanding the Warburg Effect. Science. 2009.
- Longo VD, Mattson MP. Fasting: Molecular Mechanisms and Clinical Applications. Cell Metabolism. 2014.
