Blood sugar, insulin resistance, and cancer risk
Series: The metabolic theory of cancer — post 2 of 10
Of all the metabolic factors implicated in cancer risk, chronically elevated blood glucose and the insulin resistance that so often accompanies it are among the most consistently studied — and among the most actionable. This is not a fringe hypothesis. It is the subject of hundreds of prospective cohort studies, several large meta-analyses, and a growing body of mechanistic research that helps explain why the association exists. In this post, we look at what the human evidence shows, why the biology is plausible, and what practical steps follow from it.
The science in brief: insulin, IGF-1, and the cancer connection
The biological link between insulin resistance and cancer risk operates through several overlapping mechanisms, the most well-established of which involves insulin and its close relative, insulin-like growth factor 1 (IGF-1). When cells become resistant to insulin’s signals — as occurs in type 2 diabetes, obesity, and metabolic syndrome — the pancreas compensates by producing more insulin. Chronically elevated insulin is not simply a blood sugar problem; insulin is also a potent mitogenic hormone, meaning it promotes cell growth and proliferation. Elevated circulating insulin stimulates IGF-1 signalling, which activates the same PI3K/Akt/mTOR pathways we encountered in the first post of this series — pathways that, when dysregulated, contribute to uncontrolled cell division.
The epidemiological evidence supporting this connection is substantial. A landmark systematic review and meta-analysis published in Nutrients in 2022 (PMID: 35057525) examined dietary patterns and cancer prognosis across multiple cancer types and found consistent associations between markers of poor metabolic health — including elevated fasting glucose and insulin resistance — and worse cancer outcomes. A review of the Women’s Health Initiative, published in JAMA in 2024 (DOI: 10.1186/s12933-024-02122-4), further reinforced the relationship between metabolic dysfunction and cancer risk in postmenopausal women — a population that overlaps significantly with the readership of this series.
Type 2 diabetes — the clinical endpoint of severe, sustained insulin resistance — is associated with a meaningfully increased risk of several cancers, including colorectal, liver, pancreatic, breast, and endometrial cancers. A nutrition review focused on colorectal cancer, published in Nutrients in 2021 (DOI: 10.3390/nu13010143), identifies hyperinsulinaemia as one of the most plausible mechanistic links between Western dietary patterns and colorectal cancer incidence. These are observational and review-level findings — they establish association, not causation — but the consistency of the signal across cancer types, populations, and study designs is notable.
Glycaemic load, dietary patterns, and cancer risk
It is worth being precise about what the evidence implicates here — and what it does not. The research does not suggest that eating carbohydrates causes cancer. It suggests that sustained metabolic dysfunction, characterised by chronically elevated blood glucose and insulin, creates a physiological environment that is less hostile to cancer cell proliferation. The distinction matters enormously in practice.
Dietary patterns that produce rapid, repeated spikes in blood glucose — characterised by high intakes of ultra-processed foods, refined carbohydrates, and added sugars, and low intakes of fibre, protein, and fat — are associated with greater insulin resistance over time. By contrast, dietary patterns that support stable postprandial glucose — including Mediterranean-style diets rich in vegetables, legumes, whole grains, olive oil, and oily fish — are consistently associated with reduced cancer risk and improved cancer prognosis in observational studies.
A systematic review and meta-analysis published in Nutrients in 2022 found that higher adherence to Mediterranean-style dietary patterns was associated with reduced all-cause mortality and improved prognosis across several cancer types. A review published in Experimental Gerontology in 2023 (DOI: 10.1016/j.exger.2023.112121) found the Mediterranean diet to be one of the most robustly supported dietary patterns for reducing metabolic risk factors — including insulin resistance — that sit upstream of both cancer and cardiovascular disease. These are meta-analyses and systematic reviews of observational cohort data; randomised controlled trial evidence in the cancer-specific context remains limited, but the direction of the evidence is consistent.
What this means in practice
The goal here is not glucose perfectionism. Blood glucose fluctuates naturally throughout the day, and there is no meaningful evidence that normal postprandial rises in a metabolically healthy person represent a cancer risk. What the evidence points to is the importance of avoiding the chronic, sustained metabolic dysfunction that develops over years — and of building daily habits that support insulin sensitivity rather than erode it. Here are four evidence-grounded starting points.
Prioritise fibre at every meal. Dietary fibre slows glucose absorption, blunts postprandial insulin spikes, and feeds the gut microbiome in ways that have downstream effects on systemic inflammation and metabolic health. Vegetables, legumes, whole grains, nuts, and seeds are your best sources. Aim for variety as much as quantity — different fibre types feed different bacterial populations.
Build meals around protein and fat before carbohydrate. The order in which macronutrients are consumed within a meal has a measurable effect on postprandial glucose response. Eating vegetables and protein before starchy carbohydrates consistently produces a lower and more gradual glucose rise than eating carbohydrates first. This is a low-effort, evidence-supported adjustment that requires no calorie counting.
Move after eating. Even a 10-minute walk after a meal meaningfully reduces postprandial blood glucose by enabling muscles to take up glucose independently of insulin. This is one of the most robustly supported, accessible interventions in glucose management — and it requires nothing beyond a willingness to step outside.
Reduce ultra-processed food rather than carbohydrates as a category. The evidence against ultra-processed foods — defined by their industrial formulation, high palatability, and displacement of whole foods — is far stronger than the evidence against any particular macronutrient. Whole-food carbohydrate sources such as legumes, root vegetables, and intact grains behave very differently metabolically from refined and processed equivalents, and carry fibre, polyphenols, and micronutrients that have independent health relevance.
What the evidence does not yet show
The evidence linking insulin resistance and elevated blood glucose to cancer risk is associative. We do not yet have randomised controlled trial data demonstrating that improving insulin sensitivity in previously insulin-resistant individuals reduces cancer incidence — conducting such a trial over a meaningful follow-up period would be extraordinarily difficult. What we have is a mechanistically plausible, epidemiologically consistent picture, which is a reasonable basis for action but not a guarantee of outcome.
It is also worth noting that insulin resistance is influenced by factors beyond diet — sleep quality, chronic stress, physical activity levels, genetics, and age all play meaningful roles. Dietary change alone, whilst valuable, is unlikely to fully address insulin resistance in someone whose sleep is chronically poor or whose stress response is dysregulated. We will return to those factors in posts seven and eight.
Finally, it bears repeating: no dietary intervention has been shown in a randomised controlled trial to prevent cancer or treat it as a standalone approach. The evidence discussed here relates to risk modulation and metabolic health — not to treatment.
The bottom line
Chronically elevated blood glucose and insulin resistance create a hormonal and metabolic environment that is, on the available evidence, less hostile to cancer cell proliferation — through mechanisms involving insulin, IGF-1, and the PI3K/Akt/mTOR signalling axis. The dietary patterns most consistently associated with lower cancer risk are those that support stable blood glucose and insulin sensitivity: fibre-rich, whole-food, minimally processed eating, with an emphasis on vegetables, legumes, healthy fats, and quality protein. These are not dramatic interventions. They are the kind of sustainable, daily habits that compound over years — and that have relevance not only to cancer risk, but to metabolic health, cardiovascular health, and longevity more broadly.
Scientific references
- Dietary patterns and cancer prognosis — systematic review and meta-analysis. Nutrients, 2022. PMID: 35057525
- Women’s Health Initiative — metabolic health and cancer risk review. JAMA, 2024. DOI: 10.1186/s12933-024-02122-4
- Colorectal cancer and nutrition review. Nutrients, 2021. DOI: 10.3390/nu13010143
- Mediterranean diet and metabolic risk. Experimental Gerontology, 2023. DOI: 10.1016/j.exger.2023.112121
Medical disclaimer
This article is written for educational and informational purposes only. It is not intended as medical advice and should not be used to diagnose, treat, prevent, or cure any medical condition, including cancer. If you have a cancer diagnosis or are undergoing treatment, please discuss any lifestyle or dietary changes with your oncologist or medical team before making them. The studies cited reflect current research at the time of writing; the field is evolving rapidly and findings may be updated or superseded. Chloe Archard is a nutritional health coach, not a medical doctor.
