What Your Blood Sugar Has to Do With Cancer (And Why Your Oncologist Never Mentioned It)

By Dr. Lena Suhaila, ND, FABNO

There is a conversation happening in integrative oncology that most people with cancer never get to have with their conventional medical team, and it has nothing to do with a new drug or a clinical trial. It is about glucose, the sugar in your blood, and the profound role it plays in creating the conditions that allow cancer to grow, spread, and recur.

The relationship between blood sugar dysregulation and cancer has been documented in peer-reviewed research for decades. And yet most people leave their oncologist’s office with a treatment plan that never once addresses what they are eating, what their fasting insulin looks like, or how their body is managing glucose at a cellular level. That gap matters enormously, and I want to close it for you here.

Cancer Is a Glucose-Dependent Disease

In 1931, German biochemist Otto Warburg won the Nobel Prize for discovering that cancer cells metabolize glucose in a fundamentally different way than healthy cells do. While normal cells use oxygen to produce energy efficiently through oxidative phosphorylation, cancer cells preferentially ferment glucose even when oxygen is available, a phenomenon now known as the Warburg effect and one of the most important yet most underutilized pieces of biology in the clinical management of cancer (Warburg, 1956; Hanahan and Weinberg, 2011).

What this means practically is that cancer cells are voracious consumers of sugar. They carry significantly more insulin receptors than healthy cells, which means they respond aggressively to elevated insulin levels. When blood sugar is chronically elevated and insulin is persistently high, which describes a substantial portion of the population due to the combination of diet, chronic stress, and sedentary lifestyle, the biochemical environment that results is one that cancer is exquisitely well-adapted to exploit. This is not a metaphor. It is a measurable, addressable biological reality, and it is one that almost nobody discusses in a standard oncology appointment.

Insulin Is Not Just a Diabetes Issue

Most people think of insulin as something that only matters if you have diabetes, and that framing has done a great deal of harm in the context of cancer care. Elevated insulin, even in people who have never been diagnosed with diabetes or prediabetes, is one of the most underappreciated drivers of cancer risk and cancer progression in the published literature.

Insulin is a growth-promoting hormone. When it is chronically elevated, it stimulates cell proliferation, suppresses apoptosis, which is the natural process by which damaged or abnormal cells are supposed to die, and promotes systemic inflammation. All three of these create favorable conditions for cancer to establish and maintain itself. Research has consistently shown that elevated fasting insulin and insulin resistance are associated with significantly increased risk for breast, colorectal, pancreatic, and endometrial cancers among others (Pollak, 2008; Arcidiacono et al., 2012).

And yet fasting insulin is not a standard part of most oncology lab panels. In many cases, it is not even ordered by primary care physicians unless diabetes is already suspected. This is a significant clinical blind spot, and it is one I address directly when I work with patients.

What Blood Sugar Dysregulation Actually Looks Like

You do not have to have a diabetes diagnosis for any of this to be relevant to you. Blood sugar dysregulation exists on a spectrum, and most of it goes undetected because the markers that reveal it are not routinely ordered in a standard medical workup, let alone an oncology workup.

Insulin resistance is the state in which your cells have stopped responding efficiently to insulin, so your pancreas compensates by producing more of it. Your fasting glucose may still look entirely normal on a standard lab panel while your fasting insulin is significantly elevated, meaning the dysregulation is already present and already driving the biology, just not yet visible through the markers most doctors are looking at. Reactive hypoglycemia describes the pattern where blood sugar drops sharply after meals, triggering a cortisol and adrenaline response that further stresses the body and perpetuates the glucose-insulin cycle. Many people experience this as an afternoon energy crash, irritability between meals, or an intense craving for carbohydrates after eating, and they rarely connect it to their cancer biology.

Elevated fasting glucose and a high HbA1c, which reflects average blood sugar over the preceding three months, tell you how sustained that dysregulation has been. Neither of these markers is routinely ordered in a standard oncology workup, which means a patient can be sitting across from their oncologist with a significant metabolic problem that is actively feeding their cancer’s preferred environment and nobody in that room is aware of it.

The Cortisol Connection

There is another layer to this that rarely gets discussed, and it connects the metabolic picture directly to the nervous system. Chronic stress elevates cortisol, and cortisol raises blood sugar. This is one of cortisol’s primary physiological functions, mobilizing glucose to fuel a fight or flight response. In a body under sustained psychological or physical stress, blood sugar is being driven upward not just by diet but by the stress response itself.

For someone navigating a cancer diagnosis, chronic stress is not a background variable. It is often a primary feature of daily life. And the downstream metabolic consequence of that stress, persistently elevated cortisol driving persistently elevated glucose and insulin, is directly relevant to the biological environment their cancer is living in. Addressing stress physiology is not a separate conversation from addressing metabolic health. In this context they are the same conversation.

The Corticosteroid Problem Nobody Is Talking About

There is something else worth naming directly, because it affects a significant number of people in active cancer treatment. Corticosteroids, particularly dexamethasone, are among the most commonly prescribed drugs in oncology. They are given routinely as antiemetics before chemotherapy, to manage inflammatory side effects, and increasingly to treat the immune-related reactions that checkpoint inhibitors can trigger in healthy tissue.

The problem is that corticosteroids raise blood glucose significantly and do so predictably. Research shows that all corticosteroids increase glucose concentrations, with dexamethasone and methylprednisolone producing the most pronounced spikes, and that between 10 and 30 percent of cancer patients experience acute hyperglycemia episodes during steroid use (Frontiers in Pharmacology, 2025). For a patient whose cancer is already thriving in a glucose-rich environment, a drug that reliably elevates blood sugar is not a neutral intervention from a metabolic standpoint.

What most patients are not told is that corticosteroids are not always the only option. A growing body of oncology research is actively investigating steroid-minimizing approaches for nausea management, including 5-HT3 antagonists, NK1 receptor antagonists, and olanzapine, precisely because of concerns about their immunosuppressive and metabolic effects in patients on immunotherapy. These are not experimental ideas. They are being discussed at the highest levels of oncology right now and increasingly supported in the literature (Ottaiano et al., 2025).

This does not mean corticosteroids are never appropriate. There are clinical situations where they are necessary and where the benefit clearly outweighs the tradeoff. But that tradeoff deserves to be named out loud and discussed explicitly, and in my experience it rarely is.

What I Look at and Why

When I work with a patient, blood sugar regulation is one of the first areas I assess. This includes fasting glucose, fasting insulin, HbA1c, and a careful review of dietary patterns that may be driving dysregulation without the patient recognizing it. I am also looking at cortisol patterns, sleep quality, and the chronic stressors that may be feeding the glucose-insulin cycle from the nervous system end.

From there a protocol is built around the specific picture in front of me. This may include a low-glycemic or ketogenic dietary approach tailored to the individual’s cancer type, metabolic status, and treatment context. It may include berberine, which works through AMPK activation to improve insulin sensitivity and has meaningful evidence base in both metabolic and oncological contexts. In some patients, I also use metformin, which has accumulated a genuinely compelling body of research as a metabolic intervention in cancer, including data suggesting it may reduce cancer cell proliferation, lower circulating insulin, and improve outcomes in certain cancer types. These are clinical tools with a growing evidence base that most patients navigating cancer will never hear about unless they are working with someone who is specifically looking at the metabolic picture.

The Ketogenic Diet in the Cancer Context

A well-formulated ketogenic diet with a high vegetable content is one of the most evidence-supported dietary strategies in integrative oncology for exactly the reasons we have been discussing. By significantly reducing carbohydrate intake and shifting the body’s primary fuel source to fat-derived ketones, you remove the chronic glucose and insulin signaling that cancer cells depend on while healthy cells, which are considerably more metabolically flexible than cancer cells, adapt effectively to fat-based fuel.

Beta hydroxybutyrate, the primary ketone produced during nutritional ketosis, also directly inhibits the NLRP3 inflammasome and suppresses NF-kB signaling, two of the central molecular drivers of the chronic inflammation that promotes cancer progression (Youm et al., 2015). A ketogenic dietary approach, therefore, works on multiple levels at once: it removes a primary fuel source for cancer cells, reduces the inflammatory signaling that supports tumor survival, and improves the metabolic conditions under which both healthy cells and immune cells operate.

Wherever you are right now in your treatment, it is not too late to shift this. I have seen patients transform their metabolic health within weeks simply by changing what they eat. The body wants to heal. It just needs the right conditions.

The Question Worth Asking

If cancer cells are preferentially fueled by glucose, and if elevated insulin creates a biochemical environment that actively promotes cancer growth, then addressing blood sugar is not a lifestyle suggestion. It is a metabolic strategy with real and well-documented clinical implications, and it belongs at the center of your cancer care, not as an afterthought.

You deserve to have this conversation. If you are ready to look at your metabolic terrain and understand what your blood sugar is actually doing in the context of your cancer, I would welcome that conversation.

Schedule a consultation with Dr. Lena at naturallywellwithin.com/contact

References

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2. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646-674. https://doi.org/10.1016/j.cell.2011.02.013

3. Pollak M. Insulin and insulin-like growth factor signalling in neoplasia. Nature Reviews Cancer. 2008;8(12):915-928. https://doi.org/10.1038/nrc2536

4. Arcidiacono B, Iiritano S, Nocera A, et al. Insulin resistance and cancer risk: an overview of the pathogenetic mechanisms. Experimental Diabetes Research. 2012;2012:789174. https://doi.org/10.1155/2012/789174

5. Klement RJ, Kämmerer U. Is there a role for carbohydrate restriction in the treatment and prevention of cancer? Nutrition and Metabolism. 2011;8:75. https://doi.org/10.1186/1743-7075-8-75

6. Youm YH, et al. The ketone metabolite beta-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease. Nature Medicine. 2015;21(3):263-269. https://doi.org/10.1038/nm.3804

7. Hadad SM, et al. Evidence for biological effects of metformin in operable breast cancer. British Journal of Cancer. 2011;104(7):1054-1058. https://doi.org/10.1038/bjc.2011.64

8. Coyle C, Cafferty FH, Vale C, Langley RE. Metformin as an adjuvant treatment for cancer: a systematic review and meta-analysis. Annals of Oncology. 2016;27(12):2184-2195. https://doi.org/10.1093/annonc/mdw410

9. Ottaiano A, Santorsola M, Capuozzo M, Scala S. Balancing immunotherapy and corticosteroids in cancer treatment: dilemma or paradox? The Oncologist. 2025;30(3):oyaf045. https://doi.org/10.1093/oncolo/oyaf045

   Frontiers in Pharmacology. Rethinking corticosteroids use in oncology. 2025. https://doi.org/10.3389/fphar.2025.1551111

Dr. Lena Suhaila is a naturopathic oncologist and the founder of Naturally Well Within. To learn more about her work, visit her About page.