The idea that “sugar feeds cancer” is one of those health claims that sounds convincing because it contains a grain of truth.

Many cancer cells do indeed take up and metabolize large amounts of glucose. This characteristic of tumor metabolism is well established and even contributes to the way some cancers can be detected using FDG PET/CT imaging.2, 3, 4, 5

However, the conclusion that is often drawn from this — that eating sugar selectively “feeds” a tumor, or that removing sugar from the diet can starve cancer cells — is not supported by the scientific evidence.

Cancer metabolism is far more complex.

First, What Is Cancer?

Cancer is not a single disease. It is a large group of diseases that share certain biological characteristics, including uncontrolled cell growth and, in the case of malignant tumors, the ability to invade nearby tissues and potentially spread to other parts of the body.1

Cancer development is usually a multistep process. Genetic and epigenetic changes accumulate over time and affect biological pathways that regulate cell growth, survival, metabolism, and interactions between cells and the surrounding tissue.1

There is no single biology or single metabolic pattern that characterizes every cancer.

Do Cancer Cells Feed Exclusively on Sugar?

This claim is misleading.

Many cancer cells increase their uptake of glucose and rely heavily on glycolysis, even when oxygen is available. This phenomenon is associated with what is known as the Warburg effect.2, 3

Glucose can support rapidly dividing cells in more than one way. It can provide energy, but intermediates produced during glucose metabolism can also be used to generate molecules needed to build new cells, including nucleotides, amino acids, and lipids.2, 3, 4

So yes, glucose can be an important nutrient source for many tumors.

Cancer Cells Are Not the Only Cells That Use Glucose

Glucose is a normal energy source used throughout the entire body.

The brain and many other tissues depend heavily on glucose under normal physiological conditions. Other cells can use combinations of glucose, fatty acids, amino acids, and other substrates depending on their function and the body’s metabolic state.

This is one reason why simply removing added sugar from the diet does not remove glucose from the bloodstream.

Even when carbohydrate intake is severely restricted, the body has mechanisms that help maintain blood glucose levels. Stored glycogen may initially be broken down, while during fasting or prolonged carbohydrate restriction the body increasingly produces glucose from non-carbohydrate precursors through gluconeogenesis, mainly in the liver.8

It is not possible to selectively remove glucose from a tumor while continuing to provide glucose to the rest of the body.

And the available scientific evidence does not show that removing sugar from the diet causes an existing cancer to shrink or disappear.17

There Is No Single Cancer Metabolism

Tumors show substantial metabolic heterogeneity.

Although increased glycolysis is common in cancer, many tumors retain functional mitochondria and use oxidative phosphorylation alongside glycolysis.2, 3, 4, 5

Even tumors of the same type can behave differently.

Researchers have administered nutrient substrates labeled with stable isotopes to patients immediately before or during tumor-removal surgery in order to observe how human tumors actually metabolize nutrients in vivo, meaning inside the human body.

In patients with non-small cell lung cancer, these studies revealed substantial metabolic heterogeneity and showed that glucose can enter mitochondrial metabolic pathways rather than being used exclusively through glycolysis.5

Another human study showed that lung tumors could take up and use circulating lactate as a carbon source. In the tumors that were studied, lactate made a substantial contribution to mitochondrial metabolism.6

Kidney cancers showed yet another metabolic pattern, with high glycolytic activity but comparatively suppressed glucose oxidation through the tricarboxylic acid (TCA) cycle.7

These findings highlight that different tumors can meet their metabolic needs in different ways.

Depending on the type of cancer, tumor genetics, tissue of origin, and tumor microenvironment, cancer cells may use glucose, glutamine, fatty acids, lactate, and other available nutrient substrates.2, 4, 5, 6, 7

This ability to switch between different metabolic pathways and substrates is often described as metabolic flexibility or metabolic plasticity.2, 4

This makes the idea that every form of cancer can be “starved” by removing a single nutrient biologically unrealistic.

What About Low-Carbohydrate and Ketogenic Diets?

Because many tumors show increased glucose uptake, researchers have investigated whether significantly reducing dietary carbohydrates — particularly through ketogenic diets — could affect tumor metabolism or improve outcomes in people with cancer.

This is a reasonable research question.

A systematic review of clinical studies examining ketogenic diets in cancer patients found substantial heterogeneity in the available evidence, while many of the studies had a high risk of bias. The authors found no definitive evidence that ketogenic diets have anticancer effects or improve overall survival.9

More recent evidence, including a systematic review and meta-analysis of randomized controlled trials, continues to investigate the effects of ketogenic diets on glucose levels, metabolic markers, body weight, quality of life, and other cancer-related outcomes.10

Randomized trials and feasibility studies in patients with malignant gliomas and glioblastoma have also shown that ketogenic dietary interventions can be studied alongside conventional treatment. However, these trials were small and have not established ketogenic diets as a treatment that reliably controls tumors or improves survival.11, 12, 13

Current clinical nutrition guidelines therefore do not recommend restrictive diets as a substitute for evidence-based cancer treatments. This is particularly important because some cancer patients are already at risk of unintentional weight loss and malnutrition.14

Does PET/CT Prove That Cancer Feeds on Sugar?

This is another common argument:

“PET scans use sugar to find cancer, so that proves cancer feeds on sugar.”

Once again, there is a grain of truth followed by an incorrect conclusion.

A widely used tracer in oncology is 18F-fluorodeoxyglucose (18F-FDG), a radioactive glucose analogue. After entering cells, FDG can accumulate in tissues with increased glucose uptake and metabolism.15

Many tumors show increased FDG uptake, which is why FDG PET/CT can be useful for detecting, staging, and monitoring certain types of cancer.15

However, FDG uptake is not specific to cancer.

Normal tissues can also show substantial uptake. The brain, for example, naturally consumes large amounts of glucose. Uptake can also occur in the heart and skeletal muscles depending on physiological conditions.15

Inflammation, infections, healing tissues, and recent surgery can also produce increased FDG uptake, creating findings that may resemble malignancy.15, 16

The reverse is also true. Not all cancers show strong FDG uptake. Some tumors have relatively low or variable uptake and may therefore be less visible on FDG PET imaging.15

For this reason, PET findings are not interpreted in isolation. They are assessed together with the CT component of the scan, the pattern and location of uptake, previous imaging studies, and the patient’s clinical information.15

PET/CT therefore provides important information about glucose metabolism in tissues.

It does not prove that cancer cells survive exclusively because of the sugar we eat.

References

1. Hanahan D. Hallmarks of Cancer: New Dimensions. Cancer Discov. 2022;12(1):31–46.

2. Pavlova NN, Zhu J, Thompson CB. The hallmarks of cancer metabolism: Still emerging. Cell Metab. 2022;34(3):355–377.

3. Vander Heiden MG, Cantley LC, Thompson CB. Understanding the Warburg effect: The metabolic requirements of cell proliferation. Science. 2009;324(5930):1029–1033.

4. DeBerardinis RJ, Chandel NS. Fundamentals of cancer metabolism. Sci Adv. 2016;2(5).

5. Hensley CT, Faubert B, Yuan Q, et al. Metabolic heterogeneity in human lung tumors. Cell. 2016;164(4):681–694.

6. Faubert B, Li KY, Cai L, et al. Lactate metabolism in human lung tumors. Cell. 2017;171(2):358–371.e9.

7. Courtney KD, Bezwada D, Mashimo T, et al. Isotope tracing of human clear cell renal cell carcinomas demonstrates suppressed glucose oxidation in vivo. Cell Metab. 2018;28(5):793–800.e2.

8. Landau BR, Wahren J, Chandramouli V, Schumann WC, Ekberg K, Kalhan SC. Contributions of gluconeogenesis to glucose production in the fasted state. J Clin Invest. 1996;98(2):378–385.

9. Römer M, Dörfler J, Huebner J. The use of ketogenic diets in cancer patients: A systematic review. Clin Exp Med. 2021;21(4):501–536.

10. Salido-Bueno B, Gil-Hernandez E, Rueda-Ruzafa L, Gomez-Chica P, Roman P, Cardona D. Effects of ketogenic diets on cancer-related variables: A systematic review and meta-analysis of randomized controlled trials. Nutr Bull. 2024;49(3):264–277.

11. Voss M, Wagner M, von Mettenheim N, et al. ERGO2: A prospective, randomized trial of calorie-restricted ketogenic diet and fasting in addition to reirradiation for malignant glioma. Int J Radiat Oncol Biol Phys. 2020;108(4):987–995.

12. Martin-McGill KJ, Marson AG, Tudur Smith C, et al. Ketogenic diets as an adjuvant therapy for glioblastoma (KEATING): A randomized, mixed methods, feasibility study. J Neurooncol. 2020;147(1):213–227.

13. Amaral LJ, et al. A phase 1 safety and feasibility trial of a ketogenic diet plus standard of care for patients with recently diagnosed glioblastoma. Sci Rep. 2025;15:21064.

14. Muscaritoli M, Arends J, Bachmann P, et al. ESPEN practical guideline: Clinical nutrition in cancer. Clin Nutr. 2021;40(5):2898–2913.

15. Boellaard R, Delgado-Bolton R, Oyen WJG, et al. FDG PET/CT: EANM procedure guidelines for tumour imaging: version 2.0. Eur J Nucl Med Mol Imaging. 2015;42(2):328–354.

16. Pijl JP, Nienhuis PH, Kwee TC, Glaudemans AWJM, Slart RHJA, Gormsen LC. Limitations and pitfalls of FDG-PET/CT in infection and inflammation. Semin Nucl Med. 2021;51(6):633–645.

17. National Cancer Institute. Common Cancer Myths and Misconceptions: Will Eating Sugar Make My Cancer Worse? Updated July 24, 2024.