Cancer can push blood sugar in both directions, sometimes raising it and sometimes dropping it dangerously low, depending on the type of cancer, where it is in the body, and how it is being treated. The relationship is not a single mechanism but a tangle of overlapping ones: tumors that guzzle glucose, tumors that secrete hormones mimicking insulin, cancer treatments that trigger insulin resistance, and the body’s own stress response to the disease. For anyone living with cancer or caring for someone who is, understanding these pathways matters because blood sugar swings can affect treatment decisions, quality of life, and outcomes.
How Tumors Consume Glucose
Most healthy cells get the bulk of their energy by breaking down glucose through a process that requires oxygen. Cancer cells tend to do something different. Even when oxygen is plentiful, many tumors shift to a less efficient form of glucose processing that converts sugar into lactate. This behavior, known as the Warburg effect, has been observed across a wide range of cancers and was first described nearly a century ago, yet it remains a defining feature of tumor metabolism today.1PubMed Central. The Warburg Effect: How Does it Benefit Cancer Cells?
Because this metabolic shortcut extracts less energy per molecule of glucose, cancer cells compensate by taking in far more glucose than normal cells do.2PubMed Central. Understanding the Warburg effect: the metabolic requirements of cell proliferation That heightened appetite for sugar is the whole basis of PET scans, which detect tumors by tracking where a radioactive glucose tracer accumulates. But does that local sugar consumption actually lower your blood sugar readings? In most cases, no. The body’s glucose regulation systems are powerful enough to keep pace with even a fast-growing tumor’s demands. Blood sugar disruptions from cancer usually arise through more specific mechanisms than simple overconsumption alone.
Pancreatic Cancer and New-Onset Diabetes
The pancreas manufactures insulin, so it is no surprise that cancers arising there can wreck blood sugar control. What is surprising is the timing. Older adults who develop diabetes seemingly out of nowhere have roughly an eightfold higher risk of harboring pancreatic cancer compared to the general population.3PubMed Central. New-onset diabetes: a potential clue to the early diagnosis of pancreatic cancer In many of these people, the rising blood sugar is the first detectable sign of a tumor that has not yet caused pain, weight loss, or jaundice.
Researchers believe the tumor disrupts insulin production and insulin signaling in the surrounding pancreatic tissue, essentially triggering a form of diabetes that appears months before other symptoms surface. This has prompted ongoing interest in using unexplained new-onset diabetes in older adults as a screening signal for pancreatic cancer. The challenge is that type 2 diabetes is extremely common in that age group for other reasons, so sorting out which new cases warrant further investigation remains an active area of research.
Tumors That Drop Blood Sugar
While high blood sugar gets most of the attention in cancer care, some tumors cause dangerously low blood sugar instead. The clearest example involves insulinomas, rare tumors of the insulin-producing cells in the pancreas. They pump out excess insulin regardless of what your blood sugar is doing, which can send glucose levels plummeting. These tumors are uncommon, affecting roughly one to four people per million, but they are the most frequent cause of low blood sugar from the body overproducing its own insulin.4PubMed Central. Diagnosis and management of insulinoma
A separate and even rarer phenomenon involves tumors that do not arise in the pancreas at all. In non-islet cell tumor hypoglycemia, a tumor secretes a large form of a molecule called IGF-II, which acts like insulin and drives blood sugar down.5PubMed Central. Management of non-islet-cell tumor hypoglycemia: a clinical review These tumors are typically large, arising from connective tissue or, less commonly, from epithelial organs.6PubMed Central. IGF-2-mediated hypoglycemia: a case series and review of the medical therapies for refractory hypoglycemia The hypoglycemia they produce can be severe and resistant to treatment, sometimes requiring continuous glucose infusion or surgical removal of the tumor to resolve.
On the opposite end of the spectrum, glucagonomas are rare pancreatic tumors that overproduce glucagon, a hormone that raises blood sugar. People with glucagonomas can develop diabetes as part of a broader syndrome that also includes skin rashes, weight loss, and blood clots.7PubMed. The glucagonoma syndrome and its management These tumors illustrate that the pancreas can harbor cancers pulling blood sugar in either direction, depending on which cell type has gone rogue.
When Cancer Spreads to the Liver
The liver is the body’s main glucose warehouse, storing it as glycogen and releasing it between meals to keep blood sugar steady. When cancer metastasizes to the liver and replaces a large volume of normal tissue, the organ can lose its ability to fulfill that role. Patients in this situation sometimes develop severe hypoglycemia because there is simply not enough functional liver tissue left to produce or store glucose.8PubMed Central. Persistent hypoglycemia in patients with liver cancer
Documented cases paint a vivid picture. In one report, a patient with extensive liver metastases required 500 grams of glucose per day, roughly five times the normal amount, to maintain consciousness. The hypoglycemia only resolved after chemotherapy shrank the tumor burden enough for the remaining liver tissue to resume its job.9PubMed. Hypoglycemia secondary to metastases to the liver. A case report and review of the literature In another case, a patient with gastric cancer that had spread to the liver developed hypoglycemic coma linked to IGF-II production by the cancer cells themselves, compounding the metabolic failure caused by the loss of liver tissue.10Internal Medicine. Severe Hypoglycemia and Hypokalemia in Association with Liver Metastases of Gastric Cancer
These scenarios are most often seen in advanced disease, when liver involvement is extensive. For people with smaller or fewer liver metastases, blood sugar control typically remains intact because the liver has a large functional reserve.
Cancer Treatments That Raise Blood Sugar
Even when the cancer itself is not driving blood sugar changes, the treatments frequently do. Several classes of cancer therapy are well known to push glucose levels up, and in some patients, the effect is severe enough to require its own management plan.
Steroids
Corticosteroids like dexamethasone and prednisone are given alongside many chemotherapy regimens to prevent nausea and reduce inflammation. They are effective at both jobs, but they also make cells more resistant to insulin. In one study of cancer patients receiving dexamethasone as an antiemetic, about a fifth developed steroid-induced diabetes within the first few months of chemotherapy, and the risk rose with higher cumulative steroid doses.11Cancer Research and Treatment. A Pilot Study Evaluating Steroid-Induced Diabetes after Antiemetic Dexamethasone Therapy in Chemotherapy-Treated Cancer Patients For people with blood cancers like lymphoma or myeloma, high-dose prednisone is often part of the cancer treatment itself, making hyperglycemia an expected side effect that oncology teams actively monitor.12PubMed. Metformin’s effectiveness in preventing prednisone-induced hyperglycemia in hematological cancers
PI3K and AKT Inhibitors
A newer class of targeted cancer drugs works by blocking a signaling pathway called PI3K/AKT. That pathway happens to play a central role in how your body responds to insulin: it helps muscle and fat cells absorb glucose. Block the pathway to starve a tumor, and you may also block the pathway that keeps blood sugar in check.13PubMed Central. Hyperglycemia secondary to phosphatidylinositol-3 kinase (PI3K) inhibition In phase I trials of drugs targeting this pathway, nearly nine out of ten patients developed some degree of elevated blood sugar during treatment, though most cases were mild.14The Oncologist. Hyperglycemia and Phosphatidylinositol 3-Kinase/Protein Kinase B/Mammalian Target of Rapamycin (PI3K/AKT/mTOR) Inhibitors in Phase I Trials: Incidence, Predictive Factors, and Management Patients with pre-existing diabetes or prediabetes are at particular risk for more serious blood sugar spikes on these drugs.15PubMed Central. Characterization, management, and risk factors of hyperglycemia during PI3K or AKT inhibitor treatment
Immune Checkpoint Inhibitors
Immunotherapy drugs that release the brakes on the immune system have transformed cancer treatment, but they can also cause the immune system to attack healthy tissue. In rare cases, that includes the insulin-producing cells of the pancreas, leading to a form of type 1 diabetes that requires lifelong insulin. One large study found this happened in about 0.45% of patients treated with immune checkpoint inhibitors, with the risk roughly doubling in patients receiving combination immunotherapy.16JAMA Oncology. Identification of Immune Checkpoint Inhibitor–Induced Diabetes People with pre-existing type 2 diabetes faced about six times the odds of developing this complication. When it occurs, onset can be sudden and dramatic, sometimes presenting with diabetic ketoacidosis that requires emergency treatment.
Androgen Deprivation Therapy
Men treated for prostate cancer with androgen deprivation therapy (ADT) frequently develop metabolic side effects, including elevated blood sugar and insulin resistance. In one study, men on ADT had fasting glucose levels averaging around 131 mg/dL, well above the roughly 100 mg/dL seen in men with prostate cancer who were not on the therapy.17PubMed. Hyperglycemia and insulin resistance in men with prostate carcinoma who receive androgen-deprivation therapy These metabolic changes have been confirmed in multiple studies and appear to be a direct consequence of testosterone suppression, which affects how the body handles fat, insulin, and glucose.18PubMed Central. Changes in blood glucose and cholesterol levels due to androgen deprivation therapy in men with non-metastatic prostate cancer19The Journal of Clinical Endocrinology & Metabolism. The Influence of Androgen Deprivation Therapy on Metabolism in Patients with Prostate Cancer
Cachexia and the Body’s Glucose Recycling Problem
Advanced cancer often triggers cachexia, a wasting syndrome marked by severe loss of muscle and fat that does not reverse with normal eating. Cachexia is not simple starvation; it involves a deep metabolic reprogramming driven by signals from the tumor. Part of that reprogramming accelerates a glucose recycling loop between the liver and muscles. The liver works overtime to convert lactate from the tumor and other tissues back into glucose, a process that burns extra energy and contributes to the relentless weight loss seen in cachectic patients.20PubMed Central. Walker-256 Tumour-Induced Cachexia Altered Liver Metabolomic Profile and Function in Weanling and Adult Rats
Research has shown that tumors can send signals that ramp up glucose production in the liver, and higher levels of these liver-based glucose-production genes correlate with more severe weight loss in animal models.21PubMed Central. Tumor Cytokine-Induced Hepatic Gluconeogenesis Contributes to Cancer Cachexia: Insights from Full Body Single Nuclei Sequencing For patients, this can mean wild swings in blood sugar. Some cachectic patients have persistently high glucose levels because the liver keeps pumping it out, while others may swing low because the tumor and the recycling loop consume it faster than the body can replenish. It is one reason why blood sugar monitoring in advanced cancer is especially important and often unpredictable.
Stress, Cortisol, and Blood Sugar During Cancer
A cancer diagnosis does not just change your biology; it also floods your body with stress hormones. Chronic psychological stress activates the hypothalamic-pituitary-adrenal axis, leading to sustained elevations in cortisol. Cortisol, in turn, promotes glucose release from the liver and makes cells more resistant to insulin, both of which push blood sugar up. This stress response can also amplify the sympathetic nervous system, raising catecholamine levels that further worsen insulin resistance.22PubMed Central. The Influence of Psychological Stress on the Initiation and Progression of Diabetes and Cancer
For people undergoing cancer treatment, this creates a layered problem. A steroid-based antiemetic raises blood sugar on its own. Chronic stress adds to the insulin resistance. Reduced physical activity during treatment further lowers insulin sensitivity. And if the patient is eating irregularly because of nausea or appetite loss, blood sugar becomes even harder to predict. The medical team can address the pharmacological causes, but the stress-cortisol component often goes underrecognized.
Glucose Competition Inside the Tumor
There is an interesting wrinkle in the relationship between tumors and glucose that has practical implications for cancer treatment. Immune cells that are trying to attack a tumor also need glucose to function. Early research in mouse models suggested that tumors could starve nearby immune cells by hogging the local glucose supply, weakening the immune response and helping the cancer grow unchecked.23PubMed Central. Metabolic competition in the tumor microenvironment is a driver of cancer progression
More recent work, though, has complicated this picture. When researchers directly measured which cells inside tumors were consuming the most glucose, they found it was actually immune cells, specifically myeloid cells, that were the biggest consumers, not the cancer cells themselves. The cancer cells turned out to prefer glutamine over glucose in several mouse models. Blocking glutamine uptake caused all cell types to take up more glucose, suggesting that the sugar supply inside a tumor may not be as limited as originally thought.24Cancer Cell. Metabolic heterogeneity in the tumor microenvironment This matters because some experimental treatment strategies aim to cut off a tumor’s glucose supply. If the tumor is not actually as glucose-dependent as assumed, those strategies might need rethinking.
Why High Blood Sugar Worsens Cancer Outcomes
The relationship runs in both directions. Cancer affects blood sugar, and blood sugar affects cancer. Elevated glucose has been linked to worse outcomes in several cancer types. In colorectal cancer, patients with fasting blood glucose above 110 mg/dL had roughly twice the risk of dying compared to those with normal levels, and that association held even after adjusting for tumor stage and other known risk factors.25PubMed Central. High blood sugar levels significantly impact the prognosis of colorectal cancer patients through down-regulation of microRNA-16 by targeting Myb and VEGFR2 A similar pattern appears in lung cancer, where patients with fasting glucose at or above 126 mg/dL had about 69% higher risk of dying from any cause.26PubMed. Fasting blood glucose level and prognosis in non-small cell lung cancer (NSCLC) patients
The biological mechanisms behind this are not fully settled, but several leading explanations have emerged. High insulin levels promote cell growth signals through the insulin and IGF-1 pathways, which can accelerate tumor proliferation.27PubMed Central. Diabetes and cancer: Epidemiological and biological links Systemic inflammation and insulin resistance frequently travel together in cancer patients and are both independently associated with poorer prognosis.28PubMed Central. Prognostic importance of systemic inflammation and insulin resistance in patients with cancer: a prospective multicenter study The implication for patients and oncologists is practical: keeping blood sugar well controlled during cancer treatment may matter for outcomes, not just for comfort.
The Ketogenic Diet and Cancer
Given how much tumors depend on glucose, a natural question is whether restricting sugar intake could help fight cancer. The ketogenic diet, which sharply limits carbohydrates and forces the body to burn fat for fuel, has attracted attention as a possible adjunct to standard cancer treatment. The rationale is straightforward: if you lower the body’s circulating glucose and insulin, you might slow tumor growth while also making cancer cells more vulnerable to chemotherapy and radiation.
Preclinical studies and a limited number of clinical trials have shown some promise. The diet appears to be generally safe and well tolerated in cancer patients, and some studies suggest it can enhance the effects of standard treatments.29PubMed Central. Ketogenic diet in the treatment of cancer – Where do we stand? However, it is not a standalone therapy, and the clinical evidence is still early-stage. For people who are already losing weight from cachexia or struggling to eat because of treatment side effects, a restrictive diet could do more harm than good. Anyone considering dietary changes during cancer treatment should work closely with their medical team to weigh the potential benefits against the very real nutritional needs of a body fighting both cancer and the side effects of treatment.
Practical Monitoring for People Living With Cancer
Given how many mechanisms can push blood sugar around during cancer, routine glucose monitoring makes sense even for patients who have never had diabetes. A few situations warrant extra vigilance:
- New diabetes symptoms: If you are over 50 and develop unexplained diabetes or a rapid worsening of existing diabetes, it is worth mentioning this to your doctor as something that could occasionally signal pancreatic cancer, especially if accompanied by unintended weight loss or digestive changes.
- Starting steroids: Blood sugar often spikes within hours of a steroid dose. If you are receiving dexamethasone or prednisone as part of your treatment, ask your oncology team about monitoring, particularly if you already have borderline glucose levels.
- Targeted therapies: If your treatment plan includes a PI3K or AKT inhibitor, expect your team to check glucose frequently. Most elevations are mild and manageable, but some require medication adjustment or treatment interruption.
- Immunotherapy: While immunotherapy-induced diabetes is uncommon, its onset is often abrupt. Unusual thirst, frequent urination, or unexplained fatigue during immunotherapy should be flagged immediately.
- Advanced liver disease: Patients with extensive liver metastases may experience episodes of low blood sugar that worsen with poor nutrition. Frequent small meals and close glucose tracking become especially important in this setting.
Blood sugar management during cancer is rarely about a single cause and a single fix. It is about recognizing that the disease, the treatments, the stress response, and the body’s metabolic changes all converge on the same glucose-regulating systems. The patients who fare best tend to be the ones whose medical teams treat blood sugar as a vital sign worth watching throughout the cancer journey, not just as a side issue for the endocrinologist.