Can Fasting Improve Chemotherapy for Ovarian Cancer?

By. Dr. Lena Suhaila, ND, FABNO

In a 2026 randomized trial, women with advanced ovarian cancer who fasted briefly around each chemotherapy infusion had lower insulin, a stronger response to chemotherapy, and a longer time before their cancer progressed, compared with women who ate normally. It's a small, single-center study, so these are early findings. They're also consistent and striking enough to take seriously, and they point straight at insulin and the metabolic environment your body brings to treatment.

If you're preparing for chemotherapy for ovarian cancer, you've probably gotten detailed instructions about your infusions and almost nothing about what to eat around them. It's a question that rarely comes up in the appointment, and the answer turns out to be more interesting than just keeping your strength up.

How the trial was designed

Researchers in Rome enrolled women with newly diagnosed, advanced high-grade serous ovarian cancer who weren't candidates for surgery first and needed neoadjuvant chemotherapy. To take part, women needed a stable body weight, and the trial excluded anyone with diabetes, malnutrition, or a history of eating disorders. Everyone got the same standard carboplatin and paclitaxel. From there, the women were split at random into two groups: one fasted around each chemotherapy cycle, the other ate normally with no changes.

The fasting was short and specific. Those women ate almost nothing, capped at 350 calories a day, from 36 hours before each infusion until 24 hours after the cycle finished. Water, herbal tea, vegetable juice, and a little light broth were allowed. Between cycles, they went back to eating normally. Thirty-six women finished three cycles and were included in the analysis, eighteen in each group.

The insulin finding came first

The study was built around one question: what happens to insulin. After three cycles, insulin went up in the free-diet group by nearly 10 µIU/mL. In the fasting group, it edged down a little. That gap was statistically significant, and it was the primary result the trial was designed to find.

Insulin does more than manage your blood sugar. It works as a growth signal too. When insulin locks onto its receptor, and the closely related one for IGF-1, it switches on the PI3K-AKT-mTOR pathway, the cascade that tells a cell to grow, divide, and hold off on the signals that would normally retire a worn-out cell (Pollak, 2008). Many tumor cells carry insulin receptors of their own. Circulating insulin reaches them the way it reaches your healthy cells, and on a tumor studded with those receptors, extra insulin acts like Miracle-Gro (Pollak, 2012; Gallagher and LeRoith, 2020).

This is why I pay attention to where insulin sits, not just whether a lab calls it normal. I want to see a fasting insulin around 2 to 3 µIU/mL. Most people land far above that without ever being told, because the standard lab range runs all the way up to about 25. Someone sitting at the top of that range reads as normal on paper while already deep into insulin resistance, and once fasting insulin climbs past 10, that resistance is well underway.

Chemotherapy adds a twist of its own. A lot of regimens, including the taxane-based ones in this trial, are given alongside corticosteroids like dexamethasone to prevent reactions and nausea, and both those steroids and the cortisol your body releases under stress push blood sugar and insulin up. So even while you work to bring insulin down, parts of treatment and ordinary life are pushing it the other way, which is exactly why the metabolic side of care deserves real attention.

One more detail stood out to me. The women whose insulin climbed the most were also the ones who didn't make it to interval surgery. The metabolism and the outcome moved together.

Response and survival signals

By the time of surgery, the fasting group showed a near-complete or complete response to chemotherapy in about 59% of cases, against roughly 18% in the free-diet group. Median progression-free survival came in at 38 months with fasting and 24 months without.

These are strong results for a first trial. A near-complete response in well over half the fasting group, compared with fewer than one in five on the free diet, is a wide gap, and progression-free survival moved in the same direction. The study is small and the follow-up is still young, so the survival figure will firm up over time. And the signal held across every measure they looked at, which is why this work is heading into larger trials.

The women tolerated the fasting well, with no increase in chemotherapy side effects, and their blood showed fewer of the immune cells that blunt a treatment response. For a short fast, it was an easy thing to live with.

How I think about strengthening the terrain

My work centers on strengthening the terrain, the internal environment your whole body brings to treatment. My attention goes to the conditions the tumor grew in, and to changing them so it's less likely to keep growing. Insulin and IGF-1 are part of those conditions, and changing what, how, and when you eat is one of the most direct ways we have to shift them. Fasting is one form of that.

The science here isn't new, we've understood the basic mechanism for years. When you fast, your healthy cells drop into a protected, low-energy state. Cancer cells, which are wired to keep eating and dividing, can't downshift the same way, and that difference leaves them more exposed. Researchers call it differential stress resistance, and it's why fasting cycles have made a range of cancers more sensitive to chemotherapy in lab studies while protecting normal tissue (Raffaghello et al., 2008; Lee et al., 2012). A drop in IGF-1 looks like a big part of why (Lee et al., 2010).

The strongest human evidence so far is in breast cancer. In the randomized DIRECT trial, a fasting-mimicking diet alongside neoadjuvant chemotherapy improved how well tumors responded on imaging and under the microscope (de Groot et al., 2020). There's also preclinical work showing fasting can change the immune environment around a tumor and make immunotherapy work better, though that's still in animals for now (Cortellino et al., 2022). This ovarian study is one more early human piece, and it points the same way as the rest.

The ketogenic arm, and why diet in cancer is never one-size-fits-all

The trial started out with a third group on a ketogenic diet. That arm got shut down early. Part of it was that the women struggled to stick with it, and part of it was preclinical data hinting that, in this specific advanced ovarian setting, keto might not work the way it does in other situations.

It's a reminder that metabolic strategy in cancer depends on the person and the disease in front of you. There's no single move that fits everyone. What helped these women was bringing insulin and IGF-1 down through brief, timed fasting. There are other ways to reach the same goal, and the right one for you depends on your cancer, your treatment, your weight, your nutrition, and the rest of your clinical picture. Something that helps one person can set another back, which is why this works best when it's matched to your own body and circumstances.

Why your team may be wary of fasting

If you raise fasting with your oncologist, your nurse, or your family, there's a fair chance you'll meet hesitation, and sometimes a flat no. It helps to understand where that comes from, because most of it isn't about this research.

Oncology has spent decades, for good reason, worried about weight loss. Cancer and its treatment can waste the body, and a patient who is losing weight and muscle is in real danger. So the instinct to keep calories up and never skip a meal runs deep in cancer care. That instinct protects the person who is depleted, and it tends to get applied to everyone, including the well-nourished patient who could safely do a short fast around chemotherapy. That's where it stops fitting the evidence.

There's also a lot of fear around food that has nothing to do with biology. Feeding someone is how we care for them. When a daughter or a partner can't put a plate in front of you, they can feel like they're failing you, and that worry often comes out as resistance. Sometimes the clinician carries a quieter version of the same fear. And much of what people still believe about fasting and cancer is simply old, formed before the differential stress resistance research and the human trials that followed it.

The caution makes sense for the patient it was built for. It falls short when it gets applied to everyone, no matter how well-nourished and steady someone is. The data is consistent enough now that fasting deserves a real conversation about whether it fits you.

What this means for you

A brief fast around chemotherapy is a gentle, manageable thing for most people, not something to fear. The research backs up taking this seriously. The metabolic environment your treatment works in can change, and it's something you can take an active hand in. If you want the fuller picture of how fasting and chemotherapy fit together across different cancers, I've written more about that here.

And if you want to really understand the ground your cancer is growing in, and bring that understanding into your treatment decisions, that's the kind of work I do with patients. You can work with me here.

References

1. Marchetti C, et al. Short-term fasting compared to free diet in ovarian cancer. 2026 ASCO Annual Meeting; Abstract 5517. Presented May 30, 2026.

2. de Groot S, Lugtenberg RT, Cohen D, et al. Fasting mimicking diet as an adjunct to neoadjuvant chemotherapy for breast cancer in the multicentre randomized phase 2 DIRECT trial. Nature Communications. 2020;11:3083. https://doi.org/10.1038/s41467-020-16138-3

3. Lee C, Raffaghello L, Brandhorst S, et al. Fasting cycles retard growth of tumors and sensitize a range of cancer cell types to chemotherapy. Science Translational Medicine. 2012;4(124):124ra27. https://doi.org/10.1126/scitranslmed.3003293

4. Raffaghello L, Lee C, Safdie FM, et al. Starvation-dependent differential stress resistance protects normal but not cancer cells against high-dose chemotherapy. Proceedings of the National Academy of Sciences. 2008;105(24):8215-8220. https://doi.org/10.1073/pnas.0708100105

5. Lee C, Safdie FM, Raffaghello L, et al. Reduced levels of IGF-I mediate differential protection of normal and cancer cells in response to fasting and improve chemotherapeutic index. Cancer Research. 2010;70(4):1564-1572. https://doi.org/10.1158/0008-5472.CAN-09-3228

6. 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

7. Pollak M. The insulin and insulin-like growth factor receptor family in neoplasia: an update. Nature Reviews Cancer. 2012;12(3):159-169. https://doi.org/10.1038/nrc3215

8. Gallagher EJ, LeRoith D. Hyperinsulinaemia in cancer. Nature Reviews Cancer. 2020;20(11):629-644. https://doi.org/10.1038/s41568-020-0295-5

9. Cortellino S, Raveane A, Chiodoni C, et al. Fasting renders immunotherapy effective against low-immunogenic breast cancer while reducing side effects. Cell Reports. 2022;40(8):111256. https://doi.org/10.1016/j.celrep.2022.111256

10. Kikomeko J, Schutte T, van Velzen MJM, et al. Short-term fasting and fasting mimicking diets combined with chemotherapy: a narrative review. Therapeutic Advances in Medical Oncology. 2023;15:17588359231161418. https://doi.org/10.1177/17588359231161418