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The Benefits of Fasting During Cancer Treatment: A Powerful Metabolic Strategy

  • Writer: Dr. Lena Suhaila
    Dr. Lena Suhaila
  • Mar 17, 2025
  • 6 min read

Updated: Mar 30


Fasting During Cancer Treatment: What the Research Actually Shows




By Dr. Lena Suhaila, ND, FABNO


Most people going through chemotherapy are told to eat as much as they can. Maintain your weight. Keep your strength up. The intention is good. But it does not account for what we now know about how fasting changes the biology of cancer treatment in ways that can meaningfully shift your outcomes. This is not a fringe idea. It is an evidence-based metabolic strategy that has been studied in randomized controlled trials, peer-reviewed, and published in journals like Nature Communications and Cancer Research. If you are in active treatment and you have never heard this discussed, that is worth sitting with.

Let me walk you through what the science actually shows.


The Core Mechanism: Differential Stress Resistance


The foundational research here comes from the laboratory of Valter Longo, PhD at the University of Southern California, and it centers on a phenomenon called Differential Stress Resistance (DSR). The premise is elegantly simple once you understand it.


When you fast, your healthy cells receive a signal to slow down. They reduce metabolic activity, downregulate growth pathways, and shift into a protective, low-resource state. This is an ancient adaptive response, conserved across species from yeast to mammals. Your cells know how to do this. What cancer cells cannot do is follow.


Most cancer cells carry mutations in growth-signaling oncogenes, including Ras, Akt, and mTOR. These mutations keep cancer cells locked in a constitutive grow-or-die mode. They cannot downregulate. They cannot shift into protection. So when you fast before and during chemotherapy, you create a divergence: your healthy cells become more resilient to the cytotoxic insult, while cancer cells remain fully exposed to it. This has been demonstrated in animal models across a wide range of tumor types and chemotherapy agents, including doxorubicin, cyclophosphamide, and etoposide (Raffaghello et al., 2008).

Does this translate to humans? Increasingly, yes!


The Role of IGF-1, Glucose, and the Warburg Effect


Part of what makes fasting so metabolically interesting in the context of cancer is the cascade of changes it triggers in your blood chemistry. Research shows that 72 hours of fasting reduces circulating glucose by approximately 41% and drops IGF-1 levels by as much as 70%, while the IGF-1 inhibitor IGFBP-1 increases more than elevenfold (Lee et al., 2010).


This matters because cancer cells are overwhelmingly dependent on glucose and IGF-1 for fuel and growth signaling. You may have heard of the Warburg effect, the well-documented phenomenon by which cancer cells preferentially rely on glycolysis for energy production even when oxygen is abundant. This metabolic preference is a vulnerability. When you fast and glucose availability drops, cancer cells lose their primary energy substrate. At the same time, fasting shifts your body toward ketone body production, and unlike glucose, ketones are not efficiently used by most cancer cells. Your healthy tissues, which retain metabolic flexibility, adapt. Cancer cells, which do not, become increasingly stressed and sensitized to treatment.


What the Clinical Trials Show


The most rigorous human data comes from the DIRECT trial, a randomized phase II study published in Nature Communications in 2020 (de Groot et al.). One hundred thirty-one patients with HER2-negative stage II and III breast cancer were randomized to receive either a fasting-mimicking diet or their regular diet for three days before and during neoadjuvant chemotherapy. The fasting group showed significantly higher rates of radiological response. In per-protocol analysis, pathological response showing 90 to 100% tumor cell loss was more than four times more likely in the fasting group. The fasting group also showed significantly reduced DNA damage in T-lymphocytes during treatment, meaning their immune cells were measurably better protected.


A 2024 systematic review published in BRASPEN Journal analyzed seven randomized controlled trials evaluating fasting or fasting-mimicking diets during chemotherapy (Ribeiro et al.). The findings were clinically meaningful. Stomatitis, nausea, vomiting, diarrhea, mucositis, weakness, and chemotherapy delay were all significantly reduced in fasting patients. No grade V adverse events were observed across any of the trials. A separate 2023 narrative review in Therapeutic Advances in Medical Oncology identified nine active clinical trials currently enrolling across breast, lung, ovarian, prostate, and colorectal cancer, reflecting just how seriously the oncology research community is now taking this question (Kikomeko et al., 2023).


Immune Recovery and the Hematopoietic Argument


There is one more mechanism I want you to know about, because it matters beyond the infusion day. Research from Cheng et al. (2014) published in Cell Stem Cell showed that prolonged fasting reduces IGF-1 and PKA activity in ways that promote hematopoietic stem cell regeneration and reverse chemotherapy-induced immunosuppression. What this means in practice is that fasting may not only reduce damage during a cycle of treatment but actively support immune system recovery between cycles. For patients who are watching their white cell counts, experiencing repeated delays, or trying to hold together immune resilience across a long treatment course, this is not a trivial finding.

Chemotherapy does not discriminate between the immune cells it damages and the cancer cells it targets. The immune system is collateral damage in most cytotoxic regimens. Anything that supports its regeneration between cycles belongs in the conversation.


How I Use This Protocol in Clinical Practice


In my integrative oncology practice, I recommend fasting from 48 hours before chemotherapy through 24 hours after the infusion. During this window, I ask patients to keep calories at 500 or under, focused on low-carbohydrate, mineral-rich broths. This is the window where the biology is most relevant, and most of the clinical data clusters around this timing.


Bone broth is an excellent option during this period. Beyond its role in the fasting protocol, it provides collagen, glycine, proline, and bioavailable minerals that support gut lining integrity, which matters significantly during chemotherapy when the gastrointestinal epithelium is under direct cytotoxic assault. A healing vegetable broth built around shiitake mushrooms, garlic, ginger, fresh turmeric, and parsley addresses the same goals through a plant-based lens. Shiitake beta-glucans have documented natural killer cell-activating properties. Curcumin, the active compound in turmeric, is one of the best-studied NF-kB inhibitors we have. These are not incidental additions to a broth recipe. They are deliberate, evidence-informed choices.


If you experience light-headedness during the fast, a pinch of Himalayan sea salt in your water will usually resolve it within minutes by restoring mineral balance.

This protocol is not appropriate for everyone. Patients with cachexia, a BMI below 18.5, insulin-dependent diabetes, or a history of eating disorders need individual assessment before implementing any fasting protocol. And it should always be coordinated with your oncology team.


The Bigger Picture


The question I want you to sit with is this: if the research shows that short-term fasting before chemotherapy can reduce side effects, protect your immune cells, lower treatment-related DNA damage, and in at least one randomized trial produce significantly better pathological tumor response, why is it not part of the standard conversation?


Part of the answer is time. The research is compelling but still maturing. Larger trials are underway. Part of the answer is the deeply ingrained clinical habit of prioritizing caloric intake during cancer treatment, which made sense before this mechanism was understood and still applies to patients with nutritional compromise, but does not account for the metabolic biology of a well-nourished patient in active treatment.


This is the work of integrative oncology: to look at the full picture, to hold the clinical nuance, and to offer you tools that conventional care has not yet integrated. Fasting during chemotherapy is one of those tools. Used appropriately and supported well, it is one of the most powerful metabolic levers you have access to during treatment.


Ready to explore how fasting and metabolic strategy could be integrated into your cancer care? Reach out here.


References

Raffaghello L, Lee C, Safdie FM, Wei M, Madia F, Bianchi G, Longo VD. Starvation-dependent differential stress resistance protects normal but not cancer cells against high-dose chemotherapy. PNAS. 2008;105(24):8215-8220. https://doi.org/10.1073/pnas.0708100105

Lee C, Safdie FM, Raffaghello L, Wei M, Madia F, Parrella E, Hwang D, Cohen P, Bianchi G, Longo VD. 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

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

Ribeiro RP, et al. Fasting or fasting mimicking diet as a strategy for managing adverse effects in patients undergoing chemotherapy. BRASPEN Journal. 2024;39(2):e202439117. https://doi.org/10.37111/braspenj.2024.39.1.17

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

Cheng CW, Adams GB, Perin L, et al. Prolonged fasting reduces IGF-1/PKA to promote hematopoietic stem cell-based regeneration and reverse immunosuppression. Cell Stem Cell. 2014;14(6):810-823. https://doi.org/10.1016/j.stem.2014.04.014

 
 

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