Cancer and Metabolic Health


Cancer risk and progression are strongly linked to insulin resistance, impaired mitochondrial function, and metabolic dysfunction.

Evidence from review articles, clinical trials, and case reports suggests that metabolic therapies, in particular the ketogenic diet and calorie restriction, can disrupt the energy pathways that cancer cells depend on. Cancer cells rely almost exclusively on glucose and glutamine for fuel, a vulnerability that can be targeted through dietary and metabolic interventions.

  • reducing tumour glucose availability
  • lowering insulin and insulin-like growth factor signalling
  • inducing ketosis to starve cancer cells of their primary fuel
  • reducing systemic inflammation
  • improving quality of life during conventional treatment.


While metabolic therapy is not a replacement for conventional oncology care, growing evidence supports its role as a complementary approach that may improve outcomes when combined with standard treatment.


Cancer as a Metabolic Disease

A growing body of peer-reviewed research supports the view that cancer is, at its core, a metabolic disease. Rather than arising solely from genetic mutations, cancer is increasingly understood to originate from impaired mitochondrial function and disrupted cellular energy metabolism. This perspective, first proposed by Otto Warburg and now supported by contemporary researchers including Professor Thomas Seyfried, has significant implications for how cancer may be prevented and treated.

The evidence presented on this page draws on review articles, randomised controlled trials, clinical studies, and case reports to highlight the role of metabolic therapies, particularly the ketogenic diet and calorie restriction, as complementary approaches in cancer care.

Key messages from clinical and research evidence

  • Cancer is primarily a metabolic disease involving disturbances in mitochondrial energy production. Genomic instability and other hallmarks of cancer are considered downstream consequences of this initial metabolic disruption, not the primary cause.
  • Cancer cells rely almost exclusively on glucose and glutamine for energy, a phenomenon known as the Warburg effect. This metabolic dependency creates a targetable vulnerability that dietary and pharmacological interventions can exploit.
  • The ketogenic diet creates a metabolic environment that is unfavourable for tumour growth by reducing circulating glucose and insulin, elevating ketone bodies, and shifting the body toward fat-based metabolism that healthy cells can use but most cancer cells cannot.
  • The Press-Pulse strategy combines a chronic dietary “press” with acute therapeutic “pulses” such as fasting or chemotherapy, to maximise metabolic stress on tumour cells while protecting normal tissue, with the goal of improving outcomes and reducing toxicity.
  • Insulin resistance and elevated insulin signalling promote tumour growth and progression. Reducing insulin levels through carbohydrate restriction may therefore reduce a key driver of cancer cell proliferation.
  • The Glucose Ketone Index (GKI) is a practical monitoring tool that allows patients and clinicians to track the depth of the metabolic state achieved during ketogenic therapy, with lower values associated with greater therapeutic effect.
  • Clinical evidence supports ketogenic metabolic therapy as a complementary intervention in cancers including glioblastoma and breast cancer, with studies demonstrating improvements in tumour markers, quality of life, and in some cases survival outcomes.
  • Orthomolecular agents, including high-dose vitamin C, show cytotoxic effects on cancer cells, inhibit glycolysis and glutamine synthesis, and may target cancer stem cells, offering additional avenues for metabolic combination therapy.

Together, these findings support the position that metabolic therapy, when used alongside conventional oncology care, may improve outcomes by targeting the fundamental energy vulnerabilities of cancer cells.


Cancer: combining traditional and metabolic treatment paradigms

This presentation is from Low Carb Down Under 2023.

Dr. Alex Petrushevski graduated from the University of Tasmania in 2008, attaining Honours in the MBBS. He has worked in various teaching hospitals across two states, including several years within Sydney Cancer services, and has had his research published in an international journal. His postgraduate qualifications include the Fellowship of the Royal Australian College of General Practitioners and the Diploma of Child Health from the University of Sydney.

He currently works in general practice and within Sydney Low Carb Specialists. He is passionate about preventative health, improving the lifestyle of his patients, and treating chronic disease without medication where possible.

Having witnessed the profound benefits that low carbohydrate nutrition has provided for many of his patients, Dr. Petrushevski is committed to sharing this evidence-based approach with a wider audience. In this presentation, he explores how the metabolic theory of cancer can be practically applied alongside conventional oncology treatment, including the use of the ketogenic diet, fasting, and the Glucose Ketone Index as a monitoring tool.


Key evidence

Review article examining cancer as a metabolic disease and implications for novel therapeutics. 
Seyfried et al., Carcinogenesis (2013)


Cancer is primarily a metabolic disease involving disturbances in energy production through respiration and fermentation. Genomic instability and other hallmarks of cancer are considered downstream consequences of initial disruptions to cellular energy metabolism. Cancer growth and progression can be managed by transitioning tumour cells away from fermentable metabolites such as glucose and glutamine toward respiratory metabolites such as ketone bodies.

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Review article on targeting the mitochondrial-stem cell connection in cancer treatment using a hybrid orthomolecular protocol.
Baghli et al., Journal of Orthomolecular Medicine (2024)


This review introduces a hybrid orthomolecular protocol based on the mitochondrial-stem cell connection theory, which proposes that cancer originates from chronic impairment of oxidative phosphorylation in stem cells. The protocol combines orthomolecular agents, repurposed drugs, dietary change, and lifestyle interventions to enhance mitochondrial function, inhibit cancer cell fuels (glucose and glutamine), and target cancer stem cells. High-dose vitamin C is highlighted for its cytotoxic effects on cancer cells and its ability to inhibit glycolysis and glutamine synthesis.

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Review article on molecular mechanisms for ketone body metabolism, signalling functions, and therapeutic potential in cancer.
Hwang et al., Nutrients (2022)


Ketone bodies serve as alternative energy sources and play important signalling roles in regulating inflammation and oxidative stress. Targeting cancer cell metabolism through dietary interventions such as fasting and the ketogenic diet shows beneficial effects in cancer therapy. This review explores the molecular mechanisms by which ketone body metabolism may be leveraged as a therapeutic strategy in oncology.

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Review article on the ketogenic diet in cancer prevention and therapy: molecular targets and therapeutic opportunities.
Talib et al., Current Issues in Molecular Biology (2021)


The ketogenic diet has emerged as a metabolic therapy in cancer treatment, targeting cancer cell metabolism by reducing the energy supply available to tumour cells and thereby inhibiting tumour growth. This review highlights the key mechanisms underlying the antitumour effects of the ketogenic diet and explores its potential as an adjuvant in combination cancer therapies.

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Randomised controlled trial evaluating the effects of ketogenic metabolic therapy in patients with breast cancer.
Khodabakhshi et al., Clinical Nutrition (2021)


Ketogenic metabolic therapy in breast cancer patients significantly decreased tumour necrosis factor-alpha and insulin levels while increasing the anti-inflammatory marker interleukin-10. The ketogenic diet led to a reduction in tumour size and downstaging in patients with locally advanced disease. These findings support the role of ketogenic metabolic therapy as a complementary intervention alongside conventional breast cancer treatment.

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Clinical study on the successful application of dietary ketogenic metabolic therapy in patients with glioblastoma.
Kiryttopoulos et al., Frontiers in Nutrition (2025)


Among 18 patients with glioblastoma, those who adhered to the ketogenic diet for more than six months demonstrated a survival rate of 66.7%, compared with 8.3% in non-adherent patients, a statistically significant difference. These findings suggest that dietary ketogenic metabolic therapy may meaningfully improve survival outcomes in patients with this aggressive brain cancer.

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Case reports

Case report: ketogenic metabolic therapy in conjunction with standard treatment for glioblastoma.
Phillips et al., Oncology Letters (2024)


A 64-year-old woman with glioblastoma underwent standard treatment combined with an intensive, multimodal ketogenic metabolic therapy program. During the first two years of treatment, she maintained a low Glucose Ketone Index, which coincided with complete clinical improvement, a healthy body mass index, a high quality of life, and no visible tumour progression on imaging. This case highlights the potential therapeutic benefit of achieving and sustaining a low Glucose Ketone Index as part of a combined metabolic and conventional treatment approach.

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Case report: ketogenic metabolic therapy, without chemotherapy or radiation, for the long-term management of IDH1-mutant glioblastoma, an 80-month follow-up.
Seyfried et al., Frontiers in Nutrition (2021)


A patient with IDH1-mutant glioblastoma remained alive with good quality of life 80 months after diagnosis, with only slow tumour progression, despite declining standard chemotherapy and radiotherapy. Management consisted solely of ketogenic metabolic therapy and surgical debulking. The findings suggest a potential therapeutic synergy between ketogenic metabolic therapy and the IDH1 mutation, and indicate that this non-toxic nutritional intervention may support long-term management of glioblastoma.

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