Sarah Rice BSC. (Hons), Mcoptom (UK), MHP, NNP
The role of the ketogenic diet in cancer treatment is a controversial issue that requires a sensitive and subtle discussion. Different metabolic phenotypes of tumor tissue and individual responses, along with heterogeneity between study types and dietary interventions, have made progress in this area a challenge.
Such a type of cancer that responds favorably to a ketogenic diet is glioblastoma (GBM). A recent document deserves special attention as it is the most comprehensive overview I have seen to date (1). A global team of researchers who experienced the Ketogenic diet and cancer research worked on this document to develop an extensive consensus treatment protocol that covers the mechanisms and biochemistry of cancer as mitochondrial metabolic metabolic disease, the projection of the protocols.
THE Duraj et al. The paper serves as a framework for a development based on evidence of observational and invasive studies that are critical to the progress of this area. In this work, they use the term ketogenic metabolic therapy (KMT) to reflect that this approach is not the same as an ad libitum isochecal ketogenic diet that can be used for other clinical conditions such as obesity or type 2 diabetes.
The concept of pulse type has its roots in a model of evolution of extinction, where, in this example, tumor cells can be considered compared to healthy cells (2). One “type” describes an environmental pressure, such as the loss of habitat, which favors a species (or cellular type) that is best able to adapt to change. An “pulse” event is short and focused, causing high mortality. In this context, in the most vulnerable type of cell. This concept in the treatment of cancer concerns the preferences of energy metabolism, which are used to increase the sensitivity of the tumor to therapeutic interventions. KMT creates an “type” environment by reducing the availability of preferred fuels for the type of GBM volume. Mitochondrial metabolic theory of cancer supports the theory of metabolic cancer of metabolism. In the damaged mitochondria of cancer cells, energy metabolism is impaired and the ATP synthesis through oxidative phosphorylation (Oxphos) gradually decreases, forcing a transition to the ATP composition through the fermentation road, which fails upwards as the Oxphos road fails. This fermentation route reflects the “survival state” as Oxphos is the preferred energy route.
Cancer cells, such as those in GBM, depend on the fermentation road, which uses fermentable fuels such as glucose and glutamine to produce energy. The microenvail of the tumor tends to have elevated levels of these substrates.
Ketogenic treatments show a promise due to the displacement of metabolism that occurs when individuals enter the ketosis. Tumor cells are less likely to use non -fermented fuel such as ketone, fatty acids and lactic. This decrease in preferred fuels can inhibit tumor growth. This is the ‘press’ item.
The use of ketogenic diets (the “type”) alongside other treatments such as drug treatments and radiation (“pulse”) can make the tumor more sensitive to these treatments, helping to reduce volume load. The presence of non -fermentable ketone bodies is easily used by healthy cells. In fact, metabolism of the ketone body offers additional durability and an advantage for normal cells over cancer cells. Through these mechanisms, the microenval of the tumor becomes less favorable, while healthy cells are more protected.
Individual nutritional needs, type of treatment, cancer stage and personal preference should guide the formulation of an ketogenic approach. The KMT may include different variations of a ketogenic diet, calorie restriction, fasting or combination.
Glucose-Ketone (GKI) is a biomarker that evaluates the adhesion and biological effects of ketogenic treatment and indicates the ratio of glucose to β-hydroxybutyry (ketones). This indicator, along with other measurements of metabolic and volume repulsions, allows ketogen intervention to be adapted for the best therapeutic effect. The proposed goals for GKI are <2.0, with the optimal target being close to 1.0. It is important to recognize the KMT should be personalized as clinically indicated and according to the needs and preferences of patients.
Key features of the KMT approach suggested by Duraj et al. include:
- Carbohydrates <20-50 g/day
- Fixed levels BG <5 mmol/L (90 mg/dl) (aims at lower levels feasible normal safe glucose and insulin levels)
- GKI ≤2.0 target, ideally ≤1.0
- Sufficient protein intake (initially 0.8 g/kg and adjust GKI: AV ~ 1.2 and 1.5 g/kg)
- Watch body mass and adjust the diet according to needs
- Adequate intake of micronutrients and vitamins
- Focus on dense foods of nutrients, e.g. eggs, beef, fatty fish and bypass
Support from an experienced professional and examining patient preferences are important factors for success. Other important lifestyle factors that need to be examined include stress exercise and management.
In conclusion, by focusing on energy metabolism, tumor cells can be actively at stake through ketogenic interventions that reduce the preferred fuel availability and therefore reduce the energy available for the growth and survival of the tumor.
Combined with standard treatments, KMT’s synergy with these other interventions has the ability to improve the effects of cancer treatment.
This article represents the collective experience of the leading experts in the KMT application for GBM and the detailed framework for further research will bring hope to bring the required clarity in the field. This document requires reading for those interested in ketogenic therapies as additional cancer management strategies.
The food network reference resource has an extensive list where you can read more about the application of the therapeutic restraint of carbohydrates (TCR) as a complementary treatment for cancer management (in the “Metabolic Ingredient” department). Look at our training options to find out how to support others using this approach. If you are particularly interesting, education “Cancer: A Metabolic Disease” is a comprehensive program that includes teachers who were colleagues of the document discussed in this article.
- Duraj, T. et al. (2024) “Proposal of clinical research for ketogenic metabolic treatment in glioblastoma”, BMC drug22 (1), p. 578. Available in: https://doi.org/10.1186/s12916-024-03775-4.
- Seyfried, tn et al. (2017) ‘Press-Pulse: a new therapeutic strategy for metabolic cancer management’, Diet and metabolism14 (1), p. 19 Available in: https://doi.org/10.1186/s12986-017-0178-2.
