Updated: Nov 8, 2022
Cancer is a complex disease that involves the uncontrolled replication of cells that have a resistance to normal cell death and the ability to spread to other parts of the body. These rapidly multiplying cells can clump together and form tumours. The most common types of cancers are breast, lung, colon and prostate.
The metabolic requirements of proliferating cells, including cancer cells, differ from those of non-proliferating cells. Rapidly multiplying cells must get enough fuels to meet the demands of replication. As early as the 1920’s it has been known that cancer cells have an increased affinity for using glucose as a fuel source and the rate of use is thought to be 10-15 times that of normal cells.
In fact, most cells in our body prefer to use glucose (from the carbohydrates we eat) as a fuel for energy. However, when carbohydrates are restricted, normal cells shift from burning predominantly glucose to burning fat; this is call ketosis. For humans, ketosis is a normal physiological state that occurs when food intake is limited, such as in fasting. In ketosis, ketones are produced from the breakdown of fats in the liver. 
This adaptive ability our body to shift between burning carbohydrates and burning fat help us to survive when food resources are scarce. Unlike normal healthy cells, many malignant cells are unable metabolise ketones for energy.
Glucose consumed through the diet stimulates cells in the pancreas to release the hormone insulin. Insulin in turn signals the liver to produce insulin-like growth factors 1 and 2 (IGF-1 and 2). A function of IGF-1 is to promote cell growth and proliferation, and in cancer, it can lead to the overgrowth of tumour cells by stimulating hyperproliferation.  Insulin-like growth factors can also inhibit normal cell death (apoptosis) and this makes them more resistant to standard treatments.
In light of this, the ketogenic diet has recently been used as an adjunct therapy in cancer. These clinical studies have indeed shown beneficial outcomes in a variety of cancers including limiting cancer growth and improving quality of life.   A Ketogenic diet is very low in carbohydrates, high in fat, and moderate in protein. Providing a fat-rich, low-carbohydrate diet reduces the amount of glucose available to the tumour cells. With the decrease of glucose from the diet there is less insulin signalling and less IGF-1 is created, and this may account for the beneficial effects found in these trials. By reducing the blood levels of IGF-1 there is the possibility that cancer cells may also become more sensitive to standard treatments.
Simply addressing glucose metabolism, however, may not provide us with the whole picture. Whilst cancer cells utilise glucose at a very high rate, when carbohydrates are restricted their survival often depends on a having ready supply of certain amino acids.  Key amino acids include glutamine, asparagine, serine, methionine and the branched-chain amino acids.    
Amino acids play a number of important roles in the initiation, growth and metastasis of tumours. Cancer cells require amino acid for not only for energy but many of the mechanisms that promote their aberrant proliferation and survival. For example, they provide building blocks for the synthesis of proteins and other compounds needed for DNA replication, cell division, and tumour growth.  Animal protein (from meat egg, fish and dairy) is richer in the amino acids that upregulate these mechanisms than plant foods.
The concept of ‘metabolic fasting’ for cancer, explained in more detail in my book Nutritious, provides a dietary approach that utilizes the potential benefits of a ketogenic diet while at the same time limiting the supply of the amino acids from the diet to make conditions less favourable for cancer to grow or spread. Conventional fasting (calorie restriction) has been shown to lead to improved chemotherapy response rates.   The approach in Nutritious does not restrict calories but takes advantage of the inability of many cancer cells to get energy from ketones while also limiting the ready supply of alternative fuels. It therefore may help to improve conventional cancer therapy outcomes and survival while still providing balanced energy and nutrition to normal cells to support your health.
 Puchalska P, Crawford PA.Multi-dimensional roles of ketone bodies in fuel metabolism, signaling, and therapeutics. Cell metabolism. 2017 Feb 7; 25(2): 262-284 PMC [article] PMCID: PMC5313038, PMID: 28178565, DOI: 10.1016/j.cmet.2016.12.022  Hopkins BD, Goncalves MD, Cantley LC. Insulin-PI3K signalling: an evolutionarily insulated metabolic driver of cancer. Nat Rev Endocrinol. 2020 May;16(5):276-283. doi: 10.1038/s41574-020-0329-9. Epub 2020 Mar 3. PMID: 32127696; PMCID: PMC7286536.  Yang L, Tan Z, Li Y, Zhang X, Wu Y, Xu B, Wang M. Insulin-like growth factor 1 promotes proliferation and invasion of papillary thyroid cancer through the STAT3 pathway. J Clin Lab Anal. 2020 Dec;34(12):e23531. doi: 10.1002/jcla.23531. Epub 2020 Aug 26. PMID: 32851683; PMCID: PMC7755808.  Hua H, Kong Q, Yin J, Zhang J, Jiang Y. Insulin-like growth factor receptor signaling in tumorigenesis and drug resistance: a challenge for cancer therapy. J Hematol Oncol. 2020 Jun 3;13(1):64. doi: 10.1186/s13045-020-00904-3. PMID: 32493414; PMCID: PMC7268628.  Branca JJ, Pacini S, Ruggiero M. Effects of Pre-surgical Vitamin D Supplementation and Ketogenic Diet in a Patient with Recurrent Breast Cancer. Anticancer Res. 2015 Oct;35(10):5525-32. PMID: 26408720.  Furukawa K, Shigematus K, Iwase Y, Mikami W, Hoshi H, Nishiyama T, Ohtuka A, Abe H. Clinical effects of one year of chemotherapy with a modified medium-chain triglyceride ketogenic diet on the recurrence of stage IV colon cancer. Journal of Clinical Oncology 2018 36:15_suppl, e15709-e15709  Plotti F, Terranova C, Luvero D, Bartolone M, Messina G, Feole L, Cianci S, Scaletta G, Marchetti C, Di Donato V, Fagotti A, Scambia G, Benedetti Panici P, Angioli R. Diet and Chemotherapy: The Effects of Fasting and Ketogenic Diet on Cancer Treatment. Chemotherapy. 2020;65(3-4):77-84. doi: 10.1159/000510839. Epub 2020 Nov 16. PMID: 33197913.  Lieu, E.L., Nguyen, T., Rhyne, S. et al. Amino acids in cancer. Exp Mol Med 52, 15–30 (2020). https://doi.org/10.1038/s12276-020-0375-3  Vettore, L., Westbrook, R.L. & Tennant, D.A. New aspects of amino acid metabolism in cancer. Br J Cancer 122, 150–156 (2020). https://doi.org/10.1038/s41416-019-0620-5  Labuschagne CF, van den Broek NJ, Mackay GM, Vousden KH, Maddocks OD. Serine, but not glycine, supports one-carbon metabolism and proliferation of cancer cells. Cell Rep. 2014 May 22;7(4):1248-58. doi:  Simon R. V. Knott, Elvin Wagenblast, Showkhin Khan, Sun Y. Kim, Mar Soto, Michel Wagner, Marc-Olivier Turgeon, Lisa Fish, Nicolas Erard, Annika L. Gable, Ashley R. Maceli, Steffen Dickopf, Evangelia K. Papachristou, Clive S. D’Santos, Lisa A. Carey, John E. Wilkinson, J. Chuck Harrell, Charles M. Perou, Hani Goodarzi, George Poulogiannis, Gregory J. Hannon. Asparagine bioavailability governs metastasis in a model of breast cancer. Nature, 2018; DOI: 10.1038/nature25465.  Sivanand S, Vander Heiden MG. Emerging Roles for Branched-Chain Amino Acid Metabolism in Cancer. Cancer Cell. 2020 Feb 10;37(2):147-156. doi: 10.1016/j.ccell.2019.12.011. PMID: 32049045; PMCID: PMC7082774.  Zhang J, Pavlova NN, Thompson CB. Cancer cell metabolism: the essential role of the nonessential amino acid, glutamine. EMBO J. 2017 May 15;36(10):1302-1315. doi: 10.15252/embj.201696151. Epub 2017 Apr 18. PMID: 28420743; PMCID: PMC5430235.  Locasale JW. Serine, glycine and one-carbon units: cancer metabolism in full circle. Nat Rev Cancer. 2013 Aug;13(8):572-83. doi: 10.1038/nrc3557. Epub 2013 Jul 4. PMID: 23822983; PMCID: PMC3806315.  de Groot, S., Pijl, H., van der Hoeven, J., & Kroep, J. R. (2019). Effects of short-term fasting on cancer treatment. Journal of experimental & clinical cancer research : CR, 38(1), 209. https://doi.org/10.1186/s13046-019-1189-9  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. Proc Natl Acad Sci U S A. 2008 Jun 17;105(24):8215-20. doi: 10.1073/pnas.0708100105. Epub 2008 Mar 31. PMID: 18378900; PMCID: PMC2448817.