Suggesting that people fast or starve themselves to kill a tumor has been the domain of dubious and exaggerated claims over the years, and that is not the suggestion now. In recent trials, metabolic pathways have been targeted though various approaches to changing what people eat. Some research has involved minimizing sugar intake. Indeed, some cancer cells metabolize glucose at higher than normal levels (to support the process of aerobic glycolysis), and depleting their access to sugar can slow growth.
Read: Preventing cancer through good food and exercise
Last year, Siddhartha Mukherjee, the Columbia University researcher and author of The Emperor of All Maladies, and his colleagues found that at least one particular chemotherapy drug can be made more effective by combining its use with eating a low-sugar, protein-and-fat-heavy “ketogenic” diet. In a paper in Nature, the researchers suggest that the effect was related to decreasing the levels of insulin that the pancreas releases into the blood in response to eating.
Around the same time, an international team of researchers concluded in the journal Science Signaling that “only some cancer cells are acutely sensitive to glucose withdrawal, and the underlying mechanism of this selective sensitivity is unclear.” In other words, a low-sugar diet could help combat some cancers, but it’s certainly not as simple as Cancers eat sugar, so low sugar stops cancer.
While the sugar-and-insulin angle has shown promise, more of the research has focused on dietary protein—or, specifically, individual amino acids that make up that protein. Studies have shown that the restriction of the amino acids serine and glycine can modulate cancer outcomes. According to a 2018 study in Nature, the chemotherapy drug methotrexate is affected by the amino acid histidine. Another, asparagine, is involved in the progression of breast cancer metastasis.
The most interest has gone to methionine, which is found in high levels in eggs and red meat. In 2018, a review of existing evidence from the Rutgers Cancer Institute of New Jersey deemed restricting methionine “a promising anti-tumor strategy.” That promise has also shown itself in brain tumors and melanomas, as the UC San Diego surgeon Robert Hoffman detailed in February. Methionine is made in normal cells—out of homocysteine, folate, and vitamin B12. However, many types of cancer cells lack the enzyme that makes cellular manufacturing of methionine possible. So they require extra methionine from outside the body—via food we eat—for survival. Cut off that supply, and it should help to slow the tumor without starving the person.
This month, Locasale and his colleagues at Duke released findings showing that restricting methionine decreased tumor growth in mice and human subjects. Locasale’s particular area of research, known as metabolomics, uses enormous data sets to quantify metabolic activity. This allows the controversial field of nutrition research to operate with new levels of precision, where specific metabolic pathways can be monitored. Most nutrition research relies on self-reported data, in which people who say they eat almonds are found to have lower rates of some sort of cancer, and the best we can do is assume these two things are related. Locasale’s paper, by contrast, is full of complex statistical calculus involving “Euclidian distances” and “multidimensional scaling.”