Those following ketogenic (keto) diets consume large amounts of fat and minimal carbohydrates and protein. A lack of carbohydrates prompts the body to convert fat into molecules called ketones. When in circulation, ketones provide most of the energy our bodies need to function, potentially leading to positive health outcomes.
Keto diets have become increasingly popular over the past decade. The popularity of these diets has been encouraged by social media trends and mainstream news. Further, diet trends, in general, have gained momentum due partly to the growing obesity crisis in the United States. As of 2022, 22 states report at least 35% of the adult population as obese. Notably, just one decade ago, 0 states had an adult obesity prevalence above 35%.
Some evidence from the early twentieth century supported keto diets for the treatment of epilepsy. Around this time, some scientists believed low carbohydrate diets could also help fight cancer based on the “Warburg Effect.” Discovered by German physiologist Otto Warburg, the Warburg Effect describes how cancer cells require glucose to survive. Typically, cancer cells derive glucose from carbohydrates, and thus, scientists theorized that minimizing carbohydrate intake could kill cancer cells, essentially through starvation. In other words, the Warburg Effect suggests that cancer cells have a unique metabolic preference for glucose, which could be exploited by reducing carbohydrate intake in the diet.
Despite some noted benefits to high fat/low carbohydrate diets, particularly for weight loss, other reports suggest that long-term keto diet consumption can negatively affect tissues in the heart and kidney.
A recent study in Science Advances aimed to better understand the effects of a keto diet using mouse models. The rigorous research process involved in this study provides a solid foundation for the findings. Senescence , a state where cells stop dividing and growing, occurred in mice eating a keto diet. Researchers observed this effect throughout several organs, including the heart and kidney, further reinforcing the credibility of the study's results.
The study also showed that a keto diet led to an accumulation of p53, a gene that regulates cell division and cell death. Known as a tumor suppressor gene, p53 can control cell growth, and thus, mutations in p53 can promote cancer growth. Because p53 helps prevent the development of cancer by regulating the growth and death of cells, an accumulation of p53, as observed in the study, could have significant implications for cancer treatment.
The researchers also detected elevated levels of senescence biomarkers in mice on a keto diet. These biomarkers are specific molecules that indicate the presence of senescence, a state where cells stop dividing and growing. Importantly, plasma samples from patients on keto diets also showed increased levels of these biomarkers. An intermittent keto diet, consisting of cycles of four days of keto and seven days of standard diet, prevented the onset of cellular senescence. This suggests that taking a "break" from a keto diet, could present a tool for individually controlling cycles of senescence.
The researchers conclude that the science underlying keto diets may be more complex than currently thought. Thus, including a keto diet as part of a treatment plan may require personalized context for each patient. This underscores the importance of individualized care and the potential for dietary interventions to become a crucial aspect of personalized medicine regimens, making each patient feel valued and integral to their own health journey.
Sources: Mo Med, Front Neurosci, JAMA, Fed Pract, Trends Biochem Sci, Science, Nature, Biochem Biophys Res Commun, Sci Adv