By Kirsten West ND, LAc
A recent study has called into question the use of a high fat diet in those with cancer. The article was debuted in the Journal “Nature.”[i] On first read, the use of a high fat (ketogenic diet) in those with cancer may seem to promote cancer. However, when diving deeper there is more to this study and its outcome.
Prior to discussing the study’s drawbacks, it is important to give the study methods, a quick review. The cellular protein CD36 has been identified as a marker on cancer cells and is associated with metastasis. Tumor cells without the propensity to metastasize (spread), do not appear to have this protein. With this knowledge, researchers then decided to elucidate the role of dietary intake on this marker itself. More specifically, mice were injected with cancer cells that displayed the CD36 marker. Half of these mice were fed a dietary intake high in palmitic acid (a saturated fat high in palm oil) and half were fed a “standard mouse” diet. Those mice that were fed a dietary intake high in palmitic acid developed metastasis as compared to only half of those that were fed a standard “mouse” diet. The research team then came to the conclusion that unrestricted fat intake may promote disease spread.
There are several caveats to this conclusion and the study, itself.
First and foremost, this study was not a clinical trial but instead, an in vivo study. The study was not performed on human subjects but instead on mice. The ability to cleanly extrapolate this data to human subjects is far from easy. In fact, scientists and doctors would never assume a drug testing safe in a mouse, is safe in humans and vice versa.
Second, the standard dietary intake of a mouse is not one that is high in fats. In fact, mice tend to eat fruit, seeds, and grains.[ii] The ability of their inherent metabolism to utilize high fat dietary intake is not normal. Whereas humans have been given an evolutionary advantage here. In times of famine, we were given the ability to produce ketones from fats and fasting which enabled our survival. Accordingly, a significant amount of research has been done on the use of ketosis and cancer management – in humans.[iii] The data continues to be substantial and highly intriguing.
Third and very importantly, the mice fed high fat diets are almost always fed other components. In fact, the “high fat rodent diet” U.S. researchers most commonly use is high in fat and sugar.[iv] So although these mice were fed a dietary intake high in fat, palmitic acid, they were likely also given sugar as an additional component. The research regarding the role of sugar and cancer progression is huge. Not to mention the speed of progression when high sugar and saturated fats are combined. This is not the method of a high fat therapeutic diet (the ketogenic diet) as used in cancer research and now cancer management. The inherent nature of the ketogenic diet is the restriction of sugars and carbohydrates. Otherwise, ketosis is not obtained and the therapeutic value of the diet itself, useless.
In conclusion, it is imperative that we always beg the questions, with any study, to determine its utility and also what it means for humans and cancer. Negative studies tend to hold more weight than several positive studies. Overall, this makes sense, as safety is key. Unfortunately, this has also resulted in the unwarranted attention to a study with questionable methodology. This is why we must always dig deeper. The truth is always somewhere in between.
[i] Pascual G, Avgustinova A, Mejetta S, Martín M, Castellanos A, Attolini CS, Berenguer A, Prats N, Toll A, Hueto JA, Bescós C, Di Croce L, Benitah SA.Targeting metastasis-initiating cells through the fatty acid receptor CD36. Nature. 2016 Dec 7. doi: 10.1038/nature20791. [Epub ahead of print]
[iii] Bryan G. Allen,⁎,1 Sudershan K. Bhatia,1 Carryn M. Anderson, Julie M. Eichenberger-Gilmore, Zita A. Sibenaller, Kranti A. Mapuskar, Joshua D. Schoenfeld, John M. Buatti, Douglas R. Spitz, and Melissa A. Fath. Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism. Redox Biol. 2014; 2: 963–970.
Seyfried T, Shelton L. Cancer as a Metabolic Disease (2010). Retrieved December 20, 2016 from: http://download.springer.com/static/pdf/494/art%253A10.1186%252F1743-7075-7-7.pdf?originUrl=http%3A%2F%2Fnutritionandmetabolism.biomedcentral.com%2Farticle%2F10.1186%2F1743-7075-7-7&token2=exp=1482198764~acl=%2Fstatic%2Fpdf%2F494%2Fart%25253A10.1186%25252F1743-7075-7-7.pdf*~hmac=a651f8a5ffdd6cfe08598d0c6aed2d0f591b9cc4e74dd021a44ab1416e7e963a
Seyfriend T, Kiebish M, Marsh J, Shelton, L, et al. Metbolic Management of Brain Cancer. Bioenergetics. 2011; 6: 577-594
[iv] Yandell K. Inside a Lab Mouses’s High-Fat Diet (2015). Retrieved on December 20, 2016 from: http://mobile.the-scientist.com/article/44600/inside-a-lab-mouse-s-high-fat-diet