Cancer & Keto
Today, 4th February 2020 is WORLD CANCER DAY.
A day where we honor all cancer fighters, medical staff, and researchers who are involved in the front line.
Cancer is a worldwide disease, that appears to arise at times without logical reason or cause, leaving many researchers, doctors and scientists confused in identifying its origin, treatment, and prevention.
But as far back as 1922 Dr. A Braunstein (1) it was already recorded that glucose was absent from the urine of diabetic patients who had been diagnosed with cancer, suggesting an accelerated use of glucose at higher than normal rates. In 1924, Nobel laureate Dr. Otto Warburg (2) found that cancer cells thrive on glycolysis and fermentation, producing high acidic lactate levels, even in the presence of abundant oxygen.
Fast forward almost 100 years, and the idea that cancer is a metabolic disease is only recently becoming widely accepted. And, as research progresses, it seems cancer is not just one disease, but many diseases that have very different characteristics and responses to intervention strategies. At any one time, we may have up to 7.5 million cancer cells in our body that are kept under control through tight regulation of our complex biochem system. So how do we keep it like that?
So, without getting too scientific and trying to unpack a multitude of possibilities on a very complex and multi-factorial disease, I’ve chosen to highlight some of the key reasons research is supporting low carb (Keto included) and Intermittent Fasting (IF) in both management and prevention. For clarity’s sake, there is also research indicating beneficial outcomes for certain types of cancers on plant-based diets, but comparative trials have not been conclusive.
Cancer Prevention is two-fold, either referring to the inhibition of carcinogenesis, or, if the cell(s) made the transition to being a malignant cancerous cell, that the tumor growth remains slow and undetected, causing no issue or harm.
Research shows that reducing the number of dietary carbohydrates (CHOs) one could suppress, or at least delay, the emergence of cancer and that the growth rate of already existing tumor cells could be slowed. CHOs or ultimately, glucose, which complex carbohydrates are ultimately digested as, can have direct and indirect effects on tumor cells: first, most malignant cells need glucose for energy and can’t metabolize significant amounts of fatty acids or ketone bodies due to mitochondrial dysfunction within their cell (unlike healthy cells and a few specific cells of the brain, renal and retina). Second, high insulin and insulin-like growth factor 1 (IGF-1) levels resulting from chronic ingestion of CHO-rich Western foods, can directly influence tumor cell proliferation via the insulin/IGF1 signaling pathway. Lastly, ketone bodies that rise when insulin and blood glucose levels are low, have been shown to reduce the growth of malignant cells in vitro.
Glucose and Insulin
Without lots of insulin, IGF-1 is reduced, which reduces in most instances the fuel (glucose) to the malignant cell. If IF is done (say a 16:8; or even a 24hr fast), the probability for apoptosis (cell death) to occur increases. If a cell has already crossed to the dark side (ie malignant), having a high carb diet will increase insulin and IGF1 levels, causing increased growth of the cell(s) to forming a more aggressive, glycolytic type of mass. Lower insulin levels may increase the chance of intermittent ketosis, in particular, if CHO restriction is combined with exercise, calorie restriction or intermittent fasting. Researchers (3) looked at the role of ketone bodies to help in cancer prevention through mitochondrial protection from inflammation and oxidative byproducts of metabolism (which, increases if cancer cells increase). A low CHO diet would make it easier to manage fasting cycles and/or to implement intermittent fasting as an additional lifestyle change (4).
Inflammation is a well-known co-morbidity that accompanies most cancers, and a low CHO diet can promote such an inflammatory state in leukocytes and endothelial cells (5). Even moderate CHO restriction has been shown to effectively target several important biochemical markers of atherosclerosis and type II diabetes, both of which are associated with chronic inflammation (5)
Grains and Gluten
A low CHO diet often reduces grain intake, which can induce inflammation with increased omega-6 fatty acids, lectins and gluten. Gluten might even be a key contributor in the development of auto-immune and inflammatory disorders when it relates to zonulin, a regulatory junction protein in the lining of the gut and blood-brain barrier (that regulates the tight junctions between epithelial cells and therefore intestinal, but also blood-brain barrier function. Recent evidence suggests that excess zonulin in certain individuals could disrupt cell communication, allowing tumor development at specific sites (6).
Where to now?
Preliminary studies on animals are showing some positive ketogenic diet for prostate, colon, pancreatic, ovarian, endometrial, and lung cancers, though more research is needed before researchers can draw any conclusions (7). You only have to search IG for many long-term success stories of effective management of cancer using low carb and Keto interventions.
It’s important to note there’s no single standardized ketogenic diet or formalized adaption period from a standard diet, which makes studying a high-fat, carb-restricted model challenging in oncology and research care; and may also be a barrier to seeing the
There is a high incidence of diabetes or metabolic dysfunction like being overweight in the cancer population. Ketogenic or low carb diets based on whole foods can dramatically improve both glycemia, insulin resistance, and inflammation. So, it would be beneficial to use medical nutritional therapy such as these during cancer treatment and this is an emerging area of research. Unfortunately, many cancer patients don’t have the luxury of time to wait for this research to be completed. Although the current clinical evidence isn’t robust, it does show that the diet is safe and tolerable if implemented correctly under the supervision of a supportive medical practitioner.
This article is for information purposes only and is not meant to diagnose, treat or take the place of your professional primary health care provider.
If you would like any more information, please feel free to contact me.
Virchows Archiv f Pathol Anatom und Physiol 1922, 23: 1-19.
WARBURG O Science (New York, N.Y.), (1956 Aug 10) Vol. 124, No. 3215, pp. 269-70. Journal code: 0404511. ISSN: 0036-8075. L-ISSN: 0036-8075. Report No.: CLML-5630:60227.
Seyfried TN, Shelton LM: Cancer as a metabolic disease. Nutr Metab (Lond)2010, 7: 7. 10.1186/1743-7075-7-7
Mavropoulos JC, Isaacs WB, Pizzo SV, Freedland SJ: Is there a role for a low-carbohydrate ketogenic diet in the management of prostate cancer?Urology 2006, 68: 15-18.
Mantovani A, Allavena P, Sica A, Balkwill F: Cancer-related inflammation.Nature 2008, 454: 436-444. 10.1038/nature07205
Fasano A: Zonulin and it's regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiol Rev2011, 91: 151-175. 10.1152/physrev.00003.2008
Weber DD, Aminazdeh-Gohari S, Kofler B. Ketogenic diet in cancer therapy. Aging. 2018;10(2):164-165.