By David Seaman, DC, MS, DABCN
Texts and papers that discuss cancer often illustrate how a normal cell is transformed into a cancerous cell. Normal cells should die off; however, they instead go through metaplastic and dysplastic changes, which leads to the transformation of normal cells into cancerous cells that proliferate and do not die.1 One of the chemicals that pushes the transformation of normal cells into cancer cells is prostaglandin E2,1 which is derived from arachidonic acid. In fact, we eat an excess of arachidonic acid indirectly and directly. We eat an excess of linoleic acid from refined foods, fast foods, and packaged foods. Some of the worst culprits are French fries and the various chips that have been cooked in linoleic acid-rich oils (corn, sunflower, safflower, cottonseed).
Our bodies convert linoleic acid into arachidonic acid. We also eat arachidonic acid excessively in excessively fatty meats and farm-raised fish, such as tilapia and catfish, which have subsisted almost exclusively on feed that contains linoleic acid. Arachidonic acid from the various sources is then converted into PGE2 by the COX1 and COX2 enzymes in the human body. (Interestingly, an image showing the conversion of arachidonic acid into PGE2 is provided in an article about fatty acids, PGE2 and other eicosanoids, and brain cancer.)2
A recent news piece on Medscape discussed why aspirin helps to prevent cancer: it blocks the conversion of arachidonic acid into PGE2.3 This is actually not new news; the cancer-modulating effects of NSAIDs has been known for years.4-7 Of course, nothing is ever mentioned in these articles about the fact that we get arachidonic acid in unhealthy foods and that we should stop eating these foods in excessive amounts.
Images in certain papers actually show us that PGE2 is involved in cancer promotion, such as esophageal and breast cancer.1,8 Bulun even provides an image of how PGE2 inhibits BRCA, which is a famous anti-cancer gene related to breast cancer expression.8 Another paper explains that patients with brain cancer have measured levels of linoleic acid and arachidonic acid that are excessive.2
The bottom line is that an excess consumption of linoleic acid and arachidonic acid represents the pursuit of cancer because cancer transformation, in part, requires PGE2. And it is well-known that modern man consumes excessive levels of omega-6 fatty acids. In fact over 20 percent of our calories come from omega-6-rich refined oils and obese meat,9 which means the modern diet is really the "PGE2/cancer diet."
It is also well-known that modern man consumes excessive amounts of refined carbohydrates with high glycemic indexes/loads. Approximately 20 percent of our calories come from sugar and another 20 percent from refined flour.9 Research has demonstrated that cancer cells actually survive on sugar. In fact, "cancer cells are addicted to aerobic glycolysis."10 The details of the chemistry related to this phenomenon are elegantly described in two excellent papers.10-11
The short story is that mitochondria are the key executors of normal cell turnover. Without normal functioning mitochondria, cell apoptosis is prevented. The cancerous process involves the "silencing" of mitochondria, such that they are unable to push apoptosis and so cancer cells become immortal.11 Cancer cells can only survive on glycolysis, so they require a constant supply of sugar, which is generously supplied by the modern diet. Interestingly, fasting and ketogenic diets appear to have cancer-preventing properties.10
Sixty percent of calories in the current modern diet come from refined omega-6 oils, sugar, and flour, all of which feed the cancerous process. This means that the average American is pursuing cancer as a dietary goal. If you, colleagues, or patients, find this to be a disagreeable concept, read the cited papers and you will see that it is true, which means that much suffering on the part of patients and family members can be prevented. We need to stop feeding cancer and other chronic diseases the food they love.
This type of information is no longer relegated to conspiracy theorists in health food stores, as made evident by the relevant citations in this paper. Additionally (and surprisingly), even the mainstream media is now reporting that sugar is a driver of cancer and stimulates the same "addiction pathways" in the brain as cocaine.12
- Buttar NS, Wang KK. Mechanisms of disease: carcinogenesis in Barrett's esophagus. Nat Clin Pract Gastroenterol Hepatol, 2004;1(2):106-12.
- Nathoo N, Barnett GH, Golubic M. The eicosanoid cascade: possible role in gliomas and meningiomas. J Clin Pathol, 2004;57;6-13.
- Kerr DJ. "Can Aspirin Slow Cancer Progression?" Medscape Today, Feb. 12, 2012.
- Rosenberg L, Palmer JR, Zauber AG, Warshauer ME, Stolley PD, Shapiro S. A hypothesis: nonsteroidal anti-inflammatory drugs reduce the incidence of large-bowel cancer. J Natl Cancer Inst, 1991;83(5):355-8.
- Norrish AE, Jackson RT, McRae CU. Non-steroidal anti-inflammatory drugs and prostate cancer progression. Int J Cancer, 1998;77(4):511-5.
- Smalley W, Ray WA, Daugherty J, Griffin. MR. Use of nonsteroidal anti-inflammatory drugs and incidence of colorectal cancer: a population-based study. Arch Intern Med, 1999;25;159(2):161-6.
- Langman MJ, Cheng KK, Gilman EA, Lancashire RJ. Effect of anti-inflammatory drugs on overall risk of common cancer: case-control study in general practice research database. Brit Med J, 2000;320:1642-46.
- Bulun SE, et al. Regulation of aromatase expression in breast cancer tissue. Ann NY Acad Sci, 2009;115:121-31.
- Cordain L, et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr, 2005;81(2):341-54.
- Klement RJ, Kammerer U. Is there a role for carbohydrate restriction in the treatment and prevention of cancer? Nutr Metab, 2011;8:75.
- Seyfried TN, Shelton LM. Cancer as a metabolic disease. Nutr Metab, 2010;7:7.
- "60 Minutes." Dr. Sanjay Gupta reporting the on the disease-driving nature of refined sugar. www.cbsnews.com/video/watch/?id=7403942n
Dr. David Seaman is the author of Clinical Nutrition for Pain, Inflammation and Tissue Healing and a longtime columnist for DC, writing on clinical nutrition (his current column focus) and the subluxation. He is a professor of clinical sci-ences at National University of Health Sciences (St. Petersburg, Fla. campus). For more information including a printable version of this article and a link to previous articles, visit www.dynamicchiropractic.com/columnist/seaman.