Nutrition & Cancer: Understanding the Power of Information | Part II

Last month, I wrote briefly on the marketing history and impact of one food item:  dairy and estrogen-sensitive cancers. This week, I want you to understand that at the intersection of nutrition and cancer, other dietary factors must be considered.

  1. Blood sugar:  Both elevated glucose and insulin levels (remember, insulin is given to “correct” high blood sugar in diabetics) set the stage for the unchecked growth of cancer cells (Amadou 2013). Our bodies were never designed to consume the amount of sugar we do on a daily basis. More on this here.
  2. Excess weight:  Central obesity (“tummy fat”) increases the risk of dying from breast cancer by 34%, and is a source of excess estrogen that fuels many cancers (Amadou, 2013). Excessive body fat, weight gain and/or obesity is responsible for one of every five diagnoses of cancer in the U.S. (Bähr, 2017). Losing weight by correcting your diet improves natural killer cells, critical components of a robust immune system (Bähr, 2017). The ideal cancer host is an obese (i.e. inflamed) individual, living on packaged foods, and using popular skin care products that contain estrogen-like chemicals. Returning to a healthy weight helps reduce risk of cancer.
  3. Alcohol:  Although many people have heard that small amounts of wine may be cardioprotective, it’s a mistake to assume the health benefits of alcoholic beverages can be extended to non-cardiac diseases. The more a person drinks alcohol, the higher the risk for breast, gastric, and pancreatic cancers (Brennan 2010; Ma 2017), likely due to the fact that alcohol blocks liver function—including removal of excess estrogen, which we know promotes cancer growth (Hankinson et al., 1994). Alcohol consumption also inactivates the vital tumor suppressor gene, BRCA1. Hence, with a weakened ability to terminate defective cells plus a rise in hormones, estrogen naturally does its job to increase responsiveness in the breast tissue (Yi et al., 2017). When the timing is off, the information becomes a death sentence.

Alcohol also induces a specific enzyme, called cytochrome P450 2E1 (CYP2E1), which is highly expressed in the liver to clear toxicants from the body (Shimada et al., 1994; Bieche et al., 2007). When CYP2E1 and other cytochrome P450 enzymes are activated, they can inadvertently generate excessive reactive oxygen species (ROS), resulting in a rise of lipid peroxidation (damage to fat membranes) as well as protein and DNA oxidation (damage to our information code) (Porubsky et al., 2008; Yi et al., 2017). 

This may be why a recent study found that alcohol consumption leads to an 8% rise of new cancer cases, even in light-to-moderate alcohol drinking groups. Yet, it was estimated that a 10% drop in alcohol consumption would have prevented over 2,000 new cancers from developing (Yi et al., 2017). When you consider the pesticides used to grow crops that turn into alcohol, you also increase your exposure to toxic agrochemicals. Thus, your chemical cocktail is anything but an elixir, as it further hinders your body’s ability to function.

Red meat:  Most studies linking red meat and cancer have evaluated commercial, grain-fed meat (i.e. not grass-fed beef, which is higher in anti-inflammatory fats, precursors for Vitamin A and E, and other “cancer fighting antioxidants”) (Daley 2010). I submit to you that commercially grown meat is probably one of the most important things to remove from your diet. 

Cattle, sheep, deer, and their relatives’ stomachs are designed to turn fresh foliage into nutrients; the problem is when these ruminants are fed grains, they become inflamed. How? Due to a pathogenic shift in their gut bacteria. 

Commercially grown, grain-fed cattle are loaded with a pathogenic type of bacteria in their gut, which can then shed toxic byproducts into the cow’s milk and muscle tissue. Furthermore, pasteurization does not directly take care of the remaining bacterial byproducts in either milk or meat (Zhang, 2016). When you drink milk or eat meat, your body gets information that it, too, is under attack (as a consequence of consuming inflammatory byproducts). A cow’s and human’s response to a grain-filled diet is the same: systemic inflammation

To add fuel to the fire, rBGH and estrogens given to commercial cows (to increase milk production) can then stimulate cancer growth when the immune system is busy fighting off bacterial byproducts from a pathogenic gut. 

The solution is not to consume grass-fed animals, contrary to what most people believe. Regardless of the source, when an animal is butchered, its meat gets wrapped in plastics (which migrate easily into fat stores and mimic estrogen in the body when consumed). After the meat is then cooked at excessively high temperatures, and then consumed, the meat sends the wrong message to our cells from estrogen-like compounds in meat It leads to an unchecked growth of inflammation and cellular damage from fried proteins, and eventually, unchecked growth of cancer cells.

Pivoting from diet, at the intersection of other lifestyle factors and cancer, practice the following:

Stress less:  This is easier said than done, but you can at least promote a positive outlook on life every moment you are consciously aware of your stress. This is something we can all take control of. “Stressing less” looks different for different people, but my favorites include spending time with loved ones, having a good belly laugh, getting the much needed “me time” massage, taking a nap on a warm summer afternoon, watching a funny movie, meditating, and being hugged. These all immediately increase natural killer cell activity—part of your body’s ability to fight cancer and infected cells (Hayashi 2007).

Move:  Regular physical activity reduces the risk of dying from all cancer types. Risk of breast cancer decreases by 3% for each 4-hour-per-week spent walking at 2 miles per hour or 1-hour-per-week spent jogging at 10-minute miles. Risk of breast cancer decreases 5% for more vigorous exercise (Wu 2013). Low intensity, longer duration and high intensity, shorter duration physical activity can increase the quality and length of one’s lifespan by protecting against all causes of illness and death (Kopperstad 2017). In other words, it doesn’t matter what you do, it matters that you do. If swimming isn’t your thing, that’s okay. Moving in a way that you love is an excellent way to stress less. There’s no wrong option when you’re moving.

Don’t fear the sun:  Vitamin D is an excellent cellular communicator and deserves a book on it own.  Not only does it have the ability to poke holes in certain viruses, but it also regulates the cell’s ability to break down and recycle dysfunctional or unused parts in a process called autophagy (Tavera-Mendoza, 2017). This is critical when cells become sick. Doctors worldwide measure vitamin D status by assessing 25-hydroxyvitamin D (25[OH]D), a prohormone that is produced in the liver (via hydroxylation of vitamin D₃ by the enzyme cholecalciferol 25-hydroxylase). Analyzing 10 years of data from almost 27,000 individuals, the farther serum 25[OH]D drops below 50 nmol/L: (1) the greater risk of developing cancer; (2) the greater the risk of having a more advanced cancer; (3) the greater the risk of having a larger cancer; (4) the greater the risk of having metastatic cancers; (5) the greater the risk of having a treated cancer come back; (6) the greater the risk of dying from cancer; and (7) the greater the risk of dying from cardiovascular complications. People with very high 25[OH]D (serum values greater than 125 nmol/L) had comparably good health to those around 75 nmol/L (30 ng/mL) (Gaksch, 2017), which is the ideal range.

SleepToo little sleep (under 7 hours per night) or too much sleep (more than 10 hours per night) is associated with a higher risk of death from all causes (Collins 2017). Individuals who habitually sleep less than 6 hours nightly had a 62% greater risk of dying from cancer than those who snooze at least 7 hours each night.

Restore the thyroid:  Repairing years of damage to one of the most sensitive organs, the thyroid, and balancing thyroid hormone levels can be done with diligent work and effort. It’s better to do this naturally rather than take thyroid hormone medications. While hypothyroid individuals have greater risk of cancer, it’s worth considering the possibility that thyroid hormone treatment may increase pancreatic cancer cell division, migration, and invasion, and reduce the chances of beating cancer (Sarosiek 2016). This cannot justifiably be generalized to people without cancer, but research efforts should focus here in the future, as with estrogen hormone levels and breast cancer.

If you or a loved one is facing the diagnosis of cancer, please CONTACT US as soon as you can. Advanced Health is here to help confront the root causes of your illness. Let’s work together to get you on the path to lifelong wellness.



Amadou, A., Hainaut, P., & Romieu, I. (2013). Role of Obesity in the Risk of Breast Cancer: Lessons from Anthropometry. Journal of Oncology, 2013, 906495.

Bähr, I., Goritz, V., Doberstein, H., Hiller, G. G. R., Rosenstock, P., Jahn, J., … Kielstein, H. (2017). Diet-Induced Obesity Is Associated with an Impaired NK Cell Function and an Increased Colon Cancer Incidence. Journal of Nutrition and Metabolism, 2017, 4297025.

Bieche, I., Narjoz, C., Asselah, T., Vacher, S., Marcellin, P., Lidereau, R., ... & de Waziers, I. (2007). Reverse transcriptase-PCR quantification of mRNA levels from cytochrome (CYP) 1, CYP2 and CYP3 families in 22 different human tissues. Pharmacogenetics and genomics, 17(9), 731-742.

Brennan, S. F., Cantwell, M. M., Cardwell, C. R., Velentzis, L. S., & Woodside, J. V. (2010) Dietary patterns and breast cancer risk: a systematic review and meta-analysis. American Journal of Clinical Nutrition 91(5), 1294-1302

Collins K.P., Geller D.A., Antoni M., Donnell D.M., Tsung A., Marsh J.W., … Steele, J.L. (2017) Sleep duration is associated with survival in advanced cancer patients. Sleep Medicine. 32, 208-212. Epub 2017 Jan 20.

Daley, C. A., Abbott, A., Doyle, P. S., Nader, G. A., & Larson, S. (2010). A review of fatty acid profiles and antioxidant content in grass-fed and grain-fed beef. Nutrition Journal, 9, 10.

Gaksch, M., Jorde, R., Grimnes, G., Joakimsen, R., Schirmer, H., Wilsgaard, T., … Pilz, S. (2017). Vitamin D and mortality: Individual participant data meta-analysis of standardized 25-hydroxyvitamin D in 26916 individuals from a European consortium. PLoS ONE, 12(2), e0170791.

Hankinson, S. E., Manson, J. E., London, S. J., Willett, W. C., & Speizer, F. E. (1994). Laboratory reproducibility of endogenous hormone levels in postmenopausal women. Cancer Epidemiology and Prevention Biomarkers, 3(1), 51-56.

Hayashi, T., Tsujii, S., Iburi, T., Tamanaha, T., Yamagami, K., Ishibashi, R., … Murakami, K. (2007) Laughter up-regulates the genes related to NK cell activity in diabetes. Biomedical Research, 28, 281-285.

Kopperstad Ø, Skogen JC, Sivertsen B, Tell GS, Sæther SMM (2017) Physical activity is independently associated with reduced mortality: 15-years follow-up of the Hordaland Health Study (HUSK). PLoS ONE, 12(3): e0172932.

Ma, K., Baloch, Z., He, T.-T., & Xia, X. (2017). Alcohol Consumption and Gastric Cancer Risk: A Meta-Analysis. Medical Science Monitor: International Medical Journal of Experimental and Clinical Research, 23, 238–246.

Porubsky, P. R., Meneely, K. M., & Scott, E. E. (2008). Structures of human cytochrome P-450 2E1 insights into the binding of inhibitors and both small molecular weight and fatty acid substrates. Journal of Biological Chemistry, 283(48), 33698-33707.

Sarosiek, K., Gandhi, A. V., Saxena, S., Kang, C. Y., Chipitsyna, G. I., Yeo, C. J., & Arafat, H. A. (2016). Hypothyroidism in Pancreatic Cancer: Role of Exogenous Thyroid Hormone in Tumor Invasion—Preliminary Observations. Journal of Thyroid Research, 2016, 2454989.

Shimada, T., Yamazaki, H., Mimura, M., Inui, Y., & Guengerich, F. P. (1994). Interindividual variations in human liver cytochrome P-450 enzymes involved in the oxidation of drugs, carcinogens and toxic chemicals: studies with liver microsomes of 30 Japanese and 30 Caucasians. Journal of Pharmacology and Experimental Therapeutics, 270(1), 414-423.

Tavera-Mendoza, L. E., Westerling, T., Libby, E., Marusyk, A., Cato, L., Cassani, R., … Brown, M. (2017). Vitamin D receptor regulates autophagy in the normal mammary gland and in luminal breast cancer cells. Proceedings of the National Academy of Sciences of the United States of America, 114(11), E2186–E2194.

Zhang, K., Chang, G., Xu, T., Xu, L., Guo, J., Jin, D., & Shen, X. (2016). Lipopolysaccharide derived from the digestive tract activates inflammatory gene expression and inhibits casein synthesis in the mammary glands of lactating dairy cows. Oncotarget, 7(9), 9652–9665.

Wu, Y., Zhang, D. & Kang, S. (2013) Physical activity and risk of breast cancer: a meta-analysis of prospective studies. Breast Cancer Research and Treatment 137(3), 869–882.

Yi, Y., Huang, C., Zhang, Y., Tian, S., Lei, J., Chen, S., . . . Zhong, S. (2017). Exploring a common mechanism of alcohol-induced deregulation of RNA pol III genes in liver and breast cells. Gene, 626, 309-318.

Dr. Payal Bhandari Dr. Payal Bhandari M.D. is a leading practitioner of integrative and functional medicine in San Francisco.

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