The Etiology and Prevention of Colorectal Cancer

Volume 4, Part 2

In Part 1 of this series, we surveyed various non-toxic, holistic approaches to cancer treatment, which serve as viable alternatives or adjuncts to traditional allopathic approaches. In Part 2, we will focus on colorectal cancer, to understand its etiology and the range of effective interventions for its prevention and treatment.

Colorectal cancer is the 2nd leading cause of cancer deaths with an estimated 1,360,000 new cases annually, worldwide, and 694,000 deaths.1 Most colorectal cancers begin as growths, known as polyps, which appear on the inner lining of the colon or rectum. Some, but not all, polyps become cancerous during the course of several years. The two main types of polyps are:

  • Adenomatous polyps (adenomas): considered to be pre-cancerous, adenomas become more common as we age
  • Hyperplastic polyps and inflammatory polyps: more common than adenomas, even in younger people, but generally not considered to be pre-cancerous

In Part 1, we discussed the role of inflammation in cancer, noting that inflammation plays a greater role in some forms of cancer compared to others. Colorectal cancer is among those whereby inflammation factors heavily. Maintaining a healthy gut environment, absent chronic inflammation, therefore becomes paramount to colorectal cancer prevention. Specifically, this is accomplished by maintaining a healthy, balanced gut microbiome.

There is growing evidence that colorectal cancer is a microbial mediated cancer. Scientists involved with this theory of colorectal cancer etiology have identified the following two pathways by which microbes mediate colorectal cancer:2

  • Direct contact with infectious agents, including Streptococcus bovis, Helicobacter pylori, and Escherichia coli
  • The indirect effects of microbial metabolism of exogenous and endogenous materials

Hullar et al., for a 2015 study published in Cancer Treatment and Research, explain, «These pathways alter inflammation, modify DNA leading to mutations, or influence epigenetics and gene silencing».3

Regarding the first pathway, infectious agents represent a common cause of many types of cancer. For example, cervical, anal, penile, oropharyngeal, liver, and stomach cancers, along with certain types of lymphomas, all have well-established infectious etiologies.4 It is estimated that around 20% of the global cancer burden is linked to infectious agents, including viruses, bacteria and parasites.5 Scientists have described a variety of mechanisms by which a weakened gut microbiome could enable direct, local infections, which then promote the development of adenomas.

Regarding indirect pathways, research suggests that gut microbiome bacteria can a) produce metabolites from exogenous sources (such as diet) that may influence the creation of tumors, or b) alter exposure to circulating levels of endogenous compounds, such as steroid hormones or bile acids, that influence the creation of tumors.6, 7

The Epigenetics of Colorectal Cancer

Epigenetics represents another exciting area of research with respect to colorectal cancer. Epigenetics refers to changes in gene expression, which do not involve changes to the underlying DNA sequence. In other words, it involves «programs» that are built into one’s genetic code, but are not necessarily active. Environmental triggers, such as persistent exposure to certain toxins, can activate genes epigenetically. Ageing, stress, lifestyle, and disease are other triggers that exhibit epigenetic effects.

Epigenetics has been identified as one of the most important pathways for the genesis of colorectal cancer.8 Chronic stress leads to chronic inflammation, which can cause detrimental epigenetic aberrations, including DNA methylation, histone modifications, chromatin remodeling and non-coding RNAs, all of which promote tumor development.9 Stated in simpler terms, chronic stress can activate cancer cells, thereby triggering the growth of polyps, which can eventually become cancerous.

Preventative Colorectal Cancer Regimen

Research on colorectal cancer is progressing fast, as is research on both epigenetics and the microbiome. Within the next decade, the nature of this disease will likely be much better understood. Regardless, it’s safe to say that chronic stress, chronic inflammation, and gut dysbiosis, particularly with respect to the microbiome, all play significant contributory roles to the development of the disease. With this in mind, a diet/nutrition regimen addressing the aforementioned factors is strongly advised. This would include:

  • Eat plenty of fiber-rich foods, including sources of soluble and insoluble fiber
  • Consume fermented foods like natto, tempeh, sauerkraut, kim chi, etc.
  • Consume probiotic supplements, as prescribed by your practitioner
  • Avoid antibiotics unless absolutely necessary
  • Avoid all antimicrobial soaps and skincare products
  • Take proactive measures to minimize stress and mitigate its effects, including the consumption of adaptogenic herbs, as prescribed by your practitioner, which modulate the HPA axis, thereby modulating the microbiome
  • Eliminate gluten from the diet entirely, given its propensity to damage the gut lining, thereby promoting gut dysbiosis
  • Avoid all dairy foods, with the exception of butter
  • Eliminate all sugar
  • Eliminate all trans fats and hydrogenated oils

Additional Superfoods, Botanicals, and Nutraceuticals for Colorectal Cancer Prevention


Aloe vera is highly beneficial for the gut. Aloe/200x is a concentrated product, which requires 100 pounds of aloe vera gel to make 1 pound of the product. Aloe soothes inflammation internally, including within the stomach and lower portions of the gastrointestinal tract. Aloe also exhibits antioxidant and antibacterial properties, which may account for its immune-modulating effects. Research indicates that aloe may be a useful adjunct in helping combat gastrointestinal inflammation caused by excessive stress, including both psychological/mental stress and physical stress derived from improper diet and lifestyle choices (particularly alcohol consumption).

Artemis Plus

Also known as sweet wormwood, Artemisia annua, has a long history of use in Traditional Chinese Medicine. In the West, the plant became better known during the 1970s after scientists demonstrated that its extracts have antimalarial properties.10 Thereafter, scientists demonstrated that artemisinin, the natural endoperoxide of Artemisia annua, and its derivatives exhibit anti-cancer activity. Specifically, artemisinin-related endoperoxides were found to significantly inhibit angiogenesis and to induce apoptosis.11, 12

Artemis Plus, a formula that Karim uses in his practice, combines a concentrated (8:1) whole herb extract of Artemisia annua with a 99% artemisinin extract from the whole herb. Together, the whole herb and the artemisinin combine to exert a strong therapeutic synergy. Moreover, the formula contains additional herbs that modulate stress and reduce inflammation, including burdock root, red clover, and celandine.

C3 Curcumin Complex

C3 Curcumin Complex is a patented, unique formula comprised of three bioactive, health-promoting curcuminoids: curcumin, bisdemethoxy curcumin, and demethoxy curcumin. These are the strongest, most protective and best-researched constituents of the turmeric root. Naturally occurring turmeric root powder contains only 5-7% curcumin, while the C3 Curcumin Complex extract is concentrated to contain 95% cur- cuminoids, among which curcumin represents 70% of the total extract. This means supplementing with C3 Curcumin Complex is far more therapeutic than simply adding turmeric to foods.

Curcumin was shown to be more effective than certain NSAIDs in reducing inflammation and pain associated with rheumatoid arthritis or post-operative trauma.13 It has a better cardiovascular safety profile than aspirin because unlike aspirin, it does not inhibit the arterial protective factor prostacyclin. Curcumin acts on the mother compound NF Kappa beta. By suppressing this inflammatory marker, curcumin has a domino effect that reduces the entire cascade of inflammatory compounds that would be produced thereafter.


Digestzymes is a practitioner-grade product comprised of a proprietary blend of digestive enzymes along with betaine HCl to support optimal digestion of food. It contains the special protease DPP IV (dipeptidyl peptidase IV), which aids in the breakdown of difficult-to-digest food molecules. This product strengthens digestion, thereby promoting gut microbiome health.

The pancreas produces enzymes that are required for digestion and absorption of food. Enzymes secreted by the pancreas include lipases that digest fats, proteases that digest proteins, and amylases that digest starch. The health of the digestive tract is crucial for the overall health of the body. If food is not digested properly and toxins are not eliminated, it becomes very difficult to achieve optimal health. In addition, virtually every chronic condition will be exacerbated if the intestinal tract accumulates toxic by-products. Digestive enzymes decline 1% every three years after age thirty. Therefore, it is understandable why so many people need to supplement them for optimal digestion and assimilation of nutrients from food. Deficiency of endogenous production of digestive enzymes can lead to gas, bloating, constipation, malabsorption and a feeling of fullness after eating only a small quantity of food.

  1. Ferlay J, et al. (2015). Cancer incidence and mortality worldwide: sources, methods and major patterns in GLOBOCAN 2012. Int J Cancer., 136(5).
  2. Hullar M, et al. (2015). Gut Microbes, Diet, and Cancer. Cancer Treat Res., 159.
  3. Hullar M, et al. (2015). Gut Microbes, Diet, and Cancer. Cancer Treat Res., 159.
  4. DeFlora S, et al. (Jun 2011). The prevention of infection-associated cancers. Carcinogenesis, 32(6).
  5. Zur Hausen H. (Sep 2009). The search for infectious causes of human cancers: where and why. Virology, 392(1).
  6. Hullar M, et al. (2015). Gut Microbes, Diet, and Cancer. Cancer Treat Res., 159.
  7. Brennan CA, et al. (Sep 2016). Gut Microbiota, Inflammation, and Colorectal Cancer. Annu Rev Microbiol., 8(70).
  8. Wong JJ, et al. (2007). Epigenetics has been identified as one of the important pathways for CRC carcinogenesis. Gut, 56(1).
  9. Vaiopoulos AG, et al. (Jul 2014). Epigenetic modifications in colorectal cancer: Molecular insights and therapeutic challenges. Biochimica et Biophysica Acta (BBA), 1842(7).
  10. Van Agtmael MA, et al. (May 1999). Artemisinin drugs in the treatment of malaria: from medicinal herb to registered medication. Trends Pharmacol Sci., 20(5).
  11. Firestone GL, et al. (Oct 2009). Anticancer activities of artemisinin and its bioactive derivatives. Expert Rev Mol Med., 11.
  12. Chen HH, et al. (May 2004). Inhibitory effects of artesunate on angiogenesis and on expressions of vascular endothelial growth factor and VEGF receptor KDR/flk-1. Pharmacology, 71(1).
  13. Satoskar RR, et al. (Dec 1986). Evaluation of anti-inflammatory property of curcumin (diferuloyl methane) in patients with postoperative inflammation. Int J Clin Pharmacol Ther Toxicol., 24(12).