Melanie Chen ’22 and Rachel Kroll ’22

There are a lot of delicious foods in the world: from a hot bowl of noodle soup on a cold day to a breakfast sandwich and a coffee in the morning. You have probably thought about how what you eat impacts your predisposition to acquire various diseases. But what about your predisposition to develop cancer, specifically? All of the foods that we eat have an impact on our bodily functions, including how our genes are expressed and regulated.The means by which this happens is what the field of nutriepigentics aims to uncover. 

There are many ways food can impact your health, and one of the lesser-talked-about ways is by modifying your susceptibility to colorectal cancer. Colorectal cancer, or CRC for short, is a type of gastrointestinal (GI) cancer. These cancers are among the most common cancers in the world, and include types like gastric, esophageal, and, of course, colorectal cancer (CRC). Common symptoms include pain or discomfort, nausea and vomiting, loss of appetite, and uniquely a condition called early satiety, this “full” feeling6

Unfortunately, GI cancers are on the rise, as evidenced by colorectal cancer cases increasing by 1-2% each year in a 4-year period from 2012 to 20162. One in twenty individuals in the U.S. will develop this disease at some point during their life3. The prevalence of CRC in our country makes efforts of prevention all the more important. 

You may hear a doctor who is conscientious about this ask, “Do you have a family history of cancer?” One of the reasons for this inquiry is that some people are genetically predisposed to cancer. This means that their cells can become cancerous, forming their own cancer sites within the GI tract. These sites can quickly become a tumor, which can then advance to invasive carcinoma and stage 4 cancer5. Due to this, depending on your family history, colonoscopies and other screenings are recommended, especially for individuals above the age of 452.

But let’s backtrack a little. How does this part actually work? What causes cancer sites to be formed, and what does it mean to be predisposed? 

The primary culprit is a phenomenon called DNA methylation. It’s a type of marker for our cells that lowers the amount of genes expressed. Think of it as a cap – like one you would put on a water bottle – that controls the possibilities for movement of water out of the bottle. With the cap tightly on (more methylation, in our example), there will be less possibilities for the contents of the bottle to move in various directions. Likewise, with more methylation, there are overall fewer potential actions for our cells to take in regards to DNA. With the cap off (with less methylation), there will be more potential movement for the water, and therefore more possibilities for ways the water can move. In other words, in the presence of methylation, certain actions our bodies undergo are reduced, and certain genes may be expressed more or less depending on how tight the cap is, or how much methylation there is. 

In genetics, DNA methylation is a marker that can be passed from one generation to the next. Naturally, we want our bodies to make adjustments based on our environments. For example, when we are stuck outside in cold weather, we want our bodies to shiver to warm ourselves up. While we’re not sure if this shivering action can be passed to our children, if we could, wouldn’t that be a good thing? We would want our children to be already adaptive to the environment. This same concept can be applied to risk factors, or lack thereof, for how CRC comes to be. 

There is an enzyme, or tool, that does this methylation, known as DNA methyltransferase 1 (DNMT1). An army of these enzymes regulates the amount of methylation in our DNA so that we don’t have too much or too little. They control the caps’ tightness for the water bottles of our genes. These machine-like proteins can tag something called tumor suppressor genes using DNA methylation, in which abnormalities may cause some serious problems. 

But what are tumor suppressor genes anyhow? They are exactly what their name suggests: genes that suppress tumors, or the overgrowth of cells. These genes are essential for the maintenance of healthy tissue. When we get a cut, our bodies respond by undergoing actions like cell division to replace the cells lost. The process and products of cell replication need to be tightly regulated to ensure the proper amount of cells are produced and that each cell is functional. The tumor suppressor genes reduce the amount of cells being created so as to not have an overgrowth of any such cells. They also send signals telling cells to initiate apoptosis, or programmed cell death, when their life span is over or if they are exhibiting dangerous abnormalities. 

Now, occasionally there are mutations, or problems, with DNMT1. Like any other machine, sometimes it can be rendered non-functional. This leads to abnormalities in DNA methylation, sometimes increasing the amount of DNA methylation. And when there is an increase in DNA methylation on the tumor suppressor genes (aka more marks) the overall action of increasing the reduction of excessive cell growth is capped, which actually increases the number of cells being created to replace lost cells. As a result, the tumor suppressor genes are not able to do their job properly – they can’t show up to work, so to speak – allowing cells to replicate in an uncontrolled fashion. Inevitably, with so many new cells being created and rogue cells not being caught early, cells with these mutations accumulate, eventually forming tumors. 

It is hypothesized that people with CRC have more mutations related to the expression of DNMT1 – mutations which would result in tumor growth, as we just discussed8. For individuals with CR cancer, inflammation within the GI tract induces the need to replicate cells. And unfortunately, someone who is predisposed to CRC is generally found to have more of this DNA methylation, or that tighter cap, on the tumor suppressor genes.

So why did we bring up food in the first place? Well, a number of environmental factors are known to influence the amount of methylation of our genetic material, with diet being one of these major factors. There is slowly mounting evidence that environmental factors, such as diet, may play a role in CRC development. To someone already genetically predisposed based on how much methylation there is already, food can affect the level of risk for developing CRC. 

When we focus on the role of diet in CRC specifically, potential danger arises when dealing with low amounts of folate, a vitamin notably found in leafy greens, broccoli, and chickpeas. The “Western” diet lacks sufficient qualities of many of these types of foods; it is typically composed of red meat products and highly processed foods in place of folate-rich foods. Such dietary changes are significant because folate is involved in many cellular processes, including acting upstream to decrease methylation of – and subsequently activate – some genes.

Studies have found that differences in folate intake can have an effect as early as periconception, a critical time period during fetal development7. Based on this study, eating more foods with folate and consuming less of a Western-style diet ensures an adequate supply of materials to produce normal amounts of methylation, leading to regular gene expression. In essence, if someone eats well, that person will have given their child an advantage, where their child won’t be as primed for developing cancer sites. This standard expression of your genes and gene products means a fetus with someone’s genes of this type of diet will be better equipped to deal with excessive methylation and have reduced abnormalities when it comes to tumor suppressor genes and DNMT1. 

On a similar vein, those who adhere to more of a Western diet – with their high intakes of meat, fats, refined grains, and sugar – are at a significantly higher risk for developing CRC, regardless of weight or physical activity level. In a giant study assessing cancer risk in over 10,000 twins, approximately 80% of the predisposition for colorectal cancer was due to environmental factors, including types of food eaten4. The twin who ate more meat, fats, and the like had significantly higher rates of cancer than their twin. Nonshared environment factors were estimated to account for 60% of the CRC development risk. Simply put, when individuals with the same gene pool and relatively same upbringing are exposed to a “bad” diet in place of a “good” diet, those with the former type of diet are shown to be at a higher risk.

Overall, we continuously see those who eat diets high in folate are typically less likely to have CRC. Be careful not to think of this as a causality, as the studies here only observed an association between low folate diets and CRC. Nonetheless, working more folate-rich foods into your diet based on the findings here can certainly aid in defending against CRC, especially in those with family histories of cancer. As with many things in life, it is a question of maintaining a proper equilibrium between methylation and demethylation, activation and deactivation of genes, growth and apoptosis – all influenced by striking a balance with folates and other nutrients in your diet. What an empowering thought: that your attentiveness to your intake of nutrients can lower your risk, and even your children’s risk, for cancer.


  1. Colorectal Cancer Guideline | How Often to Have Screening Tests. (2020, November 17). American Cancer Society. Retrieved from ations.html 
  2. Colorectal Cancer Statistics | How Common Is Colorectal Cancer? (2022, January 12). American Cancer Society. Retrieved from
  3. Gabre, J. (2022, March 22). Colon Cancer Is Skewing Younger. Columbia University Irving Medical Center. Retrieved from,if%20a%20cancer%20is%20caught 
  4. Lichtenstein, P., Holm, N. V., Verkasalo, P. K., Iliadou, A., Kaprio, J., Koskenvuo, M., … Hemminki, K. (2000). Environmental and Heritable Factors in the Causation of Cancer — Analyses of Cohorts of Twins from Sweden, Denmark, and Finland. New England Journal of Medicine, 343(2), 78–85. 
  5. Nyström, M., & Mutanen, M. (2009). Diet and epigenetics in colon cancer. World Journal of Gastroenterology, 15(3), 257. 
  6. Rupawala, A., & Tamerisa, R. (n.d.). Gastrointestinal Cancers – American College of Gastroenterology. American College of Gastroenterology. Retrieved from 
  7. Tobi, E. W., Lumey, L. H., Talens, R. P., Kremer, D., Putter, H., Stein, A. D., … Heijmans, B. T. (2009). DNA methylation differences after exposure to prenatal famine are common and timing and sex-specific. Human Molecular Genetics, 18(21), 4046–4053.
  8. Zhu, Y.-M., Huang, Q., Lin, J., Hu, Y., Chen, J., & Lai, M.-D. (2006). Expression of human DNA methyltransferase 1 in colorectal cancer tissues and their corresponding distant normal tissues. International Journal of Colorectal Disease, 22(6), 661–666.


  1. Folate Graphic:
  2. Water Bottle Graphic: =612×612&w=0&h=5P367dCqJf7XDeCs7tUdTfrbQpzoA6UoNJAXHJJLP7I=

Featured Image Source

Desai, N., & Rabinowitz, L. (2022, June 15). Colon cancer screening decisions: What’s the best option and when? Harvard Health. Retrieved September 7, 2022, from