Gut Health and Cancer


Incidences of cancer in America are on the rise, with your probability of being diagnosed in your lifetime greater than 1 in 3 - a statistic supported by the nearly 5,000 people who are diagnosed with some form of cancer each day. Although the number of cancer deaths has slowly been declining over the last 30 years (thanks to advancements in treatment) cancer mortality is still at nearly 40%, a number that is all too high. 3

Understanding cancer is a multifactorial process. In order to prevent it, we must understand how it happens, what it is, and how to treat it. Researchers have been hard at work chipping away at these topics, attempting to shine the light on cancer and eliminate it once and for all. However, it’s been a strenuous quest for many. The more scientists learn, the more questions that appear before them. Cancer has become one of the most researched areas in science, but we have yet to find a cure. Recently, some studies have suggested that the gut microbiome may have a larger part to play with cancer development and outcome than previously thought. Here, we’ll explore some of the new research that has exposed this link - but first we’ll discuss where cancer comes from and what it really is.

From One Mutation to Many

Cancer doesn’t happen overnight. It can take a lifetime of environmental assaults on our DNA, or a series of traumatic, biological events to develop a mass of cancerous cells. In truth, the term cancer simply refers to a grouping of human cells that experience uncontrolled growth – or simply put, a group of cells that can’t stop replicating. 4 Just like any organism on earth, our cells have a natural life cycle. They are “born” – they grow and do their specific function (like whether they’re a skin cell or a kidney cell) – they replicate – and then they die. It is this normal process that allows our body the ability to control our own growth, function properly, and heal. This cycle of replication and renewal keeps our skin healthy, our organs functioning normally, and our biological processes regulated as we age. When our cells are healthy, this normal cycle occurs to keep old cells from making mistakes at their job and keeping a line of new ones ready to take their place when they die.

However, mutations can affect our DNA at certain spots and halt the normal cell life cycle process. The genes affected by these mutations are called oncogenes, which means when mutated, they can increase your risk of developing cancerous cells. 5 When enough of these oncogenes have been mutated, the cell no longer functions as a normal cell, going through its usual job and natural life cycle – instead, it becomes immortal with one goal in mind: reproducing. 6 This mutated cell then begins acting abnormally and replicates over, and over, and over again, making more and more mutated copies of itself. As it replicates, it acquires even more mutations, until the mass of immortal cells forms a cancerous tumor.

One of the incredible traits of cancerous tumors, is that the cells then begin to act as one and attempt to grow, replicate, and spread throughout the body. The metastasis of cancer, or its ability to spread to other areas, is where the name “cancer” came from – based on the crab-like movement of the tumor as it spreads. 3 Once it has reached this point, it can be exceedingly more difficult to treat as multiple tumors can be found in various regions of the body.

Cancer Risk and What That Means for You

There are a number of reasons why we develop cancer. Researchers have suggested that how many cancerous toxins we’re exposed to in our environment, our age, stress, our level of inflammation, and our nutrition are some of the most well supported areas. Our diet, however, has proven not only to increase our risk – when poor – but it can also decrease our risk of cancer. 7 Some of the studies that have shown the connection between our food and our health have also suggested a healthy gut microbiome may have a role to play.

Our Gut Microbes Work With What You Give Them

Without food, we wouldn’t have the energy or the building blocks to heal ourselves. Without proper nutrition, we lack beneficial antioxidants and nutrients that also help regulate inflammation, fight illness, and keep beneficial microbes in our gut healthy as well. If your diet is off the mark – even just a little – you’re affecting the gut microbes that interact daily with your immune system. When it comes to cancer, your level of inflammation and your immune response could be the difference between life or death.

How? Well it all comes back to those mutations.

Normally, if a cell’s DNA gets too many mutations, there are protective ways that our body has already integrated to safeguard against cancer. If your cells were a computer, it would be like your DNA is the operating system, controlling the software that’s keeping all tasks running smoothly. You can imagine these protective measures are like your standard anti-virus software. They routinely check whether the operating system (your DNA) is being corrupted by an intercepting virus (those mutations). When too many of the viruses overload the system, it can lock up the whole computer and get it stuck running one dangerous program over and over again – sound familiar?

However, your cell’s early warning “anti-virus” system catches most of these mutations and works to eliminate any errors before they inflict too much damage.

There are many different ways we can protect our DNA operating system. Some “anti-virus software programs” work to eliminate the mutations once they have integrated into our DNA by self-destructing the cell and preventing it from making any more cells just like it. This is called apoptosis and means programmed cell death. Some cancer research focuses on trying to jumpstart this mechanism that cancer cells have lost. 8 Others, however, act as a guardian and prevent these mutations from even occurring. Certain metabolites from gut microbes – like short-chain fatty acid butyrate – act as a natural anti-inflammatory agent that reduces the mutations that might occur from high levels of gut inflammation in the digestive tract. This works to prevent any disruptions to cellular DNA from our gut and many other sites, like the breasts and lungs. 9

Our gut microbes are powerful microscopic work horses that do their best to keep their environment - our gut – safe. Scientists have found they’re quite capable of many ways of helping when it comes to cancer like improving the effectiveness of chemotherapy, but the best way to tackle it may not be just curing it. It might be eliminating it from our dictionary in the first place, which aligns perfectly with what Viome is trying to accomplish. By supporting scientists who are focused on cancer research and exploring the roles of the gut microbiome, Viome is taking the steps necessary to make chronic disease a thing of the past.

This is what we stand for. Our mission is to use innovative research to optimize our health and remove words like “cancer” straight from the global vocabulary.

*The information on the Viome website is provided for informational purposes only and with the understanding that Viome is not engaged in rendering medical advice or recommendations. Viome is providing this educational information to share the exciting developments being reported in the scientific literature about the human microbiome and your health. Viome products are not intended to diagnose, treat, or prevent any disease.




4.     Bertram JS. The molecular biology of cancer. Mol Aspects Med. 2000;21:167-223.

5.     Lee EY, Muller WJ. Oncogenes and tumor suppressor genes. Cold Spring Harb Perspect Biol. 2010;2:a003236.

6.     Seyfried TN, Huysentruyt LC. On the origin of cancer metastasis. Crit Rev Oncog. 2013;18:43-73.

7.     Wiseman MJ. Nutrition and cancer: prevention and survival. Br J Nutr. 2018:1-7.

8.     Fernald K, Kurokawa M. Evading apoptosis in cancer. Trends Cell Biol. 2013;23:620-633.

9.     De Almeida CV, de Camargo MR, Russo E, Amedei A. Role of diet and gut microbiota on colorectal cancer immunomodulation. World J Gastroenterol. 2019;25:151-162.