Although the risk of developing colorectal cancer increases with age — more than ninety percent of cases occur in people ages fifty or older — recent research shows that the incidence of colorectal cancer has been increasing one to three percent annually for people younger than age fifty years while decreasing in older individuals.
How common is colorectal cancer? In the United States, it is the third most prevalent and lethal cancer among both men and women. Although the risk of developing colorectal cancer increases with age — more than ninety percent of cases occur in people fifty or older — recent research shows that the incidence of colorectal cancer has been increasing one to three percent per year for those under age fifty, while decreasing in older individuals.
Since 1994, cases of young-onset colorectal cancer — defined as colorectal cancer diagnosed before the age of 50 — have increased by 51%, according to the National Cancer Institute.
Recognizing this striking rise in the incidence of colorectal cancer among young adults, the American Cancer Society changed (in 2018) its recom-mendations for the start of colorectal screening from age fifty to age forty-five for individuals at average risk. In addition, research by the American Cancer Society has found that people younger than age fifty-five are 58% more likely to be diagnosed with late-stage disease than older adults, making cure more challenging.
The increase in colon and rectal cancer risk for young adults is clear. What is less clear is why we are seeing the rise. We have had a rise in obesity in the USA, and we wonder about other common risk factors, including diet, inactivity, and family history, may be playing in the early onset of this disease. Now comes a novel theory: Perhaps the gut microenvironment, or microbiome, is central.
Georgetown University (USA) researchers Dr. Benjamin Weinberg and colleagues hypothesized that the microbiome may be behind this rise because certain bacteria disrupt colon luminal integrity and promote inflammation, which leads to cancer-related genetic mutations in colon epithelial (lining) cells.
Before we get to the study, a brief detour. The Harvard T.H. Chan School of Public Health does a fabulous job explaining the microbiome:
Picture a bustling city on a weekday morning, the sidewalks flooded with people rushing to get to work or to appointments. Now imagine this at a microscopic level and you have an idea of what the microbiome looks like inside our bodies, consisting of trillions of microorganisms (also called microbiota or microbes) of thousands of different species.
These include not only bacteria but fungi, parasites, and viruses. In a healthy person, these “bugs” coexist peacefully, with the largest numbers found in the small and large intestines but also throughout the body. The microbiome is even labeled a supporting organ because it plays so many key roles in promoting the smooth daily operations of the human body.
Each person has an entirely unique network of microbiota that is originally determined by one’s DNA. A person is first exposed to microorganisms as an infant, during delivery in the birth canal and through the mother’s breast milk. Exactly which microorganisms the infant is exposed to depends solely on the species found in the mother. Later on, environmental exposures and diet can change one’s microbiome to be either beneficial to health or place one at greater risk for disease.
The microbiome consists of microbes that are both helpful and potentially harmful. Most are symbiotic (where both the human body and microbiota benefit) and some, in smaller numbers, are pathogenic (promoting disease). In a healthy body, pathogenic and symbiotic microbiota coexist without problems. But if there is a disturbance in that balance — brought on by infectious illnesses, certain diets, or the prolonged use of antibiotics or other bacteria-destroying medications — dysbiosis occurs, stopping these normal interactions. As a result, the body may become more susceptible to disease.
The Current Study
The researchs belived that Specifically, F. nucleatum bacteria may promote colorectal cancer by suppressing immune response within the tumor microenvironment, triggering a pathway that induces chemoresistance due to autophagy. Autophagy is the body’s way of cleaning out damaged cells.
The researchers analyzed the DNA and microbiome of tumors from eighteen younger patients (median age, 39.2 years; range, 18.2–44.6; 61 percent women) and thirteen older patients (median age, 72.8 years; range, 65.9–85; 62% women). They extracted and evaluated DNA.
Primary tumors constituted the vast majority of those analyzed in both groups (94% vs. 100%). Researchers compared the frequency of F. nucleatum and other bacterial and fungal DNA in tumors of younger and older patients.
Results showed that, among 478 unique bacterial and fungal species detected, F. nucleatum appeared in tumors of five younger patients (28%), including four left-sided tumors and one right-sided tumor, and three older patients (23%), including one left-sided and two right-sided tumors.
Compared with older patients, younger patients had a significantly lower rate of Moraxella osloensis (11% vs. 46% P = .04), another bacterium that has been found to be nearly four times more common in tumors of people aged older than 75 years compared with those aged younger than 45 years.
Further studies involving more tumors are needed to determine whether microbiome difference might help to explain the rising incidence of young-onset colorectal cancer, according to the researchers. To me, the authors really haven’t given us any good answers, but I wanted to share with you how researchers are exploring the gut microbiome to try to better understand colon cancer, as well as a myriad of other diseases.
Source : Medium