The rise of colon cancer in young people is far from just anecdotal. The American Cancer Society reports that in 2019, 20 percent of U.S. colorectal cancer cases (which includes both colon and rectal cancer) were in people aged 54 or younger, up from 11 percent in 1995. Furthermore, they note that the death rate for colorectal cancer in people under 55 has been increasing by about one percent each year since the mid-2000s. This trend has also been reported in at least 27 other countries—and if it continues, experts predict it will become the leading cause of cancer-related death among young people by 2030.
Conversely, colon cancer rates and deaths have been declining in people older than 55, mainly due to increased screenings and healthier lifestyle habits. So, what’s to blame for this stark contrast? Scientists and doctors have presented several theories in recent years, the most widely accepted of which is that younger generations consumed a diet high in processed foods when they were growing up.
Now, a groundbreaking new discovery also ties this rise in colon cancer to a childhood factor, which could be related to antibiotic use, diet, or even early childcare.
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Scientists found a link between colorectal cancer and exposure to a bacterial toxin in childhood.
The new study, published in the journal Nature, “identified a potential microbial culprit behind the alarming rise in early-onset colorectal cancer: a bacterial toxin called colibactin,” according to a press release.
Colibactin is a toxin that’s capable of altering DNA. It’s produced by certain strains of E. coli that reside in the colon and rectum.
The researchers analyzed 981 colorectal cancer genomes from patients across 11 countries. These cases accounted for both early- and late-onset cancer as well as varying colorectal cancer risk levels. They discovered the following consistencies:
- Colibactin-related DNA mutations were 3.3. times more common in colon cancer cases under age 40 than they were in those over age 70
- Around 50 percent of colon cancer cases under age 40 exhibited evidence of colibactin exposure
- Colibactin-related mutations arise early in tumor development, consistent with prior studies showing that such mutations occur within the first 10 years of life
- Colibactin-related mutations account for 15 percent of APC driver mutations—”some of the earliest genetic alterations that directly promote cancer development—in colorectal cancer”
“These mutation patterns are a kind of historical record in the genome, and they point to early-life exposure to colibactin as a driving force behind early-onset disease,” explained senior study author Ludmil Alexandrov, professor in the Shu Chien-Gene Lay Department of Bioengineering and the Department of Cellular and Molecular Medicine at UC San Diego. “If someone acquires one of these driver mutations by the time they’re 10 years old, they could be decades ahead of schedule for developing colorectal cancer, getting it at age 40 instead of 60.”
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How are children exposed to colibactin?
The study only determined a link between colibactin and colorectal cancer but did not investigate what’s driving this exposure. However, in speaking with NBC News, Alexandrov shared a few theories.
“There are several plausible hypotheses, including early-life antibiotic use, which may allow these strains to establish more easily; dietary shifts such as increased consumption of processed foods or reduced fiber consumption; increased rates of C-section births or reduced breastfeeding; and wider use of early group childcare which could facilitate microbial transmission during a critical developmental window,” he explained. “Collectively these shifts may be tipping the balance towards early-life acquisition of these microbes.”
How can the discovery inform future cancer prevention and treatment?
First, the researchers note that more research is needed to understand how children are exposed to colibactin-producing bacteria. Specifically, they want to learn more about whether certain environments (countries), diet, and other lifestyle behaviors are more conducive to colibactin production.
More immediately, the researchers are developing a stool sampling test to detect colibactin-related mutations.
“The goal is to identify people who are at elevated risk for developing early-onset colorectal cancer, ideally before any disease has developed,” Alexandrov told NBC News. “We would want to have these people regularly checked.”
His team is also exploring whether probiotics could potentially eliminate these bacterial strains.
“This reshapes how we think about cancer,” Alexandrov concluded in the press release. “It might not be just about what happens in adulthood—cancer could potentially be influenced by events in early life, perhaps even the first few years. Sustained investment in this type of research will be critical in the global effort to prevent and treat cancer before it’s too late.”
Content shared from bestlifeonline.com.