How childhood diet may lead to a rise in bowel cancer among young adults
The global incidence of early-onset colorectal cancer in individuals under the age of 50 has doubled in the past 20 years.
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New evidence suggests that what we eat in childhood - particularly diets high in sugar and ultra-processed foods-may cause serious health issues decades later, including colorectal (bowel) cancer.
Lifestyle choices, such as high intake of sugary drinks, alcohol, and processed foods, have already been linked to a rise in young-onset colorectal cancer.
However, new research raises the possibility that early-life environmental and biological factors, including microbial activity in the gut, could be playing an even more influential role than previously thought.
Scientists have shed new light on a bacterial toxin called colibactin that may further explain the rapid rise of this cancer in younger adults, especially those exposed early in life.
According to a new report published in Nature, the global incidence of early-onset colorectal cancer - defined as occurring in individuals under the age of 50 - has doubled in the past 20 years.
If this trend continues, bowel cancer is expected to become the leading cause of cancer-related deaths in young adults within the next few years.
An international research team analysed tissue samples from 981 patients across 11 countries, looking for cancer-driving mutations in the DNA.
In over half of the early-onset cases, scientists found mutation patterns linked to colibactin, a toxin produced by certain strains of Escherichia coli (e. coli) in the gut. These mutations, often referred to as “molecular scars,” point to early-life exposure as a potential cause.
“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,” explains Professor Ludmil Alexandrov, a computational biologist at the University of California San Diego.
Although the exact source of this early exposure remains unclear, researchers believe it most likely occurs within the first ten years of life, possibly through gut infections involving colibactin-producing bacteria.
Once the toxin damages the DNA in the bowel, it can set in motion a process that leads to cancer years, or even decades, later.
The study found that DNA mutations associated with colibactin were more than three times as common in patients diagnosed before the age of 40 compared to those diagnosed at 70 or older.
Older adults were more likely to exhibit DNA changes linked to natural ageing rather than bacterial exposure.
“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 40 instead of 60,” says Alexandrov.
Scientists are also investigating how the risk factors for colorectal cancer may vary from country to country.
“There may be unknown causes specific to certain regions,” says Dr Marcos Díaz-Gay of Spain’s National Cancer Research Center, that could lead to more targeted, localised prevention strategies.
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