Why Are so Many Young People Getting Colon Cancer? the Answer Could Trace Back to Infancy
NEWS | 30 December 2025
This story is available exclusively to Business Insider subscribers. Become an Insider and start reading now. Five years ago, Tim Cannon, a cancer doctor in Virginia, saw that his colon cancer patients were getting younger and their cancer was more aggressive. He had just diagnosed three people in their 30s with late-stage colon cancer. More perplexing, all three were athletes who competed in long-distance, endurance sports. "Within a six-month period, I saw three extreme athletes in their 30s with metastatic, very advanced, incurable colon cancer," Cannon told Business Insider. All three patients died. Cannon had a hunch that this pattern wasn't an anomaly. He examined 100 more long-distance runners between 35 and 50 years old and found that 39 had developed precancerous tumors in their colons. Fifteen of those cases were advanced — far more than the expected 1.2%. Nearly one-sixth of all the runners were at risk of developing colon cancer. It was startling. Cannon's research, which is still in its early stages, points to broader questions that have confounded the medical community: Why are so many young, fit adults getting sick and dying from colon and rectal cancer? And why are these patients — people who are younger than 45, the age at which screening is first recommended — getting the most aggressive forms of the disease? "The steepest rise is in people in their 20s and 30s," said Dr. Kimmie Ng, director of Dana-Farber's Young-Onset Colorectal Cancer Center. "They're younger, they're healthier, they don't have comorbidities, they get more treatment — and yet they're not living longer." In January, Business Insider reported on the leading scientific theories for why people with clean diets get colon cancer. Possible answers ranged from microplastics to antibiotics. Leading theories generally pinpointed the modern diet, including too much sugar, and other facts of modern life, like staring into the blue light of our phones late at night, which can disrupt our natural rhythms. These factors are likely part of the picture, oncologists say. But there's more to explore. Clusters of early-onset cancers like the one that Cannon says he identified are helping us gain a better understanding of the disease — and some answers for what ordinary people can do about it. Cancer researchers are discovering how different environmental factors interact with our systems in complex ways and at different points of our development. And they're increasingly zeroing in on the first year of life — from birth itself to our first months out of the womb — for answers about young cancer. Some early research is scratching at the idea that a vulnerability to colorectal cancer could start in infancy — suggesting the first months and years of life could be a key window for intervention. "Something that happened at age six months, you don't even consider when you're 35. That disconnect is extremely problematic." At UC San Diego, molecular biologist Ludmil Alexandrov recently identified a mutational signature in more than half of colorectal tumors found in patients under 40 that appears to be caused by colibactin, a toxin produced by a specific strain of E. coli. What startled researchers was the timing of the damage. Cancer researchers typically find DNA damage building up in the adult body. Smoking, grilling meats, work like mining or asbestos-spraying — these well-trodden cancer triggers are typically ignited when our DNA is already becoming more decrepit and unstable, with time and age. Here — according to the paper Alexandrov published in Nature in April — the infection had occurred before babies reached their ninth month of life. Alexandrov's research, while preliminary, suggests infants can be hit with DNA mutations just months into their lives that might leave them predisposed to developing cancer within a few decades. "You get your first hit at age 1 instead of age 30," Alexandrov said. "So you are about 20 to 30 years ahead of schedule for cancer." "Something that happened at age 6 months," Alexandrov added, "you don't even consider when you're 35." "That disconnect is extremely problematic." If Alexandrov's finding is confirmed in bigger studies, it could reframe the mystery of early-onset colorectal cancer. The rise could be rooted in early life, with early adulthood simply being the point at which the long incubation period finally comes to a head. If colibactin infections are a major early trigger, the most effective strategy may be preventing that mutational DNA damage in the first place. The next generation of cancer prevention may involve targeted microbial restoration and dietary strategies designed for an infant's developing immune system. Alexandrov envisions targeted probiotics for infants that neutralize colibactin-producing bacteria. "If we can monitor the mutations and see that the ones exposed to the probiotic don't appear," he said, it could mean "we're eliminating the cause." Ng says Alexandrov's findings "cement a role of the microbiome in this disease." Shifts in how babies eat, including more ultra-processed food and fewer fiber-rich ingredients, could drive up colibactin infection rates. While researchers suspect that colibactin infections in infants have been on the rise in recent decades, there isn't enough data yet to say for sure. More study is also needed to confirm the link of any such rise to colon cancer. It's not just diet that could be playing a role in the rise. Researchers are also looking at shifting trends in how babies are born. Our first moments of life are a pivotal training ground for the gut — a baby's welcome party to our diverse world of bacteria, fungi, and viruses. Babies born vaginally pass through the birth canal and pick up critical microbial communities from their mothers — microbes that help train the immune system. C-section babies start life with different microbes, and the evidence is mounting that these early differences may have an impact. "There is strong evidence that early-life microbial disruption can influence long-term health risk," said Dr. Maria Gloria Domínguez-Bello, a professor at Rutgers University who has pioneered infant microbiome research and looked at the links between an infant's microbiome and their risk for adult diseases, including IBS, ulcerative colitis, and colon cancer. She noted that modern changes to birth and feeding practices may lead to subtle yet consequential disruptions to the microbiome. In 2016, Domínguez-Bello launched a landmark study on "vaginal seeding" — taking babies born via C-section and coating them with bacteria from the mother's vaginal canal. It will be years before we know the effectiveness of this approach, but the hope is that this small intervention may have bolstered their microbiome from day one. Then, there's feeding. Breastfeeding is one of the ways infants acquire early protective microbes. Breastmilk is packed with complex sugars — human milk oligosaccharides — that babies' gut bacteria can feed on, shaping the early immune system. It can also contain traces of what the mother ingests or has been exposed to. Multiple large-scale studies have found that the gut bacteria of formula-fed babies tend to differ from those of breastfed babies. While questions remain, this research is reshaping the infant formula market. Companies like Biomilq and Helaina are developing "microbiome-friendly" formulas that contain synthetic versions of the complex sugars found in breastmilk. Early clinical trials show these products can nudge a baby's gut bacteria to look more breastfed, though whether that matters decades later remains unknown. Still, these formulas have become one of the fastest-growing segments of the infant nutrition industry. Consuming too much sugar is emerging as a key culprit that may be shaping what happens to our microbiome. Ng's group has found that sugary diets — especially sugary drinks including soda, juice, and sports drinks — are associated with a higher risk of early-onset colon cancer. Food that spikes insulin or glucose "is linked with a higher risk of colorectal cancer," too, she said. Dr. Andrea Cercek at Memorial Sloan Kettering noticed something else: Among her youngest patients with stage 4 cancer, sugar consumption stood out. "There were slight differences in risk factors — and sugars in particular," Cercek said. The idea aligns with prior studies showing that fructose can accelerate polyp growth in animal models. "A high fiber diet produces metabolites that suppress colon cancer risk. A high saturated meat diet produces metabolites that are inflammatory and carcinogenic." It doesn't mean sugar "causes" cancer. But modern, ultra-high levels of sugar intake may be accelerating disease in people whose risk was primed early. And they're crowding out what people once used to balance out sugar's effect on the body, improving blood sugar and aiding digestion at the same time: fiber. Sugar can be great for a quick burst of energy, but in the long run, we need fiber to slow it down and promote good gut health. This is especially true of resistant starch (beans, lentils, oats), the type that ferments in the gut and produces short-chain fatty acids that suppress inflammation. Dr. Stephen O'Keefe, who studies Alaska Native communities with historically high colorectal cancer rates, recently found that adding a resistant starch supplement to people's diets for just four weeks had measurable effects. "The supplementation did suppress cancer biomarkers," he said, discussing the findings he presented to colleagues at Digestive Disease Week 2025. "A high fiber diet produces metabolites that suppress colon cancer risk," he said. "A high saturated meat diet produces metabolites that are inflammatory and carcinogenic." He's seen this kind of thing before, noting important, negative microbial changes occurred quite rapidly when he fed rural, bean-eating South Africans typical American foods like hamburgers and hash browns for two weeks. O'Keefe believes increasing fiber intake could meaningfully offset other dietary risks, and perhaps reshape the microbiome in protective ways. Once researchers began looking beyond diet, they started interrogating other environmental changes as possible multipliers of an individual's risk of colorectal cancer. Artificial light at night — particularly from phones — disrupts circadian rhythms that regulate DNA repair. Long periods of sitting can slow gut motility and increase inflammation. Air pollution inflames the gut lining and introduces carcinogenic particles directly to the colon. These aren't "causes" in isolation. But, together with nutrition and metabolism, they can disrupt how genes operate. Over time, these changes can trigger more disease. This is the focus of Dr. Heinz-Josef Lenz's research at the University of Southern California Cancer Center. As a gastroenterologist, he has been troubled by a rise in young Latino men developing colon cancer in high school and college — many of them are athletic and healthy with no known risk factors. Lenz says their higher-than-average occurrence of young colon cancer is not due to any particular genetics. "What can it be when it's not genetic? It could be epigenetic," he said. "Meaning, what you do, what you eat, what you drink, and related to your parents — how they acted and behaved." Already, he's seeing clues that young Latino athletes with colon cancer might be suffering from nutritional changes that span multiple generations, based on changes that are inherited. For one 15-year-old in Los Angeles, it's possible that a daily Gatorade is enough to promote tumor growth in the colon, while for someone else with a different background, it's not such a big deal. Though Lenz has seen some interesting data on fructose pathways that appear dysregulated in young colon cancer patients, he is cautious to point out that nothing has emerged that is definitively an "it" cancer-causer just yet. "The data should be becoming available in the next one or two years," he said. The hope is that, with time and some more research, Lenz will be able to better tailor treatments to a patient's genetics and background, making each one more effective. One promising target is the circadian rhythm, or a person's body clock. Lenz recently teamed up with top body clock researcher Dr. Steve Kay to examine the effects of manipulating the body clock on cancer treatment. "What we found is that some circadian clock proteins our lab has been researching for many years are the 'gas pedal' to cancer," Kay said in a press release. "Out of that came a whole set of experiments that started to really blow all of us away. Drugs that my lab developed to target the circadian clock showed they could kill colorectal cancer cells." For oncologists, the rise in young cases is not just a scientific challenge. Young patients often arrive confused and ashamed because they believe cancer is strongly associated with their own lifestyle choices. Cannon says this misconception adds to the pain. "The public understands cancer as more related to personal behavior than oncologists do," he said. "You don't have total control over this, as far as I can tell." All of the researchers we spoke to for this story cautioned that people shouldn't misinterpret this emerging science as a lifestyle playbook just yet. They did encourage some lifestyle modifications. This includes more fiber, less sugar, more movement, and better sleep. When it comes to the extreme athletes Cannon is studying, his own leading hypothesis is that the stress of extreme endurance training might starve intestinal tissue of oxygen and create more opportunities for cancerous mutations. His research is far from conclusive. "The theories are all over the place," he said. "I don't want to overstate how much you can control this with any behavior," he said. "In the end, it's still a chance event."
Author: Mia De Graaf. Hilary Brueck.
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