Opinion: I’ve seen the rise in colon cancer cases. As doctors, we must take young people more seriously.

Colorectal cancer is now the number one cause of cancer death among young men and the second leading cause among young women.

(NCI Center for Cancer Research | The Associated Press) This microscope image made available by the National Cancer Institute Center for Cancer Research in 2015 shows human colon cancer cells with the nuclei stained red. On Friday, May 29, 2020, doctors are reporting success with newer drugs that control certain types of cancer better, reduce the risk it will come back and make treatment simpler and easier to bear.

It was movie night on a Friday in the summer of 2020 when my phone rang.

I had been watching “Black Panther” with my son when one of my friends called to see if I had heard the news about actor Chadwick Boseman. With a sense of foreboding, I asked what he meant.

After a pregnant pause, he responded: “Mark, he died.”

And the reason my friend was calling me — a gastrointestinal oncologist — was that the cause of death was colon cancer.

I stared in disbelief at the screen where I had paused the movie, and where Chadwick Boseman was frozen, literally portraying a superhero.

Even with a newly clinical eye, I could only perceive a fit actor at the peak of his powers. It was hard to imagine that he was in anything other than perfect health.

And yet there was a part of me that could make sense of this cognitive dissonance, because in my professional life I had been taking care of younger and younger patients with the same cancer type.

This troubling rise in cases is sometimes described as a “birth cohort effect,” which means that patients born in 1990 have double the risk of colon cancer (and quadruple the risk of rectal cancer!) versus what patients born in 1950 faced at a comparable age.

Colorectal cancer is now the number one cause of cancer death among young men and the second leading cause among young women (defined as no older than 49).

There is a common misconception that cancer is solely a result of getting older. While it is true that cellular senescence is the driver of aging, cancer is almost precisely the opposite, perhaps the closest we can come to immortality on a microscopic scale: cells that can divide indefinitely.

In fact, the very lack of growth inhibition is a hallmark of cancer.

So why is this happening? In his book, “The Gene,” author Siddhartha Mukherjee proposed this formula summing the causes of any disease, including cancer: heredity + environment + triggers + chance.

Looking at the component parts of that formula, we estimate that up to a quarter of early-onset cases can be attributed to inherited risk, e.g. syndromes that can be transmitted from generation to generation like familial adenomatous polyposis (FAP) or hereditary non-polyposis colorectal cancer (more commonly known as Lynch syndrome).

But that still leaves most cases to be explained by other causes, which we often refer to as “sporadic” because they occur in the absence of a pathogenic family history.

One way of conceiving this acquired risk is the “exposome,” which in colorectal cancer aims to measure the biologic effect of everything that passes through the gut during our lifetime, ranging from foods to antibiotics.

Nutritional epidemiology — the effect of diet on diseases at the level of entire populations — is notoriously difficult to study but some researchers have suggested that the high-temperature preparation of red meat can generate carcinogens like heterocylic amines and polycyclic aromatic hydrocarbons.

A study within the National Health Service in the United Kingdom suggested that young-onset colorectal cancer patients were more likely to have been prescribed antibiotics in childhood, presumably then changing the bacteria within their intestinal microbiome to favor carcinogenic species.

Partly in response to this shifting demography, the United States Preventive Services Task Force — the government body most responsible for issuing screening recommendations — in 2021 lowered the age of first screening for colorectal cancer for average-risk individuals from 50 to 45.

While at-home fecal testing is increasingly prevalent, the gold standard for screening likely remains colonoscopy, because during that procedure doctors — typically gastroenterologists or surgeons — don’t just identify pre-cancerous polyps but can remove them, interrupting what we call the adenoma-to-carcinoma sequence. Put another way, a polyp that is completely removed during colonoscopy no longer has the chance to invade and grow into a true cancer.

And yet, even this earlier screening may not be enough to “catch” some patients’ colorectal cancer.

Just over 70% of young-onset cases are stage III (locally advanced) or stage IV (metastatic) at the time of diagnosis, and as such frequently require chemotherapy.

As recently as this spring, Melissa Inouye — a religious scholar and historian for the Church of Jesus Christ of Latter-Day Saints — died at age 44 of metastatic colon cancer, initially diagnosed when she was 37 and, as she wrote with near-disbelief in one of her books, otherwise in terrific shape, running marathons and eating organic produce she grew in her own garden.

Tragic cases like Chadwick Boseman and Melissa Inouye’s are a call to action, to take young patients’ gastrointestinal concerns (especially bleeding but also changes in bathroom habits like narrower stools and pain on defecation, or even unintentional weight loss) more seriously.

Screening is different than diagnosis, and any symptomatic patient at any age should merit medical attention.

(Photo courtesy of Intermountain Health) Mark Lewis

Mark Lewis, MD, is the director of gastrointestinal oncology at Intermountain Health.

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