I got my colonoscopy last year. Sitting in the prep room, I kept thinking about something most gastroenterologists still aren’t talking about.
Twice a year, you sit in a dental chair and let someone examine your mouth for an hour.
They chart your gum pockets, note your bleeding, photograph your recession. They know your mouth better than anyone in healthcare — and they see you more regularly than your doctor does.
Almost none of them know that what they’re looking at may be one of the earliest warning signs of colon cancer.
In January, the American Cancer Society published 30 years of U.S. cancer death data in JAMA. The number that floored me: colorectal cancer is now the #1 cause of cancer death in Americans under 50, as of 2023. It was fifth in 1990. Every other major cancer in that age group — breast, lung, leukemia, brain — is declining. This is the only one going the wrong direction.
Five things your mouth may be telling you right now
1. Your gums bleed when you brush or floss. This is the most important signal on this list. Bleeding gums mean the barrier between your oral microbiome and your bloodstream is broken — every day, with every meal. Harvard researchers found that people with periodontal disease have a 17-21% higher risk of precancerous colon polyps. The bleeding isn’t just a symptom. It’s the mechanism.
2. You have bad breath that brushing doesn’t fix. Fusobacterium nucleatum — the oral bacterium now found living inside colon tumors — is one of the primary producers of the volatile sulfur compounds behind chronic bad breath. If brushing helps temporarily but the problem keeps returning, your anaerobic bacterial load may be elevated.
3. Your tongue has a persistent white or yellowish coating. Fn colonizes tongue biofilm heavily. Most people never touch their tongue during their oral care routine. That coating is like a reservoir. You swallow roughly a liter of saliva every day, and everything living on that tongue goes with it.
4. Your gums look puffy, or your gumline is receding. Recession signals years of accumulated periodontal damage. Puffy, tender gums without visible bleeding is early gingival inflammation — almost entirely asymptomatic, which is exactly why it goes unaddressed for years.
5. You’ve lost teeth. People who have lost four or more teeth — a proxy for decades of untreated periodontal disease — have a 20% higher risk of precancerous colon polyps, per Harvard and AACR data. Losing even one to three teeth raises the risk of advanced adenomas by 28%.
None of this means you have cancer. But these are signals that your oral microbiome is out of balance in ways that go far beyond your mouth.
What the research actually shows
A 2024 study published in Nature identified a specific subtype of Fn that appears to have evolved to make the journey from mouth to colon. It survives stomach acid that kills most other oral bacteria. It navigates the full length of the digestive tract. It hides inside tumor cells. And in more than 40% of colorectal cancer cases studied, the strain found inside the tumor was genetically identical to the strain in that same person’s saliva.
The rest of what we know:
- Fn has been found not just in primary tumors, but in distant metastases — tumors that had already spread to other organs. It appears to travel with the cancer
- Fn is associated with resistance to standard chemotherapy — meaning oral bacteria may influence not just whether you develop colorectal cancer, but whether treatment works if you do (Yu et al., Cell Host & Microbe, 2017)
- A 2024 meta-analysis of 16.6 million people across 19 studies found a 21% higher colorectal cancer risk in people with periodontal disease
- The same Harvard researcher found gum disease raises stomach cancer risk by 52%
- Colorectal cancer caught early: survival above 90%. Three out of four people under 50 are currently diagnosed at advanced stage — because nobody told them to look sooner
Columbia University researchers added one more layer. Fn doesn’t attack healthy colon cells. It only accelerates cancerous ones — because cancer cells produce a specific protein called Annexin A1 that Fn latches onto. Fn then triggers more Annexin A1 production, attracting more Fn, in a feedback loop that makes an already dangerous situation dramatically worse. They called it a two-hit model: genetic mutations are hit one. Fn is hit two.
My theory
Researchers are still working on the “why.” But I want to share a hypothesis I’ve been turning over for a while — one that I think deserves to be said out loud, even if we can’t fully prove it yet.
Colorectal cancer typically develops slowly. An early polyp takes 10 to 15 years to progress to invasive disease. That timeline matters, because it means the cancers we’re diagnosing in 2025 and 2026 didn’t start recently. They started brewing a decade ago — or longer.
But Fusobacterium nucleatum doesn’t appear to start cancer. It accelerates it. The research increasingly points to Fn as a tumor promoter — something that finds an existing precancerous lesion and speeds it toward malignancy. That distinction changes the math.
Here’s what I think may be happening.
By 2020, roughly 30% of American adults aged 30–44 already met clinical criteria for periodontitis. Many of them had Fn-laden biofilm in their mouths and had no idea. Then COVID hit — and with it came a global, simultaneous disruption to every behavior that protects the oral microbiome. Prolonged stress. Ultra-processed snacking at home. Disrupted sleep and routines. More mouth breathing from anxiety and congestion. Windows closed and poor indoor air quality driving even more mouth breathing. Reduced access to fresh food. And in many cases, delayed or skipped dental care for months at a time.
Every one of those factors pushes the oral microbiome toward dysbiosis. And dysbiosis means more Fn — not just in the mouth, but in the gut, and potentially in precancerous tissue that was already there, waiting.
If polyps existed before 2020 — and statistically, many of them did — a 4 to 6 year window of accelerated microbial activity could plausibly explain a surge in diagnoses right now. The timing isn’t wrong for this theory. It may actually be the evidence.
I want to be clear: I can’t prove this chain of events. Nobody can yet. The data connecting COVID-era oral disruption to downstream cancer acceleration simply doesn’t exist in the form we’d need to be certain. But thinking this way changes what prevention looks like — and it makes the case for catching oral dysbiosis early, with actual molecular testing rather than waiting for a pocket depth of 4mm and visible bleeding. If we can identify and correct the microbial imbalance before it becomes periodontitis, we may not just be protecting gums and teeth. We may be doing something far more significant.
What else aren’t we seeing?
That’s the question that keeps me up at night…
We know COVID was a systemic inflammatory event. We know it disrupted the oral microbiome in ways that persisted long after the acute infection resolved. We know the oral microbiome communicates with the gut, the cardiovascular system, the brain, and the immune system — constantly, through saliva, through the bloodstream, through the gut-oral axis.
We have good data on what COVID did to lungs. We have reasonable data on the heart. We have almost no long-term data on what it did to the oral microbiome — and through that, what ripple effects may still be moving through the body right now.
Colorectal cancer may be the first signal. I doubt it will be the last.
“So why not just get a colonoscopy and skip the flossing?”
It’s a fair question…
A colonoscopy happens every five to ten years. Your mouth does something to your body every single day — swallowing Fn, potentially releasing it into your bloodstream through bleeding gums, 365 days a year for decades.
Oral health is working upstream of where colonoscopy operates, continuously, in ways no screening appointment can reach.
But the more important answer: even if you get a colonoscopy and they find cancer, elevated Fn in the tumor is associated with worse chemotherapy response and worse survival. Oral health may affect not just whether you develop colorectal cancer, but whether treatment works if you do. It’s not either/or. It’s both.
What you can do — starting tonight
Know what’s actually in your mouth. This spit test tests your saliva and gives you real Fn levels — without this, we’re flying blind. I serve as the scientific advisor for this company because measuring what’s there, rather than guessing, is where dentistry needs to go.
Replace mouthwash with oil pulling. Standard antiseptic mouthwashes kill indiscriminately — including the beneficial bacteria that keep Fn in check. Oil pulling with a blend formulated with the oral microbiome in mind, like Oragin, reduces pathogenic anaerobes without that collateral damage. Just a minute or two before brushing. Pair it with a stainless steel tongue scraper every morning — I made one, but any works…I prefer stainless steel. These two habits together meaningfully change what your mouth sends downstream before breakfast.
Support your gum tissue from the inside. There’s a well-documented connection between CoQ10 deficiency and periodontal disease — gum tissue depends on it for basic cellular function. This is the CoQ10 I take. If you’re thinking about gum health systemically, it belongs in the picture.
Rebuild your oral ecosystem. Oral probiotics with Streptococcus salivarius K12 — this is the one I recommend — shift the bacterial balance away from Fn and toward beneficial species. Think less about evicting one tenant, more about making the neighborhood inhospitable.
Find a dentist who takes this seriously. My Functional Dentist Directory connects you with dental practitioners who understand the oral-systemic connection. If you have any of the signs from the list above, it’s also worth a direct conversation with your doctor about earlier colorectal screening — bring this research to that appointment.
Get the colonoscopy. Oral health is not a substitute for screening. It’s what you do alongside it. The prep is one bad day. Catching this early is a completely different conversation from catching it late.
The bacteria made a journey. It survived stomach acid, traveled the full length of the digestive tract, found the one type of cell it could latch onto — not healthy colon cells, only cancerous ones — and fed the fire. In nearly half of cases studied, researchers can prove it came from that same person’s mouth.
The mouth is an active participant in your body. And unlike most cancer risk factors, this one is right there in your bathroom cabinet every morning. What are you going to do about it?
See you next week,
Mark
Further Reading & Citations
Colorectal Cancer Incidence and Mortality Trends Siegel RL, Giaquinto AN, Jemal A. Cancer statistics, 2026. CA: A Cancer Journal for Clinicians. 2026 Jan 22.
Fusobacterium nucleatum and Colorectal Cancer Zepeda-Rivera M, Minot SS, Bouzek H, et al. A distinct Fusobacterium nucleatum clade dominates the colorectal cancer niche. Nature. 2024;628(8007):424–432. doi:10.1038/s41586-024-07182-w. PMID: 38509359
Yu T, Guo F, Yu Y, et al. Fusobacterium nucleatum promotes chemoresistance to colorectal cancer by modulating autophagy. Cell. 2017;170(3):548–563. PMID: 28753429
Rubinstein MR, Baik JE, Lagana SM, et al. Fusobacterium nucleatum promotes colorectal cancer by inducing Wnt/β-catenin modulator Annexin A1. EMBO Reports. 2019;20(4):e47638. doi:10.15252/embr.201847638. PMID: 30833345
Komiya Y, Shimomura Y, Higurashi T, et al. Patients with colorectal cancer have identical strains of Fusobacterium nucleatum in their colorectal cancer and oral cavity. Gut. 2019;68(7):1335–1337. PMID: 29934439
Periodontal Disease and Colorectal Cancer Risk Lo CH, Nguyen LH, Wu K, et al. Periodontal disease, tooth loss, and risk of serrated polyps and conventional adenomas. Cancer Prevention Research. 2020;13(8):699–706. PMID: 32727821
Periodontal Disease and Upper GI Cancer Risk Lo CH, Kwon S, Wang L, et al. Periodontal disease, tooth loss, and risk of oesophageal and gastric adenocarcinoma: a prospective study. Gut. 2021;70(3):620–621. PMID: 32690603