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Smoking is rarely linked to health benefits, but it has long been observed to ease colitis while worsening Crohn’s disease. New research suggests the difference comes down to how bacteria move within the gut—a finding that could lead to better treatments.
Scientists Puzzled by 40-Year Smoking Paradox in Colitis and Crohn’s Disease
Researchers at Japan’s RIKEN Center for Integrative Medical Sciences note that scientists and patients have recognized this smoking paradox for about 40 years. Both ulcerative colitis and Crohn’s disease fall under inflammatory bowel diseases (IBDs), making it puzzling that smoking eases one but worsens the other. Ulcerative colitis involves inflammation of the colon’s lining, while Crohn’s can appear as inflamed patches throughout the digestive tract and may affect every layer of the bowel wall.
Like much of modern biology, the RIKEN team looked to the gut microbiome to investigate the paradox. They wanted to see whether smoking encourages certain gut bacteria to flourish in ways that might explain its effects on IBDs.
Their findings showed that in smokers, bacteria such as Streptococcus—normally found in the mouth—were thriving in the mucus layer of the intestinal wall. Typically, these mouth-dwelling microbes pass harmlessly through the digestive system without settling in the colon. Smoking, however, appeared to give them the ability to take hold in the gut.
Gut Metabolites Reveal Why Smoking Helps Colitis but Harms Crohn’s
To understand why, the researchers examined gut metabolites—the byproducts of digestion. In smokers, they detected elevated levels of hydroquinone, a compound that allowed oral bacteria like Streptococcus to survive and multiply in the gut.
But why would these mouth bacteria benefit people with ulcerative colitis while worsening Crohn’s disease?
Mouse studies provided the answer. The researchers discovered that when oral bacteria thrived in the gut, they activated helper Th1 cells—immune cells that help fight infections. In colitis patients, these Th1 cells suppressed the immune response that normally triggers colon inflammation, easing symptoms. In Crohn’s patients, however, Th1 cells are themselves the drivers of inflammation, so their activation only made the condition worse.
Naturally, the researchers stress they are not recommending smoking as a treatment for ulcerative colitis, given its well-documented health risks. Instead, they believe their findings shed new light on IBDs and point toward potential therapies.
“Our results suggest that the movement of bacteria from the mouth to the gut—particularly Streptococcus—and the resulting immune response in the gut is the mechanism by which smoking offers protection against the disease,” explained lead researcher Hiroshi Ohno. “This means that directly introducing these bacteria, or indirectly using hydroquinone, could replicate smoking’s benefits without its harmful effects.”
Read the original article on: New Atlas
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