Diarrhea sucks. It can create unpleasant bathroom emergencies, and — all jokes aside — if you lack access to healthcare, it can be life-threatening.
But even though diarrhea has existed throughout time, it’s only now being understood why our bodies get the squirts.
In a study conducted on mice and published Wednesday in the journal Cell Host and Microbe, a team of pathologists and gastroenterologists at Brigham and Women’s Hospital in Massachusetts explain that diarrhea helps clear pathogenic bacteria from your intestines.
That’s right: Diarrhea might be good for you. By infecting mice with an intestinal bacterium called Citrobacter rodentium — which is similar to E. coli that infects humans — the researchers were able to study how the mice’s intestines attempted to flush out the bacteria with diarrhea. Here’s what they found.
The cells that line your intestines have small gaps between them, called intercellular tight junctions, which also have small pores that pass through them. These pores and tight junctions are essential to intestinal function, allowing ions, nutrients, water, and waste through. Principal invesigator Jerrold Turner, a gastroenterology researcher at Brigham and Women’s Hospital and Harvard Medical Center, and his colleagues found that the smallest and most selective gap, known as the pore pathway, becomes more permeable early on in an intestinal infection. It does this as a result of a protein called claudin-2, which is upregulated by another protein called interleukin-22. This increased permeability results in sodium ions and water entering the intestines and flushing out bacteria. And while this experiment was performed on mice, humans also possess these proteins.
This is a big step forward from our previous understanding of diarrhea, explains Turner. For a long time, doctors suspected that diarrhea was the body’s way of washing bacteria out.
“The problem is there was no data to speak to that,” he tells Inverse.
With this research, though, there’s strong evidence that this is true. And again, though this experiment was performed on mice, Turner is confident that these same intestinal mechanisms hold true for humans. “I think it’s probably exactly the same,” he says. This deepened understanding of diarrhea sheds new light on conventional wisdom.
Often when diarrhea strikes, our go-to response is to grab an anti-diarrheal drug like Lomotil (diphenoxylate hydrochloride and atropine sulfate) or Imodium (loperamide). These drugs, called antimotility agents, stop the intestines from moving feces in the usual way. This gives our bodies more time to draw water out of the stool, resulting in firmer feces. And while some older studies indicated that these might slow down the body’s natural defenses, there wasn’t enough evidence to say this for sure.
With this research, we’re gaining a greater understanding of how the body’s immune response leads to diarrhea in the case of a bacterial infection.
“What we showed is that diarrhea is actually really good for you. It’s your body’s way of saying, ‘We need something,’” Turner says.
He cautions that we’ll need further research to know exactly what’s going on, though.
“I don’t know if it’s as simple as washing away the bacteria,” he tells Inverse. “You could read our data that way, but that’s an area of ongoing investigation. I don’t know that it’s that simple, as just washing bacteria off the surface.”
One thing about treating diarrhea hasn’t changed: Turner says it’s still a good idea to stay hydrated and ingest electrolytes and glucose. In other words, drink some Gatorade or Pedialyte to replace lost nutrients.
Abstract: Diarrhea is a host response to enteric pathogens, but its impact on pathogenesis remains poorly defined. By infecting mice with the attaching and effacing bac- teria Citrobacter rodentium, we defined the mecha- nisms and contributions of diarrhea and intestinal barrier loss to host defense. Increased permeability occurred within 2 days of infection and coincided with IL-22-dependent upregulation of the epithelial tight junction protein claudin-2. Permeability in- creases were limited to small molecules, as expected for the paracellular water and Na+ channel formed by claudin-2. Relative to wild-type, claudin-2-defi- cient mice experienced severe disease, including increased mucosal colonization by C. rodentium, prolonged pathogen shedding, exaggerated cyto- kine responses, and greater tissue injury. Conversely, transgenic claudin-2 overexpression reduced dis- ease severity. Chemically induced osmotic diarrhea reduced colitis severity and C. rodentium burden in claudin-2-deficient, but not transgenic, mice, demon- strating that claudin-2-mediated protection is the result of enhanced water efflux. Thus, IL-22-induced claudin-2 upregulation drives diarrhea and pathogen clearance.