Dr Chey reviews his presentation on the role of diet in disorders of gut-brain interaction from Digestive Disease Week  2024.

William Chey, MD, is the H. Marvin Pollard Professor of Gastroenterology, professor of Nutrition Sciences, and chief, Division of Gastroenterology & Hepatology, at University of Michigan Medicine in Ann Arbor, Michigan.

TRANSCRIPT:

My name is William Chey. I'm a professor of gastroenterology and nutrition sciences at Michigan Medicine in Ann Arbor, Michigan and I'm the chief of GI and Hepatology in the Division of Gastroenterology and Hepatology.

Recently I spoke about the role of food in the pathophysiology of disorders of gut -brain interaction at Digestive Diseases Week, 2024. And in that discussion, I emphasized that food is our main source of nutritional sustenance, but is also really important culturally, and further is an immense source of enjoyment.

I mean, think about last time you went on vacation and how you planned your day, right? It's really always around mealtime. So, food is an incredible source of pleasure and an important part of our culture, but for patients with disorders of gut -brain interaction—let's use the examples of functional dyspepsia and IBS—food can become quite a burden rather than just a source of enjoyment and sustenance. And there's many reasons why food can lead to symptoms in patients with disorders of gut-brain interaction like FD and IBS.

There are direct effects, so the chemical effects, the osmotic properties, the physical characteristics, as well as remember the food's not sterile, a lot of times there's bacteria in food, there are bacterial components, there are foods that encourage the growth of certain types of bacteria, so prebiotics, so there are many direct effects and then there are also indirect effects usually through the process of fermentation. So carbohydrates remember are fermented to short-chain fatty acids which create an osmotic load and lead to water secretion into the bowel. Also those short-chain fatty acids are fermented to produce gases and you can imagine that in a patient with a DGBI who has visceral hypersensitivity or motility abnormalities that creating a big osmotic load and distending the lumen of the bowel will trigger symptoms.

So think of food as a really important trigger for symptoms in patients with DGBI. If that were the end of the story it'd be interesting enough but it's not the end of the story. You know there's fascinating recent research to suggest that there may also be immune activation after the ingestion of a variety of foods.

I think people won't be surprised that there's immune activation after exposure to certain proteins. That's the whole concept between food allergy. But people might be surprised to learn that carbohydrates are increasingly showing evidence of immune activation as well.

So for example, the FODMAP hypothesis, as we predicated on the osmotic effects and the fermentation effects of FODMAPs, may be complicated by changes in the microbiota that occur in response to a high FODMAP diet that leads to the production of a variety of different mediators, like lipopolysaccharide, which can affect permeability and lead to greater exposure of the gut immune system to a variety of antigens as well as LPS, which can lead to mast cell activation. So, the story is a lot more complicated than we've given a credit for to this point. For people like me, that's super exciting because there's lots of different things that we need to do research on and learn about.

But for people at home, the take-home message is this: food is complicated. We tend to always want to oversimplify things to make it easier to understand, but understand this, and that is that we're really just to the beginning of starting to scratch the surface and our understanding of how food causes symptoms in patients with DGBI. So stay tuned, we have a lot to learn.