Currently, 250,000 people suffer from chronic inflammatory bowel disease (IBD) in France. For so long, gastroenterologists refused to see a correlation between diet and these diseases (Crohn’s disease and UC), things are starting to change. The role of the intestinal microbiota is now much better known.
Benoît Chassaing, research director at Inserm, has made it his specialty. 20 minutes met him at the national IBD fair, to understand the link between ultra-processed food, microbiota and intestinal diseases.
Does ultra-processed food have an impact on the evolution of chronic intestinal diseases?
Several clinical trials show that diet plays either a protective or negative role in the onset and chronicity of Crohn’s disease and UC. And it goes through the microbiota. These studies show that processed and ultra-processed diets tend to promote the onset and chronicity of IBD, while a rich and balanced diet with fiber consumption, without additives and not processed, is associated with a decrease in the incidence of IBD.
For example, we were interested in emulsifying agents. Not all of them are necessarily bad. Soy lecithin or mono and diglycerides of fatty acids, two emulsifiers that are widely used in France, seem completely harmless. Unlike carrageenans, which are widely used in chocolate dessert creams for their gelatinous side, soy milk or coconut milk, and whose pro-inflammatory power is known and recognized.
Does the diet we received at an early age also play a role in the occurrence of these diseases?
Yes, some studies show that people who will develop IBD consume more emulsifying agents and ultra-processed foods than people who will not develop the pathology. We know that there is a genetic factor in these diseases. The Japanese, for example, had very few IBD. One could think that they had a genetic ground which made them more resistant. But we have realized, during waves of migration, that when these populations arrive in countries where there are many IBD, in one generation, the children have a risk of IBD equivalent to the country in which they have immigrant. The genes didn’t mutate on the plane, so there’s clearly an environmental factor. We believe that processed food will impact the microbiota and will therefore reveal the pathology in people who were at risk of developing it.
Cooking and stopping eating processed foods is fine. But I live in Paris. I have two children. I know it’s complicated. In fact, ideally, patients at risk should be identified and they should be very careful. The other patients, having a disease caused by other factors, would be left alone. That is the key to personalized medicine.
You mean not all people with IBD are impacted by ultra-processed food?
No, especially concerning emulsifying agents. We saw this with mouse models, then with the first clinical study in humans. When given a particular emulsifying agent to healthy humans, some do not respond at all and others have a very sensitive microbiota, which becomes pro-inflammatory. It is a pilot study and short in time, so these are not patients who have developed a pathology. But some people are thought to have microbiota that, if brought into daily contact with food additives, could lead to chronic inflammatory disease after two, five or ten years.
Can the microbiota also play a role in the way the treatment will react on the patient?
Yes. At the level of Crohn’s disease and UC, it is still at the research stage, but where it is much more advanced is at the level of cancer treatments. Research shows that in certain therapies related to certain cancers, there are responders and non-responders. Example with patients with the same cancer, taking the same drug: for some, it does not work at all while for neighbors it works. This research has shown that differences in microbiota lead to the effectiveness or ineffectiveness of treatment.
If the microbiota allows the effectiveness of the treatment, we do the treatment. If we have a microbiota that does not allow efficacy, we will do a fecal transplant from a donor which will allow the efficacy of the treatment. Preliminary data shows it works. It’s still extraordinary to be able to modulate the microbiota in order to promote the therapeutic response.
Precisely, where are we in terms of fecal transplantation?
For now, it’s only at the research level. Today, I really advise against fecal transplants done at home, because you have to be very careful about the donor you use. We will take the microbiota from a donor who is healthy and we will transplant it into someone who is at risk, having a pathology. Some bacteria can carry resistance to antibiotics, for example. We must be careful to take donors who do not have these bacteria. In the United States, there were mistakes made because the regulations had changed. And there were two deaths. These patients should never have received these microbiota. But I really think that in the longer term, fecal transplantation can benefit patients. When we have identified the good recipients, the good donors, the good donor-recipient couples, that can help them.