PARIS, February 29, 2024 – A mother’s diet during and before pregnancy can subtly reshape her child’s gut bacteria, potentially increasing their risk of inflammatory bowel disease and obesity-even if the child never directly consumes the same foods. That’s the takeaway from new research in mice, raising questions about the long-term impact of common food additives on future generations.
Gut Changes Start in the Womb
Table of Contents
Early alterations to gut microbiota,even without direct exposure to the altering agent,can have lasting health consequences,according to a study published in Nature Communications. Here are the key findings:
- Emulsifiers consumed by mothers can alter the gut bacteria of their offspring.
- These changes occur even if the offspring don’t consume the emulsifiers themselves.
- The altered gut bacteria are linked to increased inflammation and a higher risk of obesity and inflammatory bowel disease.
- The study highlights the need for research into the impact of food additives, particularly in infant formula.
Emulsifiers-additives used to improve texture and extend the shelf life of processed foods-are ubiquitous in modern diets. You’ll find them in dairy products, baked goods, ice cream, and even some powdered baby formulas. While widely used, the full extent of their impact on human health, particularly the delicate balance of the gut microbiota, remains largely unknown.
How the Study Worked
Researchers at the Institut Pasteur and Inserm, led by Benoit Chassaing, Inserm Research Director and Head of the Microbiome-Host Interactions laboratory, investigated this connection in mice. Female mice were fed two common emulsifiers-carboxymethyl cellulose (E466) and polysorbate 80 (E433)-for ten weeks before becoming pregnant, throughout their pregnancy, and while breastfeeding. The researchers then analyzed the gut microbiota of the pups, who had never been directly exposed to these emulsifiers.
Within the first few weeks of life, the young mice exhibited notable changes in their gut bacteria. This early period is critical, as mothers naturally transfer their microbiota to their offspring through close contact.The altered microbiota in the pups included elevated levels of flagellated bacteria, known to trigger the immune system and promote inflammation.
Disrupted Gut-Immune Dialog
The research team also observed increased contact between bacteria and the gut lining-a process they termed “bacterial encroachment.” This encroachment caused certain pathways in the gut to close prematurely. These pathways are normally responsible for allowing small bacterial fragments to interact with the immune system, enabling it to learn to tolerate the body’s own microbial inhabitants.
What happens when these pathways close too early? When these pathways closed prematurely in the offspring of mothers exposed to emulsifiers, communication between the gut microbiota and the immune system was disrupted. As the mice matured, this disruption manifested as an overactive immune response and chronic inflammation, substantially increasing their susceptibility to inflammatory gut diseases and obesity.
What Does This Mean for Humans?
“It is crucial for us to develop a better understanding of how what we eat can influence future generations’ health,” said Chassaing. “These findings highlight how critically importent it is indeed to regulate the use of food additives, especially in powdered baby formulas, which frequently enough contain such additives and are consumed at a critical moment for microbiota establishment. We want to continue this research with clinical trials to study mother-to-infant microbiota transmission, both in cases of maternal nutrition with or without food additives and in cases of infants directly exposed to these substances in baby formula.”
the study, published in Nature Communications, underscores the potential for dietary factors to have transgenerational health effects and emphasizes the need for further examination into the role of emulsifiers and other food additives in human health.
This work was funded by a Starting Grant and a Consolidator Grant from the European Research Council (ERC).
