New publication · npj Science of Food
How Human Milk and Formula Shape What Gut Bacteria Make
A new MUSC lab study shows that six species of helpful gut bacteria respond to human milk and infant formula in their own distinct ways.
By Katie Chetta, MD · Chetta Lab · September 2026

The study in plain language
Soon after birth, a baby’s gut fills with bacteria, including a group called lactobacilli that help keep the body healthy. These bacteria make small molecules, called metabolites, that can affect the body. It has not been clear how different lactobacilli species respond to what babies are fed.
In this study, first author Alyssa (Aly) Gutierrez, Dr. Chetta and senior author Melinda (Mindy) Engevik, all at MUSC, worked with colleagues at Baylor College of Medicine and Texas Children’s Hospital. The team grew six lactobacilli species in the lab with human milk, infant formula or water added. They then used a technique called untargeted metabolomics to measure the molecules each culture produced.
Each species had its own chemical “fingerprint,” and that fingerprint changed with the diet. Human milk boosted several compounds, including hydroxyphenyllactic acid, the amino acid tyrosine, indoles, the fatty acid vaccenic acid and di-peptides (tiny protein pieces). Infant formula raised a different set, including isonicotinic acid.
The results show that human milk and formula shape these bacteria in different ways, that each species responds differently, and that human milk prompts more potentially beneficial compounds. Understanding these diet–microbe interactions could help improve newborn gut health.
This was a lab study, not a study in babies. The human milk was pasteurized, like the donor milk used in the NICU, so the authors note the results may not fully reflect fresh breast milk.
Read the paper
Gutierrez A, Chetta KE, Puckett B, Haidacher SJ, Horvath TD, Engevik MA. Human milk and infant formula influence lactobacilli metabolism in a species-specific manner. NPJ Sci Food. 2026 Apr 2;10(1):168. doi: 10.1038/s41538-026-00759-x. PMID: 41927583; PMCID: PMC13216266. Open access.
This plain-language summary is based on the published abstract and article. For full details, please see the original paper.
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