Still, that may be a risk worth taking for children with stunting who are not helped by diet alone, Dr. Ahmed said.
To identify this population, the researchers recruited more than 500 children from an urban district in Dhaka, Bangladesh, from 2016 to 2018; all were around 18 months old and at high risk of stunting. For three months, each child was given eggs, milk, vitamins and minerals, as well as antiparasitic medications to purge unwanted infections from their gut.
Most of the children in the study gained weight and grew, but just over one-fifth of them stayed obstinately small. Most of their small intestines showed signs of inflammation, the researchers found, a possible indicator of E.E.D.
An analysis of their gut contents also revealed that many of the children harbored several of the same types of bacteria in their small intestines. None of the microbial members of this “core group” of bugs was “what you’d call a classic pathogen,” Dr. Gordon said. And yet, “the more of these bacterial strains you had, the worse the stunting,” he said. “That to us was an amazing surprise.”
The team then transferred a subset of these bacteria into germ-free mice, each one bred without gut microbes of its own. Shortly after the microbes set up shop in the animals’ small intestines, the tissues began to deteriorate — an apparent mimicry of the inflammatory friendly fire seen in many children with signs of stunting.
That bacteria alone can give mice gut inflammation is “huge, in my mind,” said Honorine Ward, a microbiologist and immunologist at Tufts University who was not involved in the study.
Although it is still unclear whether these dynamics will play out the same way in people, “this is very convincing, and a really good start,” said Ana Maria Porras, a microbiologist and tissue engineer at Cornell University who also was not a part of the research team.