Researchers are a step closer to understanding the role gut bugs may play in the development of type 1 diabetes.
A major international study has charted the developing gut bug populations of babies and toddlers who were later
diagnosed with the condition, which affects an estimated 10,000-20,000 New Zealanders.
Children who get type 1 diabetes have certain kinds of genes, but not everyone with these genes develop the condition.
Scientists are looking at whether the development of the gut microbiome from birth to childhood may play a protective,
predisposing or even triggering role – potentially offering a kind of microbial ‘security blanket’.
The latest results come from an umbrella study called TEDDY (The Environmental Determinants of Diabetes in the Young),
in which researchers collected monthly stool samples, as well as blood samples and diet, health and lifestyle records to
generate the richest data set of its kind to date. The children were far-flung, living in Finland, Sweden, Germany, and
three United States states - Washington, Colorado and Georgia - where the TEDDY’s six collaborating research centres are
based.
The new study, one of two analyses out of TEDDY just published in Nature, used bacterial gene sequencing to track the
gut microbiome of mostly Caucasian children with type 1 diabetes from three months of age until they were diagnosed –
usually at two to five years old – and compared it to that of healthy children without diabetes. A third group of
children had a pre-diagnostic stage called islet autoimmunity, or IA.
Analysis of nearly 11,000 stool samples from the 783 children revealed how much the variety and mix of gut bugs change
and develop in early childhood. Researchers found pronounced individual differences – suggesting unique gut bug
populations evolve from a very young age – but also subtle group differences.
Compared to the IA children, the healthy cohort had more Lactobacillus rhamnosus, common in fermented milk products such
as yoghurt, and linked to better gut digestion. They also harboured more bacterial genes that fuel short-chain
fatty-acid production, compared to both the IA and type 1 diabetes children. Short-chain fatty-acids are beneficial to
gut health and immune function and are produced only by gut microbes.
Lead author Dr Tommi Vatanen says: “Past, smaller studies have identified shifts in the gut microbiome before the onset
of type 1 diabetes, suggesting that the gut microbiome might be a predisposing or even a triggering factor.”
Dr Vatanen conducted the study while based at the Broad Institute of MIT and Harvard, and has since joined the Liggins
Institute at the University of Auckland, New Zealand as a Research Fellow.
Previous investigations in TEDDY have also raised the idea that probiotics may be protective against type 1 diabetes in
children with the highest genetic risk. In Nordic countries, probiotics are sometimes recommended for babies and young
children, and many parents give their babies Vitamin D and probiotics drops with breastmilk.
“We cannot say with certainty that probiotics are protective yet, though,” says Dr Vatanen.
“First, we need to run controlled clinical trials of, for example, carefully selected pro- and/or pre-biotic
supplements. It also may be possible to protect children from type 1 diabetes by radically changing their gut microbiome
by way of a gut bugs transfer – another exciting research direction.”
The researchers also found geographical differences in children’s gut bugs. For example, Finnish children had, on
average, more Bifidobacterium breve, which is sometimes used as a probiotic and belongs to a family of bacteria known to
be beneficial to gut health.
Dr Vatanen: “This could be due to differences in the mothers’ gut microbiome, which she transfers to the baby, or to
differences in breast milk and early feeding in general.”
Dr Vatanen was also one of the authors of a second TEDDY study published in the same issue of Nature, which analysed
12,500 stool samples from 903 children and identified three distinct phases of gut microbiome development, influenced by
breastfeeding and other environmental factors.