In an article published in the August Lancet, Finnish
researchers have summarized the recent findings between islet
autoimmunity, type 1 diabetes, and the intestinal microbiota.
Professors Heli Siljander, Jarno Honkanen and Mikael Knip report
that the steep increase in the incidence of type 1 diabetes in the
Western world after World War II cannot be explained solely by
genetic factors. They state that this rise implies crucial
interactions between predisposing genes and environmental
"Three parallel phenomena in early childhood - the dynamic
development of the immune system, maturation of the gut microbiome,
and the appearance of the first T1D-associated autoantibodies -
raise the question whether these phenomena might reflect causative
relationships," they wrote.
Steep increase in incidence
As an example of the rise in type 1, the researchers said in
Finland the incidence among children under the age of 15 years has
increased from 12 to 65 new cases/100,000/year in five decades.
Research areas summarised include intestinal bacterial
microbiota, including interactions between the genetic profile,
nutrition, and susceptibility to islet autoimmunity; intestinal
virome and the relationship between virus and type 1 diabetes;
intestinal fungal community; microbiota in other sites; and causal
Based on their evaluations of those areas, the professors
hypothesized that intestinal microbiota may contribute to the
development of type 1 via a two-phased process.
The first phase starts at birth and ends with the appearance of
the first type 1-associated antibodies. During that phase, a
successful training of the developing immune system is required to
establish self-tolerance and control of inflammatory responses.
Gut imbalance = auto-immune issues
If during that phase the gut microbiome becomes unbalanced, the
immune system's development becomes distorted and susceptibility to
auto-immune diseases increases.
"The second phase … [transitioning] to overt T1D seems to be
characterized by a reduced microbial diversity and a
proinflammatory intestinal dysbiosis. The mechanisms behind the
spreading of the relatively local intestinal inflammation towards
extra-intestinal autoimmunity remains to be explored in the
future," they wrote.
"We are only at the beginning of learning about the role of the
intestinal microbiome in the development of T1D and other
immune-mediated diseases. Further efforts should be directed to
studies on the role of the intestinal mycrobiota and virome, their
interplay, and their interaction with the host and other