Gut health and type 1 diabetes
Friday, 6 December 2019
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 changes.
“Three parallel phenomena in early childhood – the dynamic development of the immune system, maturation of the gut microbiome, and the appearance of the first type 1 diabetes -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 phenomena.
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 = autoimmune issues
If during that phase the gut microbiome becomes unbalanced, the immune system’s development becomes distorted and susceptibility to autoimmune diseases increases.
“The second phase … [transitioning] to overt Type 1 diabetes 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 type 1 diabetes 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 microbes.”