Professor Oluf Pedersen
Novo Nordisk Foundation Center for Basic Metabolic Research
University of Copenhagen
MedicalResearch.com: What is the background for this study?
Response: We focused our study on healthy people due to the world-wide bottom-up movement among healthy adults to live gluten-free or on a low-gluten diet.
Therefore, we undertook a randomised, controlled, cross-over trial involving 60 middle-aged healthy Danish adults with two eight week interventions comparing a low-gluten diet (2 g gluten per day) and a high-gluten diet (18 g gluten per day), separated by a washout period of at least six weeks with habitual diet (12 g gluten per day).
The two diets were balanced in number of calories and nutrients including the same total amount of dietary fibres. However, the composition of fibres differed markedly between the two diets.
When the low-gluten trend started years back the trend was without any scientific evidence for health benefits. Now we bring pieces of evidence that a low-gluten diet in healthy people may be related to improved intestinal wellbeing due to changes in the intestinal microbiota which to our surprise is NOT induced by gluten itself but by the concomitant change in the type of dietary fibres linked to a low-gluten intake.
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: In a large population of pregnant women, we found that the risk of the offspring being diagnosed with type 1 diabetes before the age of 15.6 years (the follow up period) was doubled in the group of women ingesting the highest amounts of gluten (20-66 g/day) versus the group of women ingesting the lowest amounts of gluten (0-7 g/day). For every additional 10 grams of gluten ingested, the risk for type 1 diabetes in the child increased by a factor of 1.31.
It the sense that it was a hypothesis that we specifically tested, we were not surprised. We had seen in animal experiments that a gluten-free diet during pregnancy protected the offspring from diabetes, and we wanted to see if we could prove the same pattern in humans. There could be many reasons why we would not be able to show the association, even if it was there (sample size, low quality data, covariates we could not correct for and so on), but we were off course pleasantly surprised that we found the association that we were looking for, in particular because it is quite robust Continue reading →