Could a Low-Gluten Diet During Pregnancy Protect Offspring from Diabetes?

MedicalResearch.com Interview with:
Knud Josefsen, senior researcher
Bartholin Institute, Rigshospitalet,
Copenhagen K, Denmark

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

Bacterial Infections in Pregnancy May Lead To Brain Changes in Baby

MedicalResearch.com Interview with:

Elaine Tuomanen, MD Chair and Full Member Dept of Infectious Diseases St Jude Children’s Research Hospital 262 Danny Thomas Place Memphis, TN 38105

Dr. Elaine Tuomanen

Elaine Tuomanen, MD
Chair and Full Member
Dept of Infectious Diseases
St Jude Children’s Research Hospital
262 Danny Thomas Place
Memphis, TN 38105

MedicalResearch.com: What is the background for this study? What are the main findings?

Dr. Tuomanen: While investigating mechanisms of brain repair during infection in a mouse model system, we found that components from the surfaces of bacteria could traffic from the mother to the fetus. The bacterial components moved across the placenta and into the fetal brain. To our surprise, the fetal brain did not respond with neuronal death like we see in children with meningitis. Rather, fetal neurons proliferated. This response involved the innate immune system (TLR2) inducing the neuronal transcription factor, FoxG1, which is known to drive proliferation. The newly born neurons migrated appropriately to the cortical plate, the area on the surface of the fetal brain that forms the cortex, a major part of the adult brain. Although the neurons moved to the right place in the brain, there were too many and they crowded together in the cortex, changing the architecture of the brain. At birth, affected mice seemed to have no abnormalities. However, when we tested if this change in architecture would affect brain function after birth, mice were shown to progressively develop defects in learning, memory and other cognitive functions. This indicates there is a window during pregnancy where components of bacteria from the mother can change fetal brain architecture and subsequent postnatal behavior

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