The study, published in the Journal of the American Medical Association (JAMA), brought together a multinational team to decipher whether celiac disease depended on gluten consumption in the first five years of life.
Subjects of the study were part of a ‘prospective observational birth cohort’ focused on the environmental triggers of diabetes and celiac, known as The Environmental Determinants of Diabetes in the Young (TEDDY).
Researchers at six clinical centers in Finland, Germany, Sweden and the US enrolled more than 8,600 newborns between 2004 and 2010, each carrying a genetic makeup connected to Type 1 diabetes and celiac disease.
The team began running tests for the two autoimmune deficiencies starting at age two, ultimately testing more than 6,700 male and female children each year.
Testing every year, through age 5
Researchers analyzed parental reports on what their children consumed over three-day periods in the first 12 months of life – first at six months, then at nine months and finally at age one. From that point until age five, they ran tests twice a year.
They reconnected with the children at median age nine to test for the potential presence of celiac disease.
Nearly 20% of the children showed signs of celiac disease autoimmunity, meaning they tested positive twice in a row. A full 7% had developed the disease, with incidents ‘peaking’ between ages two and three.
Notably, for every 1g per day in the increase of gluten consumption, children were 34% more likely to develop celiac as an adolescent.
The risk remained even if the children in the study consumed the reference amount of gluten: 28% were still at risk.
Conclusions and importance
“Higher gluten intake during the first five years of life was associated with increased risk of celiac disease autoimmunity and celiac disease among genetically predisposed children,” wrote the study's authors.
Scientists can pinpoint which genes cause celiac disease and what environmental triggers cause it to inflame (i.e. gluten), so it makes for an interesting autoimmune case study, according to an adjunct statement in JAMA.
There, Dr Maureen M. Leonard and Dr Alessio Fasano from the Harvard Media School in Boston, Massachusetts, said medical professionals have identified nearly 60 alleles (mutations of a gene) and HLA genes (human leukocyte antigen genes, which regulate the immune system) that ‘confer risk.’
Despite the importance of this ‘crucial’ information, they noted, “it cannot explain the substantial increase in the prevalence of celiac disease from 0.21% to 0.95% in the US between 1974 and 2003.” Nor does it explain away the fact that more than 19 out of 100,000 Europeans suffered from celiac in 2011, compared to just five in 1990.
“There is substantial interest in the environmental trigger – gluten – particularly related to the timing of its introduction and amount ingested as the driving factors associated with this increased prevalence.”
More research needed
In 2017, the US Preventive Services Task Force dug into the opportunity for celiac screenings to better treat the disease. Researchers noted the rate of diagnosis had indeed spiked since the 1990s, “explained by increased awareness but perhaps also by a true increase in the disease.”
They recommended screening – especially for predisposed patients – as a way of detecting the disease early, even if symptoms were not yet present.
The task force determined there was insufficient evidence to determine the value of such screening, adding more research could benefit the diagnosis and treatment of this autoimmune disease and its rising prevalence.
Authors: C. Andrén Aronsson, H.S. Lee, E.M. Hård, et al.
JAMA: Issue 322, Volume 6, pg. 514-523 – 2019
Authors: M.M. Leonard and A. Fasano
JAMA: Issue 322, Volume 6, pg. 510-511 – 2019
Authors: R.S. Choung and J.A. Murray
JAMA: Issue 317, Volume 12, pg. 1221-1223 – 2017