Evidence map›Paper›PMID 31451871›Full record

ReviewDiabetologia2019

Early-life factors contributing to type 1 diabetes.

Maria E Craig, Ki Wook Kim, Sonia R Isaacs, Megan A Penno, Emma E Hamilton-Williams, Jennifer J Couper, William D Rawlinson

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Diabetologia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 5 pooled it
9.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 5 syntheses or guidelines pooled it, 105 citations in OpenAlex.

  1. Pooled it
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  5. Association BetweenFrontiers in endocrinology · 2021
    Pooled it
  6. Review
  7. Article
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  9. Article
  10. Sex as a modifier of genetic risk for type 1 diabetes.Diabetes, obesity & metabolism · 2025
    Review
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6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 1 country.

Maria E CraigSchool of Women's and Children's Health, University of New South Wales Faculty of Medicine, Sydney, NSW, Australia. m.craig@unsw.edu.au.ORCID 0000-0001-6004-576X
Ki Wook KimSchool of Women's and Children's Health, University of New South Wales Faculty of Medicine, Sydney, NSW, Australia.
Sonia R IsaacsSchool of Women's and Children's Health, University of New South Wales Faculty of Medicine, Sydney, NSW, Australia.
Megan A PennoRobinson Research Institute, School of Paediatrics and Reproductive Health, University of Adelaide, Adelaide, SA, Australia.
Emma E Hamilton-WilliamsUniversity of Queensland Diamantina Institute, University of Queensland, Translational Research Institute, Brisbane, QLD, Australia.
Jennifer J CouperRobinson Research Institute, School of Paediatrics and Reproductive Health, University of Adelaide, Adelaide, SA, Australia.
William D RawlinsonSchool of Women's and Children's Health, University of New South Wales Faculty of Medicine, Sydney, NSW, Australia.
UNSW Sydney · AUWomen's and Children's Hospital · AUNew South Wales Department of Health · AUThe University of Sydney · AUTranslational Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of type 1 diabetes has increased since the mid-twentieth century at a rate that is too rapid to be attributed to genetic predisposition alone. While the disease can occur at any age, mounting evidence from longitudinal cohort studies of at-risk children indicate that type 1 diabetes associated autoantibodies can be present from the first year of life, and that those who develop type 1 diabetes at a young age have a more aggressive form of the disease. This corroborates the hypothesis that environmental exposures in early life contribute to type 1 diabetes risk, whether related to maternal influences on the fetus during pregnancy, neonatal factors or later effects during infancy and early childhood. Studies to date show a range of environmental triggers acting at different time points, suggesting a multifactorial model of genetic and environmental factors in the pathogenesis of type 1 diabetes, which integrally involves a dialogue between the immune system and pancreatic beta cells. For example, breastfeeding may have a weak protective effect on type 1 diabetes risk, while use of an extensively hydrolysed formula does not. Additionally, exposure to being overweight pre-conception, both in utero and postnatally, is associated with increased risk of type 1 diabetes. Epidemiological, clinical and pathological studies in humans support a role for viral infections, particularly enteroviruses, in type 1 diabetes, but definitive proof is lacking. The role of the early microbiome and its perturbations in islet autoimmunity and type 1 diabetes is the subject of investigation in ongoing cohort studies. Understanding the interactions between environmental exposures and the human genome and metagenome, particularly across ethnically diverse populations, will be critical for the development of future strategies for primary prevention of type 1 diabetes.

Indexed as

AutoantibodiesAutoimmunityDiabetes Mellitus, Type 1FemaleHumansInsulin-Secreting CellsLongitudinal StudiesAutoantibodiesChildDietEnterovirusGene–environment interactionLife course developmentMicrobiomePregnancyReviewType 1 diabetesVirus

Identifiers

PMID31451871
OpenAlexW2971071832

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.