Evidence map›Paper›PMID 33474583›Full record

ArticleDiabetologia2021

Growth and development of islet autoimmunity and type 1 diabetes in children genetically at risk.

Anita M Nucci, Suvi M Virtanen, David Cuthbertson, Johnny Ludvigsson, Ulle Einberg, Celine Huot, Luis Castano, Bärbel Aschemeier, Dorothy J Becker, Mikael Knip and 2 more

Registry-linked trialOpen access · bronzeAbstract readMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Diabetologia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00179777 (TRIGR - Trial to Reduce IDDM in the Genetically at Risk), which is not on this map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 7% 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.

NCT00179777 nacompletednot on this map

TRIGR - Trial to Reduce IDDM in the Genetically at Risk

TypeinterventionalSponsorUniversity of HelsinkiRan2002 to 2017Enrolled5,156ConditionsDiabetes Mellitus, Type 1ArmsHydrolysed infant formula, Nonhydrolysed infant formula
3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Article
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  11. Review
  12. Article
  13. Growth in Children with HLA-Conferred Susceptibility to Type 1 Diabetes.Endocrinology and metabolism (Seoul, Korea) · 2022
    Article
  14. Observational
  15. Review
  16. Review
  17. Article
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

12 authors at 12 institutions in 7 countries.

Anita M NucciDepartment of Nutrition, Georgia State University, Atlanta, GA, USA. anucci@gsu.edu.ORCID 0000-0001-8823-7384
Suvi M VirtanenWelfare and Health Promotion Unit, Finnish Institute for Health and Welfare, Helsinki, Finland.ORCID 0000-0001-8928-0878
David CuthbertsonPediatrics Epidemiology Center, University of South Florida, Tampa, FL, USA.ORCID 0000-0002-3785-9834
Johnny LudvigssonCrown Princess Victoria Children's Hospital and Division of Pediatrics, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.ORCID 0000-0003-1695-5234
Ulle EinbergTallinn Children's Hospital, Tallinn, Estonia.
Celine HuotCHU Ste. Justine, Montreal, QC, Canada.ORCID 0000-0003-3821-009X
Luis CastanoCruces, University Hospital, Biocruces Bizkaia Research Institute, UPV/EHU, CIBERDEM, CIBERER, Endo-ERN, Bilbao, Bizkaia, Spain.ORCID 0000-0003-0437-9401
Bärbel AschemeierDiabetes Centre for Children and Adolescents, Children's and Adolescent's Hospital AUF DER BULT, Hannover, Germany.ORCID 0000-0002-4016-8321
Dorothy J BeckerDivision of Endocrinology, University of Pittsburgh and UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, USA.ORCID 0000-0002-1311-351X
Mikael KnipPediatric Research Center, Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.ORCID 0000-0003-0474-0033
Jeffrey P KrischerPediatrics Epidemiology Center, University of South Florida, Tampa, FL, USA.ORCID 0000-0003-4526-888X
TRIGR Investigators
University of South Florida · USUniversity of Pittsburgh · USCentre Hospitalier Universitaire Sainte-Justine · CALinköping University Hospital · SEBioCruces Health research Institute · ESGeorgia State University · USKinderkrankenhaus auf der Bult · DETallinn Health Care College · EEUniversity of Helsinki · FITampere University · FITampere University Hospital · FIPirkanmaa Hospital District · FI

Funding

Trial to Reduce IDDM in the Genetically at Risk StudyU01HD040364 · NICHD · UNIVERSITY OF HELSINKI · PI KNIP, MIKAEL · 2001 to 2015
$32.7M
Trial to Reduce IDDM in the Genetically at Risk: A Nutritional primary preventionU01HD042444 · NICHD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BECKER, DOROTHY J · 2001 to 2015
$24.4M
Trial to Reduce IDDM in the Genetically at Risk (TRIGR) Data Management UnitU01HD051997 · NICHD · UNIVERSITY OF SOUTH FLORIDA · PI KRISCHER, JEFFREY P · 2006 to 2015
$7.1M
Trial to Reduce IDDM in the Genetically at Risk (TRIGR) Data Management UnitR01HD051997 · NICHD · UNIVERSITY OF SOUTH FLORIDA · PI KRISCHER, JEFFREY P · 2016 to 2018
$2.3M
CIHRNICHD NIH HHS R01 HD051997NICHD NIH HHS U01 HD040364NICHD NIH HHS U01 HD042444NICHD NIH HHS U01 HD051997
6 · The paper itself

Abstract

aims/hypothesisWe aimed to evaluate the relationship between childhood growth measures and risk of developing islet autoimmunity (IA) and type 1 diabetes in children with an affected first-degree relative and increased HLA-conferred risk. We hypothesised that being overweight or obese during childhood is associated with a greater risk of IA and type 1 diabetes.

methodsParticipants in a randomised infant feeding trial (N = 2149) were measured at 12 month intervals for weight and length/height and followed for IA (at least one positive out of insulin autoantibodies, islet antigen-2 autoantibody, GAD autoantibody and zinc transporter 8 autoantibody) and development of type 1 diabetes from birth to 10-14 years. In this secondary analysis, Cox proportional hazard regression models were adjusted for birthweight and length z score, sex, HLA risk, maternal type 1 diabetes, mode of delivery and breastfeeding duration, and stratified by residence region (Australia, Canada, Northern Europe, Southern Europe, Central Europe and the USA). Longitudinal exposures were studied both by time-varying Cox proportional hazard regression and by joint modelling. Multiple testing was considered using family-wise error rate at 0.05.

resultsIn the Trial to Reduce IDDM in the Genetically at Risk (TRIGR) population, 305 (14.2%) developed IA and 172 (8%) developed type 1 diabetes. The proportions of children overweight (including obese) and obese only were 28% and 9% at 10 years, respectively. Annual growth measures were not associated with IA, but being overweight at 2-10 years of life was associated with a twofold increase in the development of type 1 diabetes (HR 2.39; 95% CI 1.46, 3.92; p < 0.001 in time-varying Cox regression), and similarly with joint modelling. CONCLUSIONS/

interpretationIn children at genetic risk of type 1 diabetes, being overweight at 2-10 years of age is associated with increased risk of progression from multiple IA to type 1 diabetes and with development of type 1 diabetes, but not with development of IA. Future studies should assess the impact of weight management strategies on these outcomes.

trial registrationClinicalTrials.gov NCT00179777.

Indexed as

Adolescent DevelopmentChild DevelopmentAdolescentAge FactorsAustraliaAutoimmunityBottle FeedingChildChild, PreschoolDiabetes Mellitus, Type 1EuropeFemaleGenetic Predisposition to DiseaseHeredityHumansIncidenceBeta cell autoimmunityChildhood growthGenetic riskLengthType 1 diabetesWeight

Identifiers

PMID33474583
PMCPMC7940594
OpenAlexW3122792694

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.