Evidence map›Paper›PMID 39313195›Full record

ArticleThe Journal of nutrition2024

Food Consumption and Risk of Islet Autoimmunity and Type 1 Diabetes in Children at Increased Genetic Susceptibility for Type 1 Diabetes.

Suvi M Virtanen, Essi J Peltonen, Leena Hakola, Sari Niinistö, Hanna-Mari Takkinen, Suvi Ahonen, Mari Åkerlund, Ulla Uusitalo, Markus Mattila, Tuuli Ei Salo and 5 more

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In one paragraph

Article in The Journal of nutrition, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. 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

15 authors.

Suvi M VirtanenUnit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland; Wellbeing Services County of Pirkanmaa, Tampere University Hospital, Tampere, Finland; Department of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland. Electronic address: suvi.virtanen@thl.fi.
Essi J PeltonenUnit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland; Wellbeing Services County of Pirkanmaa, Tampere University Hospital, Tampere, Finland.
Leena HakolaUnit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland; Wellbeing Services County of Pirkanmaa, Tampere University Hospital, Tampere, Finland; Department of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland.
Sari NiinistöDepartment of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland.
Hanna-Mari TakkinenUnit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland; Wellbeing Services County of Pirkanmaa, Tampere University Hospital, Tampere, Finland; Department of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland.
Suvi AhonenUnit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland; Wellbeing Services County of Pirkanmaa, Tampere University Hospital, Tampere, Finland; Department of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland.
Mari ÅkerlundUnit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland; Wellbeing Services County of Pirkanmaa, Tampere University Hospital, Tampere, Finland; Department of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland.
Ulla UusitaloHealth Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, FL, United States.
Markus MattilaUnit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland; Wellbeing Services County of Pirkanmaa, Tampere University Hospital, Tampere, Finland; Department of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland.
Tuuli Ei SaloUnit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland; Department of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland.
Jorma IlonenInstitute of Biomedicine, Immunogenetics Laboratory, University of Turku, Turku, Finland.
Jorma ToppariInstitute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, and Centre for Population Health Research, University of Turku, Turku, Finland; Department of Pediatrics, Turku University Hospital, Turku, Finland.
Riitta VeijolaDepartment of Paediatrics, Research Unit of Clinical Medicine, Medical Research Centre, University of Oulu, Oulu, Finland; Department of Children and Adolescents, Oulu University Hospital, Oulu, Finland.
Mikael KnipResearch Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland; Department of Pediatrics, Tampere University Hospital, Tampere, Finland.
Jaakko NevalainenUnit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProspective longitudinal evidence considering the entire childhood food consumption in relation to the development of islet autoimmunity (IA or) type 1 diabetes is lacking.

objectivesWe studied the associations of consumption of various foods and their combinations with IA and type 1 diabetes risk.

methodsChildren with genetic susceptibility to type 1 diabetes born in 1996-2004 were followed from birth up to ≤6 y of age in the prospective birth cohort type 1 diabetes prediction and prevention study (n = 5674). Exposure variables included 34 food groups covering the entire diet based on repeated 3-d food records at ages 3 mo to 6 y. Endpoints were islet cell antibodies plus biochemical IA (n = 247), multiple biochemical IA (n = 206), and type 1 diabetes (n = 94). We analyzed associations between longitudinally observed foods and risk of IA/type 1 diabetes using a Bayesian approach to joint models in 1-food and multi-food models adjusted for energy intake, sex, human leukocyte antigen genotype, and familial diabetes.

resultsThe final multi-food model for islet cell antibodies plus biochemical IA included oats [hazard ratio (HR): 1.09; 95% credible interval (CI): 1.04, 1.14], banana (HR: 1.07; 95% CI: 1.03, 1.11), and cruciferous vegetables (HR: 0.83; 95% CI: 0.73, 0.94). The final model for multiple biochemical IA included, in addition to the above-mentioned foods, fermented dairy (HR: 1.42; 95% CI: 1.12, 1.78) and wheat (HR: 1.10; 95% CI: 1.03, 1.18). The final multi-food model for type 1 diabetes included rye (HR: 1.27; 95% CI: 1.07, 1.50), oats (HR: 1.15; 95% CI: 1.03, 1.26), fruits (HR: 1.05; 95% CI: 1.01, 1.09), and berries (HR: 0.67; 95% CI: 0.50, 0.93).

conclusionsHigher consumption of oats, gluten-containing cereals, and fruits was associated with increased that of cruciferous vegetables with decreased risk of several type 1 diabetes-related endpoints when considering all the foods in combination. Further etiological and mechanistic studies are warranted.

Indexed as

AutoimmunityDiabetes Mellitus, Type 1DietGenetic Predisposition to DiseaseIslets of LangerhansChildChild, PreschoolFemaleHumansInfantLongitudinal StudiesMaleProspective StudiesRisk Factorschilddiabetes mellitusdietfood consumptionislet autoimmunitymultivariate joint modelssurvival analysistype 1

Identifiers

PMID39313195
PMCPMC11600112

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Registered trials

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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.