Evidence map›Paper›PMID 38795745›Full record

ArticleThe Journal of nutrition2024

Gut Inflammation Markers, Diet, and Risk of Islet Autoimmunity in Finnish Children - A Nested Case-Control Study.

Tuuli Ei Salo, Leena Hakola, Sari Niinistö, Hanna-Mari Takkinen, Suvi Ahonen, Leena Puustinen, Jorma Ilonen, Jorma Toppari, Riitta Veijola, Heikki Hyöty and 2 more

Abstract read
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 2 papers.

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0cells of the map it votes in
2citing papers in PubMed
–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

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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

2 citing papers in PubMed.

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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.

Tuuli Ei SaloDepartment of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland; Unit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland. Electronic address: tuuli.salo@thl.fi.
Leena HakolaDepartment of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland; Unit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland; Tampere University Hospital, Wellbeing Services County of Pirkanmaa, Tampere, Finland.
Sari NiinistöDepartment of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland.
Hanna-Mari TakkinenDepartment of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland; Unit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland; Tampere University Hospital, Wellbeing Services County of Pirkanmaa, Tampere, Finland.
Suvi AhonenDepartment of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland; Unit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland; Tampere University Hospital, Wellbeing Services County of Pirkanmaa, Tampere, Finland.
Leena PuustinenDepartment of Virology, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Jorma IlonenImmunogenetics Laboratory, Institute of Biomedicine, University of Turku, Turku, Finland.
Jorma ToppariResearch Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, and Centre for Population Health Research, University of Turku, Turku, Finland; Department of Pediatrics, Turku University Hospital, Turku, Finland.
Riitta VeijolaDepartment of Pediatrics, PEDEGO Research Unit, Medical Research Center Oulu, University of Oulu and Oulu University Hospital, Oulu, Finland; Department of Children and Adolescents, Oulu University Hospital, Oulu, Finland.
Heikki HyötyDepartment of Virology, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland; Fimlab laboratories, Tampere, Finland.
Mikael KnipPediatric Research Center, Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland; Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland; Department of Pediatrics, Tampere University Hospital, Tampere, Finland.
Suvi M VirtanenDepartment of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland; Unit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland; Tampere University Hospital, Wellbeing Services County of Pirkanmaa, Tampere, Finland; Center for Child Health Research, Tampere University and Tampere University Hospital, Tampere, Finland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGut dysbiosis and increased intestinal permeability have been reported to precede type 1 diabetes-related autoimmunity. The role of gut inflammation in autoimmunity is not understood.

objectivesThis study aimed to assess whether gut inflammation markers are associated with risk of islet autoimmunity and whether diet is associated with gut inflammation markers.

methodsA nested case-control sample of 75 case children with islet autoimmunity and 88 control children was acquired from the Finnish Type 1 Diabetes Prediction and Prevention cohort. Diet was assessed with 3-d food records, and calprotectin and human β-defensin-2 (HBD-2) were analyzed from stool samples at 6 and 12 mo of age. Conditional logistic regression analysis was used in a matched case-control setting to assess risk of autoimmunity. Analysis of variance, independent samples t test, and a general linear model were used in secondary analyses to test associations of background characteristics and dietary factors with inflammation markers.

resultsIn unadjusted analyses, calprotectin was not associated with risk of islet autoimmunity, whereas HBD-2 in the middle (odds ratio [OR]: 3.23; 95% confidence interval [CI]: 1.03, 10.08) or highest tertile (OR: 3.02; 95% CI: 1.05, 8.69) in comparison to the lowest at 12 mo of age showed borderline association (P-trend = 0.063) with higher risk of islet autoimmunity. Excluding children with cow milk allergy in sensitivity analyses strengthened the association of HBD-2 with islet autoimmunity, whereas adjusting for dietary factors and maternal education weakened it. At age 12 mo, higher fat intake was associated with higher HBD-2 (β: 0.219; 95% CI: 0.110, 0.328) and higher intake of dietary fiber (β: -0.294; 95% CI: -0.510, -0.078), magnesium (β: -0.036; 95% CI: -0.059, -0.014), and potassium (β: -0.003; 95% CI: -0.005, -0.001) with lower HBD-2.

conclusionsHigher HBD-2 in infancy may be associated with higher risk of islet autoimmunity. Dietary factors play a role in gut inflammatory status.

Indexed as

Autoimmunitybeta-DefensinsBiomarkersDiabetes Mellitus, Type 1DietIslets of LangerhansLeukocyte L1 Antigen ComplexCase-Control StudiesFecesFemaleFinlandHumansInfantInflammationMaleRisk Factorsbeta-DefensinsBiomarkersDEFB4A protein, humanLeukocyte L1 Antigen Complexcalprotectindietgut inflammationhuman β-defensin-2islet autoimmunity

Identifiers

PMID38795745
PMCPMC11282497

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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.