Evidence map›Paper›PMID 37709841›Full record

ArticleScientific reports2023

Interaction between genetic susceptibility to obesity and food intake on BMI in Finnish school-aged children.

Heli Viljakainen, Jose V Sorlí, Emma Dahlström, Nitin Agrawal, Olga Portolés, Dolores Corella

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Genetics of Common Obesity in Children and Adolescents.Annals of the New York Academy of Sciences · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. 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

6 authors at 4 institutions in 2 countries.

Heli ViljakainenFolkhälsan Research Center, Topeliuksenkatu 20, 00250, Helsinki, Finland. heli.viljakainen@helsinki.fi.
Jose V SorlíDepartment of Preventive Medicine and Public Health, University of Valencia, Valencia, Spain.
Emma DahlströmFolkhälsan Research Center, Topeliuksenkatu 20, 00250, Helsinki, Finland.
Nitin AgrawalFolkhälsan Research Center, Topeliuksenkatu 20, 00250, Helsinki, Finland.
Olga PortolésDepartment of Preventive Medicine and Public Health, University of Valencia, Valencia, Spain.
Dolores CorellaDepartment of Preventive Medicine and Public Health, University of Valencia, Valencia, Spain.
Centro de Investigación Biomédica en Red · ESFolkhälsans Forskningscentrum · FIUniversitat de València · ESUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diet modulates the genetic risk of obesity, but the modulation has been rarely studied using genetic risk scores (GRSs) in children. Our objectives were to identify single nucleotide polymorphisms (SNPs) that drive the interaction of specific foods with obesity and combine these into GRSs. Genetic and food frequency data from Finnish Health in Teens study was utilized. In total, 1142 11-year-old subjects were genotyped on the Metabochip array. BMI-GRS with 30 well-known SNPs was computed and the interaction of individual SNPs with food items and their summary dietary scores were examined in relation to age- and sex-specific BMI z-score (BMIz). The whole BMI-GRS interacted with several foods on BMIz. We identified 7-11 SNPs responsible for each interaction and these were combined into food-specific GRS. The most predominant interaction was witnessed for pizza (p < 0.001): the effect on BMIz was b - 0.130 (95% CI - 0.23; - 0.031) in those with low-risk, and 0.153 (95% CI 0.072; 0.234) in high-risk. Corresponding, but weaker interactions were verified for sweets and chocolate, sugary juice drink, and hamburger and hotdog. In total 5 SNPs close to genes NEGR1, SEC16B, TMEM18, GNPDA2, and FTO were shared between these interactions. Our results suggested that children genetically prone to obesity showed a stronger association of unhealthy foods with BMIz than those with lower genetic susceptibility. Shared SNPs of the interactions suggest common differences in metabolic gene-diet interactions, which warrants further investigation.

Indexed as

Genetic Predisposition to DiseaseObesityAdolescentAlpha-Ketoglutarate-Dependent Dioxygenase FTOBody Mass IndexChildEatingFemaleFinlandHumansMaleAlpha-Ketoglutarate-Dependent Dioxygenase FTOFTO protein, human

Identifiers

PMID37709841
PMCPMC10502078
OpenAlexW4386736700

What Socratic holds

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LicenceCC BY
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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 Socratic graph.