Evidence map›Paper›PMID 25523644›Full record

ArticleAppetite2015

Relation of the multilocus genetic composite reflecting high dopamine signaling capacity to future increases in BMI.

Sonja Yokum, C Nathan Marti, Andrew Smolen, Eric Stice

Abstract read
In one paragraph

Article in Appetite, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

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

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Neural vulnerability factors for obesity.Clinical psychology review · 2019
    Review
  12. Article
  13. Review
  14. Article
  15. Association betweenNeuropsychiatric disease and treatment · 2017
    Article
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  17. Review
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

4 authors.

Sonja YokumOregon Research Institute, 1776 Millrace Drive, Eugene, OR 97403, USA. Electronic address: sonjay@ori.org.
C Nathan MartiOregon Research Institute, 1776 Millrace Drive, Eugene, OR 97403, USA.
Andrew SmolenInstitute for Behavioral Genetics, University of Colorado, 1480 30th Street, Boulder, CO 80303.
Eric SticeOregon Research Institute, 1776 Millrace Drive, Eugene, OR 97403, USA.

Funding

Relation of Consummatory and Anticipatory Food Reward to ObesityR01DK080760 · NIDDK · OREGON RESEARCH INSTITUTE · PI STICE, ERIC M, YOKUM, SONJA · 2009 to 2013
$3.3M
NIDDK NIH HHS R01 DK080760NIDDK NIH HHS R01 DK80760
6 · The paper itself

Abstract

Because food intake exerts its rewarding effect by increasing dopamine (DA) signaling in reward circuitry, it theoretically follows that individuals with a greater number of genotypes putatively associated with high DA signaling capacity are at increased risk for overeating and subsequent weight gain. We tested the association between the multilocus genetic composite risk score, defined by the total number of genotypes putatively associated with greater DA signaling capacity (i.e. TaqIA A2 allele, DRD2-141C Ins/Del and Del/Del genotypes, DRD4-S allele, DAT1-S allele, and COMT Val/Val genotype), and future increases in Body Mass Index (BMI) in three prospective studies. Participants in Study 1 (N = 30; M age = 15.2; M baseline BMI = 26.9), Study 2 (N = 34; M age = 20.9; M baseline BMI = 28.2), and Study 3 (N = 162; M age = 15.3, M baseline BMI = 20.8) provided saliva samples from which epithelial cells were collected, permitting DNA extraction. The multilocus genetic composite risk score was associated with future increases in BMI in all three studies (Study 1, r = 0.37; Study 2, r = 0.22; Study 3, r = 0.14) and the overall sample (r = 0.19). DRD4-S was associated with increases in BMI in Study 1 (r = 0.42), Study 2 (r = 0.27), and in the overall sample (r = 0.17). DAT1-S was associated with increases in BMI in Study 3 (r = 0.17) and in the overall sample (r = 0.12). There were no associations between the other genotypes (TaqIA, COMT, and DRD2-141C) and change in BMI over 2-year follow-up. Data suggest that individuals with a genetic propensity for greater DA signaling capacity are at risk for future weight gain and that combining alleles that theoretically have a similar function may provide a more reliable method of modeling genetic risk associated with future weight gain than individual genotypes.

Indexed as

Body Mass IndexRewardAdolescentAdultAllelesDopamineEatingEnergy IntakeFemaleGenotypeHumansHyperphagiaMaleObesityProspective StudiesRisk FactorsDopamineBody mass indexDopamineMultilocus genetic compositeObesityWeight gain

Identifiers

PMID25523644
PMCPMC4333052

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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.