Evidence map›Paper›PMID 30005279›Full record

ArticlePsychoneuroendocrinology2018

Polymorphic variation in the SLC5A7 gene influences infant autonomic reactivity and self-regulation: A neurobiological model for ANS stress responsivity and infant temperament.

Christopher W Jones, Sarah A O Gray, Katherine P Theall, Stacy S Drury

Open access · greenAbstract read
In one paragraph

Article in Psychoneuroendocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. 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

4 authors at 1 institution in 1 country.

Christopher W JonesNew Orleans, LA, Neuroscience Program, Department of Neuroscience, Tulane Brain Institute, Tulane University, United States.
Sarah A O GrayNew Orleans, LA, Department of Psychology, Tulane University, School of Science and Engineering, United States.
Katherine P TheallNew Orleans, LA, Department of Global Community Health and Behavioral Sciences, Tulane University School of Public Health and Tropical Medicine, United States.
Stacy S DruryNew Orleans, LA, Neuroscience Program, Department of Neuroscience, Tulane Brain Institute, Tulane University, United States; New Orleans, LA, Department of Psychiatry and Behavioral Sciences, Tulane University School of Medicine, Division of Child and Adolescent Psychiatry, 1430 Tulane Ave #8055, 70112, United States. Electronic address: sdrury@tulane.edu.
Tulane University · US

Funding

Tulane Building Interdisciplinary Research Careers in Women's Health (BIRCWH)K12HD043451 · NICHD · TULANE UNIVERSITY OF LOUISIANA · PI KROUSEL-WOOD, MARIE · 2002 to 2023
$9.9M
Setting the trajectoryR01MH101533 · NIMH · TULANE UNIVERSITY OF LOUISIANA · PI DRURY, STACY SCHMIDT · 2013 to 2017
$2.7M
NICHD NIH HHS K12 HD043451NICHD NIH HHS L30 HD085275NIMH NIH HHS R01 MH101533
6 · The paper itself

Abstract

objectiveTo examine the impact of polymorphic variation in the solute carrier family 5 member 7 (SLC5A7) gene on autonomic nervous system (ANS) reactivity indexed by respiratory sinus arrhythmia (RSA) and heart rate (HR) in infants during a dyadic stressor, as well as maternal report of infant self-regulation. Given evidence of race differences in older individuals, race was specifically examined.

methodsRSA and HR were collected from 111 infants during the still-face paradigm (SFP). Mothers completed the Infant Behavior Questionnaire-Revised short-form. Multi-level mixed effects models examined the impact of SLC5A7 genotype on RSA and HR across the SFP. Linear models tested the influence of genotype on the relation between RSA, HR, and maternal report of infant self-regulation.

resultsSLC5A7 genotype significantly predicted RSA stress responsivity (β = -0.023; p = 0.028) and HR stress responsivity (β = 0.004; p = 0.002). T-allele carriers exhibited RSA suppression and HR acceleration in response to stress while G/G homozygotes did not suppress RSA and exhibited less HR acceleration. All infants exhibited modest RSA augmentation and HR deceleration during recovery. Race-stratified analyses revealed that White T-allele carriers drove the overall results for both RSA (β = -0.044; p = 0.007) and HR (β = 0.006; p = 0.008) with no relation between SLC5A7 genotype and RSA or HR in Black infants. Maternal report of infant orienting/regulation was predicted by the interaction of SLC5A7 genotype and both RSA recovery (β = 0.359; p = 0.001) and HR recovery (β = -1.659; p = 0.020). RSA augmentation and HR deceleration during recovery were associated with higher maternal reports of self-regulation among T-allele carriers, a finding again primarily driven by White infants.

conclusionsEarly in development, genetic contributions to ANS are evident and predict maternal report of infant self-regulation within White infants, consistent with prior literature. The lack of associations in Black infants suggest that race differences in physiological reactivity and self-regulation are emerging during the first year of life potentially providing early evidence of disparities in health risk trajectories.

Indexed as

AdultAllelesAutonomic Nervous SystemBiomarkersBlack or African AmericanChild DevelopmentFemaleGene FrequencyHeart RateHumansInfantInfant BehaviorInfant, NewbornMaleMother-Child RelationsMothersBiomarkersSLC5A7 protein, humanSymportersAcetylcholineHealth disparitiesRespiratory sinus arrhythmiaSelf-regulationSLC5A7Temperament

Identifiers

PMID30005279
PMCPMC6500559
OpenAlexW2810672718

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.