Preschool development, temperament and genetic liability as early markers of childhood ADHD: A cohort study.
ADHD
ALSPAC
developmental delay
early markers
polygenic risk scores
precursors
temperament
Journal
JCPP advances
ISSN: 2692-9384
Titre abrégé: JCPP Adv
Pays: United States
ID NLM: 9918250414706676
Informations de publication
Date de publication:
Sep 2022
Sep 2022
Historique:
received:
25
10
2021
accepted:
01
08
2022
entrez:
8
12
2022
pubmed:
9
12
2022
medline:
9
12
2022
Statut:
ppublish
Résumé
ADHD is associated with multiple adverse outcomes and early identification is important. The present study sets out to identify early markers and developmental characteristics during the first 30 months of life that are associated with ADHD 6 years later. 9201 participants from the prospective Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort were included. Outcome measures were parent-rated ADHD symptom scores (Strengths and Difficulties Questionnaire, SDQ) and ADHD diagnosis (Development and Wellbeing Assessment, DAWBA) at age 7. Seventeen putative markers were identified from previous literature and included: pre- and peri-natal risk factors, genetic liability (ADHD polygenic risk scores, PRS), early development, temperament scores and regulatory problems. Associations were examined using regression analysis. Univariable regression analysis showed that multiple early life factors were associated with future ADHD outcomes, even after controlling for sex and socio-economic status. In a multivariable linear regression model; temperament activity scores ( As well as male sex and lower socio-economic status, high temperament activity levels and motor and speech delays in the first 30 months of life, are associated with childhood ADHD. Intriguingly, given that genetic risk scores are known to explain little of the variance of ADHD outcomes, we found that ADHD PRS added useful predictive information. Future research needs to test whether predictive models incorporating aspects of early development and genetic risk scores are useful for predicting ADHD in clinical practice.
Sections du résumé
Background
UNASSIGNED
ADHD is associated with multiple adverse outcomes and early identification is important. The present study sets out to identify early markers and developmental characteristics during the first 30 months of life that are associated with ADHD 6 years later.
Methods
UNASSIGNED
9201 participants from the prospective Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort were included. Outcome measures were parent-rated ADHD symptom scores (Strengths and Difficulties Questionnaire, SDQ) and ADHD diagnosis (Development and Wellbeing Assessment, DAWBA) at age 7. Seventeen putative markers were identified from previous literature and included: pre- and peri-natal risk factors, genetic liability (ADHD polygenic risk scores, PRS), early development, temperament scores and regulatory problems. Associations were examined using regression analysis.
Results
UNASSIGNED
Univariable regression analysis showed that multiple early life factors were associated with future ADHD outcomes, even after controlling for sex and socio-economic status. In a multivariable linear regression model; temperament activity scores (
Conclusion
UNASSIGNED
As well as male sex and lower socio-economic status, high temperament activity levels and motor and speech delays in the first 30 months of life, are associated with childhood ADHD. Intriguingly, given that genetic risk scores are known to explain little of the variance of ADHD outcomes, we found that ADHD PRS added useful predictive information. Future research needs to test whether predictive models incorporating aspects of early development and genetic risk scores are useful for predicting ADHD in clinical practice.
Identifiants
pubmed: 36478889
doi: 10.1002/jcv2.12099
pii: JCV212099
pmc: PMC9716640
doi:
Types de publication
Journal Article
Langues
eng
Pagination
e12099Subventions
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Medical Research Council
ID : G9815508
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_PC_15018
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_PC_19009
Pays : United Kingdom
Informations de copyright
© 2022 The Authors. JCPP Advances published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.
Déclaration de conflit d'intérêts
The authors declares that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.
Références
J Child Psychol Psychiatry. 2000 Jul;41(5):645-55
pubmed: 10946756
Arch Dis Child. 2011 Jul;96(7):622-9
pubmed: 21508059
JAMA Psychiatry. 2021 Feb 1;78(2):210-219
pubmed: 33052393
J Am Acad Child Adolesc Psychiatry. 2022 Feb;61(2):187-226
pubmed: 33864938
Int J Epidemiol. 2013 Feb;42(1):111-27
pubmed: 22507743
J Pediatr Psychol. 2007 Jul;32(6):711-27
pubmed: 17556402
J Child Psychol Psychiatry. 2006 Mar-Apr;47(3-4):313-37
pubmed: 16492262
J Am Acad Child Adolesc Psychiatry. 2001 Nov;40(11):1337-45
pubmed: 11699809
PeerJ. 2017 May 16;5:e3323
pubmed: 28533971
Lancet. 2016 Mar 19;387(10024):1240-50
pubmed: 26386541
Soc Psychiatry Psychiatr Epidemiol. 2011 Jun;46(6):521-32
pubmed: 20376427
Paediatr Perinat Epidemiol. 2017 Jul;31(4):328-337
pubmed: 28493508
Eur Child Adolesc Psychiatry. 2016 Oct;25(10):1055-66
pubmed: 26861952
J Pediatr Psychol. 1984 Jun;9(2):205-17
pubmed: 6470903
Biol Psychiatry. 2020 Jan 15;87(2):93-94
pubmed: 31856958
JAMA Psychiatry. 2014 Apr;71(4):432-8
pubmed: 24577047
J Clin Child Adolesc Psychol. 2004 Mar;33(1):42-53
pubmed: 15028540
J Pediatr. 1967 Aug;71(2):181-91
pubmed: 6029467
Eur Child Adolesc Psychiatry. 2019 Mar;28(3):377-388
pubmed: 30027417
Early Hum Dev. 2014 Aug;90(8):399-405
pubmed: 24951075
JCPP Adv. 2022 Sep;2(3):e12099
pubmed: 36478889
Dev Psychopathol. 2017 Feb;29(1):107-120
pubmed: 26751219
J Am Acad Child Adolesc Psychiatry. 2015 Apr;54(4):322-7
pubmed: 25791149
J Child Psychol Psychiatry. 2019 Aug;60(8):866-874
pubmed: 30908655
Expert Rev Neurother. 2011 Apr;11(4):557-63
pubmed: 21469928
Nat Genet. 2019 Jan;51(1):63-75
pubmed: 30478444
J Child Psychol Psychiatry. 2004 Jan;45(1):109-34
pubmed: 14959805
J Child Psychol Psychiatry. 2013 Dec;54(12):1284-94
pubmed: 23848372
J Epidemiol Community Health. 2016 Jul;70(7):704-9
pubmed: 26767410
Res Autism Spectr Disord. 2017 Sep;41-42:57-65
pubmed: 28919924
J Child Psychol Psychiatry. 2013 Jan;54(1):3-16
pubmed: 22963644
Genome Med. 2020 May 18;12(1):44
pubmed: 32423490
Int J Epidemiol. 2013 Feb;42(1):97-110
pubmed: 22507742
Eur Child Adolesc Psychiatry. 2020 Jul;29(7):903-916
pubmed: 30798414
J Child Psychol Psychiatry. 2015 Mar;56(3):228-47
pubmed: 25266278
Paediatr Perinat Epidemiol. 2018 Sep;32(5):458-466
pubmed: 29882976
Child Dev. 2000 Mar-Apr;71(2):310-22
pubmed: 10834466
J Child Psychol Psychiatry. 2020 Apr;61(4):401-416
pubmed: 31696514
JAMA Psychiatry. 2016 Dec 01;73(12):1285-1292
pubmed: 27806167
Infancy. 2019 Sep;24(5):768-786
pubmed: 32677276
Arch Gen Psychiatry. 2011 Dec;68(12):1267-75
pubmed: 22147844
J Abnorm Child Psychol. 2014;42(5):831-43
pubmed: 24122374
J Child Psychol Psychiatry. 2017 Jun;58(6):691-701
pubmed: 28094432
Pediatrics. 2015 Sep;136(3):e599-608
pubmed: 26304830
Children (Basel). 2021 Mar 04;8(3):
pubmed: 33806289
Int J Epidemiol. 2018 Aug 1;47(4):1207-1216
pubmed: 29800128
Br J Psychiatry. 2009 Sep;195(3):249-56
pubmed: 19721116
Atten Defic Hyperact Disord. 2019 Sep;11(3):233-240
pubmed: 30515726