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Dopamine and serotonin transporter genotypes moderate sensitivity to maternal expressed emotion: the case of conduct and emotional problems in attention deficit/hyperactivity disorder
Author(s) -
SonugaBarke Edmund J.S.,
Oades Robert D.,
Psychogiou Lamprini,
Chen Wai,
Franke Barbara,
Buitelaar Jan,
Banaschewski Tobias,
Ebstein Richard P.,
Gil Michael,
Anney Richard,
Miranda Ana,
Roeyers Herbert,
Rothenberger Aribert,
Sergeant Joseph,
Steinhausen Hans Christoph,
Thompson Margaret,
Asherson Philip,
Faraone Stephen V.
Publication year - 2009
Publication title -
journal of child psychology and psychiatry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.652
H-Index - 211
eISSN - 1469-7610
pISSN - 0021-9630
DOI - 10.1111/j.1469-7610.2009.02095.x
Subject(s) - serotonin transporter , dopamine transporter , psychology , attention deficit hyperactivity disorder , dopamine , conduct disorder , 5 httlpr , emotional behavior , clinical psychology , serotonin , developmental psychology , psychiatry , neuroscience , medicine , receptor , dopaminergic
Background: Mothers’ positive emotions expressed about their children with attention deficit/hyperactivity disorder (ADHD) are associated with a reduced likelihood of comorbid conduct problems (CP). We examined whether this association with CP, and one with emotional problems (EMO), is moderated by variants within three genes, previously reported to be associated with ADHD and to moderate the impact of environmental risks on conduct and/or emotional problems; the dopamine transporter gene (SLC6A3/DAT1), the dopamine D4 receptor gene (DRD4) and the serotonin transporter gene (SLC6A4/5HTT). Methods: Seven hundred and twenty‐eight males between the ages of 5 and 17 with a DSM‐IV research diagnosis of combined type ADHD were included in these analyses. Parents and teachers rated children’s conduct and emotional problems. Positive maternal expressed emotion (PMEE) was coded by independent observers on comments made during a clinical assessment with the mother based on current or recent medication‐free periods. Results: Sensitivity to the effects of PMEE on CP was moderated by variants of the DAT1 and 5HTT genes. Only children who did not carry the DAT1 10R/10R or the 5HTT l/l genotypes showed altered levels of CP when exposed to PMEE. The effect was most marked where the child with ADHD had both these genotypes. For EMO, sensitivity to PMEE was found only with those who carried the DAT1 9R/9R. There was no effect of DRD4 on CP or EMO. Conclusion: The gene–environment interactions observed suggested that genetic make‐up can alter the degree of sensitivity an ADHD patients has to their family environment. Further research should focus on distinguishing general sensitivity genotypes from those conferring risk or protective qualities.