Etiological influences on the stability of autistic traits from childhood to early adulthood: evidence from a twin study.
BACKGROUND
Autism spectrum disorders (ASD) are persistent and lifelong conditions. Despite this, almost all twin studies focus on childhood. This twin study investigated the stability of autistic traits from childhood to early adulthood and explored the degree to which any stability could be explained by genetic or environmental factors.


METHODS
Parents of over 2500 twin pairs completed questionnaires assessing autistic traits when twins were aged either 9 or 12 years and again when twins were aged 18. Bivariate twin analysis assessed the degree of phenotypic and etiological stability in autistic traits across this period. Genetic overlap in autistic traits across development was also tested in individuals displaying a broad ASD phenotype, defined as scoring within the highest 5% of the sample.


RESULTS
Autistic traits displayed moderate phenotypic stability (r= .39). The heritability of autistic traits was 76-77% in childhood and 60-62% in adulthood. A moderate degree of genetic influences on childhood autistic traits were carried across into adulthood (genetic correlation = .49). The majority (85%) of the stability in autistic traits was attributable to genetic factors. Genetic influences on autistic traits were moderately stable from childhood to early adulthood at the extremes (genetic correlation = .64).


CONCLUSIONS
Broad autistic traits display moderate phenotypic and etiological stability from childhood to early adulthood. Genetic factors accounted for almost all phenotypic stability, although there was some phenotypic and etiological instability in autistic traits. Thus, autistic traits in adulthood are influenced by a combination of enduring and unique genetic factors.
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Nobels väg 12A, 17177 Stockholm, Sweden.
Mark J
MJ
Taylor
Gillberg Neuropsychiatry Centre, Institute of Neuroscience and Physiology, University of Gothenburg, Kungsgatan 12, 41119 Gothenburg, Sweden.
Christopher
C
Gillberg
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Nobels väg 12A, 17177 Stockholm, Sweden.
Paul
P
Lichtenstein
Gillberg Neuropsychiatry Centre, Institute of Neuroscience and Physiology, University of Gothenburg, Kungsgatan 12, 41119 Gothenburg, Sweden.|Centre for Ethics, Law, and Mental Health, Institute of Neuroscience and Physiology, University of Gothenburg, Rågården, Hus 1, SU-Östra sjukhuset, 41685 Gothenburg, Sweden.
Sebastian
S
Lundström
D000293:Adolescent; D001321:Autistic Disorder / Q000235:genetics* / Q000523:psychology*; D002648:Child; D004200:Diseases in Twins; D005260:Female; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D010641:Phenotype; D011795:Surveys and Questionnaires; D014427:Twins / Q000235:genetics*
Adulthood; Autism; Genetics; Stability; Twin study