ABSTRACT
BACKGROUND: Considering an evolutionary perspective, psychiatric conditions present us with a paradox. How can the high prevalence of those conditions be explained, given the importance of genetic factors in many of them? Evolutionary principles predict that traits with an adverse effect on reproduction undergo negative selection. AIM: To try to formulate an answer to this paradox from the perspective of evolutionary psychiatry by integrating different disciplines. METHOD: We describe some important evolutionary models: the adaptive and maladaptive model, the mismatch model, the trade-off model and the balance model. By way of illustration, we have searched the literature for evolutionary perspectives on autism spectrum disorder. RESULTS: In this narrative review we describe several evolutionary hypotheses about autism spectrum disorder with a framing within the different evolutionary models. We discuss, among others, evolutionary hypotheses regarding gender differences in social skills, the link with more recent evolutionary cognitive development, and autism spectrum disorder as an extreme cognitive outlier. CONCLUSION: We conclude that evolutionary psychiatry offers a complementary point of view on psychiatric conditions and specifically on autism spectrum disorder. A link to neurodiversity and an impetus to clinical translation is made.
Subject(s)
Autism Spectrum Disorder , Psychiatry , Humans , Autism Spectrum Disorder/psychology , Prevalence , Social Skills , Sex FactorsABSTRACT
BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) is a frequently occurring problem in child and adolescent psychiatry. Most prevalent comorbid disorders are oppositional defiant behavior, tics, autism spectrum disorder, anxiety and depression. Stimulants are the first pharmacological choice. Recently, long-acting guanfacin became available in Belgium and the Netherlands.
AIM: To investigate the efficacy of guanfacin on comorbid symptoms in ADHD.
METHOD: A systematic search in Medline and Cochrane databases for randomized controlled trials in which the effect of guanfacin on comorbid symptoms is evaluated.
RESULTS: Guanfacin had an effect on autism symptoms, oppositional defiant symptoms and possibly on tics in children and adolescents with adhd. On anxiety symptoms, no effect was reported. The effect on depression needs to be further investigated. The side effects of guanfacin are similar in comorbid disorders and pure ADHD.
CONCLUSION: Guanfacin is a treatment option for ADHD in children and adolescents with comorbid autism or behavioural symptoms and possibly also tics, as it has a demonstrated effect on these comorbid features. Further research is necessary in order to decide on the preference for a particular medication in ADHD with these various comorbid disorders.
Subject(s)
Adrenergic alpha-2 Receptor Agonists/therapeutic use , Attention Deficit Disorder with Hyperactivity/drug therapy , Attention Deficit Disorder with Hyperactivity/epidemiology , Guanfacine/therapeutic use , Adolescent , Anxiety Disorders/drug therapy , Anxiety Disorders/epidemiology , Autism Spectrum Disorder/drug therapy , Autism Spectrum Disorder/epidemiology , Child , Comorbidity , Female , Humans , Male , Tic Disorders/drug therapy , Tic Disorders/epidemiology , Treatment OutcomeABSTRACT
BACKGROUND: In the last decades, researchers often used measures to quantify autism spectrum disorder (ASD) traits, paralleling the tendency to describe psychiatric and developmental disorders more dimensionally. The broader autism phenotype (BAP) concept originates from this kind of research. AIM: The primary aim of our studies was to study the existence of the BAP and the familial transmission of quantitative autism traits (QAT). METHOD: We measured ASD-traits with interviews and questionnaires in all members of 170 families with at least one child with ASD. RESULTS: We confirmed the existence of the BAP in fathers, as well as the familial transmission of QAT. The results also suggest that what is measured with these questionnaires might depend on the population and the context. CONCLUSION: Based on our results and additional data from scientific literature, we reflect on the interpretations of research results and the use of quantitative scales in both research and clinical practice.
Subject(s)
Autism Spectrum Disorder/classification , Autism Spectrum Disorder/diagnosis , Family/psychology , Fathers/psychology , Adolescent , Autism Spectrum Disorder/psychology , Child , Child, Preschool , Female , Humans , Male , Mothers/psychology , Siblings/psychologyABSTRACT
We describe the identification and delineation of an inherited 2.07 Mb microduplication in 1q42.2 in two brothers with autism and mild mental retardation. Since this duplication was not present in 1577 Belgian persons, we consider this as an extremely rare variant which has the potential to provide further insight into the genetics of autism. The duplication contains seven genes including the DISC1 gene, an interesting candidate gene that has been associated to schizophrenia, bipolar disorder, autism and Asperger syndrome. In this report we describe additional analyses undertaken to investigate the causal relationship of the duplication to the autism phenotype. We conclude that the 1q42.2 microduplication probably confers susceptibility to autism in the current family. This study is a typical illustration of the difficult interpretation of causality of a very rare variant in neuropsychiatric disease and the challenge of genetic counselling in a particular family.
