Activiteiten per jaar
Objectives It is often claimed that ADHD is a brain-based and highly heritable disorder. However, although all behavior relates to the brain in some way, there are no physiological, neuro-chemical or anatomical studies showing differences other than on a group level. Such claims are in fact generalizations that occur also in relation to ADHD genetics. High heritability claims originate from quantitative genetics: twin, family and adoption studies. These studies are unfortunately only behaviorally and not genetically informative and very limited in their capacity to separate environmental influences from genetic ones. Studies that are genetically informative, qualitative studies, show that genes associated with ADHD occur only slightly more often in groups of individuals diagnosed with ADHD, and when aggregated they have an effect size of <10% explained variance of ADHD related behaviors. This means those diagnosed with ADHD are slightly more likely than controls to have these particular genes, and many with the diagnosis will not have them. Furthermore, many individuals without ADHD related behaviors do carry these genes. For many healthcare professionals, study books used during their professional training shape their perception of the supposedly strong genetic origins of ADHD. In this study, we examine if authors of study books do justice to the intricate difference between findings from twin/adoption/family studies on the one hand and molecular genetics on the other. Method From study guides of >50 (pre-) master’s programs taught between 2012 to 2015 on 10 Dutch universities we selected 43 prescribed study books with a section or chapter on ADHD. We scanned and analyzed chapters and (sub)sections on ADHD with atlas TI, identifying themes on which authors differed in their description of the genetic etiology of ADHD. We analyzed how often authors contrast the high effect sizes of quantitative studies with the low effect sizes from qualitative studies, if they do so at all. Results IN 49% of study books only the high effect sizes of quantitative genetics were mentioned, without contrasting them with the low effect sizes from qualitative genetics. These ‘selective quantitative’ study books likely give the impression that genes with elusive names as TPH-2, SLC6A4, CHRNA4 and GRIN2ADRD4, explain much of ADHD’s heritability. 23% of the study books in our sample demonstrate a more thoughtful approach to writing about genetics. These books name effect sizes from quantitative as well as qualitative studies and often contrast these findings. In some cases, the authors explicitly use the contrast as a dialectical tool to discuss pitfalls of heritability estimates and the interaction of genes and environment. Discussion Selecting only the high estimates from quantitative studies in ADHD genetics is arguably a form of publication bias. Especially since quantitative genetics are only behaviorally informative and do not refer directly to genes as qualitative studies do, it seems questionable to overemphasize those findings. This might be a self-reinforcing phenomenon, as authors of study books likely inspire each other. Possibly, influential writings from opinion leaders have paved the way for this approach; for instance the consensus statement on ADHD is ‘selective quantitative’. This statement scolded cultural and environmental approaches in favor of a disease model with a crucial etiological role for genetics. Molecular studies suggest that there is no proof for a strong stand-alone genetic influence. Additionally, one of the most important candidate genes associated with ADHD appears to interact with family environments, indicating that neither biology nor environment can be seen as a primal influence. Contrary to what many authors of study books suggest, the many interacting influences -each with small effect size- seem to reveal the catch-all nature of the ADHD definition.
|Status||Published - 1-okt-2016|
|Evenement||EUSARF 2016: Shaping the future : connecting knowledge and evidence to child welfare practice - Oviedo, Oviedo, Spain|
Duur: 13-sep-2016 → 16-sep-2016
|Verkorte titel||XIV EUSARF|
|Periode||13/09/2016 → 16/09/2016|