“…Furthermore, some influences act dimensionally rather than as pathogens at high levels of severity only. It has long been known, for example, that minor degrees of hypoxia after birth have only very weak associations with behavioural or cognitive abnormalities later (Taylor, 1991a). It now appears that it would be wrong to generalise this conclusion – of a high threshold for injury – to all forms of stressors.…”
Section: Discussionmentioning
confidence: 99%
“…Even a left‐sided hemispherectomy is compatible with a satisfactory development of language (though there may still be subtle deficiencies) (Pulsifer et al, 2004). The young brain when damaged is not so much resilient as plastic: it compensates for functional alteration, and that compensation can bring different sorts of dysfunction (Taylor, 1991a).…”
Background: Knowledge of genetic influences, on developmental disorders such as autism spectrum, attention deficit/hyperactivity disorder and learning disabilities, has increased the opportunities for understanding the influences of the early environment. Methods: This paper provides a selective, narrative review for clinicians of the effects of factors such as exposure to toxins and stresses in utero and in postnatal life; brain injuries and perinatal compromise; neglect, malnutrition and selective food deficiencies. It also considers what is known about the mechanisms through which early adversities operate. Results: Gaps in the research are identified and suggestions made about clinical investigations. Several types of environmental adversity have associations with later disorders that suggest a causal role. The effects are often on a broad range of psychological processes, and are not always quickly reversible. Several adversities often coexist, calling for skilled judgement about priorities in treatment. Conclusions: Individuals vary considerably in their exposure to adversity and their vulnerability to its effects, and genetic inheritance can influence both.
“…Furthermore, some influences act dimensionally rather than as pathogens at high levels of severity only. It has long been known, for example, that minor degrees of hypoxia after birth have only very weak associations with behavioural or cognitive abnormalities later (Taylor, 1991a). It now appears that it would be wrong to generalise this conclusion – of a high threshold for injury – to all forms of stressors.…”
Section: Discussionmentioning
confidence: 99%
“…Even a left‐sided hemispherectomy is compatible with a satisfactory development of language (though there may still be subtle deficiencies) (Pulsifer et al, 2004). The young brain when damaged is not so much resilient as plastic: it compensates for functional alteration, and that compensation can bring different sorts of dysfunction (Taylor, 1991a).…”
Background: Knowledge of genetic influences, on developmental disorders such as autism spectrum, attention deficit/hyperactivity disorder and learning disabilities, has increased the opportunities for understanding the influences of the early environment. Methods: This paper provides a selective, narrative review for clinicians of the effects of factors such as exposure to toxins and stresses in utero and in postnatal life; brain injuries and perinatal compromise; neglect, malnutrition and selective food deficiencies. It also considers what is known about the mechanisms through which early adversities operate. Results: Gaps in the research are identified and suggestions made about clinical investigations. Several types of environmental adversity have associations with later disorders that suggest a causal role. The effects are often on a broad range of psychological processes, and are not always quickly reversible. Several adversities often coexist, calling for skilled judgement about priorities in treatment. Conclusions: Individuals vary considerably in their exposure to adversity and their vulnerability to its effects, and genetic inheritance can influence both.
“…The scores derived from the PACS and K-SADS were combined with the Conners Teacher Rating Scale: Long version for children <18 years (Conners et al, 1998a) and the Conners Adult ADHD Rating Scale-Self Report: Long version for participants ≥18 years (Conners et al, 1997), depending on the age of the participant (cut-off 18 years). Participants originally diagnosed with ADHD, but not meeting the ADHD diagnostic criteria at follow-up anymore, were classified as remitters (Francx et al, 2015).…”
Section: Assessment Of Adhd Impulsivity and Callous Traitsmentioning
Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder that often persists into adulthood. ADHD and related personality traits, such as impulsivity and callousness, are caused by genetic and environmental factors and their interplay. Epigenetic modifications of DNA, including methylation, are thought to mediate between such factors and behavior and may behave as biomarkers for disorders. Here, we set out to study DNA methylation in persistent ADHD and related traits. We performed epigenome-wide association studies (EWASs) on peripheral whole blood from participants in the NeuroIMAGE study (age range 12-23 years). We compared participants with persistent ADHD (n = 35) with healthy controls (n = 19) and with participants with remittent ADHD (n = 19). Additionally, we performed EWASs of impulsive and callous traits derived from the Conners Parent Rating Scale and the Callous-Unemotional Inventory, respectively, across all participants. For every EWAS, the linear regression model analyzed included covariates for age, sex, smoking scores, and surrogate variables reflecting blood cell type composition and genetic background. We observed no epigenome-wide significant differences in single CpG site methylation between participants with persistent ADHD and healthy controls or participants with remittent ADHD. However, epigenome-wide analysis of differentially methylated regions provided significant findings showing that hypermethylated regions in the APOB and LPAR5 genes were associated with ADHD persistence compared to ADHD remittance (p = 1.68 * 10 −24 and p = 9.06 * 10 −7 , respectively); both genes are involved in cholesterol signaling. Both findings appeared to be linked to genetic variation in cis. We found neither significant epigenome-wide single CpG sites nor regions associated with impulsive and callous traits; the top-hits from these analyses were annotated to genes involved in neurotransmitter release and the regulation of the biological clock. No link to genetic variation was observed for these findings, which thus might reflect environmental influences. In conclusion, in this pilot study with a small sample size, we observed several DNA-methylation-disorder/trait associations of potential significance for ADHD and the related behavioral traits. Although we do not wish to draw conclusions before replication in larger, independent samples, cholesterol signaling and metabolism may be of relevance for the onset and/or persistence of ADHD.
“…Their able to the confounding presence of conduct disorder. perceived importance declined greatly with the realization that most obstetric suboptimal-There is a better established association between ADHD and family dysfunction: we ity was not a direct cause of any psychological abnormalities, but reflected psychosocial have long known that the fathers of young people with ADHD have a higher rate of de-adversity and abnormalities of fetal development (Taylor, 1991a). More recently they linquency, substance abuse, and antisociality, and that mothers are often characterized by have again become a focus for study because of imaging evidence for structural brain somatizing disorders (Cantwell, 1975).…”
mentioning
confidence: 99%
“…Seeger (1998) has reported prelimi-vary at different stages of development? Developmental neuropsychiatry, investigating nary findings of a strong association between ADHD and season of birth, but only in a sub-the effects of known brain abnormalities, has usually emphasized the variability of expres-group characterized by a variant form of the gene coding for the D4 dopamine receptor sion of congenital abnormalities (Taylor, 1991a). Lesions alter through development, (DRD4.7).…”
Recent research on the disorders of attention and activity has indicated inherited variants of
genes controlling aspects of neurotransmission, abnormalities of structure and function in regions
of frontal lobes and basal ganglia, failures to suppress inappropriate responses, and a cascade of
failures in various kinds of cognitive performance and organization of behavior. This review
integrates the neurodevelopmental findings with findings from developmental psychopathology.
It outlines several developmental tracks by which constitutional factors interact with the
psychological environment. In one set of tracks, altered brain states lead to cognitive alteration.
An understimulating environment is evoked by (and may be genetically associated with) an
inattentive and cognitively impulsive style during early childhood. In another track, impulsive
and inattentive behavior shows direct continuity through childhood into late adolescence. In yet
another track, impulsiveness evokes (and may be genetically associated with) critical expressed
emotion from parents and inefficient coping strategies, which in turn contribute to the
development of antisocial conduct. This formulation emphasizes the need for several types of
research: the mapping of biological findings onto different components of disorder, the
combination of genetically informative designs with direct measurement of relevant aspects of
the environment, and the use of longitudinal studies to examine predictive and mediating factors
separately for different aspects of outcome.
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