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•SPS captures sensitivity to environment in a heritable, evolutionary-conserved trait, associated with increased information processing in the brain.•SPS moderates sensitivity to ...environments in a for-better-and-for-worse fashion.•Interaction with negative experiences, increases risk for psychopathology.•Interaction with positive experiences (including interventions), increases positive outcomes.•Objective assessment, mechanistic understanding and evidence-based interventions for high scoring individuals on SPS need to be improved.
Sensory Processing Sensitivity (SPS) is a common, heritable and evolutionarily conserved trait describing inter-individual differences in sensitivity to both negative and positive environments. Despite societal interest in SPS, scientific knowledge is lagging behind. Here, we critically discuss how SPS relates to other theories, how to measure SPS, whether SPS is a continuous vs categorical trait, its relation to other temperament and personality traits, the underlying aetiology and neurobiological mechanisms, and relations to both typical and atypical development, including mental and sensory disorders. Drawing on the diverse expertise of the authors, we set an agenda for future research to stimulate the field. We conclude that SPS increases risk for stress-related problems in response to negative environments, but also provides greater benefit from positive and supportive experiences. The field requires more reliable and objective assessment of SPS, and deeper understanding of its mechanisms to differentiate it from other traits. Future research needs to target prevention of adverse effects associated with SPS, and exploitation of its positive potential to improve well-being and mental health.
Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) have overlapping characteristics and etiological factors, but to which extent this applies to infant- and preschool ...age is less well understood. Comparing the pathways to ASD and ADHD from the earliest possible stages is crucial for understanding how phenotypic overlap emerges and develops. Ultimately, these insights may guide preventative and therapeutic interventions. Here, we review the literature on the core symptoms, temperament and executive function in ASD and ADHD from infancy through preschool age, and draw several conclusions: (1) the co-occurrence of ASD and ADHD increases with age, severity of symptoms and lower IQ, (2) attention problems form a linking pin between early ASD and ADHD, but the behavioral, cognitive and sensory correlates of these attention problems partly diverge between the two conditions, (3) ASD and ADHD share high levels of negative affect, although the underlying motivational and behavioral tendencies seem to differ, and (4) ASD and ADHD share difficulties with control and shifting, but partly opposite behaviors seem to be involved.
Different psychiatric disorders and symptoms are highly correlated in the general population. A general psychopathology factor (or "P-factor") has been proposed to efficiently describe this ...covariance of psychopathology. Recently, genetic and neuroimaging studies also derived general dimensions that reflect densely correlated genomic and neural effects on behaviour and psychopathology. While these three types of general dimensions show striking parallels, it is unknown how they are conceptually related. Here, we provide an overview of these three general dimensions, and suggest a unified interpretation of their nature and underlying mechanisms. We propose that the general dimensions reflect, in part, a combination of heritable 'environmental' factors, driven by a dense web of gene-environment correlations. This perspective calls for an update of the traditional endophenotype framework, and encourages methodological innovations to improve models of gene-brain-environment relationships in all their complexity. We propose concrete approaches, which by taking advantage of the richness of current large databases will help to better disentangle the complex nature of causal factors underlying psychopathology.
While the negative association between ADHD symptoms and IQ is well documented, our knowledge about the direction and aetiology of this association is limited. Here, we examine the association of ...ADHD symptoms with verbal and performance IQ longitudinally in a population-based sample of twins. In a population-based sample of 4,771 twin pairs, DSM-IV ADHD symptoms were obtained from the Conners' Parent Rating Scale-Revised. Verbal (vocabulary) and performance (Raven's Progressive Matrices) IQ were assessed online. ADHD symptom ratings and IQ scores were obtained at ages 12, 14 and 16 years. Making use of the genetic sensitivity and time-ordered nature of our data, we use a cross-lagged model to examine the direction of effects, while modelling the aetiologies of the association between ADHD symptoms with vocabulary and Raven's scores over time. Although time-specific aetiological influences emerged for each trait at ages 14 and 16 years, the aetiological factors involved in the association between ADHD symptoms and IQ were stable over time. ADHD symptoms and IQ scores significantly predicted each other over time. ADHD symptoms at age 12 years were a significantly stronger predictor of vocabulary and Raven's scores at age 14 years than vice versa, whereas no differential predictive effects emerged from age 14 to 16 years. The results suggest that ADHD symptoms may put adolescents at risk for decreased IQ scores. Persistent genetic influences seem to underlie the association of ADHD symptoms and IQ over time. Early intervention is likely to be key to reducing ADHD symptoms and the associated risk for lower IQ.
All individuals on planet earth are sensitive to the environment, but some more than others. These individual differences in sensitivity to environments are seen across many animal species including ...humans, and can influence personalities as well as vulnerability and resilience to mental disorders. Yet, little is known about the underlying brain mechanisms. Key genes that contribute to individual differences in environmental sensitivity are the serotonin transporter, dopamine D4 receptor and brain-derived neurotrophic factor genes. By synthesizing neurodevelopmental findings of these genetic factors, and discussing them through the lens of mechanisms related to sensitive periods, which are phases of heightened neuronal plasticity during which a certain network is being finetuned by experiences, we propose that these genetic factors delay but extend postnatal sensitive periods. This may explain why sensitive individuals show behavioral features that are characteristic of a young brain state at the level of sensory information processing, such as reduced filtering or blockade of irrelevant information, resulting in a sensory processing system that ‘keeps all options open’.
•Dopamine D4 receptor, serotonin transporter and BDNF genes are key modulators of environmental sensitivity.•Animals lacking the genes exhibit increased environmental sensitivity.•Environmental sensitivity may rely on extended and/or prolonged sensitive periods.•Environmental sensitivity may therefore be related to a young brain state.
Attention-deficit/hyperactivity disorder (ADHD) is more frequent in males than in females. The “female protective effect” posits that females undergo greater exposure to etiological factors than ...males in order to develop ADHD, leading to the prediction that relatives of females with ADHD will display more ADHD behaviors. We thus tested whether cotwins of females displaying extreme ADHD traits would display more ADHD traits than cotwins of males displaying extreme ADHD traits.
Parents of approximately 7,000 pairs of nonidentical twins in Sweden, and approximately 4,000 pairs of twins in England and Wales, completed dimensional assessments of ADHD traits. Probands were selected on the basis of scoring within the highest 10% of the distribution in each sample. Dimensional scores of cotwins of probands, as well as the categorical recurrence rate, were investigated by proband sex.
Cotwins of female probands displayed higher mean ADHD trait scores (mean = 0.62−0.79) than cotwins of male probands (mean = 0.38−0.55) in both samples. This trend was significant in the Swedish sample (p < .01) and when the 2 samples were merged into a single, larger sample (p < .001). When the samples were merged, there was also a significant association between proband sex and cotwin’s categorical status, with more cotwins of female probands also being probands than cotwins of male probands.
These findings support a female protective effect against ADHD behaviors, suggesting that females require greater exposure to genetic and environmental factors associated with ADHD in order to develop the condition.
Attention-deficit/hyperactivity disorder (ADHD) is conceptualized as a neurodevelopmental disorder that is strongly heritable. However, to our knowledge, no study to date has examined the genetic and ...environmental influences explaining interindividual differences in the developmental course of ADHD symptoms from childhood to adolescence (ie, systematic decreases or increases with age). The reason ADHD symptoms persist in some children but decline in others is an important concern, with implications for prognosis and interventions.
To assess the proportional impact of genes and the environment on interindividual differences in the developmental course of ADHD symptom domains of hyperactivity/impulsivity and inattention between ages 8 and 16 years.
A prospective sample of 8395 twin pairs from the Twins Early Development Study, recruited from population records of births in England and Wales between January 1, 1994, and December 31, 1996. Data collection at age 8 years took place between November 2002 and November 2004; data collection at age 16 years took place between February 2011 and January 2013.
Both DSM-IV ADHD symptom subscales were rated 4 times by participants' mothers.
Estimates from latent growth curve models indicated that the developmental course of hyperactivity/impulsivity symptoms followed a sharp linear decrease (mean score of 6.0 at age 8 years to 2.9 at age 16 years). Interindividual differences in the linear change in hyperactivity/impulsivity were under strong additive genetic influences (81%; 95% CI, 73%-88%). More than half of the genetic variation was specific to the developmental course and not shared with the baseline level of hyperactivity/impulsivity. The linear decrease in inattention symptoms was less pronounced (mean score of 5.8 at age 8 years to 4.9 at age 16 years). Nonadditive genetic influences accounted for a substantial amount of variation in the developmental course of inattention symptoms (54%; 95% CI, 8%-76%), with more than half being specific to the developmental course.
The large genetic influences on the developmental course of ADHD symptoms are mostly specific and independent of those that account for variation in the baseline level of symptoms. Different sets of genes may be associated with the developmental course vs the baseline level of ADHD symptoms and explain why some children remit from ADHD, whereas others persist. Recent longitudinal imaging data indicate that the maintenance or increase in symptoms is underpinned by atypical trajectories of cortical development. This may reflect a specific genetic liability, distinct from that which contributes to baseline ADHD symptoms, and warrants closer follow-up.
Cognitive control has been strongly linked to midfrontal theta (4–8 Hz) brain activity. Such control processes are known to be impaired in individuals with psychiatric conditions and ...neurodevelopmental diagnoses, including attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Temporal variability in theta, in particular, has been associated with ADHD, with shared genetic variance underlying the relationship. Here, we investigated the phenotypic and genetic relationships between theta phase variability, theta-related signals (the N2, error-related negativity, and error positivity), reaction time, and ADHD and ASD longitudinally in a large twin study of young adults to investigate the stability of the genetic relationships between these measures over time.
Genetic multivariate liability threshold models were run on a longitudinal sample of 566 participants (283 twin pairs). Characteristics of ADHD and ASD were measured in childhood and young adulthood, while an electroencephalogram was recorded in young adulthood during an arrow flanker task.
Cross-trial theta phase variability in adulthood showed large positive phenotypic and genetic relationships with reaction time variability and both childhood and adult ADHD characteristics. Error positivity amplitude was negatively related phenotypically and genetically to ADHD and ASD at both time points.
We showed significant genetic associations between variability in theta signaling and ADHD. A novel finding from the current study is that these relationships were stable across time, indicating a core dysregulation of the temporal coordination of control processes in ADHD that persists in individuals with childhood symptoms. Error processing, indexed by the error positivity, was altered in both ADHD and ASD, with a strong genetic contribution.
The objectives of this study were to model more homogeneous subgroups within autism spectrum disorder (ASD) based on early trajectories of core symptoms; and to further characterize these subgroups ...in terms of trajectories of language, cognition, co-occurring (attention-deficit/hyperactivity disorder ADHD-related) traits and clinical outcome diagnosis.
Children (N = 203) referred for possible ASD at ages 1 to 4 years were assessed at three time points at intervals ranging from 9 months to 3 years. Assessments included standardized measures for ASD (Autism Diagnostic Observation Schedule ADOS), language (ADOS-language item), nonverbal IQ (NV-IQ; different tests adequate to chronological/mental age), and parent-reported behavioral problems (Infant-Toddler Social and Emotional Assessment, Child Behavior Checklist).
Latent-class growth curve analysis with ADOS total scores led to the identification of three main stable and two small improving groups: a severe-stable group (19.5% of sample)-the only group without considerable language improvement-showed persistent low NV-IQ and marked increase in attention problems over time; a moderate-stable group (21.7%) with below-average increasing NV-IQ; and a mild-stable group (48%) with stable-average NV-IQ and the highest scores on ADHD-related traits, whose ASD outcome diagnoses increased despite stable-low ASD scores. Two groups (each 5.4%) improved: one moved from severe to moderate ASD scores, and the other moved from moderate to mild/nonspectrum scores. Both of these groups improved on language, NV-IQ, and ADHD-related traits.
Results support the high stability of ASD symptoms into various severity levels, but also highlight the significant contribution of non-ASD domains in defining and explaining the different ASD trajectories.
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