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It is not known whether early intervention can improve long-term autism symptom outcomes. We aimed to follow-up the Preschool Autism Communication Trial (PACT), to investigate whether the PACT intervention had a long-term effect on autism symptoms and continued effects on parent and child social interaction. PACT was a randomised controlled trial of a parent-mediated social communication intervention for children aged 2–4 years with core autism. Follow-up ascertainment was done at three specialised clinical services centres in the UK (London, Manchester, and Newcastle) at a median of 5·75 years (IQR 5·42–5·92) from the original trial endpoint. The main blinded outcomes were the comparative severity score (CSS) from the Autism Diagnostic Observation Schedule (ADOS), the Dyadic Communication Assessment Measure (DCMA) of the proportion of child initiatiations when interacting with the parent, and an expressive-receptive language composite. All analyses followed the intention-to-treat principle. PACT is registered with the ISRCTN registry, number ISRCTN58133827. 121 (80%) of the 152 trial participants (59 [77%] of 77 assigned to PACT intervention vs 62 [83%] of 75 assigned to treatment as usual) were traced and consented to be assessed between July, 2013, and September, 2014. Mean age at follow-up was 10·5 years (SD 0·8). Group difference in favour of the PACT intervention based on ADOS CSS of log-odds effect size (ES) was 0·64 (95% CI 0·07 to 1·20) at treatment endpoint and ES 0·70 (95% CI −0·05 to 1·47) at follow-up, giving an overall reduction in symptom severity over the course of the whole trial and follow-up period (ES 0·55, 95% CI 0·14 to 0·91, p=0·004). Group difference in DCMA child initiations at follow-up showed a Cohen's d ES of 0·29 (95% CI −0.02 to 0.57) and was significant over the course of the study (ES 0·33, 95% CI 0·11 to 0·57, p=0·004). There were no group differences in the language composite at follow-up (ES 0·15, 95% CI −0·23 to 0·53). The results are the first to show long-term symptom reduction after a randomised controlled trial of early intervention in autism spectrum disorder. They support the clinical value of the PACT intervention and have implications for developmental theory. Medical Research Council.

Mothers' self-reported stroking of their infants over the first weeks of life modifies the association between prenatal depression and physiological and emotional reactivity at 7 months, consistent with animal studies of the effects of tactile stimulation. We now investigate whether the effects of maternal stroking persist to 2.5 years. Given animal and human evidence for sex differences in the effects of prenatal stress we compare associations in boys and girls. From a general population sample of 1233 first-time mothers recruited at 20 weeks gestation we drew a random sample of 316 for assessment at 32 weeks, stratified by reported inter-partner psychological abuse, a risk indicator for child development. Of these mothers, 243 reported at 5 and 9 weeks how often they stroked their infants, and completed the Child Behavior Checklist (CBCL) at 2.5 years post-delivery. There was a significant interaction between prenatal anxiety and maternal stroking in the prediction of CBCL internalizing (p = 0.001) and anxious/depressed scores (p < 0.001). The effects were stronger in females than males, and the three-way interaction prenatal anxiety × maternal stroking × sex of infant was significant for internalizing symptoms (p = 0.003). The interactions arose from an association between prenatal anxiety and internalizing symptoms only in the presence of low maternal stroking. The findings are consistent with stable epigenetic effects, many sex specific, reported in animal studies. While epigenetic mechanisms may be underlying the associations, it remains to be established whether stroking affects gene expression in humans.

Autism spectrum disorder (ASD) was once considered to be highly associated with intellectual disability and to show a characteristic IQ profile, with strengths in performance over verbal abilities and a distinctive pattern of 'peaks' and 'troughs' at the subtest level. However, there are few data from epidemiological studies. Comprehensive clinical assessments were conducted with 156 children aged 10-14 years [mean (s.d.)=11.7 (0.9)], seen as part of an epidemiological study (81 childhood autism, 75 other ASD). A sample weighting procedure enabled us to estimate characteristics of the total ASD population. Of the 75 children with ASD, 55% had an intellectual disability (IQ<70) but only 16% had moderate to severe intellectual disability (IQ<50); 28% had average intelligence (115>IQ>85) but only 3% were of above average intelligence (IQ>115). There was some evidence for a clinically significant Performance/Verbal IQ (PIQ/VIQ) discrepancy but discrepant verbal versus performance skills were not associated with a particular pattern of symptoms, as has been reported previously. There was mixed evidence of a characteristic subtest profile: whereas some previously reported patterns were supported (e.g. poor Comprehension), others were not (e.g. no 'peak' in Block Design). Adaptive skills were significantly lower than IQ and were associated with severity of early social impairment and also IQ. In this epidemiological sample, ASD was less strongly associated with intellectual disability than traditionally held and there was only limited evidence of a distinctive IQ profile. Adaptive outcome was significantly impaired even for those children of average intelligence.

False positive findings in science are inevitable, but are they particularly common in psychology and psychiatry? The evidence that we review suggests that while not restricted to our field, the problem is acute. We describe the concept of researcher ‘degrees-of-freedom’ to explain how many false-positive findings arise, and how the various strategies of registration, pre-specification, and reporting standards that are being adopted both reduce and make these visible. We review possible benefits and harms of proposed statistical solutions, from tougher requirements for significance, to Bayesian and machine learning approaches to analysis. Finally we consider the organisation and methods for replication and systematic review in psychology and psychiatry.

Data from a representative community sample were used to explore predictors of lifetime suicidality and to examine associations between distal adolescent and more proximal adult risks. Data are from a midlife follow-up of the Isle of Wight study, an epidemiological sample of adolescents assessed in 1968. Ratings of psychiatric symptoms and disorder, relationships and family functioning and adversity were made in adolescence; adult assessments included lifetime psychiatric history and suicidality, neuroticism and retrospective reports of childhood sexual abuse and harsh parenting. A wide range of measures of childhood psychopathology, adverse experiences and interpersonal difficulties were associated with adult suicidality; associations were particularly strong for adolescent irritability, worry and depression. In multivariate analyses, substantial proportions of these effects could be explained by their association with adult psychopathology and neuroticism, but additional effects remained for adolescent irritability and worry. Factors of importance for long-term suicidality risk are evident in adolescence. These include family and experiential adversities as well as psychopathology. In particular, markers of adolescent worry and irritability appeared both potent risks and ones with additional effects beyond associations with adult disorder and adult neuroticism.

In animal models, prenatal and postnatal stress is associated with elevated hypothalamic–pituitary axis (HPA) reactivity mediated via altered glucocorticoid receptor (GR) gene expression. Postnatal tactile stimulation is associated with reduced HPA reactivity mediated via increased GR gene expression. In this first study in humans to examine the joint effects of prenatal and postnatal environmental exposures, we report that GR gene ( NR3C1 ) 1-F promoter methylation in infants is elevated in the presence of increased maternal postnatal depression following low prenatal depression, and that this effect is reversed by self-reported stroking of the infants by their mothers over the first weeks of life.

Current prospective reports suggest a pandemic-related increase in adolescent mental health problems. We examine whether age-related change over 11–14 years accounts for this increase. Mothers and adolescents in a UK-based birth cohort (Wirral Child Health and Development Study; WCHADS; N = 737) reported on adolescent depression and behavioural problems pre-pandemic (December 2019–March 2020), mid-pandemic (June 2020–March 2021) and late pandemic (July 2021–March 2022). Analysis used repeated measures models for over-dispersed Poisson counts with an adolescent-specific intercept with age as a time-varying covariate. Maturational curves for girls, but not for boys, showed a significant increase in self-reported depression symptoms over ages 11–14 years. Behavioural problems decreased for both. After adjusting for age-related change, girls’ depression increased by only 13% at mid-pandemic and returned to near pre-pandemic level at late pandemic (mid versus late – 12%), whereas boys’ depression increased by 31% and remained elevated (mid versus late 1%). Age-adjusted behavioural problems increased for both (girls 40%, boys 41%) and worsened from mid- to late pandemic (girls 33%, boys 18%). Initial reports of a pandemic-related increase in depression in young adolescent girls could be explained by a natural maturational rise. In contrast, maturational decreases in boys’ depression and both boys’ and girls’ behavioural problems may mask an effect of the pandemic.

Background There is emerging evidence that the neuroanatomy of autism forms a spectrum which extends into the general population. However, whilst several studies have identified cortical morphology correlates of autistic traits, it is not established whether morphological differences are present in the subcortical structures of the brain. Additionally, it is not clear to what extent previously reported structural associations may be confounded by co-occurring psychopathology. To address these questions, we utilised neuroimaging data from the Adolescent Brain Cognitive Development Study to assess whether a measure of autistic traits was associated with differences in child subcortical morphology, and if any observed differences persisted after adjustment for child internalising and externalising symptoms. Methods Our analyses included data from 7005 children aged 9–10 years (female: 47.19%) participating in the Adolescent Brain Cognitive Development Study. Autistic traits were assessed using scores from the Social Responsiveness Scale (SRS). Volumes of subcortical regions of interest were derived from structural magnetic resonance imaging data. Results Overall, we did not find strong evidence for an association of autistic traits with differences in subcortical morphology in this sample of school-aged children. Whilst lower absolute volumes of the nucleus accumbens and putamen were associated with higher scores of autistic traits, these differences did not persist once a global measure of brain size was accounted for. Limitations It is important to note that autistic traits were assessed using the SRS, of which higher scores are associated with general behavioural problems, and therefore may not be wholly indicative of autism-specific symptoms. In addition, individuals with a moderate or severe autism diagnosis were excluded from the ABCD study, and thus, the average level of autistic traits will be lower than in the general population which may bias findings towards the null. Conclusions These findings from our well-powered study suggest that other metrics of brain morphology, such as cortical morphology or shape-based phenotypes, may be stronger candidates to prioritise when attempting to identify robust neuromarkers of autistic traits.

General intelligence is an important human quantitative trait that accounts for much of the variation in diverse cognitive abilities. Individual differences in intelligence are strongly associated with many important life outcomes, including educational and occupational attainments, income, health and lifespan. Data from twin and family studies are consistent with a high heritability of intelligence, but this inference has been controversial. We conducted a genome-wide analysis of 3511 unrelated adults with data on 549 692 single nucleotide polymorphisms (SNPs) and detailed phenotypes on cognitive traits. We estimate that 40% of the variation in crystallized-type intelligence and 51% of the variation in fluid-type intelligence between individuals is accounted for by linkage disequilibrium between genotyped common SNP markers and unknown causal variants. These estimates provide lower bounds for the narrow-sense heritability of the traits. We partitioned genetic variation on individual chromosomes and found that, on average, longer chromosomes explain more variation. Finally, using just SNP data we predicted ∼1% of the variance of crystallized and fluid cognitive phenotypes in an independent sample ( P =0.009 and 0.028, respectively). Our results unequivocally confirm that a substantial proportion of individual differences in human intelligence is due to genetic variation, and are consistent with many genes of small effects underlying the additive genetic influences on intelligence.

Climate change threatens natural landscapes through shifting distribution and abundance of species and attendant change in the structure and function of ecosystems. However, it remains unclear how climate-mediated variation in species' environmental niche space may lead to large-scale fragmentation of species distributions, altered meta-population dynamics and gene flow, and disrupted ecosystem integrity. Such change may be especially relevant when species distributions are restricted either spatially or to a narrow environmental niche, or when environments are rapidly changing. Here, we use range-wide environmental niche models to posit that climate-mediated range fragmentation aggravates the direct effects of climate change on species in the boreal forest of North America. We show that climate change will directly alter environmental niche suitability for boreal-obligate species of trees, birds and mammals (n = 12), with most species ranges becoming smaller and shifting northward through time. Importantly, species distributions will become increasingly fragmented, as characterized by smaller mean size and greater isolation of environmentally-suitable landscape patches. This loss is especially pronounced along the Ontario-Québec border, where the boreal forest is narrowest and roughly 78% of suitable niche space could disappear by 2080. Despite the diversity of taxa surveyed, patterns of range fragmentation are remarkably consistent, with our models predicting that spruce grouse (Dendragapus canadensis), boreal chickadee (Poecile hudsonicus), moose (Alces americanus) and caribou (Rangifer tarandus) could have entirely disjunct east-west population segments in North America. These findings reveal potentially dire consequences of climate change on population continuity and species diversity in the boreal forest, highlighting the need to better understand: 1) extent and primary drivers of anticipated climate-mediated range loss and fragmentation; 2) diversity of species to be affected by such change; 3) potential for rapid adaptation in the most strongly-affected areas; and 4) potential for invasion by replacement species.