Latent Transitions of Census-level Deprivation and Network Analysis of Conduct Problem Behaviours.

Conduct problems are more prevalent in neighbourhoods that have a vulnerable structure (e.g., high neighbourhood-level deprivation) and disarranged interpersonal characteristics (e.g., low social cohesion and informal social control at the neighbourhood level). However, as an indicator of neighbourhood structure, neighbourhood deprivation has typically not been assessed longitudinally and solely based on neighbourhood-level socioeconomic status rather than a wide variety of census-level deprivation indicators. Also, few studies have examined which CD behaviours (e.g., stealing) interplay with neighbourhood risks (e.g., low social cohesion). In this study, latent transitions of neighbourhood-level deprivation patterns, based on census-level information, were estimated between age 12.5 and 15.5 using the Avon Longitudinal Study of Parents and Children (ALSPAC). In network models, we employed multi-informant variables and estimated interplays between mother-reported CD behaviours and child-reported social cohesion, informal social control and deviant peer affiliations within different patterns of the latent neighbourhood-level deprivation transitions. We identified three constant deprivation patterns: deprived, intermediate and low pattern. In the deprived pattern, the CD behaviour "bullying" had the highest interplay with lack of social cohesions, social control, and high deviant peer affiliation. In contrast, non-violent CD behaviours: "lying" and "staying after dark ", showed importance in the intermediate and low patterns, respectively. Regardless of deprivation patterns, social cohesion played a protective role, whereas affiliation with deviant peers involved in property crime was a risk factor for CD behaviours. The identified CD behaviours can serve as a screening tool, and interventions increasing social cohesion might mitigate CD development.

Mother and father depression symptoms and child emotional difficulties: a network model.

BACKGROUND: Mother and father depression symptoms often co-occur, and together can have a substantial impact on child emotional well-being. Little is understood about symptom-level mechanisms underlying the co-occurrence of depression symptoms within families. AIMS: The objective was to use network analysis to examine depression symptoms in mothers and fathers after having a baby, and emotional symptoms in children in early adolescence. METHOD: We examined data from 4492 mother-father-child trios taken from a prospective, population-based cohort in the UK. Symptoms were examined using two unregularised partial correlation network models. The initial model was used to examine the pattern of associations, i.e. the overall network structure, for mother and father depression symptoms, and then to identify bridge symptoms that reinforce depression symptoms between parents during offspring infancy. The second model examined associations between the parent symptom network, including bridge symptoms, with later child emotional difficulties. RESULTS: The study included 4492 mother-father-child trios; 2204 (49.1%) children were female. Bridge symptoms reinforcing mother and father depression symptoms were feeling guilty and self-harm ideation. For mothers, the bridge symptom of feeling guilty, and symptoms of anhedonia, panic and sadness were highly connected with child emotional difficulties. For fathers, the symptom of feeling overwhelmed associated with child emotional difficulties. Guilt and anhedonia in fathers appeared to indirectly associate with child emotional difficulties through the same symptom in mothers. CONCLUSIONS: Our findings suggest that specific symptom cascades are central for co-occurring depression in parents and increased vulnerability in children, providing potential therapeutic targets.

The adult outcome of childhood quasi-autism arising following extreme institutional deprivation.

BACKGROUND: Rutter and colleagues' seminal observation that extended early life exposure to extreme institutional deprivation can result in what he termed quasi-autism (QA), informed both our understanding of the effects of adversity on development and the nature of autism. Here we provide the first detailed analysis of the adult outcomes of the group of institutionally deprived-then-adopted children identified as displaying QA. METHODS: Twenty-six adult adoptees identified with QA in childhood (Childhood QA+) were compared to 75 adoptees who experienced extended institutional deprivation (>6 months) but no QA (Childhood QA-), and 116 adoptees exposed to Low/No institutional deprivation. The outcomes were child-to-adult developmental trajectories of neuro-developmental symptoms (autism, attention-deficit/hyperactivity disorder (ADHD), disinhibited social engagement (DSE) and cognitive impairment), adult functioning, life satisfaction and mental health. RESULTS: Childhood QA+ was associated with elevated and persistent trajectories of broad-based autism-related difficulties, ADHD and DSE symptoms and low IQ, as well as adult mental health difficulties and functional impairment, including high rates of low educational attainment and unemployment. Life satisfaction and self-esteem were unaffected. Autism-related communication problems, in particular, predicted negative adult outcomes. Childhood QA+ was still associated with poor outcomes even when ADHD, DSE and IQ were controlled. CONCLUSIONS: Early and time-limited institutional deprivation has a critical impact on adult functioning, in part via its association with an early established and persistent variant of autism, especially related to communication difficulties. Apparent similarities and differences to non-deprivation related autism are discussed.

Epilepsy severity mediates association between mutation type and ADHD symptoms in tuberous sclerosis complex.

The association between attention-deficit/hyperactivity disorder (ADHD) and tuberous sclerosis complex (TSC) is widely reported, with support for the role of epilepsy, yet the mechanisms underlying the association across development are unclear. The Tuberous Sclerosis 2000 Study is a prospective longitudinal study of TSC. In Phase 1 of the study, baseline measures of epilepsy, cortical tuber load, and mutation were obtained with 125 children ages 0-16 years. In Phase 2, at an average of 8 years later, ADHD symptoms were measured for 81 of the participants. Structural equation modeling revealed an indirect pathway from genetic mutation, to cortical tuber load, to epileptic spasm severity in infancy, to ADHD symptoms in middle childhood and adolescence, in addition to a pathway linking current seizure severity to ADHD symptoms. Findings were retained when intelligence quotient (IQ) was entered as a correlated factor. The findings support a cascading developmental pathway to ADHD symptoms mediated by early-onset and severe epilepsy in the first 2 years of life. This warrants detailed investigation of seizure characteristics and cognitive and behavioral sequelae associated with ADHD from early in life, to further the understanding of the association between ADHD and early-onset epilepsy across syndromic and non-syndromic populations.

The Underlying Mechanisms in the Association Between Traumatic Brain Injury in Childhood and Conduct Disorder Symptoms in Late Adolescence.

The present study examined i) the direct association between traumatic brain injury (TBI) in childhood and conduct disorder symptoms in adolescence, ii) whether this effect is mediated by impulsivity and/or callous unemotional traits (CU traits), and iii) whether these indirect effects are moderated by childhood family adversity and adolescent substance use. Utilising data from the Avon Longitudinal Study of Parents and Children (ALSPAC), participants with head injury information up to 12 years (4.5 years, 5.4 years, 6.5 years, 8.6 years, 11.7 years) were identified and categorised into a TBI (n = 409), orthopaedic injury (n = 1469) or non-injury group (n = 5685). Psychosocial factors such as impulsivity at 13 years, CU traits at 13 years, childhood family adversity (between birth to 4 years) and substance use at 14 years were collated for moderated mediation analyses. Conduct disorder symptoms were assessed at 16 years of age. TBI and conduct disorder symptoms were positively associated, and this association was mediated by impulsivity but not CU traits. The indirect effects were higher in magnitude for individuals with higher levels of childhood family adversity. Adolescent substance use was not found to moderate the indirect effects between TBI and conduct disorder symptoms. These results were specific to TBI individuals, and not in participants with orthopaedic injury and no reported injuries. Targeting impulsivity and early family adversity may alleviate the risk of conduct disorder symptoms following TBI in childhood. These findings have important implications for informing neuro-rehabilitative and preventative measures in clinical and community settings.

Sensation-seeking-related DNA methylation and the development of delinquency: A longitudinal epigenome-wide study.

Heightened sensation-seeking is related to the development of delinquency. Moreover, sensation-seeking, or biological correlates of sensation-seeking, are suggested as factors linking victimization to delinquency. Here, we focused on epigenetic correlates of sensation-seeking. First, we identified DNA methylation (DNAm) patterns related to sensation-seeking. Second, we investigated the association between sensation-seeking related DNAm and the development of delinquency. Third, we examined whether victimization was related to sensation-seeking related DNAm and the development of delinquency. Participants (N = 905; 49% boys) came from the Avon Longitudinal Study of Parents and Children. DNAm was assessed at birth, age 7 and age 15-17. Sensation-seeking (self-reports) was assessed at age 11 and 14. Delinquency (self-reports) was assessed at age 17-19. Sensation-seeking epigenome-wide association study revealed that no probes reached the critical significance level. However, 20 differential methylated probes reached marginal significance. With these 20 suggestive sites, a sensation-seeking cumulative DNAm risk score was created. Results showed that this DNAm risk score at age 15-17 was related to delinquency at age 17-19. Moreover, an indirect effect of victimization to delinquency via DNAm was found. Sensation-seeking related DNAm is a potential biological correlate that can help to understand the development of delinquency, including how victimization might be associated with adolescent delinquency.

Associations of DNA Methylation With Behavioral Problems, Gray Matter Volumes, and Negative Life Events Across Adolescence: Evidence From the Longitudinal IMAGEN Study.

BACKGROUND: Negative life events (NLEs) increase the risk for externalizing behaviors (EBs) and internalizing behaviors (IBs) in adolescence and adult psychopathology. DNA methylation associated with behavioral problems may reflect this risk and long-lasting effects of NLEs. METHODS: To identify consistent associations between blood DNA methylation and EBs or IBs across adolescence, we conducted longitudinal epigenome-wide association studies (EWASs) using data from the IMAGEN cohort, collected at ages 14 and 19 years (n = 506). Significant findings were validated in a separate subsample (n = 823). Methylation risk scores were generated by 10-fold cross-validation and further tested for their associations with gray matter volumes and NLEs. RESULTS: No significant findings were obtained for the IB-EWAS. The EB-EWAS identified a genome-wide significant locus in a gene linked to attention-deficit/hyperactivity disorder (ADHD) (IQSEC1, cg01460382; p = 1.26 × 10-8). Other most significant CpG sites were near ADHD-related genes and enriched for genes regulating tumor necrosis factor and interferon-γ signaling, highlighting the relevance of EB-EWAS findings for ADHD. Analyses with the EB methylation risk scores suggested that it partly reflected comorbidity with IBs in late adolescence. Specific to EBs, EB methylation risk scores correlated with smaller gray matter volumes in medial orbitofrontal and anterior/middle cingulate cortices, brain regions known to associate with ADHD and conduct problems. Longitudinal mediation analyses indicated that EB-related DNA methylation were more likely the outcomes of problematic behaviors accentuated by NLEs, and less likely the epigenetic bases of such behaviors. CONCLUSIONS: Our findings suggest that novel epigenetic mechanisms through which NLEs exert short and longer-term effects on behavior may contribute to ADHD.

Psychological and Developmental Correlates of Paraphilic and Normophilic Sexual Interests.

The classification of sexual fantasies and behaviors (here referred to as 'sexual interests') has historically been divided into 'paraphilic' and 'normophilic'. However, studies on paraphilic interests are often limited to clinical or forensic samples and normophilic interests are rarely assessed in tandem. Previous research has found mixed results for psychological and other correlates of sexual interests, potentially due to inconsistency in operationalism and measurement of fantasies and behaviors. The aim of the current study was to quantify correlates of sexual interests via the Sexual Fantasies and Behaviors Inventory, containing factors related to general fantasies/behaviors, normophilia, power dynamics, sadomasochism, and courtship paraphilias, using a large (N = 4280) non-clinical sample. Psychological, developmental, sexual, and demographic correlates were investigated via bivariate correlations, mean difference testing, and multiple regression. Sexual interest domains were largely unrelated to psychopathology and developmental factors. Sociosexuality and more accepting attitudes towards sadomasochism was generally related to more arousal to/engagement in normophilic and paraphilic domains. More autism spectrum disorder traits were related to decreased normophilic interests. Psychopathic traits, sexual sensation seeking, and sexual compulsivity were related to paraphilia dimensions, especially courtship paraphilias and domination/sadism; the former was also associated with negative attitudes about establishing consent. Men, non-monogamous, and non-heterosexual participants indicated greater sexual fantasies and behaviors compared to women (except in the case of submission and masochism), monogamous, and heterosexual participants, respectively.

Networks of Adversity in Childhood and Adolescence and Their Relationship to Adult Mental Health.

Adverse experiences before the age of eighteen are common and include diverse events ranging from sexual abuse to parental divorce. These stressful experiences have been linked to physical and mental health issues. Previous research has focused mainly on childhood adversity, such as experiences in the family environment. Little consideration has been given to adversities that may be particularly harmful in adolescence. To understand adolescents' adverse experiences, this project used data from the Avon Longitudinal Study of Parents and Children (ALSPAC, total N = 14,901, N ≈ 1,200 - 10,000 per measure). We modelled interrelations of adversities in childhood (1-11 years) and adolescence (11-23 years) and examined adversity clusters using network analysis. We found two similar clusters in the childhood and adolescence networks: (1) direct abuse and (2) adverse family factors. We identified a third cluster of (3) educational and social adversities for adolescence. For both age groups, emotional abuse in the family environment was closely linked to mental health in early adulthood and most adversities were linked with depression in early adulthood. In adolescence, housing and academic issues and abuse by a romantic partner were particularly central to the network of adversities. Thus, we found commonalities and differences in the relevance of adverse experiences at different developmental stages. These findings highlight the need to develop age-dependent frameworks for adversity research and policymaking.

Editorial: Does the polygenic revolution herald a watershed in the study of GE interplay in developmental psychopathology? Some considerations for the Special Issue reader.

The primary goal motivating the scientific field of Developmental Psychopathology is to discover why some individuals develop mental health and neuro-developmental difficulties while others do not. This is not simply a 'blue skies' preoccupation: the underlying hope, of course, is to translate such discoveries to the benefit of individuals, families and communities, reducing poor outcomes for those at risk and - in the best case scenario - ensuring that they thrive. A core tenet of the bio-psycho-social framework within which this field of enquiry operates is that children's difficulties are determined by the interplay of predisposing genetic risk and resilience factors and the environments and experiences to which individuals are exposed. From this perspective, understanding gene-environment (GE) interplay is a necessary condition for explaining and, as importantly predicting, why one individual is at risk while another is not. If we believe this, then the risk calculators designed to show who will and will not get a particular disorder - all the rage at the moment - are doomed to fail until they can go beyond modelling the main effects of genes and environments, and reliably estimate GE processes too. Despite significant progress, we remain a considerable way off cracking this problem.

Not in education, employment and training: pathways from toddler difficult temperament.

BACKGROUND: Youths disengaged from the education system and labour force (i.e. 'Not in Education, Employment, or Training' or 'NEET') are often at reduced capacity to flourish and thrive as adults. Developmental precursors to NEET status may extend back to temperamental features, though this - and possible mediators of such associations such as attention deficit hyperactivity (ADHD) symptoms and antisocial behaviours (ASB) - have yet to be directly tested. This study investigates if i) difficult temperament in toddlerhood associates with NEET status in adulthood and ii) different subdomains of ADHD (i.e. hyperactivity-impulsivity vs. inattention) in late childhood and ASB in adolescence partially explain this pathway. METHODS: Participants were 6,240 mother-child dyads (60.7% female) from the Avon Longitudinal Study of Parents and Children. Mothers reported on their child's (a) difficult temperament (i.e. mood, intensity and adaptability) at age 2 and (b) ADHD symptoms at ages 8 and 10. Participants reported their own ASB at age 14 and NEET status in adulthood (ages 18, 20, 22 and 23). RESULTS: First, higher levels of difficult temperament in toddlerhood directly associated with an increased probability of being NEET in adulthood. Second, this effect was carried through hyperactivity-impulsivity, but not inattention, in late childhood, and ASB in adolescence; this demonstrates differential contribution to the pathway between the ADHD dimensions, with symptoms of hyperactivity-impulsivity playing a prominent role. CONCLUSIONS: Early difficult temperament is a vulnerability factor for NEET status in adulthood. Our findings suggest that one developmental pathway for this vulnerability manifests through increased hyperactivity-impulsivity in childhood and ASB in adolescence. Of note, difficult temperament, as measured here, reflects difficulties in emotional and behavioural self-control (e.g. low adaptability and high intensity negative emotional expressions). Our results, therefore, suggest a prominent developmental role for lack of self-control from toddlerhood onwards in increasing risk for NEET.

Role of polygenic and environmental factors in the co-occurrence of depression and psychosis symptoms: a network analysis.

Depression and psychosis are often comorbid; they also have overlapping genetic and environmental risk factors, including trauma and area-level exposures. The present study aimed to advance understanding of this comorbidity via a network approach, by (1) identifying bridge nodes that connect clusters of lifetime depression and psychosis symptoms and (2) evaluating the influence of polygenic and environmental risk factors in these symptoms. This study included data from European ancestry participants in UK Biobank, a large population-based sample (N = 77,650). In Step 1, a network model identified bridge nodes between lifetime symptoms of depression and psychosis and functional impairment. In Step 2, genetic and environmental risk factors were incorporated to examine the degree to which symptoms associated with polygenic risk scores for depression and schizophrenia, lifetime exposure to trauma and area-level factors (including deprivation, air pollution and greenspace). Feelings of worthlessness, beliefs in unreal conspiracy against oneself, depression impairment and psychosis impairment emerged as bridges between depression and psychosis symptoms. Polygenic risk scores for depression and schizophrenia were predominantly linked with depression and psychosis impairment, respectively, rather than with specific symptoms. Cumulative trauma emerged as a bridge node associating deprivation with feelings of worthlessness and beliefs in unreal conspiracy, indicating that the experience of trauma is prominently linked with the co-occurrence of depression and psychosis symptoms related to negative views of oneself and others. These key symptoms and risk factors provide insights into the lifetime co-occurrence of depression and psychosis.

Contribution of Innate Lymphoid Cells in Supplementing Cytokines Produced by CD4+ T Cells During Acute and Chronic SIV Infection of the Colon.

HIV/SIV (simian immunodeficiency virus) infection leads to a loss of CD4+ T helper (Th) cells in number and function that begins during the acute phase and persists through the chronic phase of infection. In particular, there is a drastic decrease of Th17 and Th22 cells in the HIV/SIV-infected gastrointestinal (GI) tract as a source of interleukin (IL)-17 and IL-22. These cytokines are vital in the immune response to extracellular pathogens and maintenance of the GI tract. However, innate lymphoid cells (ILCs) are a source of IL-17 and IL-22 during the early stages of an immune response in mucosal tissue and remain vital cytokine producers when the immune response is persistent. Here, we wanted to determine whether ILCs are a source of IL-17 and IL-22 in the SIV-infected colon and could compensate for the loss of Th17 and Th22 cells. As a control, we evaluated the frequency and number of ILCs expressing interferon-gamma (IFNγ) and tumor necrosis factor-alpha (TNFα). We determined the frequency and number of cytokine expressing ILC subsets and T cell subsets within leukocytes from the colons of uninfected as well as acute and chronic SIV-infected colons without in vitro mitogenic stimulation. In the present study, we find that: (1) the frequency of IL-22, IFNγ, and TNFα but not IL-17 producing ILCs is increased in the acutely infected colon and remains high during the chronically infected colon relative to cytokine expressing ILCs in the uninfected colon, (2) ILCs are a significant source of IL-22, IFNγ, and TNFα but not IL-17 when CD4+ T lymphocytes in the gut lose their capacity to secrete these cytokines during SIV infection, and (3) the changes in the cytokines expressed by ILCs relative to CD4+ T cells in the infected colon were not due to increases in the frequency or number of ILCs in relation to T lymphocytes found in the tissue.

Presence of Natural Killer B Cells in Simian Immunodeficiency Virus-Infected Colon That Have Properties and Functions Similar to Those of Natural Killer Cells and B Cells but Are a Distinct Cell Population.

Here, we report the appearance of natural killer B (NKB) cells within the colon during simian immunodeficiency virus (SIV) infection of susceptible monkeys. Using RNA sequencing (RNAseq) and flow cytometry, we show that NKB cells are unique cells with features and functions of both NK and B cells. NKB cells express receptors and ligands found on B cells that are important for (i) antigen presentation; (ii) activities associated with class switching, affinity maturation, and B-cell memory formation in secondary lymphoid follicles; and (iii) antigen recognition. The predominant immunoglobulins (Igs) expressed on NKB cells are IgA, although NKB cells can express surface IgM and IgG. There is dominant lambda expression over the kappa light chain characteristic of mucosal B cells. In addition to B-cell aspects, NKB cells express NK cell activation receptors and Fas ligand. We show in this study that NKB cells express perforin and granzymes and lyse cells in a lytic assay. In addition to NK cell cytolytic function, NKB cells also produce the inflammatory cytokines interferon gamma, tumor necrosis factor alpha, and interleukin-18 (IL-18). Finally, we noted the increased capacity of NKB cells to proliferate compared to NK cells and CD8+ T cells from the SIV-infected colon. The increased proliferation and inflammatory cytokine production may be related to the relatively high expression levels of IL-15 receptor beta, IL-7 receptor, IL-18 receptor, and 41BB relative to the same receptors on CD8 and NK cells. The properties of NKB cells may point to their role in the enhanced inflammation observed in the SIV-infected gut. IMPORTANCE There is low-level but significant mucosal inflammation in the gastrointestinal tract secondary to human immunodeficiency virus (HIV) infection that has long-term consequences for the infected host. This inflammation most likely originates from the immune response that appears as a consequence of HIV. Here, we show in an animal model of HIV that the chronically SIV-infected gut contains cytotoxic natural killer B cells that produce inflammatory cytokines and proliferate during infection.

Family Aggression Screening Tool (FAST): Factor structure and psychometric properties of subscales.

BACKGROUND: The Family Aggression Screening Tool (FAST) is an instrument to screen for experiences of maltreatment using primarily pictorial representations, including direct victimisation and exposure to intimate partner violence. The initial psychometric properties of the FAST were reported in the original research in the United Kingdom. OBJECTIVE: This research aimed to replicate and to extend the evaluation of the psychometric properties of FAST in Brazil. PARTICIPANTS AND SETTING: Data consisted of 648 youth aged 11 to 17 years from public schools in Brazil. METHOD: We employed confirmatory factor analysis (CFA), exploratory factor analysis (EFA) and exploratory graphical analysis (EGA). Concurrent validity was supported by strong correlations between the FAST's emotional and physical victimisation subscales and Childhood Trauma Questionnaire (CTQ) emotional and physical abuse subscales. RESULTS: CFA resulted in a solution including second and first order factors, resembling the original structure. FAST's reliability was assessed both through internal consistency and test-retest, showing favorable coefficients. CONCLUSION: Our results suggest that FAST has good psychometric properties for the Brazilian population with respect to both its validity and reliability.

Nighttime lights, urban features, household poverty, depression, and obesity.

Nighttime Light Emission (NLE) is associated with diminished mental and physical health. The present study examines how NLE and associated urban features (e.g., air pollution, low green space) impact mental and physical wellbeing. We included 200,393 UK Biobank Cohort participants with complete data. The study was carried out in two steps. In Step1, we assessed the relationship between NLE, deprivation, pollution, green space, household poverty and mental and physical symptoms. In Step2, we examined the role of NLE on environment-symptom networks. We stratified participants into high and low NLE and used gaussian graphical model to identify nodes which bridged urban features and mental and physical health problems. We then compared the global strength of these networks in high vs low NLE. We found that higher NLE associated with higher air pollution, less green space, higher economic and neighborhood deprivation, higher household poverty and higher depressed mood, higher tiredness/lethargy and obesity (Rtraining_mean = 0.2624, P training_mean < .001; Rtest_mean = 0.2619, P test_mean < .001). We also found that the interaction between environmental risk factors and mental, physical problems (overall network connectivity) was higher in the high NLE network than in the low NLE network (t = 0.7896, P < .001). In areas with high NLE, economic deprivation, household poverty and waist circumference acted as bridge factors between the key urban features and mental health symptoms. In conclusion, NLE, urban features, household poverty and mental and physical symptoms are all interrelated. In areas with high NLE, urban features associate with mental and physical health problems at a greater magnitude than in areas with low NLE. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12144-022-02754-3.

Developmental pathways from toddler difficult temperament to child generalized psychopathology and adult functioning.

BACKGROUND: Early difficult temperament and child mental health problems are consistently associated with impaired functioning in adulthood. We examined three potential pathways between difficult temperament in toddlerhood (age 2) and depressive symptoms (ages 21-23) and well-being (age 23): i) direct - early difficult temperament directly associates with these outcomes, ii) mediated - these direct effects are also mediated by a general psychopathology factor in late childhood/early adolescence (GPF; ages 7, 10,and 13), and iii) moderated-mediated - these mediated effects are also moderated by negative (age 42 months) and positive (age 33 months) parenting behaviors. METHODS: The analytic sample included 1892 mother-child dyads (33.4% male children) from the Avon Longitudinal Study of Parents and Children (ALSPAC). Mothers reported on their child's difficult temperament, negative parenting, positive parenting, and child's mental health symptoms. In adulthood, participants reported their own depressive symptoms and well-being (i.e. mental well-being, life satisfaction, happiness). RESULTS: First, early difficult temperament associated directly and positively with depressive symptoms, but negatively with well-being in adulthood. Second, the GPF in late childhood/early adolescence mediated these direct associations. Third, the mediated pathways were not moderated by negative or positive parenting. LIMITATIONS: i) low risk community sample, ii) early risks are based on maternal reports. CONCLUSIONS: Temperament is a risk factor for impaired psychosocial functioning in adulthood, manifested through increased susceptibility to psychopathology in childhood/adolescence. Although more research is needed to test their generalizability, these findings suggest that targeting early difficult temperament may alleviate the risk for later mental health difficulties and may increase general well-being.

Epigenetic profiling of social communication trajectories and co-occurring mental health problems: a prospective, methylome-wide association study.

While previous studies suggest that both genetic and environmental factors play an important role in the development of autism-related traits, little is known about potential biological mechanisms underlying these associations. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), we examined prospective associations between DNA methylation (DNAm: nbirth = 804, nage 7 = 877) and trajectories of social communication deficits at age 8-17 years. Methylomic variation at three loci across the genome (false discovery rate = 0.048) differentiated children following high (n = 80) versus low (n = 724) trajectories of social communication deficits. This differential DNAm was specific to the neonatal period and not observed at 7 years of age. Associations between DNAm and trajectory membership remained robust after controlling for co-occurring mental health problems (i.e., hyperactivity/inattention, conduct problems). The three loci identified at birth were not replicated in the Generation R Study. However, to the best of our knowledge, ALSPAC is the only study to date that is prospective enough to examine DNAm in relation to longitudinal trajectories of social communication deficits from childhood to adolescence. Although the present findings might point to potentially novel sites that differentiate between a high versus low trajectory of social communication deficits, the results should be considered tentative until further replicated.

Development and psychometric validation of the Sexual Fantasies and Behaviors Inventory.

To date, no measures of sexual fantasies and behaviors have been tested using modern structural equation modeling techniques. A total of 4,280 adults from the U.S., U.K., Canada, and Ireland completed a measure of diverse (paraphilic and normophilic) sexual fantasies and behaviors. Data were randomly split in half for a two-part analysis. First, an exploratory factor analysis (EFA) was performed to reduce the item pool and determine general factor structure. Second, we tested several models using confirmatory factor analysis (CFA) and exploratory structural equation modeling (ESEM). These were followed by tests of measurement invariance (based on sex and sexual orientation) and criterion validity. For both the fantasies and behaviors, bifactor ESEMs were the most appropriate models. Similar specific factors emerged: (a) normophilia, (b) rough sex, (c) interest of intrusion, (d) assuming power, and (e) relinquishing power. Findings suggest that sexual interests show a hierarchical measurement structure. Males and nonheterosexuals had higher general fantasy scores; nonheterosexuals had higher general behavior scores. Heterosexuals generally scored lower than nonheterosexuals. Fantasy and behavior scores were positively related to Dark Triad traits and sociosexuality, and there were weak or no relationships with depression and anxiety. Results support the psychometric validation of the Sexual Fantasies and Behaviors Inventory. Strengths of this study include a large nonclinical sample with relevant psychological correlates and the use of modern psychometric methods. However, the use of an internet sample with self-report measures may be unrepresentative, although the internet has the advantage of being able to recruit from stigmatized groups. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

The protective role of father behaviour in the relationship between maternal postnatal depression and child mental health.

Background: Maternal depression, especially when severe and long-lasting, is associated with adverse mental health outcomes in children. We aimed to assess, for children of mothers with persistent postnatal depression symptoms, whether positive father behaviours would decrease risk for conduct and emotional symptoms. Methods: Using data from 4009, mother-father-child trios from the Avon Longitudinal Study of Parents and Children we examined associations between maternal depression trajectories and positive father behavioural profiles across the postnatal period (child age: 2-21 months), and child conduct and emotional symptom trajectories across middle childhood (child age: 3.5-11 years). Results: Positive father behaviour was much less common in families where mothers experienced high-persistent depression symptoms (33%) than in families where mothers did not (56%); of note, these fathers also had higher levels of depression symptoms. Using person-level analysis, exposure to high-persistent maternal depression symptoms increased child risk for a high trajectory of both conduct (odds ratio, 2.69; 95% CI: 2.00, 3.60) and emotional symptoms (odds ratio, 2.47; 95% CI: 1.83, 3.31). However, positive father behaviour (toward child and mother) reduced the odds of following high trajectories of conduct symptoms by 9% (x = 4.52, p < .001) and of emotional symptoms by 10% (x = 4.12, p < .001), even after controlling for father depression symptoms. Using variable-level analysis, we did not identify an interaction between maternal depression and positive father behaviour. For conduct problems, we identified a direct effect of positive father behaviour and lower conduct problems. For emotional symptoms, father behaviour interacted with child age, where the largest decrease was seen at age 9, when symptoms were highest across the sample. Conclusions: Positive father behaviour can be protective against chronic mental health problems for children exposed to persistent maternal postnatal depression symptoms.