Most previous studies on the link of autistic traits (ATs) to psychotic experiences (PEs) were performed in clinical populations; hence, the need for further examination of this relationship within the extended autism-and psychosis-phenotypes in the general population. This study aimed to test the following hypotheses: (1) ATs will be positively related to PEs; (2) alexithymia will act as a mediator between ATs and PEs; (3) childhood trauma will moderate the mediation model of alexithymia between ATs and PEs. This cross-sectional research took place in 12 Arab countries among 7,646 young adults. The Autism-Spectrum Quotient-28, Prodromal Questionnaire-Brief, Toronto Alexithymia Scale, and Childhood trauma Self-Report Scale-12 were used. Analysis was done using PROCESS-Macro model-7 in SPSS. Childhood abuse significantly moderated the association between ATs and alexithymia. Higher ATs were significantly associated with higher alexithymia, and this association was stronger at lower than higher levels of childhood abuse. In turn, higher alexithymia was significantly associated with higher PEs. The direct association between ATs and PEs remained significant. The conditional indirect effect of ATs on PEs through alexithymia was significant at low, moderate, and high levels of childhood abuse. Furthermore, the index of moderated mediation was significant, indicating that childhood abuse significantly moderated the indirect association between ATs and PEs through alexithymia. The current results suggest that alexithymia and childhood trauma seem to be key factors that should be considered together as specific targets for treatment to improve the severity of psychotic symptoms and even possibly prevent psychosis in highly autistic young adults.
Reinforcement sensitivity theory (RST) most clearly relates to internalizing disorders. But a weak behavioural inhibition system (BIS as defined by RST) could underlie externalising, in general, and psychopathy in particular (Fowles, 1980). Conventional “rationally derived” RST scales (rRST) are not anchored in neurally defined RST systems (nRST). So, here, we use both rRST and nRST measures to assess psychopathy traits. We operationalised psychopathy via a four-factor model (affective | interpersonal | disinhibition | boldness). We operationalised rRST via the Heym, Ferguson & Lawrence (2008) updated version of Carver and White’s (1994) BIS/BAS scales (BAS | BIS | FFFS). We operationalised nRST (goal inhibition system, GIS; goal repulsion system, GRS) via previously validated (Shadli et al., 2021) rhythmic power in the stop signal task (SST) and (goal approach system, GAS) via previously validated ERPs in the doors task. Initial bivariate correlations of psychopathy factors with rRST scales were as expected. We found no significant associations between psychopathy factors and nRST measures. A series of post hoc exploratory repeated measures ANOVAs guarded against non-linearity between psychopathy and nRST constructs. These found that: (1) Disinhibition traits might be explained (unexpectedly) by increased sensitivity in the GIS (i.e., conflict) and GRS (i.e., repulsion) and decreased sensitivity in the GAS (i.e., attraction). (2) Affective traits might be explained, as expected, by decreased sensitivity in the GIS and GRS. But an unexpected positive association was also found in the alpha frequency range for the GRS. So, nRST systems (particularly GIS) do not explain psychopathy. rRST scales were more aligned with expectations but were explained via their “rational” basis not RST per se. Unlike internalizing, nRST does not appear strongly related to externalising disorders in general and psychopathy in particular. rRST appears distinct from nRST.
In the present paper we present psychometric properties on a Social Dominance scale from items which are embedded in the Affective Neuroscience Personality Scales 3.1. In two samples we show that psychometrics of the Social Dominance scale are sufficient and that correlations with scales measuring Panksepp’s primary emotional systems fail to consistently reach statistical significance with the exception of associations with ANGER (moderate effect size), SEEKING and CARE (small effect sizes). No associations with satisfaction with life and only small negative associations with Spirituality could be observed. We concur with Panksepp that Social Dominance is not a primary emotion but is a learned secondary emotion involving several primary emotions. We show evidence that Social Dominance is not the same as ANGER. We also briefly review mammalian (including humans) evidence that supports the view that Social Dominance is learned and also that the ANGER, SEEKING, and CARE primary mammalian emotions contribute to the learning of Social Dominance.
Shame and guilt are similar yet distinct self-conscious emotions that often facilitate the attainment of social goals and motivate behaviors that promote social acceptance. Recent studies have shown that individuals with autism or high autistic traits may tend to exhibit higher shame-proneness and lower guilt-proneness. This study examined whether this profile of self-conscious emotions can be explained by the functional organization of the brain using resting-state fMRI. Autistic traits, shame- and guilt-proneness and whole-brain resting-state fMRI data were measured in 45 neurotypical individuals. Our results revealed that the positive association between autistic traits and shame-proneness was mediated by resting-state functional connectivity between the right frontal pole and several regions among the cortical midline structures, including the precuneus, anterior cingulate and posterior cingulate. Additionally, functional connectivity between the right frontal pole and precuneus was found to mediate the negative association between autistic traits and guilt-proneness. These findings highlight the role of the cortical midline structures as a key neural substrate underlying differential experiences of negative self-conscious emotions among individuals with high autistic traits.
The aim of this study was to investigate the neurochemical differences between borderline personality disorder (BPD) and antisocial personality disorder (ASPD) using proton magnetic resonance spectroscopy (¹H-MRS) in order to explore these disorders at a neurobiological level. In this cross-sectional study, 60 individuals with BPD and 60 individuals with ASPD participated. ¹H-MRS was performed using a Discovery MR 750 Magnetic Resonance Imaging (MRI) scanner with a 3.0 Tesla field strength to measure the levels of the metabolites GABA/Cr, N-acetylaspartate (NAA)/Cr, and glutamate (Glu)/Cr in the left anterior cingulate cortex (ACC) and the left orbitofrontal cortex (OFC) of the brain. The findings indicated that concentrations of GABA/Cr and Glu/Cr in the OFC were significantly higher in BPD patients compared to those with ASPD. In the ACC, GABA/Cr levels were elevated and NAA/Cr levels were reduced in the BPD group relative to the ASPD group. No significant differences were observed in Glu/Cr concentrations in the ACC or in NAA/Cr concentrations in the OFC. This study demonstrated significant neurochemical differences between BPD and ASPD in the ACC and OFC regions. These findings may enhance our understanding of the underlying neural mechanisms of these disorders and support the development of more targeted and effective therapeutic approaches.
Social rewards (e.g. smiles) powerfully shape human behavior, starting from early childhood. Yet, the neural architecture that enables differential processing of social and nonsocial rewards remains largely unknown. Few previous studies that directly compared social vs nonsocial stimuli have used stimuli that have low ecological validity or are not matched on low-level stimulus parameters – limiting the scope of inference. To address this gap in knowledge, social and nonsocial reward images taken from the real world were matched on valence, arousal, and key low-level stimulus properties and presented to 37 adults in a functional magnetic resonance imaging (fMRI) study. Individual self-reported preference for social images was associated with the functional connectivity between the left anterior insula (LAI) and medial orbitofrontal cortex (mOFC), as well as that between the left Fusiform Gyrus (LFG) and the Anterior Cingulate Cortex (ACC). Autistic traits negatively modulated LAI – mOFC connectivity and LFG – ACC connectivity. Reduced functional connectivity between these regions may contribute to the lower social reward responsivity in individuals with high autistic traits, as also noted from their lower valence ratings to social rewards. This study provides evidence for a new experimental paradigm to test social reward processing at a behavioral and neural level, which can contribute to potential transdiagnostic biomarkers for social cognitive processes.
Autism Spectrum Disorder (ASD) is defined as a unidimensional condition, and autism traits are measured on a continuum where the high end of the spectrum represents individuals likely to have an ASD diagnosis. However, the large heterogeneity of ASD has thrown this unidimensional conceptualization into question. With the exact underlying cause(s) of autism yet to be identified, there is a pressing need to establish core, underlying dimensions of ASD that can capture heterogeneity within the autism spectrum, thereby better specifying both autistic traits and ASD symptoms. Here we describe one important transdiagnostic dimension, the cognitive rigidity-flexibility dimension, that may impact autistic traits and symptoms across symptom-relevant cognitive domains. We first discuss how diminished cognitive flexibility manifests in core autistic traits and autism symptoms in perception, attention, learning, social cognition, and communication. We then propose to supplement assessments of autistic traits in the general population and autism symptoms in individuals with an ASD diagnosis with a comprehensive batter of cognitive flexibility measures in these symptom-relevant domains. We conjecture that systematic differences in domain-general versus domain-specific cognitive flexibility can distill subgroups within the autism phenotype. While we focus on the cognitive flexibility dimension here, we believe that it is important to extend this framework to other higher order dimensions that can capture core autism symptoms and transdiagnostic symptom severity. This approach can characterize the latent, multi-faceted structure of autism, thereby yielding greater precision in diagnostic classification and the creation of more targeted interventions.
The surge of online psychological assessments have brought the autism research community both opportunities and challenges: while they enable rapid large-scale data collection and more power to characterize individual differences, they also bring concerns about data quality, generalizability beyond online samples, and whether autistic traits can be reliably characterized with self-report measures administered online. Here we tackle these concerns by providing a systematic characterization of the autistic traits variability across individuals in a large cross-sectional dataset (N=2826) as well as its temporal reliability within individuals in a test-retest dataset (N=247), with both online and in-lab samples. We measured autistic traits using the Social Responsiveness Scale, 2nd version, Adult Self Report (SRS-2-ASR) - a tool that quantifies individual differences in autistic traits along a continuum for the general adult population. Across individuals, we found elevated SRS scores in online samples and were able to trace this effect to specific subsets of SRS items. SRS scores also covaried with internalizing symptoms, decreased with age, and were lower in women compared to other genders. Within individuals, we find moderate-to-good test-retest reliability of SRS scores over long intervals, with no difference between online and in-lab samples, suggesting robust temporal stability. We conclude that there are systematic differences in autistic traits between online and in-lab samples that are partly explained by systematic population-level differences in internalizing symptoms, particularly social anxiety. Future studies that sample across different populations should measure, control for, or stratify with respect to these factors.
Traditional psychological research has often treated inter-subject variability as statistical noise (even, nuisance variance), focusing instead on averages rather than individual differences. This approach has limited our understanding of the substantial heterogeneity observed in neuropsychiatric disorders, particularly autism spectrum disorder (ASD). In this introduction to a special issue on this theme, we discuss recent advances in cognitive computational neuroscience that can lead to a more systematic notion of core symptom dimensions that differentiate between ASD subtypes. These advances include large participant databases and data-sharing initiatives to increase sample sizes of autistic individuals across a wider range of cultural and socioeconomic backgrounds. Our perspective helps to build bridges between autism symptomatology and individual differences in autistic traits in the non-autistic population and introduces finer-grained dynamic methods to capture behavioral dynamics at the individual level. We specifically focus on how cognitive computational models have emerged as powerful tools to better characterize autistic traits in the general population and autistic population, particularly with respect to social decision-making. We finally outline how we can combine and harness these recent advances, on the one hand, big data initiatives, and on the other hand, cognitive computational models, to achieve a more systematic and nuanced understanding of autism that can lead to improved diagnostic accuracy and personalized interventions.
Relative to the general population, autistic adults are at elevated risk for depression. Factors related to this risk are poorly understood, yet identifying such factors is important for improving mental health in autistic people. Emotion regulation (ER) challenges may be one such factor. However, few studies have examined ER challenges and depression in autistic adults. We examined ER challenges, depressive symptomatology and their associations in 775 (aged 18-83 years) autistic adults using network analysis, a method that permits identification of key components of ER and depression and their interrelatedness. Three non-regularized weighted undirected networks were estimated: ER challenges, depressive symptomatology, and combined ER-depressive challenges. Community structures revealed in the ER challenges and depressive symptomatology networks align with theoretical/nosological models of ER challenges/depressive symptoms as well as extant research using network analysis to examine these constructs. The combined ER challenges-depressive symptomatology network indicated that ER challenges and depressive symptomatology are interrelated but distinct constructs. These preliminary findings using cross-sectional data provide a first step in understanding associations between a candidate factor in depression vulnerability in autistic adults - ER challenges - and identify important future research directions.
Like other animals, fish have unique personalities that can affect their cognition and responses to environmental stressors. These individual personality differences are often referred to as “behavioural syndromes” or “stress coping styles” and can include personality traits such as boldness, shyness, aggression, exploration, locomotor activity, and sociability. For example, bolder or proactive fish may be more likely to take risks and present lower hypothalamo–pituitary–adrenal/interrenal axis reactivity as compared to shy or reactive individuals. Likewise, learning and memory differ between fish personalities. Reactive or shy individuals tend to have faster learning and better association recall with aversive stimuli, while proactive or bold individuals tend to learn more quickly when presented with appetitive incentives. However, the influence of personality on cognitive processes other than cognitive achievement in fish has been scarcely explored. Cognitive bias tests have been employed to investigate the interplay between emotion and cognition in both humans and animals. Fish present cognitive bias processes (CBP) in which fish’s interpretation of stimuli could be influenced by its current emotional state and open to environmental modulation. However, no study in fish has explored whether CBP, like in other species, can be interpreted as long-lasting traits and whether other individual characteristics may explain its variation. We hold the perspective that CBP could serve as a vulnerability factor for the onset, persistence, and recurrence of stress-related disorders. Therefore, studying fish’s CBP as a state or trait and its interactions with individual variations may be valuable in future efforts to enhance our understanding of anxiety and stress neurobiology in animal models and humans.
We compared Ed Diener’s Satisfaction With Life Scale (SWLS), which was designed as a purely cognitive measure of global life satisfaction, with the Affective Neuroscience Personality Scales 3.1, which provides self-report measures of Panksepp’s six primary emotions (excluding LUST), in two English-speaking samples: a main sample and a hold-out validation sample. Our data showed robust negative correlations between higher satisfaction with life and lower FEAR, lower SADNESS/Separation Distress, and positive associations (albeit less strong) between higher satisfaction with life and higher PLAY and SEEKING in both samples. The relationships between the SWLS and at least four of Panksepp’s primary emotions suggest Diener’s SWLS is not purely cognitive and includes a strong affective component. In addition, detailed analysis of the negative correlation between the SWLS and the ANPS 3.1 SADNESS scale provides insight into the importance of the low arousal end of the SADNESS/Separation Distress brain system and supports the idea of a continuum of psychological states from high SADNESS including loneliness and depression to low SADNESS psychological states characterized by social comfort, self-confidence, and social strength.
Eating disorders (ED) are severe psychiatric disorders characterized by dysfunctional behaviors related to eating or weight control, with profound impacts on health, quality of life, and the financial burden of affected individuals and society at large. Given that these disorders involve disturbances in self-perception, it is crucial to comprehend the role of self-awareness in their prevalence and maintenance. This literature review presents different self-awareness processes, discussing their functioning across different levels of complexity. By deconstructing this concept, we can gain a better understanding of how each facet of self and personality relates to the symptoms of these disorders. Understanding the absence or impairment of self-awareness in ED holds significant implications for diagnosis, treatment, and overall management. By recognizing and comprehending the characteristics of self-awareness, clinicians can develop tailored interventions and evidence-based treatments for individuals with ED. Furthermore, this narrative review underscores the importance of considering temperament and personality factors in the context of ED, as temperament traits and personality characteristics may interact with self-awareness processes, influencing the development and maintenance of ED. Ultimately, the results highlight the pressing need for further research on the development of effective interventions and support strategies grounded in the aspects of self-awareness mechanisms for individuals affected by these disorders.
Psychiatric illnesses form spectra rather than categories, with symptoms varying continuously across individuals, i.e., there is no clear break between health and disorder. Dimensional measures of behaviour and brain activity are promising targets for studying biological mechanisms that are common across disorders. Here, we assessed the extent to which neural measures of the sensitivity of the three biological systems in the reinforcement sensitivity theory (RST) could account for individual differences in a latent general factor estimated from symptom counts across externalising disorders (EXTs). RST explanatory power was pitted against reduced P300, a reliable indicator of externalising per previous research. We assessed 206 participants for DSM-5 EXTs (antisocial personality disorder, conduct disorder, attention-deficit/hyperactivity disorder, intermittent explosive disorder symptoms, alcohol use disorder, and cannabis use disorder). Of the final sample, 49% met diagnostic criteria for at least one of the EXTs. Electroencephalographic measures of the sensitivities of the behavioural activation system (BAS), the fight/flight/freeze system, and the behavioural inhibition system (BIS), as well as P300 were extracted from the gold bar-lemon and stop-signal tasks. As predicted, we found that low neural BIS sensitivity and low P300 were uniquely and negatively associated with our latent factor of externalising. Contrary to prediction, neural BAS/“dopamine” sensitivity was not associated with externalising. Our results provide empirical support for low BIS sensitivity and P300 as neural mechanisms common to disorders within the externalising spectrum; but, given the low N involved, future studies should seek to assess the replicability of our findings and, in particular, the differential involvement of the three RST systems.
Schizotypal traits include abnormalities in cognition, behavior, and interpersonal relationships that are similar, yet less severe than psychotic symptomology. It is estimated that approximately 5% of the general population displays psychotic symptoms and experiences that can be considered schizotypal in nature, but there is little research examining the neurological correlates of these traits. The mismatch negativity (MMN) event-related potential is an objective measure of auditory change detection derived from electroencephalography. The current study contributes to the limited body of evidence examining the neurobiological underpinnings of schizotypy in a non-clinical sample using the MMN. Participants were recruited from the general population and divided into high and low-schizotypy groups for comparison. Individuals with high schizotypal traits displayed reduced MMN amplitudes in response to frequency and location deviants, and longer MMN latencies in response to location deviants. Specific sub-traits of schizotypy were uniquely related to frequency and location amplitudes, suggesting the previously reported inconsistencies in the literature may be due to diverse samples and differing deviant tone types. Finally, impulsivity and sensation-seeking likely contributed to the slower processing seen in location deviance detection. Ultimately, the current results provide evidence that the neurobiological abnormalities seen in clinical populations of schizotypal personality disorder and psychosis also extend to non-clinical populations.
Dimensional psychopathology scores measure symptom severity; cutting across disorder categories. Their clinical utility is high given comorbidity, but their neural basis is unclear. We used scalp electroencephalography (EEG) to concurrently assess neural activity across internalizing and externalizing traits. “Theta rhythm” (4–7 Hz) spectral power at the frontal midline site Fz in specific goal conflict and action error phases within a trial of a Stop-Signal Task was extracted using process-specific contrasts. A final sample of 146 community participants (63 males, 83 females; mean age = 36; SD = 9; range = 18 – 56), oversampled for externalizing disorder (49% diagnosed with a DSM-5 externalizing disorder), also supplied psychopathology and personality data. We used the Minnesota Multiphasic Personality Inventory−3 (MMPI-3) to measure symptoms and traits of psychopathology. An MMPI-3 measure of the higher-order internalizing psychopathology spectrum was positively correlated with action error theta. An MMPI-3 measure of the higher-order spectrum of externalizing psychopathology was negatively correlated with goal-conflict theta. We showed that goal-conflict and error theta activity are higher-order processes that index psychopathology severity. The associations extend into the nominally healthy range, and so reflect theta-related factors that apply to the general population as well as patients with sub-threshold diagnoses.
This special issue attempts to integrate personality, psychopathology, and neuroscience as means to improve understanding of specific traits and trait structures in humans. The key strategy is to dive into comparative research using a range of species to provide simple models. This strategy has, as its foundation, the fact that the most basic functions, and their supporting neural systems, are highly conserved in evolution. The papers collected in the issue show that, from fish, through rats, to primates, the homologies in brain systems and underlying functions (despite species-specific forms of expression) allow simpler cases to provide insights into the neurobiology behind more complex ones including human. Our introductory editorial paper to this special issue took a bottom-up approach, starting with the genetics of conserved brain systems and working up to cognition. Here, we deconstruct the different aspects of personality, progressing from more complex ones in primates to least complex in fish. With the primate section, we summarize papers that discuss the factors that contribute to sociability in primates and how they apply to healthy and pathological human personality traits. In the rat section, the focus is driven by psychopathology and the way that “high” strains selected for extreme behaviors can illuminate the neurobiology of motivated responses to environmental cues. The section on fish summarizes papers that look into the most fundamental emotional reactions to the environment that are governed by primitive and conserved brain structures. This raises metatheoretical questions on the nature of traits and to a section that asks “which animals have personalities.” We believe that the issue as a whole provides a nuanced answer to this question and shines a new, comparative, light on the interpretation of personality structure and the effects on it of evolution.
Human personality generally refers to coherent individuating patterns in affect, behavior, and cognition. We can only observe and measure behavior, from which we then infer personality and other psychological processes (affect, cognition, etc.). We emphasize that the study of personality always explains or summarizes patterns not only in behavior but also in these other psychological processes inferred from behavior. We thus argue that personality should be attributed only to nonhuman animals with behaviors from which we can infer a sufficiently rich set of psychological processes. The mere inference of a biological trait that explains behavioral variability, on our view, is not sufficient to count as a personality construct and should be given a different term. Methodologically, inferring personality in nonhuman animals entails challenges in characterizing ecologically valid behaviors, doing so across rich and varied environments, and collecting enough data. We suggest that studies should gradually accumulate such corpora of data on a species through well-curated shared databases. A mixture of approaches should include both top-down fit with extant human personality theories (such as the Big Five) as well as bottom-up discovery of species-specific personality dimensions. Adopting the above framework will help us to build a comparative psychology and will provide the most informative models also for understanding human personality, its evolution, and its disorders.
An altered behavioral response to positive reinforcement has been proposed to be a core deficit in attention deficit hyperactivity disorder (ADHD). The spontaneously hypertensive rat (SHR), a congenic animal strain, displays a similarly altered response to reinforcement. The presence of this genetically determined phenotype in a rodent model allows experimental investigation of underlying neural mechanisms. Behaviorally, the SHR displays increased preference for immediate reinforcement, increased sensitivity to individual instances of reinforcement relative to integrated reinforcement history, and a steeper delay of reinforcement gradient compared to other rat strains. The SHR also shows less development of incentive to approach sensory stimuli, or cues, that predict reward after repeated cue-reward pairing. We consider the underlying neural mechanisms for these characteristics. It is well known that midbrain dopamine neurons are initially activated by unexpected reward and gradually transfer their responses to reward-predicting cues. This finding has inspired the dopamine transfer deficit (DTD) hypothesis, which predicts certain behavioral effects that would arise from a deficient transfer of dopamine responses from actual rewards to reward-predicting cues. We argue that the DTD predicts the altered responses to reinforcement seen in the SHR and individuals with ADHD. These altered responses to reinforcement in turn predict core symptoms of ADHD. We also suggest that variations in the degree of dopamine transfer may underlie variations in personality dimensions related to altered reinforcement sensitivity. In doing so, we highlight the value of rodent models to the study of human personality.
This article discusses dominance personality dimensions found in primates, particularly in the great apes, and how they compare to dominance in humans. Dominance traits are seen in virtually all primate species, and these dimensions reflect how adept an individual is at ascending within a social hierarchy. Among great apes, dominance is one of the most prominent personality factors but, in humans, dominance is usually modeled as a facet of extraversion. Social, cultural, and cognitive differences between humans and our closest ape relatives are explored, alongside humanity’s hierarchical and egalitarian heritage. The basic characteristics of dominance in humans and nonhuman great apes are then described, alongside the similarities and differences between great apes. African apes live in societies each with its own hierarchical organization. Humans were a possible exception for some of our history, but more recently, hierarchies have dominated. The general characteristics of high-dominance humans, particularly those living in industrialized nations, are described. Dominance itself can be subdivided into correlated subfactors: domineering, prestige, and leadership. Various explanations have been posed for why dominance has declined in prominence within human personality factor structures, and several possibilities are evaluated. The value of dominance in personality research is discussed: dominance has links to, for instance, age, sex, aggression, self-esteem, locus of control, stress, health, and multiple socioeconomic status indicators. The piece concludes with recommendations for researchers who wish to assess dominance in personality.
