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Growing evidence suggests the relevance of affective temperaments in the development of mood disorders. This study aims to assess their potential role as a vulnerability factor for seasonal affective disorder (SAD) and subsyndromal SAD (S-SAD) in a sample of young individuals without a history of clinical diagnosis. Eight hundred and forty-six university students were enrolled in a cross-sectional study. Participants were evaluated for exclusion and inclusion criteria and divided into Control, S-SAD, and SAD groups. They filled out two self-administered questionnaires to assess the degree of seasonality problems and the predominant type of affective temperaments, the Seasonal Pattern Assessment Questionnaire (SPAQ), and the Temperament Evaluation Instrument of Memphis, Pisa, Paris, and San Diego-Auto-questionnaire version scale (briefTEMPS-M version). We conducted a multinomial logistic regression model to explore the relationship between affective temperaments and seasonality. Our results evidenced that cyclothymic [χ2 (2) = 33.486, p < 0.001] and anxious [χ2 (2) = 86.991, p < 0.001] temperaments were significant predictors in the model, suggesting that individuals with cyclothymic and anxious temperaments are at increased risk of developing SAD, due to heightened seasonal changes in mood and behavior. In contrast, people with hyperthymic temperament appear less susceptible to experiencing seasonal problems. The homogeneity of the sample; only retrospective self-reported data were considered; measures of temperament and seasonality were simultaneously assessed. Understanding which affective temperaments may constitute a potential predisposing factor for vulnerability to seasonal changes can aid in better assessing SAD and predicting its outcome. [Display omitted] • Environmental changes associated with seasonal variations impact human behavior and mood. • Seasonal affective disorder (SAD) is a condition characterized by recurrent seasonal depression. • Cyclothymic and anxious temperaments are a factor of risk for SAD. • A comprehensive psychological evaluation is essential to managing and treating SAD. [ABSTRACT FROM AUTHOR]

Objective: Premenstrual Dysphoric Disorder is a clinically important condition that affects a significant proportion of women and causes deterioration of quality of life. In this study, it was aimed to evaluate the frequency of premenstrual dysphoric disorder and its relationship with demographic and clinical variables and affective temperaments. Method: An online survey form including sociodemographic data, Premenstrual Symptoms Screening Tool, and Temperament Evaluation of Memphis, Pisa, Paris, and San Diego Auto-questionnaire was applied to 408 healthy women participants. Results: The frequency of premenstrual dysphoric disorder and moderate to severe premenstrual syndrome were 13.2%, and 14.5%, respectively. The presence of lifetime psychiatric diagnosis, positive family history of psychiatric illness, suicide attempts, and anxious temperament were significantly higher in the premenstrual dysphoric disorder group. Cyclothymic and anxious temperaments had a positive predictive effect on the Premenstrual Symptoms Screening Tool Section A scores. Discussion: Our findings show a possible relationship between anxious and cyclothymic temperament traits and premenstrual dysphoric disorder symptom severity. Premenstrual symptoms may be more severe in women with cyclothymic and anxious temperament features. However, large-scale studies in which the diagnosis of premenstrual dysphoric disorder is determined by clinical interview are needed for this judgment. [ABSTRACT FROM AUTHOR]

BackgroundAnxious temperament (AT) is an early-life heritable trait that predisposes individuals to develop anxiety and depressive disorders. Our previous work in preadolescent children suggests alterations in the uncinate fasciculus (UF), the white matter tract that connects prefrontal with limbic regions, in boys with anxiety disorders. Here, using a nonhuman primate model of AT, we tested whether this sexually dimorphic finding is evolutionarily conserved and examined the extent to which heritable and environmental influences contribute to UF microstructure.MethodsDiffusion tensor images were collected in 581 young rhesus monkeys (1.89 ± 0.77 years old; 43.9% female). Using tract-based analyses, we assessed the relationship among AT, UF microstructure (as measured with fractional anisotropy), and sex. Heritability of tract microstructure was determined using oligogenic linkage analysis of this large multigenerational pedigree.ResultsWe predicted and found a negative relation between AT and UF fractional anisotropy in male but not female monkeys (AT × sex; p = .032, 1-tailed). Additionally, heritability analyses revealed that variation in UF fractional anisotropy was largely due to nonheritable factors (h2 = 0.185, p = .077).ConclusionsThese results demonstrate a cross-species, male-specific relation between UF microstructure and anxiety and provide a potential substrate for anxiety-related prefrontal-limbic dysregulation. The heritability analyses point to the importance of environmental influences on UF microstructure, which could be important in mediating the nonheritable components of pathological anxiety. These findings have the potential to guide new treatment strategies for childhood anxiety disorders and further support the use of nonhuman primates as a translational model to discover mechanisms underlying the development of anxiety.

BackgroundAn early-life anxious temperament (AT) is a risk factor for the development of anxiety, depression, and comorbid substance abuse. We validated a nonhuman primate model of early-life AT and identified the dorsal amygdala as a core component of AT's neural circuit. Here, we combine RNA sequencing, viral-vector gene manipulation, functional brain imaging, and behavioral phenotyping to uncover AT's molecular substrates.MethodsIn response to potential threat, AT and brain metabolism were assessed in 46 young rhesus monkeys. We identified AT-related transcripts using RNA-sequencing data from dorsal amygdala tissue (including central nucleus of the amygdala [Ce] and dorsal regions of the basal nucleus). Based on the results, we overexpressed the neurotrophin-3 gene, NTF3, in the dorsal amygdala using intraoperative magnetic resonance imaging-guided surgery (n = 5 per group).ResultsThis discovery-based approach identified AT-related alterations in the expression of well-established and novel genes, including an inverse association between NTRK3 expression and AT. NTRK3 is an interesting target because it is a relatively unexplored neurotrophic factor that modulates intracellular neuroplasticity pathways. Overexpression of the transcript for NTRK3's endogenous ligand, NTF3, in the dorsal amygdala resulted in reduced AT and altered function in AT's neural circuit.ConclusionsTogether, these data implicate neurotrophin-3/NTRK3 signaling in the dorsal amygdala in mediating primate anxiety. More generally, this approach provides an important step toward understanding the molecular underpinnings of early-life AT and will be useful in guiding the development of treatments to prevent the development of stress-related psychopathology.

Children with extreme behavioral inhibition (BI) are at a significantly greater risk to develop anxiety disorders later in life. We and others have identified similar early-life temperamental BI in nonhuman primates (NHPs), including rhesus monkeys. NHP models of BI provide a unique opportunity to study the neurobiology of BI in a species that shares biological, developmental, and socioemotional similarities with humans. Rhesus monkey models have identified a distributed brain circuit that includes the central extended amygdala (EAc) as being critical for the genesis of BI. By leveraging multimodal neuroimaging, brain lesions, RNA-sequencing, and viral vector manipulations in rhesus monkeys, these studies have identified specific brain regions, genetic factors, and molecular mechanisms that causally contribute to BI. Here, we discuss these findings from NHPs and how they fit into a translational framework that can contribute to our understanding of the neural circuits that give rise to the risk to develop anxiety and depressive disorders., (© 2024. The Author(s), under exclusive license to Springer Nature Switzerland AG.)

Children with an anxious temperament (AT) are at a substantially increased risk to develop anxiety and depression. The young rhesus monkey is ideal for studying the origin of human AT because it shares with humans the genetic, neural, and phenotypic underpinnings of complex social and emotional functioning. Heritability, functional imaging, and gene expression studies of AT in young monkeys revealed that the central nucleus of the amygdala (Ce) is a key environmentally sensitive substrate of this at risk phenotype. Because epigenetic marks (e.g., DNA methylation) can be modulated by environmental stimuli, these data led us to hypothesize a role for DNA methylation in the development of AT. To test this hypothesis, we used reduced representation bisulfite sequencing to examine the cross-sectional genome-wide methylation levels in the Ce of 23 age-matched monkeys (1.3 ± 0.2 years) phenotyped for AT. Because AT reflects a continuous trait-like variable, we used an analytical approach that is consistent with this biology to identify genes in the Ce with methylation patterns that predict AT. Expression data from the Ce of these same monkeys were then used to find differentially methylated candidates linked to altered gene regulation. Two genes particularly relevant to the AT phenotype were BCL11A and JAG1. These transcripts have well-defined roles in neurodevelopmental processes, including neurite arborization and the regulation of neurogenesis. Together, these findings represent a critical step toward understanding the effects of early environment on the neuromolecular mechanisms that underlie the risk to develop anxiety and depressive disorders.

Anxiety disorders are among the most prevalent psychiatric disorders, causing significant suffering and disability. Behavioral inhibition is a temperament that is linked to an increased risk for the later development of anxiety disorders and other stress-related psychopathology, and understanding the neural systems underlying this dispositional risk could provide insight into novel treatment targets for anxiety disorders. Nonhuman primates (NHPs) have anxiety-related temperaments that are similar to those of humans with behavioral inhibition, facilitating the design of translational models related to human psychopathology. Characterization of our NHP model of behavioral inhibition, which we term anxious temperament (AT), reveals that it is trait-like. Exploration of the neural substrates of AT in NHPs has revealed a distributed neural circuit that is linked to individual differences in AT, which includes the dorsal amygdala. AT-related metabolism in the dorsal amygdala, including the central nucleus, is stable across time and can be detected even in safe contexts, suggesting that AT has trait-like neural signatures within the brain. The use of lesioning and novel chemogenetic methods allows for mechanistic perturbation of the amygdala to determine its causal contribution to AT. Studies characterizing the molecular bases for individual differences in AT in the dorsal amygdala, which take advantage of novel methods for probing cellular and molecular systems, suggest involvement of neurotrophic systems, which point to the importance of neuroplasticity in AT. These novel methods, when used in combination with translational NHP models such as AT, promise to provide insights into the brain systems underlying the early risk for anxiety disorder development. [ABSTRACT FROM AUTHOR]

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Aim: In order to resolve the equivocal relationship between anxious temperament rated by the Temperament Evaluation of Memphis, Pisa, Paris, and San Diego‐Autoquestionnaire (TEMPS‐A) and harm avoidance rated by the Temperament and Character Inventory (TCI), the present study aimed to investigate whether the anxious temperament scale and the harm avoidance scale are significantly associated with adjustment of relevant factors. Our hypothesis was that anxious temperament might be associated with harm avoidance. Methods: From the database of our previous studies, the data of 111 healthy subjects who had both TCI and TEMPS‐A scores were extracted for the present study. Two multiple regression analyses were performed: one to predict variance in anxious temperament scores without and with harm avoidance scores, and relevant factors; and another to predict variance in harm avoidance scores without and with anxious temperament scores, and relevant factors. Results: Anxious temperament was significantly and positively associated with depressive temperament, irritable temperament, and Hamilton Rating Scale for Depression whereas harm avoidance was significantly and negatively associated with hyperthymic temperament, novelty seeking, persistence, and self‐directedness, although both were significantly and positively associated with each other. Conclusion: These findings support our hypothesis and suggest that anxious temperament may have ‘depressive proneness’ whereas harm avoidance may have ‘passive proneness.’ [ABSTRACT FROM AUTHOR]

What makes us different from one another? Why does one person jump out of airplanes for fun while another prefers to stay home and read? Why are some babies born with a predisposition to become anxious? Questions about individual differences in temperament have engaged the minds of scientists, psychologists, and philosophers for centuries. Recent technological advances in neuroimaging and genetics provide an unprecedented opportunity to answer these questions. Here we review the literature on the neurobiology of one of the most basic individual differences—the tendency to approach or avoid novelty. This trait, called inhibited temperament, is innate, heritable, and observed across species. Importantly, inhibited temperament also confers risk for psychiatric disease. Here, we provide a comprehensive review of inhibited temperament, including neuroimaging and genetic studies in human and non-human primates. We conducted a meta-analysis of neuroimaging findings in inhibited humans that points to alterations in a fronto-limbic-basal ganglia circuit; these findings provide the basis of a model of inhibited temperament neurocircuitry. Lesion and neuroimaging studies in non-human primate models of inhibited temperament highlight roles for the amygdala, hippocampus, orbitofrontal cortex, and dorsal prefrontal cortex. Genetic studies highlight a role for genes that regulate neurotransmitter function, such as the serotonin transporter polymorphisms (5-HTTLPR), as well as genes that regulate stress response, such as corticotropin-releasing hormone (CRH). Together these studies provide a foundation of knowledge about the genetic and neural substrates of this most basic of temperament traits. Future studies using novel imaging methods and genetic approaches promise to expand upon these biological bases of inhibited temperament and inform our understanding of risk for psychiatric disease. [ABSTRACT FROM AUTHOR]

Background According to previous studies, temperament predicts a large share of the variance in job stress. It may be necessary for mental health practitioners to offer intervention strategies in accordance with individual temperament. Aims To investigate the relationship between job stress and temperament among nurses in a general hospital and to provide insight into personality traits influencing their mental or physical health. Methods A questionnaire survey of nurses in a general hospital. Work stress was measured using the Japanese version of the Effort–Reward Imbalance (ERI) scale. Temperament was assessed by a Japanese version of Temperament Evaluation of Memphis, Pisa, Paris and San Diego-Autoquestionnaire (TEMPS-A). Hierarchical multiple regression analysis was used to determine the independent contribution of temperament to effort–reward ratio and over-commitment. Results Response rate was 48% (326/685). Temperament predicted part of the variance of the four ERI ratios (effort–reward ratio 26%; effort–esteem ratio 27%; effort–promotion ratio 26%; and effort–security ratio 18%) and also of over-commitment (38%). Depressive temperament influenced all four ERI ratios and over-commitment. Anxious temperament influenced only over-commitment. Conclusions Nurses with depressive or anxious temperaments should be identified, monitored for signs of job stress and offered interventions to prevent adverse physical and mental effects. [ABSTRACT FROM AUTHOR]

Abstract: Recently, described what they termed a ‘causal model’ of panic disorder (Causal modeling of panic disorder theories, Clinical Psychology Review, 29, 623–637). We examined several critical tenets of this proposed model, and offer significant revisions. Our revised causal model includes elements that have received empirical support, and exclude those with known limitations in explaining the etiology and treatment of panic disorder. Chief among these revisions are (1) an increased emphasis on anxiety sensitivity, (2) elimination of the more general psychodynamic conceptualization in favor of empirically supported findings regarding early attachment, and (3) placing biological and psychophysiological reactions as outcomes of false alarm threat, rather than causal mechanisms of panic. [Copyright &y& Elsevier]

Background: Although generalized anxiety disorder (GAD) is currently described as a time-limited state mental disorder, emerging evidence suggests that it is best considered as an exaggeration of a putative “anxious temperament” (AT). It is presently unknown whether it is a distinct or unitary construct of a mélange of anxious traits related to Cluster-C personality disorders. Methods: As part of a Franco-American collaborative study, we developed the 15-item Operational Criteria for Anxious Personality (OCAP), expanding criteria sets developed earlier by one of us (H.S.A.). The study, which was conducted in the French primary care medical sector, included 1112 young adults (18–40 years), seeking help for isolated anxious complaints, never treated before—and without any diagnosable disorder on the axis I of DSM-IV. As previous papers have reported the preliminary validity of OCAP, especially concurrent validity with the State–Trait Anxiety Inventory (STAI) (Speilberger), in this report, we focus on its full psychometric properties. Results: The present data indicate a normal distribution of AT items, a satisfactory Chronbach''s coefficient (0.64), and the presence at intake of three different subtypes of AT: “anxious-avoidant,” “anxious-phobic,” and “anxious-sensitive.” After a prospective 6-month follow-up, the major criteria of AT were stable in 80% of cases, and for specific AT items, the stability rate varied between 65% and 80%; much of the unstable items were accounted by improvement during naturalistic treatment. The latter could explain the different factor structure obtained at follow-up, which tended to be less heterogeneous, and represented by one global factor. Limitation: We used a categorical (yes/no) rather than a Likert-type gradation of frequency and intensity of anxiousness items and relatively low number of items, especially for those involving worrying about one''s own health or that of one''s loved ones. Conclusions: Anxiousness as a temperamental dimension appears to involve putative subtypes along “worrying,” “phobic,” “sensitive” (and “avoidant”) dimensions. [Copyright &y& Elsevier]