Adaptability to acute stress among women survivors of intimate partner violence : protocol for a mixed-methods cross-sectional study in a laboratory setting (BRAW study)

Altres ajuts: "La Caixa" Foundation, 2017ACUP00277; Departament de Salut de la Generalitat de Catalunya, SLT002/16/00237Intimate partner violence (IPV) is the most common and alarming form of violence against women, affecting around 30% of all women around the world. Using an integrative methodology, we approach IPV as a form of chronic exposure to severe stress that alters the stress-response system of exposed women. The aim of this study is to test the hypothesis that sustained exposure to IPV in women confers a vulnerability-to-stress profile characterised by higher neuroendocrine and behavioural responsiveness associated with a selective attentional processing bias towards threat. Women between 21 and 50 years old from the area of Barcelona (Spain) will be invited to participate. A sample of 82 women exposed to IPV and 41 women not exposed to IPV will be included and assessed for attentional bias and response to acute stress in a laboratory condition (the Trier Social Stress Task). The study will include quantitative and qualitative measures of cognitive performance, neuroendocrine activity and face-to-face interviews to obtain an integrative description of the stress-response profile of these women. Results are expected to help build resilience strategies with a long-lasting impression on women's healthy functioning. The study has obtained the approval of the local Ethics Committee ('Comité de Ética de Investigación Parc Taulí de Sabadell'; 2 018 551 V.1.2 June 2018). Besides the communication of results in peer-reviewed papers and scientific congresses, the project will inform guidelines and recommendations through policy-dialogues and workshops with relevant regional and national representatives for future work and prevention strategies. Participants will be invited to be an active part in the dissemination strategy focussed on raising awareness of coping limitations and abilities that women themselves will be able to identify throughout the study. The study has been registered at the ClinicalTrails.gov database (Identifier number: NCT03623555; Pre-results)

Social reintegration programs for former inmates in Brazil: is there a gender perspective?

Com o aumento do número de mulheres privadas de liberdade em todo o mundo, a importância da implantação de estratégias específicas que devem ser aplicadas ao suporte oferecido a essas mulheres são importantes medidas sociais. O objetivo deste estudo é analisar a oferta dos recursos para a reinserção social de egressos do sistema prisional brasileiro, com o recorte de gênero. A proposta é realizar uma análise documental sobre estratégias governamentais e não governamentais direcionadas para este público, com recorte de gênero, por meio de uma matriz analítica pelo período compreendido entre 2020 e 2021. Os resultados mostram que há no país diversos programas voltados à reinserção social de egressos do sistema prisional, entretanto poucos apresentam um recorte de gênero. O tema reinserção social e sistema prisional foi identificado em 84 notícias em sítios dos organismos governamentais visitados, sendo 20 federais e 64 estaduais. Em 11 organismos internacionais atuando no Brasil e em 12 ONGs, somente seis apresentaram recorte de gênero. O desafio do sistema penitenciário brasileiro é incluir a abordagem de cidadania e dignidade humana no sistema prisional, incluindo uma abordagem da questão de gênero.With the increasing number of women deprived of liberty worldwide, implementing specific strategies that should be applied to the support offered to these women are essential social measures. This study aims to analyze the supply of resources for the social reintegration of former inmates of the Brazilian prison system from a gender perspective. We propose to conduct a documentary analysis on governmental and non-governmental strategies aimed at this audience, with a gender perspective, through an analytical matrix for the 2020-2021 period. The results show several programs in the country aimed at the social reintegration of former prisoners; however, few have a gender perspective. The theme of social reintegration and the prison system was identified in 84 news items on government agencies’ websites, 20 of which were federal and 64 state, in 11 international organizations operating in Brazil, and 12 NGOs. Only six had a gender profile. The challenge for the Brazilian penitentiary system is to introduce the citizenship and human dignity approach in the prison system, including an approach to the gender issue.Fil: Barbosa Miranda, Raquel. Universidade do Brasília; BrasilFil: Goldberg, Alejandro. Universidad de Buenos Aires. Facultad de Filosofía y Letras. Instituto de Ciencias Antropológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Díaz Bermúdez, Ximena Pamela. Universidade do Brasília; Brasi

Childhood maltreatment and risk for suicide attempts in major depression : a sex-specific approach

Altres ajuts: This work was supported partly by a non-competitive grant from the Health Department of the Generalitat de Catalunya (PREDI-NU project, European Alliance Against Depression, 2016); Fondo Europeo de Desarrollo Regional, Unión Europea, Una manera de hacer Europa, CIBERSAM, Secretaria d'Universitats.Background : Childhood maltreatment increases the risk of suicide attempts in the general population, possibly having similar effects among patients with major depressive disorder (MDD). The few studies that have addressed this association have been restricted to specific populations (e.g. treatment-resistant depression, personality disorders) and have rarely taken sex into account. Objective : To examine the impact of childhood maltreatment on suicide attempts among MDD patients above and beyond other risk factors and potential confounders, while considering potential sex-specific effects. Methods : The study assessed 165 patients with a principal diagnosis of MDD. Neurological alterations, psychiatric comorbidities, and drug abuse were reasons for exclusion. Logistic regressions using the whole sample, and divided by sex, were run to test the association between childhood maltreatment and history of suicide attempts, controlling for symptom severity, comorbidities, and treatment-resistant depression. Results : There was a significant and clinically relevant association between childhood maltreatment and history of suicide attempts in the total sample. Patients with childhood maltreatment were 3.01 times more likely to present a history of suicide attempts than patients without childhood maltreatment. A family history of psychiatric disorders also contributed to the variance of attempted suicide, but its interaction with childhood maltreatment was not statistically significant. When testing the model separately, the effect of childhood maltreatment on suicide attempts remained for females, whereas for males, age of MDD onset and Childhood Trauma Questionnaire minimization-denial scale were predictive variables. Conclusions : Childhood maltreatment is a clear predictor of suicidal behaviour among MDD patients, and this effect remains significant after controlling for potential confounders. Also, the sex of patients emerges as a relevant factor that may model the mechanisms underlying the prediction of suicide attempts. Since suicide is the main cause of premature death among MDD patients, interventions targeting childhood maltreatment should be included in preventive and clinical strategies

An fMRI study of cognitive reappraisal in major depressive disorder and borderline personality disorder

Background: One common denominator to the clinical phenotypes of borderline personality disorder (BPD) and major depressive disorder (MDD) is emotion regulation impairment. Although these two conditions have been extensively studied separately, it remains unclear whether their emotion regulation impairments are underpinned by shared or distinct neurobiological alterations. Methods: We contrasted the neural correlates of negative emotion regulation across an adult sample of BPD patients (n = 19), MDD patients (n = 20), and healthy controls (HCs; n = 19). Emotion regulation was assessed using an established functional magnetic resonance imaging cognitive reappraisal paradigm. We assessed both task-related activations and modulations of interregional connectivity. Results: When compared to HCs, patients with BPD and MDD displayed homologous decreased activation in the right ventrolateral prefrontal cortex (vlPFC) during cognitive reappraisal. In addition, the MDD group presented decreased activations in other prefrontal areas (i.e., left dorsolateral and bilateral orbitofrontal cortices), while the BPD group was characterized by a more extended pattern of alteration in the connectivity between the vlPFC and cortices of the visual ventral stream during reappraisal. Conclusions: This study identified, for the first time, a shared neurobiological contributor to emotion regulation deficits in MDD and BPD characterized by decreased vlPFC activity, although we also observed disorder-specific alterations. In MDD, results suggest a primary deficit in the strength of prefrontal activations, while BPD is better defined by connectivity disruptions between the vlPFC and temporal emotion processing regions. These findings substantiate, in neurobiological terms, the different profiles of emotion regulation alterations observed in these disorders

Group and sex differences in social cognition in bipolar disorder, schizophrenia/schizoaffective disorder and healthy people

Background: Impairment of social cognition is documented in bipolar disorder (BD) and schizophrenia/schizoaffective disorder (SCH). In healthy individuals, women perform better than men in some of its sub-domains. However, in BD and SCH the results are mixed. Our aim was to compare emotion recognition, affective Theory of Mind (ToM) and first- and second-order cognitive ToM in BD, SCH and healthy subjects, and to investigate sex-related differences. Methods: 120 patients (BD = 60, SCH = 60) and 40 healthy subjects were recruited. Emotion recognition was assessed by the Pictures of Facial Affect (POFA) test, affective ToM by the Reading the Mind in the Eyes Test (RMET) and cognitive ToM by several false-belief stories. Group and sex differences were analyzed using parametric (POFA, RMET) and non-parametric (false-belief stories) tests. The impact of age, intelligence quotient (IQ) and clinical variables on patient performance was examined using a series of linear/logistic regressions. Results: Both groups of patients performed worse than healthy subjects on POFA, RMET and second-order falsebelief (p < 0.001), but no differences were found between them. Instead, their deficits were related to older age and/or lower IQ (p < 0.01). Subthreshold depression was associated with a 6-fold increased risk of first-order false-belief failure (p < 0.001). Sex differences were only found in healthy subjects, with women outperforming men on POFA and RMET (p ≤ 0.012), but not on first/second-order false-belief. Limitations: The cross-sectional design does not allow for causal inferences. Conclusion: BD and SCH patients had deficits in emotion recognition, affective ToM, and second-order cognitive ToM, but their performance was comparable to each other, highlighting that the differences between them may be subtler than previously thought. First-order cognitive ToM remained intact, but subthreshold depression altered their normal functioning. Our results suggest that the advantage of healthy women in the emotional and affective aspects of social cognition would not be maintained in BD and SCH

Modelos complejos de las influencias genéticas y ambientales en la cognición humana. Implicaciones para las psicosis funcionales

[eng] The general construct of human cognition implies a series of mental processes by means of which human interpret and consequently act on the world that surrounds them (Sternberg y Mio, 2009). During the last decades, the recognition of human diversity and psychological variability among individuals has encouraged challenging questions addressing inter-individual differences that make each subject unique in terms of their cognitive performance (Baddeley, 2003; Botvinick, 2008). In particular, quantitative genetic studies show that both genetic variability and environmental factors are involved in the phenotypic expression of cognitive functions (Plomin, 2011). However, the mechanisms by which genes and exposure to environmental influences may contribute to the observed variability are not yet clear. The study of the origins of inter-individual differences in cognition is strongly associated with the ontogenic development of the human brain (Tau, 2010). As a consequence, cognitive alterations are considered a central trait in those mental disorders where neurodevelopmental alterations are assumed to exist, such as schizophrenia. This disease, which affects around 1% of the world’s population, is one of the main causes of years lost due to disability (WHO, 2004), while cognitive alterations in these patients explain about 20%-60% of the variance in measures of outcome (Green, 2004). The aetiological model of neurodevelopment in schizophrenia proposes that this disease might be the expression of neurobiological compromise that could begin early in the lifespan, even before the onset of the clinical symptoms (van Os, 2009). However, and despite the scientific efforts invested in the elucidation of its aetiological underpinnings, the heterogeneous presentation of the disease has prevented a deeper comprehension of these mechanisms. Are all cognitive domains heritable? Are there long-term consequences on cognition for the early exposure to environmental impact? What is the association between genetic variability and cognitive vulnerability? Can we identify specific neurobiological pathways in the expression of the cognitive alterations of patients with schizophrenia? These questions are explored in the present thesis through the analyses of twins- and family-based samples, which constitute powerful designs to study the effects of genetic and environmental variability on human cognition. In the six chapters of results that are the body of this thesis, complex models are proposed that aim at representing the mechanisms involved in the origin of cognitive variability at the population level. The findings included indicate that this variability could be the result of the relative contribution of genetic determination and environmental modelling, which could vary in different cognitive functions following ontogenic mechanisms of neurodevelopment. Specifically, results are reported on the influences of childhood maltreatment and socioeconomic status as environmental stressors, as well as Val158Met functional polymorphism of COMT gene as a genetic factor. The aetiological implications of the study of these processes are extended to the field of mental disorders, as the results may indicate that the cognitive variability present among patients with schizophrenia could support a model of developmental compromise in this disease. Accordingly, the effects of genetic and environmental influences on behaviour may underlie the heterogeneous expression of this highly disabling mental disorder. To sum up, the phenotypic diversity of schizophrenia and human cognition, far from representing an obstacle, lays the foundations for complex models of these traits that may feed an increasing understanding of their aetiology (Belsky, 2011). These findings highlight the putative role of neurobiological liability traits in crucial aspects of clinical practice. Risk factors might be identified that could be included as potential guidelines in the assessment and management of need-adapted treatments (Leiftker, 2009). Moreover, liability traits might operate as markers in preventive interventions for targeting individuals at risk of developing particular forms of the disease (Keshavan, 2011).[spa] El constructo general de cognición humana involucra una serie de procesos mentales por medio de los cuales los individuos perciben, interpretan y, en consecuencia, actúan sobre la realidad que los rodea y sobre sus pares (Sternberg y Mio, 2009). En los últimos años, el reconocimiento de la diversidad humana y la variabilidad de los rasgos psicológicos entre los individuos ha promovido preguntas acerca de las diferencias inter-individuales que hacen a cada sujeto único en términos de cognición (Baddeley, 2003; Botvinick, 2008). En particular, los estudios de genética cuantitativa demuestran que tanto la variabilidad genética como los factores ambientales podrían estar involucrados en la expresión fenotípica de las funciones cognitivas (Plomin, 2011). Sin embargo, aún no son claros los mecanismos específicos por medio de los cuales los genes y el ambiente contribuyen a esta variabilidad. Las alteraciones cognitivas son un rasgo central en enfermedades mentales donde se presume que existen alteraciones del neurodesarrollo, como lo es la esquizofrenia. El modelo etiológico del neurodesarrollo de la esquizofrenia propone que esta enfermedad se expresaría como consecuencia de alteraciones neurobiológicas que iniciarían en una época temprana de la vida, incluso antes del desencadenamiento de los síntomas clínicos (van Os, 2009). No obstante, la presentación heterogénea de la enfermedad ha dificultado una comprensión más clara de los mecanismos involucrados en su manifestación. ¿Son todas las funciones cognitivas igualmente heredables? ¿Tienen los factores ambientales tempranos consecuencias a largo plazo sobre la cognición? ¿Cuál es la relación entre variabilidad genética y vulnerabilidad cognitiva? ¿Existen vías neurobiológicas específicas para la manifestación de las alteraciones cognitivas en pacientes con esquizofrenia? Estas preguntas se exploran en la presente tesis a partir de análisis basados en muestras de gemelos y en grupos familiares, que constituyen una manera metodológicamente potente de estudiar los efectos de la variabilidad genética y ambiental sobre la cognición humana. En este sentido, la diversidad fenotípica de la esquizofrenia y la cognición humana, lejos de representar un obstáculo para la investigación de su etiología, sienta las bases de modelos complejos que podrían fomentar una comprensión cada vez más completa de los mecanismos de vulnerabilidad y resiliencia posiblemente involucrados en su origen (Belsky, 2011)

Complex Models of Genetic and Environmental Influences on Human Cognition. Implications for Functional Psychoses / Modelos complejos de las influencias genéticas y ambientales en la cognición humana. Implicaciones para las psicosis funcionales

The general construct of human cognition implies a series of mental processes by means of which human interpret and consequently act on the world that surrounds them (Sternberg y Mio, 2009). During the last decades, the recognition of human diversity and psychological variability among individuals has encouraged challenging questions addressing inter-individual differences that make each subject unique in terms of their cognitive performance (Baddeley, 2003; Botvinick, 2008). In particular, quantitative genetic studies show that both genetic variability and environmental factors are involved in the phenotypic expression of cognitive functions (Plomin, 2011). However, the mechanisms by which genes and exposure to environmental influences may contribute to the observed variability are not yet clear. The study of the origins of inter-individual differences in cognition is strongly associated with the ontogenic development of the human brain (Tau, 2010). As a consequence, cognitive alterations are considered a central trait in those mental disorders where neurodevelopmental alterations are assumed to exist, such as schizophrenia. This disease, which affects around 1% of the world’s population, is one of the main causes of years lost due to disability (WHO, 2004), while cognitive alterations in these patients explain about 20%-60% of the variance in measures of outcome (Green, 2004). The aetiological model of neurodevelopment in schizophrenia proposes that this disease might be the expression of neurobiological compromise that could begin early in the lifespan, even before the onset of the clinical symptoms (van Os, 2009). However, and despite the scientific efforts invested in the elucidation of its aetiological underpinnings, the heterogeneous presentation of the disease has prevented a deeper comprehension of these mechanisms. Are all cognitive domains heritable? Are there long-term consequences on cognition for the early exposure to environmental impact? What is the association between genetic variability and cognitive vulnerability? Can we identify specific neurobiological pathways in the expression of the cognitive alterations of patients with schizophrenia? These questions are explored in the present thesis through the analyses of twins- and family-based samples, which constitute powerful designs to study the effects of genetic and environmental variability on human cognition. In the six chapters of results that are the body of this thesis, complex models are proposed that aim at representing the mechanisms involved in the origin of cognitive variability at the population level. The findings included indicate that this variability could be the result of the relative contribution of genetic determination and environmental modelling, which could vary in different cognitive functions following ontogenic mechanisms of neurodevelopment. Specifically, results are reported on the influences of childhood maltreatment and socioeconomic status as environmental stressors, as well as Val158Met functional polymorphism of COMT gene as a genetic factor. The aetiological implications of the study of these processes are extended to the field of mental disorders, as the results may indicate that the cognitive variability present among patients with schizophrenia could support a model of developmental compromise in this disease. Accordingly, the effects of genetic and environmental influences on behaviour may underlie the heterogeneous expression of this highly disabling mental disorder. To sum up, the phenotypic diversity of schizophrenia and human cognition, far from representing an obstacle, lays the foundations for complex models of these traits that may feed an increasing understanding of their aetiology (Belsky, 2011). These findings highlight the putative role of neurobiological liability traits in crucial aspects of clinical practice. Risk factors might be identified that could be included as potential guidelines in the assessment and management of need-adapted treatments (Leiftker, 2009). Moreover, liability traits might operate as markers in preventive interventions for targeting individuals at risk of developing particular forms of the disease (Keshavan, 2011).El constructo general de cognición humana involucra una serie de procesos mentales por medio de los cuales los individuos perciben, interpretan y, en consecuencia, actúan sobre la realidad que los rodea y sobre sus pares (Sternberg y Mio, 2009). En los últimos años, el reconocimiento de la diversidad humana y la variabilidad de los rasgos psicológicos entre los individuos ha promovido preguntas acerca de las diferencias inter-individuales que hacen a cada sujeto único en términos de cognición (Baddeley, 2003; Botvinick, 2008). En particular, los estudios de genética cuantitativa demuestran que tanto la variabilidad genética como los factores ambientales podrían estar involucrados en la expresión fenotípica de las funciones cognitivas (Plomin, 2011). Sin embargo, aún no son claros los mecanismos específicos por medio de los cuales los genes y el ambiente contribuyen a esta variabilidad. Las alteraciones cognitivas son un rasgo central en enfermedades mentales donde se presume que existen alteraciones del neurodesarrollo, como lo es la esquizofrenia. El modelo etiológico del neurodesarrollo de la esquizofrenia propone que esta enfermedad se expresaría como consecuencia de alteraciones neurobiológicas que iniciarían en una época temprana de la vida, incluso antes del desencadenamiento de los síntomas clínicos (van Os, 2009). No obstante, la presentación heterogénea de la enfermedad ha dificultado una comprensión más clara de los mecanismos involucrados en su manifestación. ¿Son todas las funciones cognitivas igualmente heredables? ¿Tienen los factores ambientales tempranos consecuencias a largo plazo sobre la cognición? ¿Cuál es la relación entre variabilidad genética y vulnerabilidad cognitiva? ¿Existen vías neurobiológicas específicas para la manifestación de las alteraciones cognitivas en pacientes con esquizofrenia? Estas preguntas se exploran en la presente tesis a partir de análisis basados en muestras de gemelos y en grupos familiares, que constituyen una manera metodológicamente potente de estudiar los efectos de la variabilidad genética y ambiental sobre la cognición humana. En este sentido, la diversidad fenotípica de la esquizofrenia y la cognición humana, lejos de representar un obstáculo para la investigación de su etiología, sienta las bases de modelos complejos que podrían fomentar una comprensión cada vez más completa de los mecanismos de vulnerabilidad y resiliencia posiblemente involucrados en su origen (Belsky, 2011)

The complex organization of human cognitive domains and their heritability: a systematic review

Una revisión sistemática de la organización compleja de los dominios cognitivos humanos y su heredabilidad. Antecedentes: se ha propuesto que la estructura de la cognición humana respondería a un sistema jerárquico, donde las secuencias propias a una acción se organizarían desde sub-unidades de análisis hasta funciones de nivel superior relativamente complejas. Esta estructura organizacional estaría reflejada en las representaciones neurales que subyacen al comportamiento humano, así como también en sus sustratos genéticos. El objetivo del presente estudio fue explorar la posible organización jerárquica de las influencias genéticas subyacentes a los dominios cognitivos humanos. Método: se revisaron treinta y cuatro estudios de la heredabilidad de la cognición en muestras de la población general, que incluyeron medidas de inteligencia, habilidades verbales y manipulativas, memoria, memoria de trabajo y velocidad de procesamiento. Resultados: diversos dominios cognitivos mostraron distintas proporciones de influencias genéticas, con las mayores estimaciones de heredabilidad halladas para las funciones cognitivas de nivel superior y las menores estimaciones para las funciones de orden medio o inferior. Conclusiones: tomando como referencia los conocimientos actuales acerca del neurodesarrollo humano, las contribuciones genéticas de las habilidades cognitivas parecen organizarse paralelamente al crecimiento ontogénico del cerebro. Se discuten estos resultados en relación a la interacción entre el control genético de las funciones cognitivas y sus influencias ambientales

Psicothema

Resumen tomado de la publicaciónAntecedentes: se ha propuesto que la estructura de la cognición humana respondería a un sistema jerárquico, donde las secuencias propias a una acción se organizarían desde sub-unidades de análisis hasta funciones de nivel superior relativamente complejas. Esta estructura organizacional estaría reflejada en las representaciones neurales que subyacen al comportamiento humano, así como también en sus sustratos genéticos. El objetivo del presente estudio fue explorar la posible organización jerárquica de las influencias genéticas subyacentes a los dominios cognitivos humanos. Método: se revisaron treinta y cuatro estudios de la heredabilidad de la cognición en muestras de la población general, que incluyeron medidas de inteligencia, habilidades verbales y manipulativas, memoria, memoria de trabajo y velocidad de procesamiento. Resultados: diversos dominios cognitivos mostraron distintas proporciones de influencias genéticas, con las mayores estimaciones de heredabilidad halladas para las funciones cognitivas de nivel superior y las menores estimaciones para las funciones de orden medio o inferior. Conclusiones: tomando como referencia los conocimientos actuales acerca del neurodesarrollo humano, las contribuciones genéticas de las habilidades cognitivas parecen organizarse paralelamente al crecimiento ontogénico del cerebro. Se discuten estos resultados en relación a la interacción entre el control genético de las funciones cognitivas y sus influencias ambientales.Universidad de Oviedo. Biblioteca de Psicología; Plaza Feijoo, s/n.; 33003 Oviedo; Tel. +34985104146; Fax +34985104126; [email protected]

The complex organization of human cognitive domains and their heritability: a systematic review

Una revisión sistemática de la organización compleja de los dominios cognitivos humanos y su heredabilidad. Antecedentes: se ha propuesto que la estructura de la cognición humana respondería a un sistema jerárquico, donde las secuencias propias a una acción se organizarían desde sub-unidades de análisis hasta funciones de nivel superior relativamente complejas. Esta estructura organizacional estaría reflejada en las representaciones neurales que subyacen al comportamiento humano, así como también en sus sustratos genéticos. El objetivo del presente estudio fue explorar la posible organización jerárquica de las influencias genéticas subyacentes a los dominios cognitivos humanos. Método: se revisaron treinta y cuatro estudios de la heredabilidad de la cognición en muestras de la población general, que incluyeron medidas de inteligencia, habilidades verbales y manipulativas, memoria, memoria de trabajo y velocidad de procesamiento. Resultados: diversos dominios cognitivos mostraron distintas proporciones de influencias genéticas, con las mayores estimaciones de heredabilidad halladas para las funciones cognitivas de nivel superior y las menores estimaciones para las funciones de orden medio o inferior. Conclusiones: tomando como referencia los conocimientos actuales acerca del neurodesarrollo humano, las contribuciones genéticas de las habilidades cognitivas parecen organizarse paralelamente al crecimiento ontogénico del cerebro. Se discuten estos resultados en relación a la interacción entre el control genético de las funciones cognitivas y sus influencias ambientales