Are People with Poor Differentiation of Self at Risk of Developing Eating Disorders? A Study of Jewish and Arab Participants

Purpose: In light of findings that Israeli Arabs report higher prevalence of eating disorders (EDs) than Israeli Jews and that higher rates of the risk of EDs have been reported by females than males, the first aim of this study was to further investigate the cultural and gender differences in differentiation of self (DoS) and risk of developing EDs among Israeli young adults. The second aim was to examine whether DoS is associated with the risk of EDs. Methods: Of the 859 participants (670 females, mean age 26.8), 440 were Jewish and 419 were Arab. Participants took the Eating Attitudes Test (EAT-26) and completed the Differentiation of Self-Revised (DSI-R) questionnaire.Results: Results revealed that Jewish participants had significantly lower diet, bulimia, and total EAT-26 scores than their Arab counterparts, while Jewish female participants had higher dieting and lower emotional cutoff scores than Jewish male participants. In addition, Jews who reported higher levels of risk of EDs showed higher levels of BMI, emotional reactivity, emotional cutoff, and fusion with others. Arabs who reported higher levels of risk of EDs reported higher levels of BMI and emotional cutoff and lower levels of I-position. Conclusion: People with high risk of EDs may have difficulty maintaining intimate family relationships. In distressing situations, they tend to disconnect rather than share with or gain support from significant others. In each culture, the risk of EDs increases for differently: among the Arab participants, when feelings and needs remain unexpressed; among the Jewish participants, even when they have symbiotic family relationships.Level of evidence: Level V, cross-sectional descriptive study

A thalamo-centric neural signature for restructuring negative self-beliefs

Negative self-beliefs are a core feature of psychopathology. Despite this, we have a limited understanding of the brain mechanisms by which negative self-beliefs are cognitively restructured. Using a novel paradigm, we had participants use Socratic questioning techniques to restructure negative beliefs during ultra-high resolution 7-Tesla functional magnetic resonance imaging (UHF 7 T fMRI) scanning. Cognitive restructuring elicited prominent activation in a fronto-striato-thalamic circuit, including the mediodorsal thalamus (MD), a group of deep subcortical nuclei believed to synchronize and integrate prefrontal cortex activity, but which has seldom been directly examined with fMRI due to its small size. Increased activity was also identified in the medial prefrontal cortex (MPFC), a region consistently activated by internally focused mental processing, as well as in lateral prefrontal regions associated with regulating emotional reactivity. Using Dynamic Causal Modelling (DCM), evidence was found to support the MD as having a strong excitatory effect on the activity of regions within the broader network mediating cognitive restructuring. Moreover, the degree to which participants modulated MPFC-to-MD effective connectivity during cognitive restructuring predicted their individual tendency to engage in repetitive negative thinking. Our findings represent a major shift from a cortico-centric framework of cognition and provide important mechanistic insights into how the MD facilitates key processes in cognitive interventions for common psychiatric disorders. In addition to relaying integrative information across basal ganglia and the cortex, we propose a multifaceted role for the MD whose broad excitatory pathways act to increase synchrony between cortical regions to sustain complex mental representations, including the self.

The Relationship between Type 2 Diabetes, Differentiation of Self, and Emotional Distress: Jews and Arabs in Israel

Type 2 diabetes mellitus (T2DM) is considered a global epidemic, and is constantly on the rise. In Israel, the percentage of diabetics in the Arab population is twice that found in the Jewish population (12% and 6.2%, respectively). Findings suggest that low differentiation of self (DoS: emotional reactivity+ fusion with others, I-position, emotional cutoff) may raise vulnerability to certain physiological pathologies by increasing susceptibility to psychological distress. The major goal of this study was to test differences in DoS and emotional distress (anxiety and depressive symptoms) between diabetic and healthy participants. The second aim was to examine cultural differences within these metrics. Another purpose was to examine the relationship between DoS and emotional distress among healthy and diabetic participants. The sample included 261 participants, of whom 154 were healthy and 107 were diabetic. Diabetics reported more severe depressive symptoms, higher levels of anxiety and emotional cutoff and lower levels of I-position than healthy individuals. The groups did not differ in their levels of emotional reactivity + fusion with others. Arabs demonstrated higher levels of emotional cutoff, anxiety and depressive symptoms and lower levels of I-position than Jews. However, Arabs and Jews did not differ in their levels of emotional reactivity + fusion with others. Emotional reactivity + fusion with others contributed the most to diabetes among Arabs, while depressive symptoms contributed the most among Jews. Finally, among Jewish participants, age was positively correlated with emotional cutoff and depressive symptoms. Emotional cutoff was positively correlated with anxiety and depressive symptoms. Emotional reactivity + fusion with others was positively correlated with anxiety. Among Arab participants, age was positively correlated with emotional cutoff, anxiety and depressive symptoms. I-position was negatively correlated with all study variables. Emotional cutoff was positively correlated, anxiety and depressive symptoms. Emotional reactivity + fusion with others was positively correlated with anxiety and depressive symptoms.

Neural Changes in Borderline Personality Disorder After Dialectical Behavior Therapy–A Review

The biological component of the biosocial theory of emotion regulation stipulates that borderline personality disorder (BPD) arises from biological vulnerabilities to heightened emotional reactivity. Comprehensive reviews have consistently implicated abnormalities in the amygdala, anterior cingulate cortex, and hippocampus in the neurobiology of BPD. While Dialectical Behavior Therapy (DBT) is the leading evidence-based psychotherapy for the treatment of BPD, there remains a paucity of literature examining changes in the neurobiology of BPD following DBT treatment. Nine studies were identified that examined neurobiological changes in BPD after the completion of DBT. Results indicated that there was significant deactivation of amygdala activity as well as the anterior cingulate cortex in patients with BPD after DBT treatment. As well, several studies found after DBT treatment, BPD patients had a decreased activity in the inferior frontal gyrus in response to arousing stimuli and increased activity in response to inhibitory control. Future research on the neurobiological change after DBT treatment can help clarify biological mechanisms of change in BPD.

Behavioural consequences of Setd1a haploinsufficiency in mice: evidence for heightened emotional reactivity and impaired sensorimotor gating

ABSTRACTA number of studies implicate the loss of function (LoF) mutations affecting the histone methyl transferase SETD1A in the aetiology of a range of neurodevelopmental disorders including schizophrenia. Here, we examined the behavioural consequences of haploinsufficiency of Setd1a in a mouse model. We find evidence for changes in a number of phenotypes of relevance to schizophrenia, including increased anxiety-related behaviour, enhanced acoustic startle response, and decreased pre-pulse inhibition of acoustic startle. The sensorimotor gating deficits in Setd1a+/- mice could not be rescued by haloperidol or risperidone, suggesting that these antipsychotics are ineffective for ameliorating schizophrenia-relevant phenotypes in Setd1a+/- mice and point to deficits in neural systems other than the monoamine system. These phenotypes are emerging as key features of a number of other mouse models of rare neurodevelopmental disorders caused by LoF mutations in genes encoding epigenome modifiers suggesting they may act in a network to modulate brain development. Taken together these data strengthen the support for the use of Setd1a haploinsufficient mice as a model for the biological basis of schizophrenia, and point towards possible underpinning neural mechanisms.