Search

To determine if suicide attempts increased during the first year of the pandemic among young adolescents in Quebec, Canada. We analyzed children aged 10–14 years who were hospitalized for a suicide attempt between January 2000 and March 2021. We calculated age-specific and sex-specific suicide attempt rates and the proportion of hospitalizations for suicide attempts before and during the pandemic and compared rates with patients aged 15–19 years. We used interrupted time series regression to measure changes in rates during the first (March 2020 to August 2020) and second (September 2020 to March 2021) waves and difference-in-difference analysis to determine if the pandemic had a greater impact on girls than boys. Suicide attempt rates decreased for children aged 10–14 years during the first wave. However, rates increased sharply during the second wave for girls, without changing for boys. Girls aged 10–14 years had an excess of 5.1 suicide attempts per 10,000 at the start of wave 2, with rates continuing to increase by 0.6 per 10,000 every month thereafter. Compared with the prepandemic period, the increase in the proportion of girls aged 10–14 years hospitalized for a suicide attempt was 2.2% greater than that of boys during wave 2. The pattern seen in girls aged 10–14 years was not present in girls aged 15–19 years. Hospitalizations for suicide attempts among girls aged 10–14 years increased considerably during the second wave of the pandemic, compared with boys and older girls. Young adolescent girls may benefit from screening and targeted interventions to address suicidal behavior. [ABSTRACT FROM AUTHOR]

Objectives Impulsivity is a construct that is strongly associated with Gambling Disorder (GD). The main objectives in the present study are: 1) to explore the role of sex and age on impulsivity levels in GD patients; 2) to identify the relationship of the different impulsivity facets with comorbid psychopathology and other personality traits in GD patients; and (3) to assess whether impulsivity is a predictor for the severity of GD. Method The final sample consisted of 406 consecutive participants. All of them were seeking treatment for GD (88.4% male and 11.6% female) and completed the South Oaks Gambling Screen (SOGS), the UPPS-P Impulsive Behavior Scale, the Symptom Checklist (SCL-90-R), the Temperament and Character Inventory-R (TCI-R) as well as other clinical and psychopathological measures. Results Results show a negative linear trend between age and lower sensation seeking levels as well as lack of premeditation (the higher the age the lower the UPPS-P scores), and a positive linear trend between age and positive urgency (UR) (the higher the age the higher the UPPS-P score). However, no sex differences were found for the assessed impulsivity dimensions. Lack of perseverance was positively associated with obsessive–compulsive symptoms and harm avoidance trait, and negatively related to persistence and self-directedness traits. Positive UR and negative UR were positively correlated with general psychopathology and the total number of DSM-IV criteria, and negatively associated to the following personality traits: self-directedness and cooperativeness. Finally, only the sensation seeking and negative UR of the UPPS-P showed predictive capacity on the severity of the disorder (the higher the impulsivity scores the higher the illness severity). Conclusions These findings highlight the association between impulsivity traits (measured by the UPPS-P) and GD in a large and consecutively recruited clinical sample with GD, taking into account the variables sex and age. [ABSTRACT FROM AUTHOR]

Epigenetic mechanisms are believed to link environmental exposures to gene expression, and in so doing, to provide a physical basis for the activation, by life experiences, of mental-health problems. This paper provides a background to the hypothesis that epigenetic mechanisms link life stresses (perinatal, childhood and adult) and effects of malnutrition to the eating disorders (EDs). The paper reviews literature bearing upon the putative link between epigenetic factors and ED development, and examines ways in which epigenetic alterations could account for risk of eating disturbances and commonly associated behavioral and emotional problems. Ultimately, we propose that epigenetic processes provide an intriguing (although hypothetical) biological “platform” upon which ED-relevant effects of perinatal insults, life stresses, and consequences of malnutrition may be registered, and argue that an epigenetically informed understanding may explain why EDs are triggered and maintained by excessive caloric restraint, why they coincide so frequently with mood- and impulse-regulation problems, and why they tend to become increasingly entrenched over time. Finally, we comment on the clinical relevance and implications of an epigenetically informed model of ED etiology. [ABSTRACT FROM AUTHOR]

Substance abuse is common in individuals with bulimia-spectrum (binge-purge) eating disturbances, a co-occurrence that has been attributed to shared neurobiological substrates--notably alterations in dopaminergic activity. We examined the implications of variations of selected, dopamine-relevant polymorphisms (DRD2 Taq1A, DRD4 7R, and COMT) for risk of substance abuse in women with binge-purge eating syndromes. We genotyped 183 women (66.1% showing full-threshold BN and 33.9% showing sub-syndromic variants), and assessed lifetime presence of alcohol, cannabis, cocaine, and stimulant abuse or dependence using structured interviews. Tests for main and interaction effects of various allele combinations revealed that individuals who carried high function COMT and low-function DRD4 7R alleles (a combination expected to be associated with higher risk) did indeed show more lifetime substance abuse and, specifically, more cannabis abuse. Our findings suggest that a gene combination that, in theory, codes for low levels of dopaminergic neurotransmission coincides with sensitivity to substance abuse in a sample displaying binge-purge eating-disorder variants. [ABSTRACT FROM AUTHOR]

Objective: Pathological gambling (PG) and eating disorders (ED) rarely co-occur. We explored the prevalence of lifetime PG in ED, compared severity of ED symptoms, personality traits, and psychopathological profiles across individuals with ED and PG (ED + PG) and without PG (ED-PG). Finally, we assessed the incremental predictive value of gender on the presentation of a comorbid PG. Method: A total sample of 1681 consecutively admitted ED patients (1576 females and 105 males), participated in the current study (25 ED + PG and 1656 ED-PG). All participants were diagnosed according to DSM-IV criteria. Assessment measures included the Symptom Checklist and the Temperament and Character Inventory-Revised, as well as other clinical and psychopathological indices. Results: The observed lifetime prevalence of PG was 1.49%. ED subtype was associated with lifetime PG (p = .003), with PG being more frequent in binge eating disorder (5.7%). ED + PG was more prevalent in males than in females (16% vs. 1.26%, respectively). Additionally, ED + PG patients exhibited more impulsive behaviours, lower impulse regulation and higher novelty seeking. Best predictors of ED + PG were novelty seeking (OR 1.030, p = .035), sex (OR 3.295, p = .048) and BMI (OR 1.081, p = .005). Conclusions: Some personality traits (novelty seeking), being male and higher BMI are strongly related to the presence of lifetime PG in specific ED subtypes (namely binge eating disorder). [ABSTRACT FROM AUTHOR]

Abstract: Objective: We explored interaction effects involving polymorphisms of targeted dopamine system genes and selected forms of childhood abuse (sexual, physical and emotional) acting upon severity of binge-eating and psychopathological symptoms in women with Bulimia-Spectrum Disorders (BSDs). Methods: Women diagnosed with a BSD (n = 216) were assessed for childhood traumata, eating-disorder (ED) symptoms, and selected psychopathological features (sensation seeking, impulsivity, compulsivity and affective instability), and then provided blood samples for genotyping of main polymorphisms of dopamine-2 receptor (DRD2), dopamine transporter (DAT1) and catechol o-methyltransferase (COMT) genes. Results: Sensation Seeking was elevated in carriers of the low-function allele of the DRD2 Taq1A polymorphism who also reported childhood sexual abuse, relative to that in individuals showing other combinations of alleles and abuse exposures. In addition, carriers of a low-function allele of COMT scored higher on compulsivity, lower on impulsivity, and marginally lower on frequency of binge-eating than did individuals in whom the allele was absent. Discussion: Our results suggest that genes acting within the dopamine system may contribute, either directly or indirectly (i.e., in interaction with traumatic childhood experiences), to variations in the presentation of comorbid traits and, possibly, of bulimic symptoms. [Copyright &y& Elsevier]

Abstract: Introduction: Evidence associates Bulimia Nervosa (BN) with altered functioning of the hypothalamic-pituitary-adrenal (HPA) axis, but the clinical implications of such alterations need to be better understood. We contrasted cortisol responses to the dexamethasone suppression test (DST) in bulimic and non-eating disordered women and examined relationships among DST cortisol responses, eating symptoms and co-morbid disturbances. Method: Sixty women with Bulimia Spectrum (BS) Disorders (either BN or normal weight Eating Disorder NOS with regular binge eating or purging) and 54 non-eating disordered women of similar age and body mass index participated in a 0.5mg DST, and completed interviews and questionnaires assessing eating symptoms and co-morbid psychopathology. Results: Compared with the normal-eater group, the BS women demonstrated significantly less DST suppression. Among BS women, DST non-suppression was associated with more severe depression, anxiety and eating preoccupations. Conclusions: Our findings show BS women to show less DST suppression compared to normal eater women, and results link extent of non-suppression, in BS individuals, to severity of depression, anxiety and eating preoccupations. [Copyright &y& Elsevier]

Abstract: We recently documented a gene-environment interaction suggesting that individuals with Bulimia Nervosa (BN) differed from normal eaters as to the combined presence of the low-function allele of the glucocorticoid receptor polymorphism, BcII, and childhood abuse. The present study examined the extent to which any such interaction effect may have been attributable to behavioral impulsivity, sensation seeking, affective instability or depression. We had 174 bulimic and 130 nonbulimic women provide blood for genetic assays, and measured psychopathological traits and childhood abuse using structured interviews and self-report questionnaires. As expected, we observed a significant BcII × abuse interaction indicating genetic and environmental susceptibilities to co-occur significantly more often in bulimic than in nonbulimic individuals. The BcII × abuse interaction was attenuated when levels of depression were accounted for, but was surprisingly unaffected by controls for motoric impulsivity, sensation seeking or affective instability. Our findings suggest that stress-induced alterations in glucocorticoid sensitivity contribute to BN and depressive disturbances—without being associated with the behavioral/affective dysregulation seen in many BN sufferers. We discuss theoretical and clinical implications of these observations. [Copyright &y& Elsevier]

Abstract: This study evaluated the hypothesis that traumatic stress can increase risk of bulimia nervosa (BN) in individuals who are genetically disposed towards lower modulation of physiological stress reactions. We explored the extent to which childhood abuse (physical or sexual), variants of a main glucocorticoid receptor (GR) polymorphism (Bcl1), or their interaction, differentiated women with and without BN. Women seeking treatment for BN (N =129) and non-eating-disordered comparison women (N =98) provided blood samples for assays of the Bcl1 polymorphism, and completed structured interviews assessing eating symptoms, psychiatric symptoms and childhood abuse. Compared to normal-eaters, bulimic women were significantly more likely to carry the low-function Bcl1 C allele (CC or CG genotypes), to report a history of childhood abuse and, more importantly, to be positive for both factors. We interpret our findings as indicating that traumatic stress, when impacting individuals disposed to lower GR modulation, can be etiological for BN. [Copyright &y& Elsevier]

Abstract: Across populations, findings suggest that rates of self-mutilation, suicidal acts, and other self-harming behaviors (SHBs) may be influenced by polymorphisms that code for activity of the serotonin transporter (e.g., 5HTTLPR) and the enzyme, monoamine oxidase A (e.g., MAOAuVNTR). SHBs being common in patients with Eating Disorders (EDs), we evaluated (in a large sample of eating-disordered women) relationships between triallelic 5HTTLPR and MAOAuVNTR variants, on the one hand, and SHBs, on the other. We had 399 eating-disordered women report on eating symptoms and lifetime history of SHBs, and provide blood samples for genotyping. Individuals carrying high-function MAOAuVNTR alleles reported a history of SHBs about twice as often as did carriers of low-function alleles. We obtained no comparable main effect of 5HTTLPR, or MAOAuVNTR×5HTTLPR interaction effect. Genetic variations did not predict severity of eating symptoms. As in other populations, our findings link the MAOAuVNTR high-function alleles with increased risk of self-directed harm in bulimic females. We discuss theoretical and clinical ramifications of our results. [ABSTRACT FROM AUTHOR]

Abstract: Context: Efforts to classify eating-disordered individuals based on concurrent personality traits have consistently converged on a typology encompassing “over-regulated”, “dysregulated”, and “low psychopathology” subgroups. In various populations, evidence has associated personality variations of an “over-regulated/dysregulated” type with differences on serotonin-system indices, and specifically, with different loadings of serotonin transporter promoter regulatory region polymorphism (5HTTLPR) genotypes and alleles. We explored the extent to which an empirical, trait-defined typology of eating-disordered individuals coincided systematically with variations in 5HTTLPR, assayed using biallelic and triallelic models. Method: We tested 185 women with a DSM-IV eating disorder (108 with Bulimia Nervosa, 17 Anorexia Nervosa, and 60 an Eating Disorder Not Otherwise Specified) and 93 with no eating disorder on measures reflecting psychopathological traits and 5HTTLPR (biallelic and triallelic) genotypes and alleles. Results: The highest-function, triallelic (LA/LA) genotype occurred significantly more frequently among eating-disordered individuals than among controls. However, a more fine-grained analysis suggested that this association was attributable to the fact that, among eating-disordered participants, those displaying an “Inhibited/Compulsive” profile (derived using latent class analysis) were more likely than those of a “Dissocial/Impulsive” or a “Low Psychopathology” group to carry the triallelic 5HTTLPR gain-of-function LA allele and to be LA/LA homozygotes. Discussion: This study’s empirically derived classes coincide with interpretable differences on genetic indices—associating an “Inhibited/Compulsive” group with 5HTTLPR gain-of-function genotypes (and alleles) that have elsewhere been linked to trait compulsivity. The findings, furthermore, suggest that 5HTTLPR, by influencing personality-trait manifestations may, in turn, influence eating-disorder risk and symptom expression. [Copyright &y& Elsevier]

Abstract: Alterations in serotonin function have been implicated in both anorexia and bulimia nervosa, and previous studies suggest associations between serotonin function and variations in pathological personality traits. Women meeting DSM-IV criteria for anorexia nervosa (AN, 16 with the restricting subtype and 14 with the binge–purge subtype) and 49 healthy control women (CW) provided blood samples for analyses of platelet [3H]paroxetine binding. Participants also filled out questionnaires tapping eating disorder symptoms, depression, and personality pathology. Compared with CW, women with restricting and binge–purge AN had significantly lower levels of paroxetine binding (respectively: 1012+487 vs. 560+253 vs. 618+217 fmol/mg protein). Simple correlation analyses showed that, within AN but not within controls, paroxetine binding was inversely related to dieting preoccupations, affective instability, anxiousness, compulsivity, restricted expression and social avoidance but independent of age, body mass index, depression, and other eating symptoms. Findings suggest that reduced peripheral serotonin transporter density in AN relates to increased dieting preoccupations, affective instability and anxiousness–fearfulness. [Copyright &y& Elsevier]

Studies of bulimia nervosa (BN) often report decreased brain serotonin (5-hydroxytryptamine: 5-HT) activity. Across populations, impulsivity has been linked to reduced 5-HT activity, but compulsivity has been associated (at least inconsistently) with an increase. We therefore became interested in the association between behavioral-trait variations and 5-HT status in BN. In 56 bulimic and 29 non-bulimic women, we measured eating symptoms, personality traits, platelet paroxetine binding, and neuroendocrine responses following oral meta-chlorophenylpiperazine (m-CPP). Relative to normal eaters, bulimic women showed reduced density (Bmax) of platelet paroxetine-binding sites, blunted prolactin (PRL) responses following m-CPP, and (as a trend) lower basal PRL levels. However, after effects of binge–purge frequencies, body mass, and other extraneous factors were controlled, PRL levels at baseline and other moments in the serial sampling varied systematically with presence of impulsive and compulsive traits. PRL was generally low in BN, but ‘high-compulsive’/‘low-impulsive’ traits were associated with higher (normal-range) PRL values. Comparable trait-related variations were not observed on paroxetine-binding indices. Our findings suggest that 5-HT status in BN may correspond to impulsive or compulsive traits, and they encourage multidimensional modeling of the pathophysiological role of 5-HT in BN. [Copyright &y& Elsevier]

Accumulating evidence supports the view that eating-disorder (ED) etiology involves the environmental regulation of genetic potentials. This presentation reviews findings from recent molecular-genetic studies that implicate genetic effects acting upon psychiatric, metabolic, and immune components in ED phenomenology. It also reviews findings from epigenetic studies that suggest, intriguingly, that a parallel array of genes may be subject to environmental regulation via epigenetic effects–resulting from perinatal, childhood and later-life stresses and (according to preliminary evidence from our lab) reversible effects owing to prolonged dietary restraint. Although the available genetic and epigenetic data are in too-nascent a state to guide innovations in treatment, findings frame a multifactorial conceptualization of ED etiopathology that helps reduce stigmatizing misconceptions, and promotes self-acceptance on the part of affected people. [ABSTRACT FROM AUTHOR]

Previous research suggests that creative art therapies can produce short-term improvements in self-concept, mood and perceived well-being in various patient populations. Evaluation of such improvements for eating disorder patients has received little attention to date. The present report describes an Art Therapy program, consisting of a visit to Montreal Museum of Fine Arts followed by an art-therapy workshop that was provided to several groups of adult patients from the Douglas Institute’s Eating Disorders Program. We evaluated the suitability the AT program for patients being treated for eating disorders (in terms of patient satisfaction and tolerability) in a sample of 78 patients. Results indicated that patients enjoyed the program, and found it interesting and enriching. They also reported that the program provided a means for self-expression and creativity. We also assessed the short-term impact of art therapy on self-reported mood using the Profile of Mood States (POMS-BI ( Lorr, McNair, & Fisher, 1982 )), eating disorder preoccupations and urges using a Visual Analog Scale, as well as body image concerns using the Body Satisfaction Scale ( Slade, Dewey, Newton, Brodie, & Kiemle, 1990 ). At the end of the program, patients were significantly more composed and slightly more tired. The findings from the current study provide data on the suitability of art therapy programs as adjuncts to standard treatments for adults with eating disorders and show no significant short-term impact, either positive or negative, on body image or eating preoccupations/urges. [ABSTRACT FROM AUTHOR]

Objectives To summarize and synthesize the growing gene x environment (GxE) research investigating the promoter region of the serotonin transporter gene (5-HTTLPR) in the eating disorders (ED) field, and overcome the common limitation of low sample size, by undertaking a systematic review followed by a secondary data meta-analysis of studies identified by the review. Method A systematic review of articles using PsycINFO, PubMed, and EMBASE was undertaken to identify studies investigating the interaction between 5-HTTLPR and an environmental or psychological factor, with an ED-related outcome variable. Seven studies were identified by the systematic review, with complete data sets of five community ( n = 1750, 64.5% female) and two clinical ( n = 426, 100% female) samples combined to perform four secondary-data analyses: 5-HTTLPR x Traumatic Life Events to predict ED status ( n = 909), 5-HTTLPR x Sexual and Physical Abuse to predict bulimic symptoms ( n = 1097), 5-HTTLPR x Depression to predict bulimic symptoms ( n = 1256), and 5-HTTLPR x Impulsiveness to predict disordered eating ( n = 1149). Results Under a multiplicative model, the low function (s) allele of 5-HTTLPR interacted with traumatic life events and experiencing both sexual and physical abuse (but not only one) to predict increased likelihood of an ED and bulimic symptoms, respectively. However, under an additive model there was also an interaction between sexual and physical abuse considered independently and 5-HTTLPR, and no interaction with traumatic life events. No other GxE interactions were significant. Conclusion Early promising results should be followed-up with continued cross-institutional collaboration in order to achieve the large sample sizes necessary for genetic research. [ABSTRACT FROM AUTHOR]

Background and aims Orexins/hypocretins are orexigenic peptides implicated in the regulation of feeding behavior and the sleep/wake cycle. Little is known about the functioning of these peptides in anorexia nervosa (AN). The aims of the current study were to evaluate the extent to which orexin-A might be linked to sleep and treatment outcome in AN. Method Fasting plasma orexin-A concentrations were measured in 48 females with AN at the start of a day hospital treatment and in 98 normal-eater/healthy-weight controls. The Pittsburgh Sleep Quality Index was administered at the beginning of the treatment as a measure of sleep quality. Other psychopathological variables were evaluated with the Symptom Checklist-Revised (SCL90R) and the Eating Disorder Inventory-2 (EDI). Patients were assessed at the start and end of treatment by means of commonly used diagnostic criteria and clinical questionnaires. Results The AN patients presented more sleep disturbances and poorer overall sleep quality than did the healthy controls ( p = .026) but there were no global differences between groups in plasma orexin-A concentrations ( p = .071). In the AN sample, orexin-A concentrations were associated with greater sleep disturbances (| r | = .30), sleep inefficiency (| r | = .22) and poorer overall sleep (| r | = .22). Structural Equation Modeling (SEM) showed that both elevated orexin-A concentrations and inadequate sleep predicted poorer treatment outcome. Conclusion Plasma orexin-A concentrations contribute to poor sleep quality in AN, and both of these variables are associated with therapy response. [ABSTRACT FROM AUTHOR]

Eating disorder (ED) variants characterized by “binge-eating/purging” symptoms differ from “restricting-only” variants along diverse clinical dimensions, but few studies have compared people with these different eating-disorder phenotypes on measures of neurocognitive function and brain activation. We tested the performances of 19 women with “restricting-only” eating syndromes and 27 with “binge-eating/purging” variants on a modified n -back task, and used functional magnetic resonance imaging (fMRI) to examine task-induced brain activations in frontal regions of interest. When compared with “binge-eating/purging” participants, “restricting-only” participants showed superior performance. Furthermore, in an intermediate-demand condition, “binge-eating/purging” participants showed significantly less event-related activation than did “restricting-only” participants in a right posterior prefrontal region spanning Brodmann areas 6–8—a region that has been linked to planning of motor responses, working memory for sequential information, and management of uncertainty. Our findings suggest that working memory is poorer in eating-disordered individuals with binge-eating/purging behaviors than in those who solely restrict food intake, and that observed performance differences coincide with interpretable group-based activation differences in a frontal region thought to subserve planning and decision making. [ABSTRACT FROM AUTHOR]

DNA methylation allows for the environmental regulation of gene expression and is believed to link environmental stressors to such mental-illness phenotypes as eating disorders. Numerous studies have shown an association between bulimia nervosa (BN) and variations in brain-derived neurotrophic factor (BDNF). BDNF has also been linked to borderline personality disorder (BPD) and to such traits as reward dependence. We examined the extent to which BDNF methylation corresponded to bulimic or normal-eater status, and also to the presence of comorbid borderline personality disorder (BPD) and childhood abuse. Our sample consisted of 64 women with BN and 32 normal-eater (NE) control women. Participants were assessed for eating-disorder symptoms, comorbid psychopathology, and childhood trauma, and then they were required to provide blood samples for methylation analyses. We observed a significant site×group (BN vs. NE) interaction indicating that women with BN showed increases in methylation at specific regions of the BDNF promoter. Furthermore, examining effects of childhood abuse and BPD, we observed significant site×group interactions such that groups composed of individuals with childhood abuse or BPD had particularly high levels of methylation at selected CpG sites. Our findings suggest that BN, especially when co-occurring with childhood abuse or BPD, is associated with a propensity towards elevated methylation at specific BDNF promoter region sites. These findings imply that hypermethylation of the BDNF gene may be related to eating disorder status, developmental stress exposure, and comorbid psychopathology. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Previous findings indicate that women with Bulimia Nervosa (BN), when compared to women with no eating disorder (NED), tend to display elevated methylation in the promoter region of the DRD2 gene. The preceding would be compatible with evidence of generally reduced dopamine activity in people with BN. However, altered DNA methylation has also been associated with adverse environmental exposures (such as to childhood abuse) and with psychiatric disturbances (such as Borderline Personality Disorder: BPD). In this study, we examined the extent to which DRD2 methylation was associated with the presence or absence of a bulimic eating disorder, to childhood abuse exposure, or to comorbid BPD. Method: Women with a bulimia-spectrum disorder (BSD) and women with NED were assessed for childhood traumata, eating-disorder symptoms and BPD, and provided blood samples for methylation analyzes. Results: BSD and NED groups did not differ as to mean percent DRD2 promoter methylation. However, among the women with a BSD, those with BPD showed small, but significant increases in DRD2 methylation levels compared to women with NED (as indicated by Hochberg's post-hoc tests). Similarly, women with a BSD who reported a history of childhood sexual abuse showed a trend-level elevation of DRD2 methylation compared to our NED group. Discussion: Our findings imply that, in people with a BSD, increased methylation of the DRD2 gene promoter may be more strongly characteristic of comorbid psychopathology than it is a global correlate of the eating disorder per se. We discuss theoretical implications of our findings. [Copyright &y& Elsevier]

Summary: Depressive, anxiety and obsessive symptoms frequently co-occur with anorexia nervosa (AN). The relationship between these clinical manifestations and the biological changes caused by starvation is not well understood. It has been hypothesised that reduced availability of tryptophan (TRP) could reduce serotonin activity and thus trigger these comorbid symptoms. The aim of this study, during re-feeding in individuals with AN, was to analyse covariations across measures of nutritional status, depressive and anxiety symptoms, and peripheral serotonin markers. Depressive and anxiety symptoms, nutritional status and serotonin markers – whole blood serotonin content, plasma TRP and the ratio between TRP and large neutral amino acids – were assessed for 42 AN participants at admission to inpatient treatment and after re-feeding. Biological measures were compared to those obtained in 42 non-eating disordered subjects. For those with AN, psychological, nutritional and biological parameters improved significantly during hospitalisation. Levels of serotonin markers were significantly lower in the AN group compared to the control group, at admission and at discharge. Increase in the TRP/LNAA ratio was correlated with a decrease in depressive symptoms. In addition, there was a positive correlation between serotonin levels and symptoms of both anxiety and depression at discharge. We speculate that enhanced TRP availability during re-feeding, as a result of the increase in the TRP/LNAA ratio, could restore serotonin neurotransmission and lead to a decrease in depressive symptoms. The association between serotonin and anxiety and depressive symptoms would be consistent with numerous observations indicating abnormal functioning of the serotoninergic system in AN. [Copyright &y& Elsevier]

Abstract: We explored the influence of interactions between polymorphisms acting upon postsynaptic receptors (DRD2 TaqA1 rs1800497 and DRD4 7R) and dopamine regulators (COMT rs4680 and DAT1) on the expression of eating symptoms and personality traits in women with bulimia-spectrum eating disorders. We had 269 bulimic women provide blood for genetic assays, and measured eating-disorder symptoms and psychopathological traits using structured interviews and self-report questionnaires. We observed two epistatic interactions on symptom indices: interactions (in predicted directions) of DRD2 by DAT were seen on Body Mass Index (p =.023), and of DRD4 by COMT on self-harming behaviors (p =.014) —with genetic effects that would correspond to reduced dopamine transmission coinciding with more-pathological scores. Our findings suggest that genes acting in the dopamine system interact to influence both eating-related and personality psychopathology, with the result that lower levels of dopamine neuro-transmission correspond to increased psychopathology and body mass in women with bulimia-spectrum disorders. We discuss the implications of our observations. [Copyright &y& Elsevier]

Abstract: Past research has suggested that negative affect may be a causal factor for eating disordered behaviors. More specifically, research has shown that anger appears to be one aspect of negative affect that is particularly relevant in bulimic patients. Previous studies have also shown that the relationship between negative affect and eating disordered behaviors may partially depend upon personality variables such as impulsivity. The present study examined whether the relationship between anger and eating disordered behaviors is moderated by impulsivity. Subjects completed an ecological momentary assessment (EMA) protocol for an average of 2 weeks. Findings revealed that overall antecedent anger level and the variability of antecedent anger predicted binge-eating episodes and that these relationships were moderated by participants’ level of impulsivity. These findings suggest that personality variables impact the way that anger and eating behaviors relate. They also suggest that the variability of antecedent anger may be a fruitful avenue for future research for those interested in causal variables associated with bulimia nervosa. [Copyright &y& Elsevier]

Abstract: This study examined whether abnormal responses to neurobiological challenge tests in borderline personality disorder (BPD) are related to a history of childhood sexual abuse (CSA). We compared patients meeting BPD criteria (n =24), with and without histories of CSA, with normal controls (n =12) on the results of challenges with meta-chlorphenylpiperazine (m-CPP), pyridostigmine and clonidine. No differences were found between abused and non-abused patients with BPD. These results do not support the hypothesis that CSA is directly related to neurobiological abnormalities in BPD. [Copyright &y& Elsevier]

The purpose of the study was to test the hypothesis that borderline personality disorder (BPD) and its underlying traits are associated with abnormalities in neurotransmitter systems. Subjects were 30 women with BPD and 22 normal controls, assessed using the Diagnostic Interview for Borderlines, revised, the Hamilton Depression Scale (HAM-A) and the Hamilton Anxiety Scale (HAM-A), the Diagnostic Assessment of Personality Pathology, the Buss–Durkee Guilt-Hostility Inventory, the Barratt Impulsivity Scale (BIS), and challenge tests to measure serotonergic, cholinergic and noradrenergic activity. Borderline subjects with high HAM-A and HAM-D scores showed a faster time to peak in prolactin response to meta-chlorphenylpiperazine (m-CPP) challenge. Borderline subjects with high BIS scores showed prolactin blunting. There were no differences in cortisol response to m-CPP, or on the cholinergic and noradrenergic challenges. The results suggest that impulsive traits in borderline patients are associated with abnormalities in serotonergic systems. [Copyright &y& Elsevier]

Our objectives were to determine the extent to which symptoms in the schizophrenia patient and personality in the mother lead to a sense of subjective burden in the mother, and to explain variance in two components of Expressed Emotion. Data on symptom severity (PANSS), mothers’ personality (NEO-PI), subjective burden (SBAS), and Expressed Emotion (CFI) were gathered from 41 schizophrenia outpatients and their mothers. Approximately one quarter of the variance in Critical Comments (CCs) and Emotional Overinvolvement (EOI) was explained using path analysis. Mothers’ CCs were associated with more severe excitement in the patient, with lower Neuroticism, and greater burden in the mother. Higher EOI was explained by greater Conscientiousness and burden in the mother; patient depression had a weak indirect effect on maternal EOI. These results characterize the high EE mother as low in neuroticism and high in conscientiousness with a particular sensitivity to excitement and depression in the patient. [Copyright &y& Elsevier]