anxietydisorders. We report here that in older women these same ESR1 gene variants were
specifically associated with the risk of phobia, but current HT use could modify this association.
We also found that ESR2 rs1256049 was associated with the risk of GAD. Our study thus
contributes important new findings to this field.
Researchers emphasized significant perception of threat and more reactions of hypervigilance when anxiety is combined with IU. Certain neural dysfunctions are advanced namely the insula cor- tex, dACC and the amygdala when IU individuals are confronted with ambiguous stimuli.
Paradigms in anxietydisorders have already demonstrated impairments in hot and cold cognition. As regards cold cognition studies evidenced impairments in attentional and memory processes. Anxious individuals seem to have a facilitated attentional deployment, a difficulty to disengage al- located resources on specific stimuli (especially threatening stimuli) and they used more easily an attentional avoidance. The memory process has revealed a cognitive dysfunction in the episodic and the autobiographical memory (impairments in retrieval process). Concerning the hot cognition stud- ies demonstrated several dysregulation of thought and maladaptive knowledge in anxietydisorders given rise to a defective pattern of thinking and leading to diverse psychological vulnerabilities (e.g. poor orientation problem, avoidance, metaworry).
In addition, these behavioral indicators described by the models are clinically meaningful. The models are based off of clinician-assessed symptoms and not self-report instruments. These models include behavioral indicators that can capture clinically relevant levels of impairment. For example, the models are not concerned with whether a patient walked 9000 steps versus 10,000 steps, but if the patient has not left his house in the past week. The models use macro level behavioral features as inputs, such as distance traveled over a week, to predict symptoms that both patients and clinicians can understand and potentially intervene upon. The present models do not assume a causal link between the behavioral indicators and clinical symptoms; nevertheless, the models may be of interest to clinicians and patients regardless of their causal pathways, as a means to track and alert to changes in symptoms in real time. These models are not designed to replace clinical decision-making or diagnose a particular mental health condition, but rather to assess a number of behavioral indicators underlying mood and anxietydisorders. These models are a resource to provide clinically relevant behavioral information to augment clinical care.
also controlled for eating, drinking, smoking, and physical exertion. Subjects did not report any
particular potential additional stressors on the day they performed sampling. Although our study
could be considered exploratory, the differences observed more likely result from the effect of
anxietydisorders on the response to the stressor. Despite multiple analyses, Bonferroni corrections
This study brings new elements on educational inequalities in depressive and anxietydisorders among both the working and general populations. The associations between educational level and the two disorders were stronger among the general population than among the working population and for depressive disorders more than for anxietydisorders. We clearly demonstrated that non- working status may contribute to explain educational inequalities in mental disorders in the general population. More research may be needed to better understand these inequalities and to confirm the differences between the working and general populations and between the two disorders. Furthermore, as non-working status may play a substantial role in explaining social inequalities in mental health, effort towards preserving jobs and facilitating the return to employment may help to reduce these inequalities.
initially described using CD-RISC-25 . Lower resilience scores were reported in psychiatric outpatients and in GAD patients compared to the general population. In PTSD patients, a greater global clinical improvement after pharmacologic treatment was associated with a greater increase in CD-RISC resilience scores . Our data confirm and extend these findings in non- psychiatric patients using CD-RISC-10. We did not find a significant association between past psychiatric diagnoses and resilience levels, suggesting that global resilience scores could be a reversible state-like index of mental health as also suggested by two randomized placebo-controlled trials of antidepressants in Alzhei- mer’s caregivers and PTSD patients [29,30]. Interestingly, the association was only significant with current anxietydisorders (especially GAD), comorbid with mood disorder or not, but not with mood disorder without anxiety. No previous studies have examined the relationship between resilience and depressive and anxious symptomatology simultaneously. In a prospective be- reavement study, Bonnano observed a large resilient group with a relatively healthy mental profile prior to the loss, but also a small group of resilient participants who were highly depressed before bereavement suggesting that numerous pathways to resilience may exist, independently of depression. Unfortunately, anxiety was not examined in this study . The capacity to tolerate high levels of fear and still perform efficiently within a military context has been
Examination of two- and three-marker haplotypes supported the single-point findings in ALAD, CDH2, and PSAP ( Table 4 ). In addition, DYNLL2 was implicated by the haplotype-based anal- ysis, even though SNPs within this gene did not show evidence for association at p ⱕ .01 in the single marker analysis. Haplo- types in ALAD and PSAP were associated not only with social phobia and panic disorder, respectively, but also with all anxietydisorders combined. We did not find haplotype associations with empirical p values of ⬍ .01 for any combination of adjacent markers in the genes PTGDS and EPB41L4A in analysis of sliding windows. However, when performing a combined analysis of two non-adjacent EPB41L4A markers showing single-point asso- ciations (rs7719346 and rs1464766, 83 kb apart), we identified haplotypes associated with either increased or decreased risk for social phobia. All genes with SNPs and/or haplotypes associated to anxietydisorders with p ⱕ .01 are depicted in Figure 1 .
Background: Our aim was to examine whether comorbid mood and anxietydisorders influence patterns of treatment or the perceived unmet need for treatment among those not receiving treatment for illegal drug use disorders. Methods: Data came from the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC, 2001–2002 and 2004–2005, n = 34,653). Lifetime DSM-IV illegal drug use disorder (abuse and dependence), as well as comorbid mood (major depression, dysthymia, manic disorder, hypomanic disorder) and anxietydisorders (panic disorder, agoraphobia, social phobia, specific phobia, generalized anxiety) were ascertained by a standardized psychiatric interview. Treatment for illegal drug use disorders and perceived unmet need for treatment were assessed among individuals with illegal drug use disorder. Odds of treatment and odds of perceived unmet need for treatment were assessed using logistic regression, adjusting for socio-demographic characteristics, treatment for mood and anxietydisorders, and comorbid alcohol use disorder.
Mental disorders, and among them the two most com- mon disorders of depression and anxiety, are an important issue in occupational health because of the high costs and heavy impact on absenteeism, presenteeism, and other work-related outcomes such as reduced work perform- ance and turnover [1,2]. Improving the knowledge on occupational risk factors for mental disorders is there- fore crucial. Some psychosocial work factors have been identified as risk factors for common mental disorders or mental health outcomes in reviews or meta-analysis of prospective studies [3-7], these studies being often limited to well-known factors or classical factors such as those re- lated to the job strain and effort-reward imbalance models [8,9]. Thus, these reviews and meta-analysis demonstrated that the risk of mental health outcomes, especially depres- sion or depressive symptoms, may increase with high psy- chological demands, low decision latitude (comprising low skill discretion and low decision authority), the combin- ation of high demands and low latitude, and low social support (job strain model), and with the combination of high effort and low reward (effort-reward imbalance model). The literature appears more seldom for other fac- tors not covered by these two models that we may call emergent factors, and there is a need to explore the psy- chosocial work environment more widely .
spending more than $190 per head in active labor market programs could cancel the
association between the rise in unemployment and suicide rate (Stuckler et al., 2009). Other studies found that when social protection was low, the association between unemployment and suicide or mortality rate was stronger (Bambra and Eikemo, 2009; Baumbach and Gulis, 2014; Christodoulou and Christodoulou, 2013; Gerdtham and Ruhm, 2006; Kaplan, 2012). As France has high levels of social protection (Amar et al., 2014), the effects of the economic hardship on mental health might have been moderated or attenuated. Indeed, among the EU Member States, the level of social protection expenditure in relation to GDP in 2008 was highest in France (31.3%) and Denmark (30.7%) (Source: Eurostat). An example of the role of social protection in times of economic crisis is Iceland, the government invested in social protection (active labor market programs, programs to save people from homelessness, etc.) and no rise in suicides and depressive disorders were observed, unlike Greece or Spain where huge cuts were realized (Stuckler and Basu, 2013). Concerning the working population, in our previous study, few changes were observed in psychosocial work factors among men,
Background and Objectives: Despite being common among cocaine users, mental health problems and their relationship with HIV and hepatitis C high risk injection behaviors are poorly documented. This study was undertaken to examine the relationships between mood and anxietydisorders and the sharing of drug injection equipment among cocaine users who inject drugs. Methods: The sample was drawn from a prospective cohort study and comprises 387 participants. The outcome of interest was "sharing injection material" in the past three months. The presence of mood and anxietydisorders during the past year was assessed using the CIDI questionnaire. Statistical analyses were conducted on baseline data using logistic regression. Results: Most participants were male (84.5%) and were aged 25 or over (92.2%); 43.0% qualified for an anxiety disorder diagnosis and 29.3% for a mood disorder diagnosis. Participants with anxietydisorders were more likely to share needles (Adjusted Odds Ratio (AOR): 2.13, 95%CI: 1.15-3.96) and other injection material (AOR: 1.81, 95%CI: 1.12-2.92). No significant association was found between mood disorders and sharing behaviors.
Friendship Experiences and Anxiety among Children: A Genetically Informed Study
Anxiety is one of the most prevalent mental health problems in youth (Lau, Gregory, Goldwin, Pine, & Eley, 2007). Based on a representative sample of 1420 children aged 9 to 13 years, Costello, Mustillo, Erkanli, Keeler and Angold (2003) found that 4.6% of 9 to 10 year-old children suffer from anxiety disorder. Whereas prevalence rates of anxiety disorder are comparable for boys and girls in late childhood, higher rates of anxiety are observed in females starting at around age 12 (Cohen et al., 1993). In addition to causing significant psychological distress, anxiety is associated with adjustment difficulties in school as well as with problematic family and peer relationships (Essau, Conradt, & Petermann, 2000; Ezpeleta, Keeler, Erkanli, Costello, & Angold, 2001; Woodward & Fergusson, 2001). Furthermore, anxietydisorders in childhood and adolescence have been identified as precursors of psychopathology in adulthood (Lau et al., 2007; Woodward & Fergusson, 2001). Given the breadth and severity of the negative consequences associated with anxiety, it is important to understand the mechanisms that lead to its development in order to optimize prevention and intervention efforts. To this end, the present study utilized a classical twin design to examine the role of friendship experience in the development of self-reported anxiety symptoms among children, while taking into account genetic vulnerability for such problems based on the level of genetic relatedness between identical and non-identical twins and the level of anxiety in the co-twin.
Silverman, W. K., & Treffers, P. D. A. (Eds.). (2001). Anxietydisorders in children and adolescents: Research, assessment and intervention. Cambridge, UK: Cambridge University Press.
Stassart, C. (2008). La sensibilité à l’anxiété chez l’enfant, les mécanismes d’apprentissage et de résolution de problèmes. Unpublished dissertation, Université de Liège, Liège, Belgium.
Keywords: Childbirth, Anxiety, Coping, Ante- and postnatal
Pregnancy and postpartum periods are known as sensi- tive periods in a woman’s life. This specific time-frame, encompasses a major risk of psychiatric morbidity . However, there remains a lack of longitudinal studies re- garding psychological distress and development of men- tal illness, even though this issue represents a major public health concern for women and their children. Anxiety symptoms in the perinatal period are frequent . Nonetheless, data pertaining to prevalence rates of anxietydisorders are limited and are impeded by a num- ber of factors including a deficit in research , the def- inition of anxiety during pregnancy and postnatal period as a specific category  and a heterogeneous use of psychometric data . Moreover, much of the published research has only assessed postpartum anxiety through retrospective chart reviews or cases studies, thus making
potential relation to highly negatively-toned dreams such as nightmares, little is known about how anxiety relates to everyday dream content (Skancke et al., 2014).
The only empirical study to have examined the relationship between anxiety and dream content is that of Gentil and Lader (1978) who investigated how the dream content of female outpatients diagnosed with chronic anxietydisorders (n=20) differed from the dream content of healthy women (n=25). The women’s levels of anxiety were measured with the State and Trait Anxiety Inventory (STAI; Spielberger, Corsuch, & Lushene, 1970) and the control group was subdivided into High Anxious Normals (HAN, n= 13) and Low Anxious Normals (LAN, n=12) based on their scores on the STAI. The authors coded the first three dreams reported by participants in a five-day dream diary using the content categories from the Hall and Van de Castle (H/V; 1966) coding system (e.g., fortunes, misfortunes, success, failure, aggressive interactions, characters). Among the few significant differences found between the dream content of patients versus the control groups, the patient group was found to report more negative affect and a higher frequency of failures, of overall social interactions, and of aggressive interactions than both the HAN and LAN groups. The dreams of anxious patients also included fewer successes and friendly interactions than did the dreams of both control groups. Only two differences, however, were found between dream content and the varying levels of trait anxiety across the three groups. First, the length of dream reports (i.e., the mean number of words per dream report) was longer in the HAN group than in both the LAN and the patient group, suggesting that trait anxiety is associated with longer dream reports within a healthy population but with shorter dream reports in this clinical population. Second, across the three groups, scores on the STAI-T were positively associated with a greater proportion of aggression interactions being directed toward the dreamer (0%, 46% and 60% in the LAN, HAN and patient group, respectively). Taken together, these results suggest that whereas dream content may be reactive to clinical levels of trait anxiety, it appears to be only
The available data does not allow to estimate the magnitude of the relationship between mood and anxietydisorders and high risk injection practices among cocaine users. This gap in the literature hampers the ability of clinicians to accurately assess potential significant predisposing factors of at-risk injection behaviors. Such information could also pave way to more targeted preventive interventions. This study was thus carried out to estimate the prevalence of mood and anxietydisorders and their relationship with high risk injection behaviors among street-based cocaine users who were concomitantly injecting drugs. We hypothesized that both mood and anxietydisorders would be positively associated with injection risk behaviors in this population.
The Anxiety Sensitivity Index – Revised (ASI-R) (Taylor & Cox, 1998a) is an extension of the Anxiety Sensitivity Index (Reiss, Peterson, Gursky, & McNally, 1986), which measures fears of consequences that could result from anxiety symptoms. This is a scale measuring ‘fear of fear’, that is, the belief that anxiety symptoms have negative effects. The scale is made up of 36 items, the sum of which constitutes the total score. The subjects evaluate to what extent they agree with each item on a 5-point Likert scale (0 = very little to 4 = very much), resulting in a total score of 0 to 144. The scale contains six subscales that measure the following areas: fear of cardiovascular symptoms; fear of respiratory symptoms; fear of gastrointestinal symptoms; fear of publicly visible reactions; fear of dissociative and neurological symptoms; fear of loss of cognitive control. The six subscales have good internal consistency and a high alpha. Reiss et coll. (1986) consider anxiety sensitivity to be a predisposing factor for the development of anxietydisorders. It is supposed to be an individual difference associated with agoraphobia in particular and other anxietydisorders in general. Carr et coll. (1994) have shown that asthma alone (without panic disorders) is not associated with a high ASI, but they used the 16-item version. The ASI has excellent internal consistency in clinical and nonclinical populations (range of alpha coefficient 0.79 to 0.90) and good test-retest reliability.
The current concept is to consider, besides AN and BN, the eating disorders not otherwise specified (EDNOS), also called 'partial or atypical ED' (table 1). The EDNOS may be more frequent than AN and BN, clustering the large family of disturbed behaviors in relation with feeding. Obviously, there are no unequivocal criteria defining EDNOS since those disorders include any condition that does not strictly meet the criteria of AN or BN. As illustrated schematically in figure 1, the EDNOS are currently viewed as an intermediate condition between simply dieting and full EDs . Partial EDs are often impermanent and spontaneously resolving but evolution through full ED is possible . The adolescents involved in strict dieting in order to lose weight are more likely to develop a full ED within one to three years . In a study involving 16-year-old girls with a partial ED, 7% developed full ED subsequently . The earlier treatment is initiated, the better is prognosis since the risk of developing a more complicated and persisting disorder is reduced . Therefore, prevention, screening and early management of EDNOS is recommended instead of a 'wait and see option .
Aberrant synaptic plasticity is a common feature found in a number of psychiatric disorders, including addiction. As experience-dependent changes in synaptic strength are controlled in part by rapid local translation of mRNAs at synaptic sites, it is likely that impaired local translation is a central point for abnormal synaptic function and a common feature in the mechanisms underlying psychiatric disorders. For example, impairments in mTORC1 function have been associated with a variety of psychiatric diseases such as MDD, SZ, and BD and addiction, even though each of these disorders has different characteristics and symptoms (Fig. 7). Interestingly, mTORC1 signaling is also linked to the mechanism of action of diverse classes of drugs of abuse, that is, psychostimulants, opiates, alcohol, and cannabis (Fig. 7). It is therefore intriguing that different drugs of abuse, by activating different receptors and downstream signaling pathways, converge on mTORC1 to induce maladaptive synaptic plasticity to promote addiction-related behaviors. Although the precise mechanisms underlying drug-dependent modulation of mTORC1 activity and the consequent modifications in synaptic plasticity are only beginning to be understood, all these findings point toward mTORC1 as being a key effector of drug of abuse-dependent neuroadaptations. As mTORC1 is a master regulator of local dendritic translation and synaptic plasticity, it is not surprising that impaired synaptic plasticity through mTORC1, underlies the development of numerous psychiatric disorders (Fig. 7).