To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Methamphetamine has been consistently associated with positive psychotic symptoms, but little is known about whether the reverse also occurs.
This study determined whether the relationship between methamphetamine use and positive psychotic symptoms is bidirectional over 12 months. The impact of lifetime psychotic disorders and methamphetamine dependence on these relationships was also examined.
A total of 201 regular (at least monthly) primary methamphetamine users were recruited from free needle and syringe programmes in three Australian cities. Data on the frequency of methamphetamine and other drug use (from Timeline Followback inteviews) and the severity of positive psychotic symptoms (using the Brief Psychiatric Rating Scale) in the past 2 weeks were collected in 12 contiguous monthly face-to-face interviews (mean of 9.14/11 (s.d. = 3.16) follow-ups completed). Diagnoses were derived using the Psychiatric Research Interview for DSM-IV Substance and Mental Disorders.
The mean age of participants was 31.71 years (s.d. = 8.19) and 39% (n = 77) were women. At baseline 55% (n = 110) were dependent on methamphetamine and 51% (n = 102) had a lifetime psychotic disorder. Cross-lagged dynamic panel models found a significant bidirectional relationship between psychotic symptoms and methamphetamine use (Comparative Fit Index (CFI) = 0.94, standardised root mean square residual (SRMR) = 0.05, root mean square error of approximation (RMSEA) = 0.05, 95% CI 0.04–0.06). The magnitude of the relationship in each direction was similar, and the presence of methamphetamine dependence or a lifetime psychotic disorder did not have an impact on results.
A dynamic, bidirectional relationship between methamphetamine and psychotic symptoms of similar magnitude in each direction was found over 1 year. This suggests integrated treatments that target methamphetamine, psychotic symptoms and their interrelationship may be of most benefit.
Studies have examined the association between depressive symptoms and dietary patterns; however, only few studies focused on older adults. The present study examines the association between current and past dietary patterns and depression in a community-dwelling adult population aged 55 years and over. Adults (n 4082) were recruited into the Wellbeing, Eating and Exercise for a Long Life study in Victoria, Australia. In 2010 and 2014, data were collected using self-administered questionnaires including a 111-item FFQ, the RAND thirty-six-item Short Form Health Survey of health-related quality of life and the International Physical Activity Questionnaire. Depressive symptoms were assessed using the Geriatric Depression Scale in 2014. Current (2014) and past (2010) dietary patterns were determined using principal component analysis. Association between dietary patterns and depressive symptoms was assessed using a mixed model analysis with adjustment for covariates. Two similar dietary patterns were identified in men and women (n 2142). In women, a healthy dietary pattern (characterised by frequent intake of vegetables, fruits and fish) was associated with lower levels of depressive symptoms (current diet: β = −0·260, 95 % CI −0·451, −0·070; past diet: β = −0·201, 95 % CI −0·390, −0·013). A current unhealthy dietary pattern in women (characterised by frequent intake of red and processed meat, potatoes, hot chips, cakes, deserts and ice cream) was associated with higher levels of depressive symptoms (β = 1·367, 95 % CI 0·679, 2·056). No associations were identified in men. Further research is needed to confirm these findings and to understand the differences that may occur by sex.
Background. Frequency and quantity of alcohol consumption are metrics commonly used to measure alcohol consumption behaviors. Epidemiological studies indicate that these alcohol consumption measures are differentially associated with (mental) health outcomes and socioeconomic status (SES). The current study aims to elucidate to what extent genetic risk factors are shared between frequency and quantity of alcohol consumption, and how these alcohol consumption measures are genetically associated with four broad phenotypic categories: (i) SES; (ii) substance use disorders; (iii) other psychiatric disorders; and (iv) psychological/personality traits.
Methods. Genome-Wide Association analyses were conducted to test genetic associations with alcohol consumption frequency (N = 438 308) and alcohol consumption quantity (N = 307 098 regular alcohol drinkers) within UK Biobank. For the other phenotypes, we used genome-wide association studies summary statistics. Genetic correlations (rg) between the alcohol measures and other phenotypes were estimated using LD score regression.
Results. We found a substantial genetic correlation between the frequency and quantity of alcohol consumption (rg = 0.52). Nevertheless, both measures consistently showed opposite genetic correlations with SES traits, and many substance use, psychiatric, and psychological/personality traits. High alcohol consumption frequency was genetically associated with high SES and low risk of substance use disorders and other psychiatric disorders, whereas the opposite applies for high alcohol consumption quantity.
Conclusions. Although the frequency and quantity of alcohol consumption show substantial genetic overlap, they consistently show opposite patterns of genetic associations with SES-related phenotypes. Future studies should carefully consider the potential influence of SES on the shared genetic etiology between alcohol and adverse (mental) health outcomes.
The re-emergence of debates on the decolonisation of knowledge has revived interest in the National Question, which began over a century ago and remains unresolved. Tensions that were suppressed and hidden in the past are now being openly debated. Despite this, the goal of one united nation living prosperously under a constitutional democracy remains elusive. This edited volume examines the way in which various strands of left thought have addressed the National Question, especially during the apartheid years, and goes on to discuss its relevance for South Africa today and in the future. Instead of imposing a particular understanding of the National Question, the editors identified a number of political traditions and allowed contributors the freedom to define the question as they believed appropriate – in other words, to explain what they thought was the Unresolved National Question. This has resulted in a rich tapestry of interweaving perceptions. The volume is structured in two parts. The first examines four foundational traditions: Marxism-Leninism (the Colonialism of a Special Type thesis); the Congress tradition; the Trotskyist tradition; and Africanism. The second part explores the various shifts in the debate from the 1960s onwards, and includes chapters on Afrikaner nationalism, ethnic issues, black consciousness, feminism, workerism and constitutionalism. The editors hope that by revisiting the debates not popularly known among the scholarly mainstream, this volume will become a catalyst for an enriched debate on our identity and our future.
Objectives: Existing models of trichotillomania (TTM; hair pulling disorder) rely heavily on a biological predisposition or biological pathogenesis of the disorder, but fail to capture the specific neuropsychological mechanisms involved. The present systematic review aims to scope existing neuropsychological studies of TTM to explore gaps in current models. Methods: A systematic literature search was conducted to detect all published primary studies using neuropsychological and neuroimaging measures in a cohort of individuals experiencing TTM. Studies addressing neuropsychological function were divided into domains. Findings from imaging studies were considered within brain regions and across methodology. Results: Thirty studies with a combined 591 participants with TTM, 372 healthy controls and 225 participants in other types of control group were included. Sixteen studies investigated neuropsychological parameters, and 14 studies pursued neuroimaging technologies. Available studies that used neuropsychological assessments and reported a statistically significant difference between those with TTM and controls ranged in effect size from 0.25 to 1.58. All domains except verbal ability and visual ability reported a deficit. In neuroimaging studies, several structural and functional brain changes were reported that might be of significance to TTM. Only tentative conclusions can be made due to the use of multiple methodologies across studies, a major limitation to meaningful interpretations. Conclusions: Positive neuropsychological and neuroimaging results require replication, preferably with multi-site studies using standardized methodology. Increased standardized testing and analyses across the literature, as a whole, would improve the utility and interpretability of knowledge in this field. (JINS, 2018, 24, 188–205)
Binge eating is a distressing symptom common to bulimia nervosa (BN), anorexia nervosa binge/purge subtype (AN-BP) and binge-eating disorder (BED). Over the last 40 years, many attempts have been made to conceptualise this symptom in terms of its antecedents, function, triggers, consequences, and maintaining factors. Cognitive theories of binge eating have evolved as new evidence has emerged. This literature review summarises the main and most influential cognitive models of binge eating across different eating disorder presentations. Many theories have examined binge eating in the context of restriction or compensatory behaviours, as is often observed in cases of BN. Few theories have examined binge eating as it occurs in BED specifically. The long-term efficacy of cognitive behavioural therapy (CBT) treatment based on these models leaves much to be desired, and indicates that there may be maintaining factors of binge eating not addressed in the typical CBT treatment for eating disorders. More recent cognitive models of binge eating propose possible maintaining beliefs, but further study is required to validate these models. Suggestions for future research are presented.
Social anxiety disorder (SAD) is characterised by a marked and persistent fear of social/performance situations, and a number of key environmental factors have been implicated in the aetiology of the disorder. Hence, the current article reviews theoretical and empirical evidence linking the development of SAD with parenting factors, traumatic life events, and aversive social experiences. Specifically, research suggests that the risk of developing SAD is increased by over-controlling, critical and cold parenting, an insecure attachment style, aversive social/peer experiences, emotional maltreatment, and to a lesser extent other forms of childhood maltreatment and adversity. Moreover, these factors may lead to posttraumatic reactions, distorted negative self-imagery, and internalised shame-based schemas that subsequently maintain SAD symptomatology. However, further research is necessary to clarify the nature, interactions, and relative contributions of these factors. It is likely that SAD develops via a complex interplay of biological and environmental factors, and that multiple aetiological pathways underlie the development of the disorder.
The appraisal model of obsessive-compulsive disorder (OCD) suggests that six key appraisal domains contribute to the aetiology and maintenance of OCD symptoms. An accumulating body of evidence supports this notion and suggests that modifying cognitive appraisals may be beneficial in reducing obsessive-compulsive symptomatology. This literature review first summarises the nature of OCD and its treatment, followed by a summary of the existing correlational and experimental research on the role of cognitive appraisal processes in OCD across both adult and paediatric samples. While correlational data provide some support for the relationship between cognitive appraisal domains and OCD symptoms, results are inconclusive, and experimental methods are warranted to determine the precise causal relationship between specific cognitive appraisal domains and OCD symptoms.
Social anxiety disorder (SAD) is characterised by an intense fear of social situations in which the individual believes they may be negatively evaluated (American Psychiatric Association, 2013). A number of cognitive models (Clark & Wells, 1995; Hofmann, 2007; Rapee & Heimberg, 1997) have been proposed that provide frameworks for understanding the key cognitive processes involved in SAD. Negative rumination, which can be divided into pre- and post-event rumination, appears to be a key maintaining factor in the cycle of social anxiety. However, there are mixed findings regarding the cognitive predictors of post-event rumination and a lack of research regarding the consequences and predictors of pre-event rumination. Furthermore, there has been little empirical research investigating the effects of targeting negative rumination and state anxiety in social anxiety treatment. If the cognitive predictors of negative rumination can be determined then they can be targeted when designing interventions that aim to break the vicious cycle of social anxiety. The state of research investigating the cognitive determinants of state anxiety and negative rumination is reviewed and suggestions are made for continuing research.
Social anxiety disorder (SAD) is characterised by a marked and persistent fear of social or performance situations. Cognitive models suggest that self-focused cognitive processes play a crucial role in generating and maintaining social anxiety, and that self-focused cognition occurs prior to, during, and following social situations (Clark & Wells, 1995; Rapee & Heimberg, 1997). There is a substantial body of empirical evidence demonstrating that socially anxious individuals engage in self-focused cognition during and following a social or performance situation. A smaller but growing body literature suggests that a similar process occurs prior to such situations, and that these three processes are interdependent. Furthermore, the vast majority of research to date indicates that self-focused cognitive processes are detrimental, and that they generate and maintain social anxiety in a variety of ways. However, there remains considerable scope for research to further explicate the role of these processes in the maintenance of SAD, and to enhance interventions designed to ameliorate their negative effects.