Metacognition and depressive realism: Evidence for the level-of-depression account

Introduction. The present study examined the relationship between metacognition (i.e., “thinking about thinking”) and depression. More specifically, the depressive realism hypothesis (Alloy & Abramson, 1979), which posits that depressed people have a more accurate view of reality than nondepressed people, was tested.

Methods. Nondepressed, mildly depressed, and moderately depressed individuals predicted their memory performance by making judgements of learning after each studied item. These predictions were then compared with actual performance on a free recall task to assess calibration, an index of metacognitive accuracy.

Results and conclusions. Consistent with the depressive realism hypothesis, mild depression was associated with better calibration than nondepression. However, this “sadder but wiser” phenomenon appears to only exist to point, as moderate depression and nondepression showed no calibration differences. Thus, the level-of-depression account of depressive realism is supported.     

Metacognition and depressive realism: evidence for the level-of-depression account

Introduction. The present study examined the relationship between metacognition (i.e., "thinking about thinking") and depression. More specifically, the depressive realism hypothesis (Alloy & Abramson, 1979), which posits that depressed people have a more accurate view of reality than nondepressed people, was tested. Methods. Nondepressed, mildly depressed, and moderately depressed individuals predicted their memory performance by making judgements of learning after each studied item. These predictions were then compared with actual performance on a free recall task to assess calibration, an index of metacognitive accuracy. Results and conclusions. Consistent with the depressive realism hypothesis, mild depression was associated with better calibration than nondepression. However, this "sadder but wiser" phenomenon appears to only exist to point, as moderate depression and nondepression showed no calibration differences. Thus, the level-of-depression account of depressive realism is supported.     

Subgenual anterior cingulate responses to peer rejection: a marker of adolescents' risk for depression

Extensive developmental research has linked peer rejection during adolescence with a host of psychopathological outcomes, including depression. Moreover, recent neuroimaging research has suggested that increased activity in the subgenual region of the anterior cingulate cortex (subACC), which has been consistently linked with depression, is related to heightened sensitivity to peer rejection among adolescents. The goal of the current study was to directly test the hypothesis that adolescents' subACC responses are predictive of their risk for future depression, by examining the relationship between subACC activity during peer rejection and increases in depressive symptoms during the following year. During a functional magnetic resonance imaging scan, 20 13-year-olds were ostensibly excluded by peers during an online social interaction. Participants' depressive symptoms were assessed via parental reports at the time of the scan and 1 year later. Region of interest and whole-brain analyses indicated that greater subACC activity during exclusion was associated with increases in parent-reported depressive symptoms during the following year. These findings suggest that subACC responsivity to social exclusion may serve as a neural marker of adolescents' risk for future depression and have implications for understanding the relationship between sensitivity to peer rejection and the increased risk of depression that occurs during adolescence.     

Omega-3 fatty acid deficiency in major depressive disorder is caused by the interaction between diet and a genetically determined abnormality in phospholipid metabolism

Omega-3 fatty acids are a type of polyunsaturated fatty acid (PUFA). A growing body of evidence suggests that this form PUFA is a useful and well tolerated treatment for major depressive disorder, a common and serious mental illness. The efficacy of omega-3 PUFA is routinely explained as being due to a deficiency caused by inadequate dietary intake of this class of fatty acid. The hypothesis considered states that low omega-3 PUFA abundance in patients with major depressive and related disorders is due to an underlying genetically determined abnormality. The hypothesis can explain why although a specific and consistent deficit in omega-3, but not omega-6, PUFA occurs in major depressive and related disorders, the literature does not consistently support the notion that this is due to deficient dietary intake. Specifically it is hypothesized that having genetically determined low activity of fatty acid CoA ligase 4 and/or Type IV phospholipase A(2) combined with the low dietary availability of omega-3 PUFA results in reduced cellular uptake of omega-3 PUFA and constitutes a risk factor for depression. The hypothesis also has important consequences for the pharmacological treatment of depression in that it predicts that administering agents which enhance phospholipid synthesis, particularly those containing ethanolamine such as CDP-ethanolamine, should be effective antidepressants especially when co-administered with omega-3 PUFA.     

A prospective test of the hopelessness theory of depression in children.

Providing a developmental extension of the cognitive theories of depression, researchers and theorists have suggested that during early to middle childhood, attributional styles may mediate rather than moderate the association between negative life events and the development of depression. Within the context of the hopelessness theory of depression, we tested this hypothesis in a 6-month longitudinal study of 4th- and 5th-grade children. Using path analysis, we found support for the mediating role of attributional styles among both 4th and 5th graders. Supporting recent refinements in the hopelessness theory, the best fitting mediation model was one in which depressive symptoms exhibited reciprocal relations with the other variables. Specifically, attributional styles partially mediated the link between verbal victimization and residual change in depressive symptoms. In addition, initial depressive symptoms predicted negative changes in children's attributional styles and increases in verbal victimization across the follow-up. Contrary to our hypothesis, we also found support for the moderating role of attributional styles, although this was significant only among 5th graders.     

Cognitive functioning in young and middle-aged unmedicated out-patients with major depression: testing the effort and cognitive speed hypotheses

BACKGROUND: Cognitive deficits are common in major depressive disorder, but their nature is unclear. The effort hypothesis states that performance on effortful tasks is disproportionately impaired compared with the performance on automatic tasks. The cognitive speed hypothesis states that depression is characterized by cognitive slowness, which is a source of cognitive dysfunctioning. The present study investigated both theories in unmedicated adult depressive patients. It was also investigated whether the cognitive deficits can be attributed to more general physical illness-related factors or specifically to depressive disorder. METHOD: Thirty non-psychotic depressive out-patients were compared with 38 healthy control subjects and 25 patients with severe allergic rhinitis. The effects of group on more automatic and more effortful aspects of cognitive tasks measuring cognitive speed (Concept Shifting Task, Stroop Colour Word Test, Memory Scanning Test) and memory retrieval (Visual Verbal Learning Task, Verbal Fluency Test) were evaluated by MANCOVA. Age, sex, education and pre-morbid intelligence were treated as covariates. RESULTS: The depressive group had cognitive deficits in the automatic processing subtask of the Stroop, memory scanning and memory span. Performance on more effortful tasks was not impaired. CONCLUSIONS: Our results are more consistent with the cognitive speed hypothesis. Cognitive functioning in depressive disorder seems to be characterized by a reduced speed of information processing in automatic subtasks.     

Sensitization: The sine qua non of the depressive disorders?

Available definitions of depressive disorders do not adequately distinguish depressive disorders from non-pathological mood states. When depression occurs as a reaction to life events (e.g., bereavement) a diagnosis is not usually warranted since these reactions represent normal and presumably adaptive reactions to life circumstances. Various approaches in DSM-IV such as the bereavement exclusion criterion and clinical significance criteria (addressing levels of distress and dysfunction) have not provided a fully satisfactory solution. The distinction between pathological and non-pathological expressions of depression would be facilitated were there to be a clearer understanding of the adaptive purpose of depression in its normal manifestations. Such an understanding would provide a basis for distinguishing adaptive manifestations of depression from those that represent a disorder. This paper presents the hypothesis that sensitization to life events is the core feature of depressive disorders. Sensitization may be an adaptive mechanism because it can fine-tune responses in a changing environment. Sensitization, however, may fail as an adaptive mechanism if it leads to an over-sensitized state in which a person cannot function or is intensely distressed even in a normal environment. This hypothesis predicts that a pattern of increasing reactivity to life events will be a better predictor of the need for, and response to, psychiatric treatment than current definitions.     

Is there evidence for a male depressive syndrome in inpatients with major depression?

BACKGROUND: The question is investigated whether atypical depressive symptoms such as irritability, anger attacks, aggressiveness or abusive behavior, which are hypothesized to indicate a hypothetical male depressive syndrome are more prevalent in male than in female inpatients with unipolar major depression. METHODS: Data were obtained from 2411 patients who had been consecutively admitted to the Department of Psychiatry of the Ludwig-Maximilians-University of Munich. Psychopathological symptoms had been assessed by a standardized documentation system (AMDP). RESULTS: Neither frequency nor mean scores of most of the symptoms describing a male depressive syndrome differed between males and females. There were no gender differences in symptoms with respect to severity of depression, first hospitalization and duration of illness. However, gender differences emerged when regarding symptom patterns by factor analysis. Limitations: Only inpatients were studied, and comorbidity was not considered. CONCLUSIONS: The hypothesis of a male depressive syndrome needs further research, focusing on the gradual development of (masked) depression by men in mainly non-clinical samples.     

Amelioration of Child Depression Through Behavioral Parent Training: A Preliminary Study

Child depression is an impairing condition for which tested treatments have shown relatively modest mean effects. One possible explanation is that the treatments have generally adopted an individual child focus, without addressing the dysfunctional parent–child interactions that often accompany child depression. The present study provides preliminary evidence bearing on this hypothesis, using data from a treatment outcome study in which clinically referred children with a depression diagnosis could receive individual cognitive behavioral therapy (CBT) focusing on the depression or behavioral parent training (BPT) focusing on comorbid conduct problems. Among children in the study who met criteria for Diagnostic and Statistical Manual of Mental Disorders (4th ed.) depressive disorders, we identified two groups, matched on gender and age: 15 who received only CBT focused on child depression and 15 who received only BPT focused on child conduct problems. Children were 7 to 13, 20 of whom were male, and race included Caucasian (17), Latino (5), African American (2), and multirace (6). Measures assessed depressive diagnoses and symptoms, as well as parenting stress. Analyses focused on whether BPT alone might lead to reduced depression, and if so how that reduction would compare to the depression reduction achieved through CBT that focused on depression. Both groups showed significant reductions from pre- to post-treatment in depressive diagnoses and depression symptoms, and there were no BPT versus CBT group differences at post-treatment. BPT that focuses on child conduct problems, with no emphasis on depression treatment, may produce significant depression reduction in comorbid children who meet criteria for depressive disorders.     

Major depressive disorder viewed as a dysfunction in astroglial bioenergetics

For many years scientists and physicians have pondered upon the apparent connection between depressive disorder and diabetes mellitus. Several epidemiologic studies confirm that diabetics have increased incidence of depression, and vice versa. In addition: depressive, non-diabetic patients have several insulin- and glucose-metabolism disturbances, probably exerting a compensatory reaction to the malfunction in the depressed brain as these disturbances are normalised in remission. After the discovery of PET-scanning, such studies have shown that patients with depressive disorder have reduced glucose metabolism in frontal parts of the brain. The present hypothesis regards the PET findings as observations of the primary pathophysiology of depression. Furthermore: two studies of post mortem samples from depressed patients show reduced numbers of astroglia. This is in accordance to the mentioned insulin disturbances, as only astroglia, not neurons, have insulin-sensitive glucose metabolism. Hence: the astroglia, not necessarily the neurons, are proposed to be the type of cells in which the disease resides. Most probably depressive disorder is a multitude of diseases, explaining the apparent multitude of symptoms, and the fact that different patients do respond to different drugs. Therefore: one can only formulate the hypothesis by mentioning a common denominator to these specific malfunctions, namely: disturbed glucose metabolism in the depressed brain. The present paper reviews several findings and proposes that attenuated cerebral glucose metabolism in frontal parts of the brain, in the astroglia, is the cause of depressive disorder.     

Symptoms of Depression and Anxiety in Children: Specificity of the Hopelessness Theory

The common etiology hypothesis proposes that depression and anxiety commonly co-occur because they share etiological factors. This study examined the specificity of the hopelessness theory in the development of depressive and anxious symptoms in children. Students in Grades 3 through 6 (N = 418, 47% boys) completed measures assessing inferential styles about causes, consequences, and the self, depressive symptoms, and anxious symptoms. Six weeks later, children completed measures of depressive symptoms, anxious symptoms, and hassles. All 3 inferential styles interacted with hassles to predict increases in depressive symptoms, although this relation only held for children with low levels of initial symptoms. Inferential styles about consequences and the self also predicted increases in anxious symptoms. Consistent with the common etiology hypothesis, after controlling for the association between depressive and anxious symptoms, the effects of inferential styles about consequences and the self persisted.     

Symptoms of depression and anxiety in children: specificity of the hopelessness theory.

The common etiology hypothesis proposes that depression and anxiety commonly co-occur because they share etiological factors. This study examined the specificity of the hopelessness theory in the development of depressive and anxious symptoms in children. Students in Grades 3 through 6 (N = 418, 47% boys) completed measures assessing inferential styles about causes, consequences, and the self, depressive symptoms, and anxious symptoms. Six weeks later, children completed measures of depressive symptoms, anxious symptoms, and hassles. All 3 inferential styles interacted with hassles to predict increases in depressive symptoms, although this relation only held for children with low levels of initial symptoms. Inferential styles about consequences and the self also predicted increases in anxious symptoms. Consistent with the common etiology hypothesis, after controlling for the association between depressive and anxious symptoms, the effects of inferential styles about consequences and the self persisted.     

Cognitive therapy for depressed adults with comorbid social phobia

BACKGROUND: Evidence suggests that comorbid depression influences the outcome of cognitive-behavioral treatment for patients presenting with social phobia. Little is known, however, about the influence of comorbid social phobia on the response to cognitive therapy (CT) for depression among adults presenting with recurrent major depressive disorder (MDD). These analyses seek to clarify this relationship. METHODS: Patients (N=156) with recurrent DSM-IV MDD entered CT (20% also met DSM-IV criteria for social phobia). Every week during the course of CT, clinicians assessed depressive symptoms and patients completed self-report instruments measuring severity of depression and anxiety. RESULTS: At presentation, outpatients with comorbid social phobia reported greater levels of depressive symptoms and clinicians rated their impairment as more severe, compared to their counterparts without social phobia. Patients with or without comorbid social phobia did not differ significantly in (1) attrition rates; (2) response or sustained remission rates; (3) time to response or sustained remission; or (4) rate of improvement in symptoms of depression or anxiety. LIMITATIONS: The lack of domain-specific measures limits inference with respect to the improvements in social anxiety that occur with CT of depression. CONCLUSIONS: These findings introduce the hypothesis that CT for depression may be flexible enough to treat the depressive symptoms of patients presenting with MDD who also suffer from social phobia.     

A Prospective Test of the Hopelessness Theory of Depression in Children

Providing a developmental extension of the cognitive theories of depression, researchers and theorists (e.g., Cole & Turner, 1993; Rose & Abramson, 1992) have suggested that during early to middle childhood, attributional styles may mediate rather than moderate the association between negative life events and the development of depression. Within the context of the hopelessness theory of depression (e.g., Abramson, Metalsky, & Alloy, 1989), we tested this hypothesis in a 6-month longitudinal study of 4th- and 5th-grade children. Using path analysis, we found support for the mediating role of attributional styles among both 4th and 5th graders. Supporting recent refinements in the hopelessness theory, the best fitting mediation model was one in which depressive symptoms exhibited reciprocal relations with the other variables. Specifically, attributional styles partially mediated the link between verbal victimization and residual change in depressive symptoms. In addition, initial depressive symptoms predicted negative changes in children's attributional styles and increases in verbal victimization across the follow-up. Contrary to our hypothesis, we also found support for the moderating role of attributional styles, although this was significant only among 5th graders.     

Toward a neurobehavioral trait conceptualization of depression proneness

The etiology of major depressive disorder is heterogeneous, and differing pathways leading to the development of depression are proposed to account for alternative variants of depressive illness and their distinct comorbidity patterns. The present study was undertaken as a step toward developing a model for conceptualizing and quantifying dispositional proneness to depression, marked by reduced neural sensitivity to rewarding events and more persistent occurrence of depressive symptomatology. Using data for college and community adult participants (N = 201), we sought to quantify variations in depression proneness by combining symptom indicators of persistent depressive conditions (dysthymic disorder, depressive personality) with a brain potential response that has been shown to index sensitivity to pleasurable events—the reward positivity (RewP; Proudfit, 2015). We first extended prior work on the RewP and depression by showing that the magnitude of RewP covaried negatively with symptoms of persistent depressive conditions (dysthymia, depressive personality) but not with current levels of depression. Persistent depressive symptoms and the RewP were then combined to form a composite neuroclinical index of depression proneness. Compared to persistent depressive symptoms alone, this composite dimensional index showed improved specificity of relations with diagnostic criterion measures, that is, similar‐level associations with other indicators of depression proneness but significantly lower associations with fear disorder symptomatology. These findings provide evidence that a dimension of depression proneness can be quantified effectively by combining psychological indicators of persistent depression with a neurophysiological index of a core depression‐related process (i.e., reward sensitivity).     

Heart rate variability in patients with major depression

This study compared cardiac autonomic modulation in physically healthy patients with major depressive disorder to that in mentally healthy heart transplant recipients and physically and mentally healthy comparison subjects by using a nonlinear measure and a conventional measure of heart rate variability. No significant differences in cardiac autonomic modulation were noted between the depressive group and the transplant recipients, but both of those groups had significantly lower mean values for heart rate variability measures relative to the healthy comparison subjects. The results support the hypothesis that cardiac autonomic imbalance (reduced vagal modulation) to the extent of cardiac neuropathy is present in depression.     

Effects of heavy alcohol consumption on the cardiovascular system may be mediated in part by the influence of alcohol-induced depression on the immune system

The harmful effects of heavy alcohol use are well-documented and wide-ranging. Heavy drinking may cause or exacerbate cardiovascular disorders. The author suggests that effects of heavy alcohol consumption on the cardiovascular system may be mediated in part by the influence of alcohol-induced depression on the immune system. This hypothesis is based on the following data: (1) alcohol misuse may cause or exacerbate depression; (2) depressive disorders are associated with increased incidence, morbidity, and mortality of cardiovascular disorders; (3) the immune system may mediate effects of depressive disorders on the cardiovascular system. Further studies are needed to clarify the etiopathogenesis of alcohol-related disorders and develop new treatment modalities.     

Symposium: Normal and abnormal REM sleep regulation: REM sleep in depression-an overview

Abnormalities of REM sleep, i.e. shortening of REM latency, lengthening of the duration of the first REM period and heightening of REM density, which are frequently observed in patients with a major depressive disorder (MDD), have attracted considerable interest. Initial hopes that these aberrant patterns of sleep constitute specific markers for the primary/endogenous sub-type of depression have not been fulfilled. The specificity of REM sleep disinhibition for depression in comparison with other psychopathological groups is challenged as well. Demographic variables like age and sex exert strong influences on sleep physiology and must be controlled when searching for specific markers of depressed sleep. It is still an open question whether abnormalities of sleep are state- or trait-markers of depression. Beyond baseline studies, the cholinergic REM induction test (CRIT) indicated a heightened responsitivity of the REM sleep system to cholinergic challenge in depression compared with healthy controls and other psychopathological groups, with the exception of schizophrenia. A special role for REM sleep in depression is supported by the well-known REM sleep suppressing effect of most antidepressants. The antidepressant effect of selective REM deprivation by awakenings stresses the importance of mechanisms involved in REM sleep regulation for the understanding of the pathophysiology of depressive disorders. The positive effect of total sleep deprivation on depressive mood which can be reversed by daytime naps, furthermore emphasizes relationships between sleep and depression. Experimental evidence as described above instigated several theories like the REM deprivation hypothesis, the 2-process model and the reciprocal interaction model of nonREM-REM sleep regulation to explain the deviant sleep pattern of depression. The different models will be discussed with reference to empirical data gathered in the field.     

Revisiting the Accuracy Hypothesis in Families of Young Children With Conduct Problems

Revisited the accuracy hypothesis in an examination of the relation between maternal depressive symptomatology and child conduct problems. All data were gathered as part of the pretreatment assessment in an outcome study of families with clinic-referred children with conduct problems (age 3 to 6). The mothers varied in their depressive symptomatology, from not at all symptomatic to severely symptomatic. Correlations indicated that with increasing depressive symptomatology, mothers (N = 97) displayed a higher rate of physical negative behaviors towards their child and reported more child conduct problems. Regression analyses revealed that at the lowest levels of maternal depressive symptomatology there was a discrepancy between mothers' reports of child behavior problems and child deviant behaviors observed during mother-child interaction. In contrast, at higher levels of depression, mothers' reports of child behavior were consistent with laboratory observations of their child's behavior. These findings provide evidence to support the accuracy hypothesis in reference to mothers who display a high degree of depressive symptomatology, but the results also call into question the validity of maternal report in families with children with conduct problems.