Medicine JournalFeeds

Patterns of remission, continuation and incidence of broadly defined eating disorders during early pregnancy in the Norwegian Mother and Child Cohort Study (MoBa) – Corrigendum.

Psychol Med. 2012 Feb 3;:1

Authors:

PMID: 22300810 [PubMed - as supplied by publisher]

Dissociable patterns of medial prefrontal and amygdala activity to face identity versus emotion in bipolar disorder.

Psychol Med. 2012 Jan 25;:1-12

Authors: Keener MT, Fournier JC, Mullin BC, Kronhaus D, Perlman SB, Labarbara E, Almeida JC, Phillips ML

Abstract

BACKGROUND: Individuals with bipolar disorder demonstrate abnormal social function. Neuroimaging studies in bipolar disorder have shown functional abnormalities in neural circuitry supporting face emotion processing, but have not examined face identity processing, a key component of social function. We aimed to elucidate functional abnormalities in neural circuitry supporting face emotion and face identity processing in bipolar disorder.MethodTwenty-seven individuals with bipolar disorder I currently euthymic and 27 healthy controls participated in an implicit face processing, block-design paradigm. Participants labeled color flashes that were superimposed on dynamically changing background faces comprising morphs either from neutral to prototypical emotion (happy, sad, angry and fearful) or from one identity to another identity depicting a neutral face. Whole-brain and amygdala region-of-interest (ROI) activities were compared between groups. RESULTS: There was no significant between-group difference looking across both emerging face emotion and identity. During processing of all emerging emotions, euthymic individuals with bipolar disorder showed significantly greater amygdala activity. During facial identity and also happy face processing, euthymic individuals with bipolar disorder showed significantly greater amygdala and medial prefrontal cortical activity compared with controls. CONCLUSIONS: This is the first study to examine neural circuitry supporting face identity and face emotion processing in bipolar disorder. Our findings of abnormally elevated activity in amygdala and medial prefrontal cortex (mPFC) during face identity and happy face emotion processing suggest functional abnormalities in key regions previously implicated in social processing. This may be of future importance toward examining the abnormal self-related processing, grandiosity and social dysfunction seen in bipolar disorder.

PMID: 22273442 [PubMed - as supplied by publisher]

Disentangling the causal inter-relationship between negative life events and depressive symptoms in women: a longitudinal twin study.

Psychol Med. 2012 Jan 25;:1-14

Authors: Wichers M, Maes HH, Jacobs N, Derom C, Thiery E, Kendler KS

Abstract

BACKGROUND: Negative life events are strongly associated with the development of depression. However, the etiologic relationship between life events and depression is complex. Evidence suggests that life events can cause depression, and depression increases the risk for life events. Additionally, third factors influencing both phenotypes may be involved. In this work we sought to disentangle these relationships using a genetically informative longitudinal design.MethodAdult female twins (n=536, including 281 twin pairs) were followed up for measurements of negative life event exposure and depressive symptoms. Four follow-ups were completed, each approximately 3 months apart. Model fitting was carried out using the Mx program. RESULTS: The best-fitting model included causal paths from life events to depressive symptoms for genetic and shared environmental risk factors, whereas paths from depressive symptoms to life events were apparent for shared environmental factors. Shared latent influence on both phenotypes was found for individual-specific effects. CONCLUSIONS: Life events and depressive symptoms have complex inter-relationships that differ across sources of variance. The results of the model, if replicated, indicate that reducing life event exposure would reduce depressive symptoms and that lowering depressive symptoms would decrease the occurrence of negative life events.

PMID: 22273464 [PubMed - as supplied by publisher]

Lifetime co-morbidity of DSM-IV disorders in the US National Comorbidity Survey Replication Adolescent Supplement (NCS-A).

Psychol Med. 2012 Jan 25;:1-14

Authors: Kessler RC, Avenevoli S, McLaughlin KA, Green JG, Lakoma MD, Petukhova M, Pine DS, Sampson NA, Zaslavsky AM, Merikangas KR

Abstract

BACKGROUND: Research on the structure of co-morbidity among common mental disorders has largely focused on current prevalence rather than on the development of co-morbidity. This report presents preliminary results of the latter type of analysis based on the US National Comorbidity Survey Replication Adolescent Supplement (NCS-A).MethodA national survey was carried out of adolescent mental disorders. DSM-IV diagnoses were based on the Composite International Diagnostic Interview (CIDI) administered to adolescents and questionnaires self-administered to parents. Factor analysis examined co-morbidity among 15 lifetime DSM-IV disorders. Discrete-time survival analysis was used to predict first onset of each disorder from information about prior history of the other 14 disorders. RESULTS: Factor analysis found four factors representing fear, distress, behavior and substance disorders. Associations of temporally primary disorders with the subsequent onset of other disorders, dated using retrospective age-of-onset (AOO) reports, were almost entirely positive. Within-class associations (e.g. distress disorders predicting subsequent onset of other distress disorders) were more consistently significant (63.2%) than between-class associations (33.0%). Strength of associations decreased as co-morbidity among disorders increased. The percentage of lifetime disorders explained (in a predictive rather than a causal sense) by temporally prior disorders was in the range 3.7-6.9% for earliest-onset disorders [specific phobia and attention deficit hyperactivity disorder (ADHD)] and much higher (23.1-64.3%) for later-onset disorders. Fear disorders were the strongest predictors of most other subsequent disorders. CONCLUSIONS: Adolescent mental disorders are highly co-morbid. The strong associations of temporally primary fear disorders with many other later-onset disorders suggest that fear disorders might be promising targets for early interventions.

PMID: 22273480 [PubMed - as supplied by publisher]

Do subthreshold psychotic experiences predict clinical outcomes in unselected non-help-seeking population-based samples? A systematic review and meta-analysis, enriched with new results.

Psychol Med. 2012 Jan 20;:1-15

Authors: Kaymaz N, Drukker M, Lieb R, Wittchen HU, Werbeloff N, Weiser M, Lataster T, van Os J

Abstract

BACKGROUND: The base rate of transition from subthreshold psychotic experiences (the exposure) to clinical psychotic disorder (the outcome) in unselected, representative and non-help-seeking population-based samples is unknown.MethodA systematic review and meta-analysis was conducted of representative, longitudinal population-based cohorts with baseline assessment of subthreshold psychotic experiences and follow-up assessment of psychotic and non-psychotic clinical outcomes. RESULTS: Six cohorts were identified with a 3-24-year follow-up of baseline subthreshold self-reported psychotic experiences. The yearly risk of conversion to a clinical psychotic outcome in exposed individuals (0.56%) was 3.5 times higher than for individuals without psychotic experiences (0.16%) and there was meta-analytic evidence of dose-response with severity/persistence of psychotic experiences. Individual studies also suggest a role for motivational impairment and social dysfunction. The evidence for conversion to non-psychotic outcome was weaker, although findings were similar in direction. CONCLUSIONS: Subthreshold self-reported psychotic experiences in epidemiological non-help-seeking samples index psychometric risk for psychotic disorder, with strong modifier effects of severity/persistence. These data can serve as the population reference for selected and variable samples of help-seeking individuals at ultra-high risk, for whom much higher transition rates have been indicated.

PMID: 22260930 [PubMed - as supplied by publisher]

Childhood maltreatment is associated with increased body mass index and increased C-reactive protein levels in first-episode psychosis patients.

Psychol Med. 2012 Jan 20;:1-9

Authors: Hepgul N, Pariante CM, Dipasquale S, Diforti M, Taylor H, Marques TR, Morgan C, Dazzan P, Murray RM, Mondelli V

Abstract

BACKGROUND: The high incidence of the metabolic syndrome in patients with psychosis is mainly attributed to antipsychotic treatment. However, it is also possible that psychological stress plays a role, inducing a chronic inflammatory process that may predispose to the development of metabolic abnormalities. We investigated the association between childhood maltreatment and inflammatory and metabolic biomarkers in subjects with first-episode psychosis and healthy controls.MethodBody mass index (BMI), weight and waist circumference were measured in 95 first-episode psychosis patients and 97 healthy controls. Inflammatory and metabolic markers were measured in a subsample of 28 patients and 45 controls. In all the subjects we collected information on childhood maltreatment and recent stressors. RESULTS: Patients with childhood maltreatment had higher BMI [25.0 (s.e.=0.6) kg/m2] and C-reactive protein (CRP) levels [1.1 (s.e.=0.6) mg/dl] when compared with healthy controls [23.4 (s.e.=0.4) kg/m2, p=0.030 and 0.2 (s.e.=0.1) mg/dl, p=0.009, respectively]. In contrast, patients without childhood maltreatment were not significantly different from healthy controls for either BMI [24.7 (s.e.=0.6) kg/m2, p=0.07] or CRP levels [0.5 (s.e.=0.2) mg/dl, p=0.25]. After controlling for the effect of BMI, the difference in CRP levels across the three groups remained significant (F2,58=3.6, p=0.035), suggesting that the increase in inflammation was not driven by an increase in adipose tissue. CONCLUSIONS: Childhood maltreatment is associated with higher BMI, and increased CRP levels, in patients with a first-episode psychosis. Further studies need to confirm the mechanisms underlying the putative causal relationship between childhood maltreatment and higher BMI, and whether this is indeed mediated by increased inflammation.

PMID: 22260948 [PubMed - as supplied by publisher]

Delinquent peer affiliation as an etiological moderator of childhood delinquency.

Psychol Med. 2012 Jan 20;:1-10

Authors: Burt SA, Klump KL

Abstract

BACKGROUND: Prior research has indicated that affiliation with delinquent peers activates genetic influences on delinquency during adolescence. However, because other studies have indicated that the socializing effects of delinquent peers vary dramatically across childhood and adolescence, it is unclear whether delinquent peer affiliation (DPA) also moderates genetic influences on delinquency during childhood.MethodThe current study sought to evaluate whether and how DPA moderated the etiology of delinquency in a sample of 726 child twins from the Michigan State University Twin Registry (MSUTR). RESULTS: The results robustly supported etiological moderation of childhood delinquency by DPA. However, this effect was observed for shared environmental, rather than genetic, influences. Shared environmental influences on delinquency were found to be several-fold larger in those with higher levels of DPA as compared to those with lower levels. This pattern of results persisted even when controlling for the overlap between delinquency and DPA. CONCLUSIONS: Our findings bolster prior work in suggesting that, during childhood, the association between DPA and delinquency is largely (although not solely) attributable to the effects of socialization as compared to selection. They also suggest that the process of etiological moderation is not specific to genetic influences. Latent environmental influences are also amenable to moderation by measured environmental factors.

PMID: 22260983 [PubMed - as supplied by publisher]

Psychological and physiological effects of caring for patients with treatment-resistant depression.

Psychol Med. 2012 Jan 17;:1-9

Authors: Rane LJ, Fekadu A, Papadopoulos AS, Wooderson SC, Poon L, Markopoulou K, Cleare AJ

Abstract

BACKGROUND: Carers of patients with psychiatric disorders show high levels of anxiety and depression, possibly mediated through disruption of the hypothalamo-pituitary-adrenal (HPA) axis. Among carers of patients with treatment-resistant depression (TRD), we set out to determine the psychological and physiological (HPA axis) consequences of caring, and the association of these consequences with long-term outcome in patients.MethodThirty-five informal carers of patients with severe TRD requiring in-patient treatment were recruited and compared with 23 controls. HPA-axis activity was assessed by measuring post-awaking salivary cortisol. The Involvement Evaluation Questionnaire (IEQ) and the General Health Questionnaire-12 (GHQ-12) were administered to measure carer burden and psychiatric caseness respectively. Independent t tests were used to compare differences between carers and controls and a linear regression model was used to determine the association of post-awakening cortisol with carer status while controlling for confounding variables. Data on long-term patient outcome (12 to 83 months), measured using the Hamilton Depression Rating Scale (HAMD), were also obtained and linear regression was used to determine the association between cortisol output in carers and remission status in patients. RESULTS: Carers experienced high carer burden and high psychiatric caseness. Carers showed reduced cortisol output after awakening, calculated as the area under the curve with respect to ground (AUCg), which remained significant after controlling for potential confounders. In a linear regression model, non-remission in patients was associated with reduced cortisol output in carers. CONCLUSIONS: Caring for patients with TRD is associated with adverse psychological and physiological changes suggesting hypocortisolism post-awakening. These changes are associated with poor patient outcome.

PMID: 22251699 [PubMed - as supplied by publisher]

A U-shaped relationship between systolic blood pressure and panic symptoms: the HUNT study.

Psychol Med. 2012 Jan 17;:1-8

Authors: Davies SJ, Bjerkeset O, Nutt DJ, Lewis G

Abstract

BACKGROUND: Previous studies on the relationship between blood pressure (BP) and psychological morbidity are conflicting. To resolve this confusing picture we examined the hypothesis that there is a non-linear relationship between panic and systolic BP (SBP) and explored the association of generalized anxiety symptoms with SBP.MethodWe used data from the population-based Nord-Trøndelag health study (HUNT) in which all 92 936 individuals aged ⩾20 years residing in one Norwegian county were invited to participate. Panic was assessed using one item from the anxiety subscale of the Hospital Anxiety and Depression Scale (HADS) and generalized anxiety with the remaining six items of this subscale. SBP was the mean of two measurements by an automatic device. RESULTS: A total of 64 871 respondents had SBP recorded (70%). Both unadjusted (n=61 408) and adjusted analyses provided evidence for a non-linear relationship between panic and SBP, represented by a U-shaped curve with a minimum prevalence of panic at around 140 mmHg. The relationship was strengthened after adjustment for confounders, with the quadratic term significantly associated with panic (p=0.03). Generalized anxiety symptoms were associated only with low SBP. CONCLUSIONS: The U-shaped relationship between SBP and panic provides a unifying explanation for the separate strands of published literature in this area. The results support the hypothesis that high BP and panic disorder could share brainstem autonomic and serotonergic abnormalities. By contrast, generalized anxiety symptoms were more common only at lower BPs, suggesting that any biological link between panic and high BP does not extend to generalized anxiety.

PMID: 22251707 [PubMed - as supplied by publisher]

Variants within the GABA transaminase (ABAT) gene region are associated with somatosensory evoked EEG potentials in families at high risk for affective disorders.

Psychol Med. 2012 Jan 9;:1-11

Authors: Wegerer M, Adena S, Pfennig A, Czamara D, Sailer U, Bettecken T, Müller-Myhsok B, Modell S, Ising M

Abstract

BACKGROUND: Depression frequently co-occurs with somatization, and somatic complaints have been reported as a vulnerability marker for affective disorders observable before disease onset. Somatization is thought to result from an increased attention to somatic sensations, which should be reflected in long-latency somatosensory evoked electroencephalogram (EEG) potentials (SSEPs) at the physiological level. Previous studies revealed that SSEPs are altered in depressed patients and suggested late SSEP components as vulnerability markers for affective disorders. Neurotransmitters such as serotonin, γ-aminobutyric acid (GABA) and the neuropeptide substance P may play an important role for both affective disorders and somatosensory processing.MethodWe investigated the associations between SSEPs and polymorphisms within candidate genes of the serotonergic, GABAergic as well as the substance P system in subjects at high risk for affective disorders. The sample was composed of high-risk families participating in the Munich Vulnerability Study and genetic association analyses were calculated using qfam (family-based association tests for quantitative traits) implemented in PLINK 1.05. RESULTS: We observed significant associations (false discovery rate <0.05) withstanding correction for multiple testing between late SSEP components (response strength 170-370 ms after stimulation) and four single nucleotide polymorphisms within the GABA transaminase (ABAT) gene region coding for a protein responsible for GABA degradation. No effects were found with the classical disease trait approach, suggesting SSEP marker specificity of the observed associations. CONCLUSIONS: Our findings point to a possible role of ABAT gene-regulated GABA catabolism for an altered processing of somatosensory stimuli as a potential vulnerability marker for affective disorders.

PMID: 22225676 [PubMed - as supplied by publisher]