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Biomedical subjects

Lydia Krabbendam

Publications and source records attributed to Lydia Krabbendam.

At least 19 recordsLinked to original sources

Attentional bias and general orienting processes in bipolar disorder.

Attentional biases for emotional stimuli and general orienting processes were examined in bipolar disorder, using a modified dot-probe task with a spatial cueing paradigm incorporated in it. Bipolar patients in a euthymic state (i.e., remission), bipolar patients in a mildly depressed state, and non-psychiatric controls participated. General orienting results showed that within the patient group as a whole, measures of depressed mood were positively associated with a relative inability to disengage attention. Attentional bias results showed that bipolar patients in a mildly depressed state, in comparison with controls, directed their attention away from depression-related words and positive words. The bias away from positive words was equally present in both patient groups and part of a trait effect, demonstrated by the comparison of patients in a euthymic state and controls. The bias away from depression-related words was mood state-dependent and within the patient group as a whole correlated negatively with measures of depressed mood. It is proposed that biases for emotional stimuli are related to the transition of mood states, characteristic for bipolar disorder.

Adult↗

The impact of subclinical psychosis on the transition from subclinicial mania to bipolar disorder.

BACKGROUND: In the general population, symptoms of mania and psychosis are more broadly distributed than their associated clinical syndromes. Little is known, however, about how these subclinical population phenotypes co-vary with and impact on each other. METHOD: In a representative population cohort of 7076 adults, prevalence of mania and psychosis symptoms and syndromes were assessed with the CIDI at baseline, at one (T1) and two years later (T2). The degree of comorbidity between subclinical mania and subclinical psychosis was examined, as well as the impact of subclinical comorbidity on social impairment and transition from subclinical mania to onset of bipolar disorder. RESULTS: The lifetime prevalence of at least one manic and one psychotic symptom was 4.1% and 4.2% respectively. Excluding individuals with any lifetime DSM-III-R bipolar or psychotic disorder (n=218), these prevalences were 2.3% (subclinical mania) and 2.8% (subclinical psychosis). Individuals with subclinical mania had a 17% risk of subclinical psychosis, compared with 2.3% in those without (P<0.000). Comorbid subclinical psychosis in individuals with subclinical mania was much more predictive of a future diagnosis of bipolar disorder (positive predictive values of 3% versus 10% respectively). CONCLUSION: Subclinical phenotypes of mania and psychosis are more prevalent than their clinical counterparts and cluster together. The risk factors for psychosis may facilitate the formation of more "toxic" combinations of subclinical mania and subclinical psychosis with a higher probability of transition to bipolar disorder. A better understanding of this pathway is crucial for the development of early interventions.

Adult↗

An experimental study of catechol-o-methyltransferase Val158Met moderation of delta-9-tetrahydrocannabinol-induced effects on psychosis and cognition.

Observational studies have suggested that psychometric psychosis liability and a functional polymorphism in the catechol-O-methyltransferase (COMT Val(158)Met) gene moderate the psychosis-inducing effect of cannabis. To replicate and extend this finding, a double-blind, placebo-controlled cross-over design was used in which patients with a psychotic disorder (n=30), relatives of patients with a psychotic disorder (n=12), and healthy controls (n=32) were exposed to Delta-9-tetrahydrocannabinol (Delta-9-THC, the principal component of cannabis) or placebo, followed by cognitive assessment and assessment of current psychotic experiences. Previous expression of psychometric psychosis liability was also assessed. Models of current psychotic experiences and cognition were examined with multilevel random regression analyses to assess (i) main effects of genotype and condition, (ii) interactions between condition and genotype, and (iii) three-way interactions between condition, genotype, and psychometric psychosis liability. Carriers of the Val allele were most sensitive to Delta-9-THC-induced psychotic experiences, but this was conditional on prior evidence of psychometric psychosis liability. Delta-9-THC impacted negatively on cognitive measures. Carriers of the Val allele were also more sensitive to Delta-9-THC-induced memory and attention impairments compared to carriers of the Met allele. Experimental effects of Delta-9-THC on cognition and psychosis are moderated by COMT Val(158)Met genotype, but the effects may in part be conditional on the additional presence of pre-existing psychosis liability. The association between cannabis and psychosis may represent higher order gene-environment and gene-gene interactions.

Adolescent↗

Associations between COMTVal158Met polymorphism and cognition: direct or indirect effects?

BACKGROUND: Previous work suggests that reaction time variability (RTV) in attentional tasks, as a measure of cognitive stability, is associated with degree of Val loading in COMT Val(158)Met genotype, and that this association may be relevant for the aetiology of schizophrenia. This study examined (i) to what degree RTV pertaining to tasks of varying cognitive complexity would be associated with increased risk for schizophrenia and (ii) to what degree this would be mediated by Val loading. METHODS: COMT genotyping was investigated in a sample of 23 patients with schizophrenia, 33 first-degree relatives, and 21 controls. All participants performed the Flanker continuous performance test. RESULTS: Schizophrenia liability was associated with number of correct trials of the Flanker test, but not with RTV, and this association was not mediated by COMT Val(158)Met genotype. Similarly, Met loading was associated with number of correct trials and with RTV, but this was not mediated by schizophrenia liability. CONCLUSIONS: Associations between COMT Val(158)Met genotype and RTV do not appear to reflect transmission of schizophrenia liability in families. Differential associations with Val and Met alleles across studies suggest indirect effects through gene-gene interactions or the influence of a functional polymorphism near COMT Val(158)Met.

Adult↗

Evidence that the urban environment specifically impacts on the psychotic but not the affective dimension of bipolar disorder.

OBJECTIVES: High rates of psychotic disorders and psychotic symptoms have been found in urban environments but reports for bipolar affective illness have been inconsistent, possibly due to failure to stratify for comorbid psychotic symptoms. It was hypothesised, therefore, that any effect of urbanicity on the bipolar phenotype would be moderated by comorbid psychotic symptoms. METHODS: In a random, representative population cohort of 7049 adults with no history of non-affective psychotic disorder, the cumulative incidence of bipolar and psychotic symptoms and syndromes, assessed with the CIDI, was examined over five levels of population density of place of residence. Similarly, the degree of comorbidity between broadly and narrowly defined bipolar phenotypes on the one hand, and the dichotomous presence of broadly (17.2%) and narrowly defined (3.8%) psychotic symptoms on the other, was examined as a function of population density of place of residence. RESULTS: The rate of bipolar disorder, however defined, was progressively higher in more urbanised areas. However, in models of bipolar phenotypes, a strong interaction between comorbid psychosis and level of urbanicity was apparent, indicating that the greater the degree of psychotic comorbidity, the greater the effect size of the urban environmental factor. For bipolar disorder without psychosis, no effect of urbanicity was apparent. CONCLUSIONS: The results suggest differential environmental causal effects on affective and cognitive dimensions of bipolar psychopathology that are nevertheless strongly comorbid within the same categorically defined disorder, possibly due to the effect of shared genetic risk factors.

Adolescent↗

Cannabis use and expression of mania in the general population.

BACKGROUND: Cannabis use is common in patients with bipolar disorder, however little is known about cannabis as a risk factor for mania. In order to investigate the association between exposure to cannabis and subsequent development of manic symptoms whilst controlling for psychotic symptoms, a longitudinal population-based study was carried out. METHODS: 4815 individuals aged 18 to 64 years were interviewed using the Composite International Diagnostic Interview at baseline, 1 year follow up and 3 year follow up, including assessment of substance use, manic symptoms and psychotic symptoms. RESULTS: Use of cannabis at baseline increased the risk for manic symptoms during follow-up (adjusted OR 2.70, 95% CI: 1.54, 4.75), adjusted for age, sex, educational level, ethnicity, single marital status, neuroticism, use of other drugs, use of alcohol, depressive symptoms and manic symptoms at baseline. The association between cannabis use and mania was independent of the prevalence and the incidence of psychotic symptoms. There was no evidence for reverse causality, as manic symptoms at baseline did not predict the onset of cannabis use during follow-up (OR = 0.35, 95% CI: 0.03, 3.49). LIMITATIONS: As 3 years is a relative short period of follow-up, long-term effects of cannabis use on mania outcomes could not be detected. CONCLUSION: The results suggest that cannabis use may affect population expression of manic symptoms (and subsequent risk to develop bipolar disorder [Regeer, E.J., Krabbendam, L., R, DE Graaf, Ten Have, M., Nolen, W.A., Van Os, J., 2006. A prospective study of the transition rates of subthreshold (hypo)mania and depression in the general population. Psychol Med, 1-9.]). These findings may not be due to the emergence of psychotic symptoms or the effects of self-medication.

Adolescent↗

Social disadvantage and schizophrenia. A combined neighbourhood and individual-level analysis.

OBJECTIVE: To study, in a geographically defined area, associations between the neighbourhood social environment and individual socioeconomic status on the one hand, and treated incidence of schizophrenia and level of subsequent service use on the other. METHOD: A combined data set of (i) patients with a case register diagnosis of schizophrenia and (ii) population controls was subjected to multilevel analyses, including neighbourhood exposures (neighbourhood socioeconomic disadvantage and social capital) and individual level confounders. Separate analyses were conducted for inpatient and outpatient psychiatric service consumption as indexed by the case register. RESULTS: Neighbourhood socioeconomic disadvantage and neighbourhood social capital did not impact on the treated incidence of schizophrenia, but quantity of inpatient service consumption was higher in neighbourhoods with higher level of social control (i.e. where it is more likely that neighbours intervene in neighbourhood-threatening situations). In addition, most indicators of lower individual socioeconomic status were associated with higher treated incidence, while treated incidence was lower when individual educational status was low. CONCLUSION: Residents of high social control neighbourhoods may seek greater levels of resolution of psychiatric disorder in patient-residents, and by consequence may induce greater levels of inpatient service consumption in patients diagnosed with schizophrenia. Individual-level indicators of social disadvantage are associated with higher risk of treated psychotic disorder, with the exception of lower educational status, which may confer a lower probability of treatment given the presence of psychotic disorder.

Adult↗

Evidence that the outcome of developmental expression of psychosis is worse for adolescents growing up in an urban environment.

BACKGROUND: The urban environment may increase the risk for psychotic disorder in interaction with pre-existing risk for psychosis, but direct confirmation has been lacking. The hypothesis was examined that the outcome of subclinical expression of psychosis during adolescence, as an indicator of psychosis-proneness, would be worse for those growing up in an urban environment, in terms of having a greater probability of psychosis persistence over a 3.5-year period. METHOD: A cohort of 918 adolescents from the Early Developmental Stages of Psychopathology Study (EDSP), aged 14-17 years (mean 15.1 years), growing up in contrasting urban and non-urban environments, completed a self-report measure of psychotic symptoms at baseline (Baseline Psychosis) and at first follow-up around 1 year post-baseline (T1). They were again interviewed by trained psychologists for the presence of psychotic symptoms at the second follow-up on average 3.5 years post-baseline (T2). RESULTS: The rate of T2 psychotic symptoms was 14.2% in those exposed to neither Baseline Psychosis nor Urbanicity, 12.1% in those exposed to Urbanicity alone, 14.9% in those exposed to Baseline Psychosis alone and 29.0% in those exposed to both Baseline Psychosis and Urbanicity. The odds ratio (OR) for the combined exposure was 2.46 [95% confidence interval (CI) 1.46-4.14], significantly greater than that expected if Urbanicity and Baseline Psychosis acted independently. CONCLUSION: These findings support the suggestion that the outcome of the developmental expression of psychosis is worse in urban environments. The environment may impact on risk for psychotic disorder by causing an abnormal persistence of a developmentally common expression of psychotic experiences.

Adolescent↗

Lower birth weight of Dutch neonates who were in utero at the time of the 9/11 attacks.

OBJECTIVE: Maternal stress during pregnancy has been reported to have an adverse influence on fetal growth. The terrorist attacks of September 11, 2001, on the United States have provoked feelings of insecurity and stress worldwide. Our aim was to test the hypothesis that maternal exposure to these acts of terrorism via the media had an unfavorable influence on mean birth weight in the Netherlands. METHODS: We compared birth weights of 1885 Dutch neonates who were in utero during the attacks with those of 1258 neonates who were in utero exactly 1 year later. RESULTS: In the exposed group, birth weight was lower than in the nonexposed group (difference, 48 g; 95% confidence interval=13.6, 82.9; P=.006). The difference in birth weight could not be explained by tobacco use, maternal age, parity, or other potential confounders or by shorter pregnancy durations. CONCLUSION: These results provide evidence supporting the hypothesis that exposure of Dutch pregnant women to the 9/11 events via the media has had an adverse effect on the birth weight of their offspring.

Birth Weight↗

Impact of psychological trauma on the development of psychotic symptoms: relationship with psychosis proneness.

BACKGROUND: The reported link between psychological trauma and onset of psychosis remains controversial. AIMS: To examine associations between self-reported psychological trauma and psychotic symptoms as a function of prior evidence of vulnerability to psychosis (psychosis proneness). METHOD: At baseline, 2524 adolescents aged 14-24 years provided self-reports on psychological trauma and psychosis proneness, and at follow-up (on average 42 months later) participants were interviewed for presence of psychotic symptoms. RESULTS: Self-reported trauma was associated with psychotic symptoms, in particular at more severe levels (adjusted OR 1.89, 95% CI1.16-3.08) and following trauma associated with intense fear, helplessness or horror. The risk difference between those with and without self-reported trauma at baseline was 7% in the group with baseline psychosis proneness, but only 1.8% in those without (adjusted test for difference between these two effect sizes: chi2=4.6, P=0.032). CONCLUSIONS: Exposure to psychological trauma may increase the risk of psychotic symptoms in people vulnerable to psychosis.

Adolescent↗

Data gathering: biased in psychosis?

This study examined whether the probabilistic reasoning bias referred to as a "jumping-to-conclusions" (JTC) style of reasoning, which, according to previous research, is associated with particular psychotic symptoms such as delusions, represents a trait that can also be detected in nonpsychotic relatives of patients with schizophrenia and in nonpsychotic individuals with a high level of psychotic experiences. Participants were, in order of level of psychosis liability, 40 patients with schizophrenia or a schizoaffective disorder, 40 first-degree nonpsychotic relatives, 41 participants from the general population with above average expression of psychotic experiences, and 53 participants from the general population with an average level of psychotic experiences. A "jumping-to-conclusions" bias was assessed using the beads task. A dose-response relationship was found in the association between level of psychosis liability and JTC (defined as needing only a single bead to complete the beads task) (odds ratio [OR] linear trend = 1.59, 95% CI: 1.13-2.24), and, independently, alinear association was apparent between JTC and level of delusional ideation (OR linear trend = 2.59, 95% CI: 1.18-5.69). In addition, the association between psychosis liability and JTC was generally much stronger as the level of delusional ideation was higher. JTC is associated with liability to psychosis (trait), in particular if the psychosis phenotype is characterized by delusional ideation (state).

Adult↗

Cognitive functioning in patients with schizophrenia and bipolar disorder: a quantitative review.

OBJECTIVE: Evidence suggests that cognitive functioning in bipolar disorder may be impaired even in euthymic states, but it is unclear if the pattern of deficits is similar to the deficits found in schizophrenia. The aim of this study was to review quantitatively the studies on cognitive performance in schizophrenia and bipolar disorder. METHODS: Articles for consideration were identified through a literature search in MEDLINE and PsycLIT in the period between 1985 and October 2004, using the keywords "schizophrenia" combined with "bipolar disorder", or "manic-depress*" or "manic" combined with "cogniti*" or "neuropsycholog*". Thirty-one studies were included that: i) evaluated cognitive performance using standardized and reliable neuropsychological testing procedures; ii) compared adult patients with schizophrenia and with bipolar disorder; iii) reported test scores of both patient groups, or exact p-values, t-values, or F-values; and iv) were published as an original article in a peer-reviewed English language journal. RESULTS: Meta-analyses of all studies indicated that patients with bipolar disorder generally perform better than patients with schizophrenia, but the distribution of effect sizes showed substantial heterogeneity. Results based on a more homogeneous subset of studies that matched patient groups on clinical and demographic characteristics pointed in the same direction, with effect sizes in the moderate range. CONCLUSIONS: Patients with bipolar disorder show better cognitive performance than patients with schizophrenia, even when matched for clinical and demographic characteristics.

Bipolar Disorder↗

Schizophrenia and urbanicity: a major environmental influence--conditional on genetic risk.

More than 10 studies have consistently shown that around one-third of all schizophrenia incidence may be related to unknown but likely unconfounded environmental factors operating in the urban environment that have an impact on developing children and adolescents to increase, relatively specifically, the later expression of psychosis-like at-risk mental states and overt psychotic disorders. The available evidence suggests that causation (urban environment causes psychosis) is more important than selection (high-risk individuals move into urban areas) and that the effect of the environmental factors in the urban environment is conditional on genetic risk (i.e., there may be gene-environment interaction). The effect associated with urbanicity has grown in more recent birth cohorts, while studies focusing on within-city contrasts have found important within-city variation in the incidence of schizophrenia associated with neighborhood social characteristics. Future approaches may focus on the complex interactions between neighborhood cognitive social capital and genetic risk as the substrate for the increased incidence of schizophrenia in the increasingly urbanized areas that children are growing up in.

Cohort Studies↗

Subtle fluctuations in psychotic phenomena as functional states of abnormal dopamine reactivity in individuals at risk.

BACKGROUND: Subjects at increased risk for psychosis experience continuous variation in the intensity of subtle psychotic experiences in response to minor stressors. It was investigated whether this psychotic reactivity in individuals at risk for psychosis is the exophenotypic expression of an underlying endophenotype characterized by a hyperreactive dopamine (DA) system. METHODS: First-degree relatives (n = 47) and control subjects (n = 49) were studied with the Experience Sampling Method (ESM), a structured diary technique assessing current context and psychopathology in daily life, to assess psychotic experiences in response to stress. A metabolic perturbation paradigm (administration of 2-deoxy-D-glucose inducing a mild state of glucoprivation) causing plasma elevation of homovanillic acid (HVA) was used as a proxy of DA reactivity. RESULTS: Multilevel regression analyses revealed that the interaction between HVA reactivity and daily stress in their effect on psychotic experiences differed according to underlying vulnerability. In the first-degree relatives, underlying HVA reactivity modified the psychotic experiences to daily stress, whereas no such effect was found in control subjects. CONCLUSIONS: These results suggest that psychotic experiences in response to minor stresses in the flow of daily life may be functional states of an underlying abnormal DA reactivity in subjects at risk to develop psychosis. The results add credence to the suggestion that abnormal DA reactivity may be part of the substrate that increases risk for psychotic symptoms in individuals at risk.

Adult↗

Familial covariation of the subclinical psychosis phenotype and verbal fluency in the general population.

OBJECTIVE: Cognitive impairments may be markers of familial transmission of liability to psychosis. This study examined to what degree the subclinical psychosis phenotype in the general population shows similar familial continuity with cognition, measured with a verbal fluency test, and whether this was similar for men and women. METHODS: Measures of the subclinical psychosis phenotype and verbal fluency were administered to a general population sample of genetically related individuals (n=425). RESULTS: In men but not women, higher levels of the subclinical psychosis phenotype were associated with worse verbal fluency performance both within and across relatives. CONCLUSION: Psychosis and verbal fluency may be more strongly linked in men than in women, and this difference is also expressed at the subclinical level of the phenotype.

Adolescent↗

Confusing thoughts and speech: source monitoring and psychosis.

To explore the idea that deficits in source monitoring may underlie positive symptoms of schizophrenia, the current study compared schizophrenic patients' performance (n=15) on an internal source-monitoring task with that of normal controls (n=15). On the basis of a source-monitoring task in which participants had to recall whether they had verbalized answers or merely thought about these answers, overall source monitoring performance, discrimination index, and response bias were calculated. In addition, participants completed cognitive tests and symptomatology questionnaires. Relative to controls, patients had significantly more difficulties with monitoring their own actions and showed a tendency towards misclassifying imagined thoughts as verbalized thoughts. Source-monitoring performance was related to selective attention, but not to other cognitive domains. No relationship was found between source-monitoring and symptomatology. Failures in internal source monitoring are a prominent feature of schizophrenia, and our results suggest that they form a more enduring characteristic of this disorder than has previously been assumed.

Adult↗

Affective processes in the onset and persistence of psychosis.

OBJECTIVES: Cognitive models suggest that beliefs and appraisal processes are crucially important in the onset and persistence of psychosis. This study investigated whether (i) neuroticism increases the risk for development of psychotic symptoms, and (ii) a delusional interpretation and/or a depressed response to hallucinatory experiences predicts the onset of psychotic disorder. METHOD: A general population sample with no lifetime evidence of any psychotic disorder was interviewed with the Composite International Diagnostic Interview Schedule (CIDI) at baseline and 1 and 3 years later. At year 3, individuals with CIDI evidence of psychotic symptoms were interviewed by clinicians to identify onset of psychotic disorder. RESULTS: Baseline level of neuroticism increases the risk for incident psychotic symptoms. Given the presence of hallucinatory experiences at baseline, the increase in risk of having the psychosis outcome was much higher in the group with delusional ideation or depressed mood at year 1 than in those without delusional ideation or depressed mood. CONCLUSION: A cognitive style characterised by a tendency to worry increases the risk for newly developed psychotic symptoms. Individuals who report hallucinatory experiences and react to these with a delusional interpretation and/or negative emotional states have an increased risk for developing clinical psychosis.

Adolescent↗

Explaining transitions over the hypothesized psychosis continuum.

OBJECTIVES: It is crucial to understand the psychological mechanisms that mediate transition from having one or two psychotic symptoms to becoming a patient with a psychotic disorder. This study investigated whether: (i) a delusional interpretation and/or a depressed response to hallucinatory experiences predicts the later onset of clinical psychotic disorder; and (ii) the presence of need for care in relation to psychotic disorder was associated with the use of particular coping strategies. METHOD: A general population sample of 4672 individuals with no lifetime evidence of any psychotic disorder were interviewed with the Composite International Diagnostic Interview Schedule (CIDI) at baseline and 1 and 3 years later. At year 3, individuals with CIDI evidence of psychotic symptoms were interviewed by clinicians to identify onset of psychotic disorder with need for care. Coping, subjective distress with and perceived control over the psychotic experience were assessed using the Maastricht Assessment of Coping Strategies (MACS). RESULTS: Given the presence of hallucinatory experiences at baseline, the increase in risk on the additive scale of having the psychosis outcome at T2 was higher in the group with delusional ideation at T1 than in those without delusional ideation at T1. Similarly, presence of depressed mood at T1 increased the risk of having the psychosis outcome at T2, but this effect overlapped partly with the risk-increasing effect of delusional ideation. Individuals with a need for care were much more likely to display symptomatic coping, whereas the presence of the other coping types was not different across the groups with and without need for care. CONCLUSION: Transitions over the psychosis continuum are, at least in part, driven by the emotional, cognitive and behavioural responses to the initial psychotic or psychosis-like experiences. Individuals who react with a delusional interpretation, negative emotional states and/or a symptomatic coping style have an increased risk for developing clinical psychosis.

Adaptation, Psychological↗