René S Kahn

University Medical Center Utrecht, Utrecht, Utrecht, Netherlands

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Publications (999)5312.97 Total impact

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    ABSTRACT: Individual variation in structural brain network topology has been associated with heritable behavioral phenotypes such as intelligence and schizophrenia, making it a candidate endophenotype. However, little is known about the genetic influences on individual variation in structural brain network topology. Moreover, the extent to which structural brain network topology overlaps with heritability for integrity and volume of white matter remains unknown. In this study, structural network topology was examined using diffusion tensor imaging at 3T. Binary connections between 82 structurally defined brain regions per subject were traced, allowing for estimation of individual topological network properties. Heritability of normalized characteristic path length (λ), normalized clustering coefficient (γ), microstructural integrity (FA), and volume of the white matter were estimated using a twin design, including 156 adult twins from the newly acquired U-TWIN cohort. Both γ and λ were estimated to be under substantial genetic influence. The heritability of γ was estimated to be 68%, the heritability estimate for λ was estimated to be 57%. Genetic influences on network measures were found to be partly overlapping with volumetric and microstructural properties of white matter, but the largest component of genetic variance was unique to both network traits. Normalized clustering coefficient and normalized characteristic path length are substantially heritable, and influenced by independent genetic factors that are largely unique to network measures, but partly also implicated in white matter directionality and volume. Thus, network measures provide information about genetic influence on brain structure, independent of global white matter characteristics such as volume and microstructural directionality. Hum Brain Mapp, 2014. © 2014 Wiley Periodicals, Inc.
    Human Brain Mapping 10/2014; 35(10). DOI:10.1002/hbm.22550 · 6.92 Impact Factor
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    ABSTRACT: AimOlfactory identification deficits (OIDs) are seen in schizophrenia patients and individuals at increased risk for psychosis but its pathophysiology remains unclear. Although dopaminergic imbalance is known to lie at the core of schizophrenia symptomatology, its role in the development of OIDs has not been elucidated yet. This study investigated the association between OIDs and symptoms of parkinsonism as a derivative of dopaminergic functioning.Methods In 320 patients diagnosed with non-affective psychosis, olfactory identification performance was assessed by means of the Sniffin' Sticks task. Level of parkinsonian symptoms was assessed by means of the Unified Parkinson's Disease Rating Scale (UPDRS-III). By means of multiple linear regression with bootstrapping, the association between UPDRS and Sniffin' Sticks score was investigated while correcting for potential confounders. A Bonferroni corrected P-value of 0.007 was used.ResultsHigher UPDRS scores significantly predicted worse olfactory identification in patients with non-affective psychosis with an unadjusted b = −0.07 (95% CI −0.10 to −0.04) and an adjusted b = −0.04 (95% CI −0.07 to −0.01).Conclusion Results provide preliminary evidence that the same vulnerability may underlie the development of parkinsonism and OIDs in patients with non-affective psychosis. Further investigation should evaluate the clinical value of OIDs as a marker of dopaminergic vulnerability that may predict psychosis.
    Early Intervention in Psychiatry 10/2014; DOI:10.1111/eip.12183 · 1.74 Impact Factor
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    ABSTRACT: Schizophrenia patients and their parents have an increased risk of immune disorders compared to population controls and their parents. This may be explained by genetic overlap in the pathogenesis of both types of disorders. The purpose of this study was to investigate the genetic overlap between schizophrenia and three immune disorders and to compare with the overlap between schizophrenia and two disorders not primarily characterized by immune dysregulation: bipolar disorder and type 2 diabetes.
    Schizophrenia Research 09/2014; 159(2-3). DOI:10.1016/j.schres.2014.09.004 · 4.43 Impact Factor
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    ABSTRACT: Background Accumulating evidence suggests that several adult mental disorders, particularly psychoses, are preceded by impairments in cognitive function, reflected in scholastic underachievement. This study investigates the association between scholastic underachievement and general mental health problems in adolescence, using delay in school progression as a marker of poor scholastic performance.Method Cross-sectional secondary school survey comprising 10,803 adolescents. Participants completed the Strengths and Difficulties Questionnaire (SDQ) to assess mental health problems. The association of delayed school progression with the SDQ was investigated using logistic regression with SDQ as outcome and delayed school progression as primary exposure of interest while adjusting for socio-demographic characteristics, adverse life events, school-related factors, risk taking behaviour, healthy lifestyle and physical health.ResultsUnadjusted analysis showed an association between delayed school progression and total mental health problems (OR 1.83, 95% CI 1.27 ¿ 2.63) in adolescents. After adjusting for other risk factors (socio-demographic factors and life events) in a logistic regression model the association between delayed school progression en mental health problems was attenuated (OR 1.33, 95% CI 0.86 ¿ 2.05).Conclusion Delayed school progression is associated with general mental health problems in adolescence, but this relationship is heavily confounded by other factors. A causal relationship between impaired cognitive function such as poor scholastic performance and general mental health at adolescence is less likely and delayed school progression may merely be considered an indicator of risk for mental health problems.
    BMC Psychiatry 09/2014; 14(1):244. DOI:10.1186/s12888-014-0244-5 · 2.24 Impact Factor
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    ABSTRACT: The European First Episode Schizophrenia Trial (EUFEST) included first-episode schizophrenia patients, assessing the efficacy of five antipsychotic drugs (haloperidol, amisulpride, olanzapine, quetiapine and ziprasidone) over one year. Baseline frequency of extrapyramidal symptoms (EPS) in this group of patients (n=490) was as follows: parkinsonism 10.8%, akathisia 10.0%, dystonia 1.8%, and dyskinesia 0.6%. The frequency of parkinsonism at baseline was greater in patients with a brief prior exposure to antipsychotics (≤2 weeks) compared with antipsychotic-naïve ones, and was positively correlated with the intensity of negative symptoms and negatively with depressive symptoms. After one month of treatment, the increase of parkinsonism was highest in patients receiving haloperidol (+13%), that of akathisia in patients treated with ziprasidone (+14%), and 10.1% of the patients were taking anticholinergic drugs, most frequently in the haloperidol group (24%). In 291 patients remaining on treatment after one year, both parkinsonism and akathisia had decreased: the frequency of parkinsonism was 3%, highest in the haloperidol group (9.1%), that of akathisia was 3%, highest in the quetiapine group (7.5%), and 4% of patients were taking anticholinergic drugs, most frequently those receiving haloperidol (10.5%). The results obtained suggest that in first-episode schizophrenia patients during the first year of antipsychotic treatment (in this case amisulpride, haloperidol in low doses, olanzapine, quetiapine and ziprasidone), EPS present as manageable clinical problems.
    European Neuropsychopharmacology 09/2014; 24(9). DOI:10.1016/j.euroneuro.2014.07.001 · 5.40 Impact Factor
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    ABSTRACT: During adolescence, functional and structural changes in the brain facilitate the transition from childhood to adulthood. Because the cortex and the striatum mature at different rates, temporary imbalances in the frontostriatal network occur. Here, we investigate the development of the subcortical and cortical components of the frontostriatal network from early adolescence to early adulthood in 60 subjects in a cross-sectional design, using functional MRI and a stop-signal task measuring two forms of inhibitory control: reactive inhibition (outright stopping) and proactive inhibition (anticipation of stopping). During development, reactive inhibition improved: older subjects were faster in reactive inhibition. In the brain, this was paralleled by an increase in motor cortex suppression. The level of proactive inhibition increased, with older subjects slowing down responding more than younger subjects when anticipating a stop-signal. Activation increased in the right striatum, right ventral and dorsal inferior frontal gyrus, and supplementary motor area. Moreover, functional connectivity during proactive inhibition increased between striatum and frontal regions with age. In conclusion, we demonstrate that developmental improvements in proactive inhibition are paralleled by increases in activation and functional connectivity of the frontostriatal network. These data serve as a stepping stone to investigate abnormal development of the frontostriatal network in disorders such as schizophrenia and attention-deficit hyperactivity disorder. Hum Brain Mapp, 2014. © 2014 Wiley Periodicals, Inc.
    Human Brain Mapping 09/2014; 35(9). DOI:10.1002/hbm.22483 · 6.92 Impact Factor
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    ABSTRACT: Background Even though traumatic stress is a major risk factor for depression, most people do not develop a depression. The effects of stress may particularly emerge after repeated exposure in vulnerable individuals. Therefore, we hypothesized that (1) increased exposure to stress across the life span is associated with an increased depression risk and (2) this effect is the most pronounced in individuals with high levels of neuroticism.Methods We investigated the effect of childhood maltreatment, major life events, daily hassles, and a composite index thereof (cumulative stress index) on depressive symptoms and major depressive disorder (MDD) including the possible moderating role of neuroticism in a discovery sample from the general population (N = 563) and an independent replication sample from the Netherlands Study of Depression and Anxiety (N = 2,274).ResultsAll stress domains were independently associated with depressive symptoms in the discovery sample. In the replication sample, we confirmed these findings for childhood maltreatment and daily hassles but not for major life events with depressive symptoms as outcome. Nevertheless, all stress domains significantly contributed to the presence of MDD in the replication sample. The cumulative stress index was significantly associated with depression in the discovery (β = 1.42, P < .001) and replication sample (β = 3.79, P < .001), especially in those individuals with high levels of trait neuroticism (discovery: β = 0.013, P < .001; replication: β = 0.367, P < .001).Conclusions This is the first study to show that cumulative stress exposure across different stress domains contributes to depressive symptoms and MDD in adulthood. Moreover, we show that increased exposure to stress across the life span has more impact on vulnerable individuals with high levels of trait neuroticism.
    Depression and Anxiety 09/2014; 31(9). DOI:10.1002/da.22262 · 4.29 Impact Factor
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    ABSTRACT: Background Shortening the duration of untreated psychosis (DUP) – with the aim of improving the prognosis of psychotic disorders – requires an understanding of the causes of treatment delay. Current findings concerning several candidate risk factors of a longer DUP are inconsistent. Our aim was to identify factors contributing to DUP in a large sample that represents the treated prevalence of non-affective psychotic disorders. Method Patients with a non-affective psychotic disorder were recruited from mental health care institutes from 2004 to 2008. Of the 1120 patients enrolled, 852 could be included in the present analysis. Examined candidate factors were gender, educational level, migration status, premorbid adjustment and age at onset of the psychotic disorder. DUP was divided into five ordinal categories: less than one month, one month to three months, three months to six months, six months to twelve months and twelve months and over. An ordinal logistic regression analysis was used to identify the risk factors of a longer DUP. Results Median DUP was less than one month (IQR 2). The factors migration status (p = 0.028), age at onset of the psychotic disorder (p = 0.003) and gender (p = 0.034) were significantly associated with DUP in our analysis. Conclusion First generation immigrant patients, patients with an early onset of their psychotic disorder and male patients seem at risk of a longer DUP. These findings can assist in designing specific interventions to shorten treatment delay.
    Schizophrenia Research 09/2014; 158(s 1–3):76–81. · 4.43 Impact Factor
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    ABSTRACT: Background / Purpose: The ability to rapidly interrupt one programmed action in favour of another is a critical aspect of flexible behaviour. Non-human primate studies have made significant contributions to understanding how reactive adjustments to an ongoing motor plan are instantiated in the brain using the oculomotor countermanding and search-step tasks. These tasks require the subject to make a speeded eye movement to a visual target. On an infrequent number of trials, a second signal is presented that instructs the subject to rapidly alter the motor plan by either inhibiting or both inhibiting and redirecting a response. Performance on this task has been modeled as a race between competing STOP and GO processes. Neurophysiology studies of countermanding performance show that frontal eye fields (FEF) and superior colliculus (SC) play a direct role in the control of gaze. Although the role of the striatum in reactive inhibition has not been explored in primate studies, it is in a position to inhibit movement-related activity in FEF and SC. Despite the rich neurophysiology literature, there is little known about the network involved in reactive saccade control in humans. Functional MRI studies investigating manual response inhibition in humans have highlighted a role of the inferior frontal cortex and medial frontal cortex (MFC). However, primate studies indicate that MFC, including supplementary eye fields (SEF), does not have a direct role in the control of gaze; rather, it is involved in response monitoring. In the current study, we investigated reactive control of gaze in human subjects using fMRI. The goals of the study were twofold: 1) to better compare mechanisms of reactive control of action in humans to non-human primates by investigating the oculomotor system; 2) to explore the role of the striatum in the reactive control of gaze. Main conclusion: Greater activation was observed in a cortical and subcortical oculomotor network, including FEF, SC, and the caudate nucleus of the striatum. Greater activation in the caudate and visual cortex predicted faster inhibition ability. Greater activation was also observed in SEF; however, this activation was in a separate, more anterior region of SEF than that activated by no-step trials. Further, activation in SEF was associated with larger error saccade amplitude on noncompensated trials. These data lend new evidence for a role of the striatum in reactive saccade control and further clarify the role of MFC in action inhibition and performance monitoring. These results and their strong links with primate neurophysiology, have implications for understanding mechanisms of the abnormal control of action that characterize several neuropsychiatric disorders.
    20th Annual Meeting of the Organization for Human Brain Mapping (OHBM) 2014; 08/2014
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    ABSTRACT: Cognitive abilities are related to (changes in) brain structure during adolescence and adulthood. Previous studies suggest that associations between cortical thickness and intelligence may be different at different ages. As both intelligence and cortical thickness are heritable traits, the question arises whether the association between cortical thickness development and intelligence is due to genes influencing both traits. We study this association in a longitudinal sample of young twins. Intelligence was assessed by standard IQ tests at age 9 in 224 twins, 190 of whom also underwent structural magnetic resonance imaging (MRI). Three years later at age 12, 177/125 twins returned for a follow-up measurement of intelligence/MRI scanning, respectively. We investigated whether cortical thickness was associated with intelligence and if so, whether this association was driven by genes. At age 9, there were no associations between cortical thickness and intelligence. At age 12, a negative relationship emerged. This association was mainly driven by verbal intelligence, and manifested itself most prominently in the left hemisphere. Cortical thickness and intelligence were explained by the same genes. As a post hoc analysis, we tested whether a specific allele (rs6265; Val66Met in the BDNF gene) contributed to this association. Met carriers showed lower intelligence and a thicker cortex, but only the association between the BDNF genotype and cortical thickness in the left superior parietal gyrus reached significance. In conclusion, it seems that brain areas contributing to (verbal) intellectual performance are specializing under the influence of genes around the onset of puberty.
    Human Brain Mapping 08/2014; DOI:10.1002/hbm.22435 · 6.92 Impact Factor
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    Schizophrenia Research 08/2014; 157(1-3):321. DOI:10.1016/j.schres.2014.06.006 · 4.43 Impact Factor
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    ABSTRACT: Post-traumatic stress disorder (PTSD) is an anxiety disorder that is associated with structural and functional alterations in several brain areas, including the anterior cingulate cortex (ACC). Here, we examine resting state functional connectivity of ACC subdivisions in PTSD, using a seed-based approach. Resting state magnetic resonance images were obtained from male veterans with (n = 31) and without (n = 25) PTSD, and healthy male civilian controls (n = 25). Veterans with and without PTSD (combat controls) had reduced functional connectivity compared to healthy controls between the caudal ACC and the precentral gyrus, and between the perigenual ACC and the superior medial gyrus and middle temporal gyrus. Combat controls had increased connectivity between the rostral ACC and precentral/middle frontal gyrus compared to PTSD patients and healthy civilian controls. The resting state functional connectivity differences in the perigenual ACC network reported here indicate that veterans differ from healthy controls, potentially due to military training, deployment, and/or trauma exposure. In addition, specific alterations in the combat controls may potentially be related to resilience. These results underline the importance of distinguishing trauma-exposed (combat) controls from healthy civilian controls when studying PTSD. Hum Brain Mapp, 2014. © 2014 Wiley Periodicals, Inc.
    Human Brain Mapping 08/2014; 36(1). DOI:10.1002/hbm.22615 · 6.92 Impact Factor
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    ABSTRACT: Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genome-wide association studies. Here we report a multi-stage schizophrenia genome-wide association study of up to 36,989 cases and 113,075 controls. We identify 128 independent associations spanning 108 conservatively defined loci that meet genome-wide significance, 83 of which have not been previously reported. Associations were enriched among genes expressed in brain, providing biological plausibility for the findings. Many findings have the potential to provide entirely new insights into aetiology, but associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses. Independent of genes expressed in brain, associations were enriched among genes expressed in tissues that have important roles in immunity, providing support for the speculated link between the immune system and schizophrenia.
    Nature 07/2014; 511(7510):421-427. DOI:10.1038/nature13595 · 42.35 Impact Factor
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    R S Kahn · I E Sommer
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    ABSTRACT: It is evident that once psychosis is present in patients with schizophrenia, the underlying biological process of the illness has already been ongoing for many years. At the time of diagnosis, patients with schizophrenia show decreased mean intracranial volume (ICV) as compared with healthy subjects. Since ICV is driven by brain growth, which reaches its maximum size at approximately 13 years of age, this finding suggests that brain development in patients with schizophrenia is stunted before that age. The smaller brain volume is expressed as decrements in both grey and white matter. After diagnosis, it is mainly the grey matter loss that progresses over time whereas white matter deficits are stable or may even improve over the course of the illness. To understand the possible causes of the brain changes in the first phase of schizophrenia, evidence from treatment studies, postmortem and neuroimaging investigations together with animal experiments needs to be incorporated. These data suggest that the pathophysiology of schizophrenia is multifactorial. Increased striatal dopamine synthesis is already evident before the time of diagnosis, starting during the at-risk mental state, and increases during the onset of frank psychosis. Cognitive impairment and negative symptoms may, in turn, result from other abnormalities, such as NMDA receptor hypofunction and low-grade inflammation of the brain. The latter two dysfunctions probably antedate increased dopamine synthesis by many years, reflecting the much earlier presence of cognitive and social dysfunction. Although correction of the hyperdopaminergic state with antipsychotic agents is generally effective in patients with a first-episode psychosis, the effects of treatments to correct NMDA receptor hypofunction or low-grade inflammation are (so far) rather modest at best. Improved efficacy of these interventions can be expected when they are applied at the onset of cognitive and social dysfunction, rather than at the onset of psychosis.Molecular Psychiatry advance online publication, 22 July 2014; doi:10.1038/mp.2014.66.
    Molecular Psychiatry 07/2014; 20(1). DOI:10.1038/mp.2014.66 · 15.15 Impact Factor
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    ABSTRACT: Background. Post-traumatic stress disorder (PTSD) is thought to be characterized by general heightened amygdala activation. However, this hypothesis is mainly based on specific studies presenting fear or trauma-related stimuli, hence, a thorough investigation of trauma-unrelated emotional processing in PTSD is needed. Methods. In this study, 31 male medication-naive veterans with PTSD, 28 male control veterans (combat controls; CC) and 25 non-military men (healthy controls; HC) were included. Participants underwent functional MRI while trauma-unrelated neutral, negative and positive emotional pictures were presented. In addition to the group analyses, PTSD patients with and without major depressive disorder (MDD) were compared. Results. All groups showed an increased amygdala response to negative and positive contrasts, but amygdala activation did not differ between groups. However, a heightened dorsal anterior cingulate cortex (dACC) response for negative contrasts was observed in PTSD patients compared to HC. The medial superior frontal gyrus was deactivated in the negative contrast in HC, but not in veterans. PTSD+MDD patients showed decreased subgenual ACC (sgACC) activation to all pictures compared to PTSD-MDD. Conclusion. Our findings do not support the hypothesis that increased amygdala activation in PTSD generalizes to trauma-unrelated emotional processing. Instead, the increased dACC response found in PTSD patients implicates an attentional bias that extends to trauma-unrelated negative stimuli. Only HC showed decreased medial superior frontal gyrus activation. Finally, decreased sgACC activation was related to MDD status within the PTSD group.
    Psychological Medicine 07/2014; DOI:10.1017/S0033291714001706 · 5.43 Impact Factor
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    ABSTRACT: Genetic polymorphisms can shape the global landscape of DNA methylation, by either changing substrates for DNA methyltransferases or altering the DNA binding affinity of cis-regulatory proteins. The interactions between CpG methylation and genetic polymorphisms have been previously investigated by methylation quantitative trait loci (mQTL) and allele-specific methylation (ASM) analysis. However, it remains unclear whether these approaches can effectively and comprehensively identify all genetic variants that contribute to the inter-individual variation of DNA methylation levels. Here we used three independent approaches to systematically investigate the influence of genetic polymorphisms on variability in DNA methylation by characterizing the methylation state of 96 whole blood samples in 52 parent-child trios from 22 nuclear pedigrees. We performed targeted bisulfite sequencing with padlock probes to quantify the absolute DNA methylation levels at a set of 411,800 CpG sites in the human genome. With mid-parent offspring analysis (MPO), we identified 10,593 CpG sites that exhibited heritable methylation patterns, among which 70.1% were SNPs directly present in methylated CpG dinucleotides. We determined the mQTL analysis identified 49.9% of heritable CpG sites for which regulation occurred in a distal cis-regulatory manner, and that ASM analysis was only able to identify 5%. Finally, we identified hundreds of clusters in the human genome for which the degree of variation of CpG methylation, as opposed to whether or not CpG sites were methylated, was associated with genetic polymorphisms, supporting a recent hypothesis on the genetic influence of phenotypic plasticity. These results show that cis-regulatory SNPs identified by mQTL do not comprise the full extent of heritable CpG methylation, and that ASM appears overall unreliable. Overall, the extent of genome-methylome interactions is well beyond what is detectible with the commonly used mQTL and ASM approaches, and is likely to include effects on plasticity.
    PLoS ONE 07/2014; 9(7):e99313. DOI:10.1371/journal.pone.0099313 · 3.23 Impact Factor
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    Iris E Sommer · René S Kahn
    The Lancet Psychiatry 07/2014; 1(2):111. DOI:10.1016/S2215-0366(14)70288-3

Publication Stats

31k Citations
5,312.97 Total Impact Points

Institutions

  • 1996–2015
    • University Medical Center Utrecht
      • • Department of Psychiatry
      • • Department of Child and Adolescent Psychiatry
      Utrecht, Utrecht, Netherlands
    • Nathan Kline Institute
      Orangeburg, New York, United States
  • 1982–2014
    • Universiteit Utrecht
      • • Department of Psychiatry
      • • Rudolf Magnus Institute
      Utrecht, Utrecht, Netherlands
  • 2013
    • Tergooiziekenhuizen
      Blarikum, North Holland, Netherlands
  • 2003–2012
    • Netherlands Institute for Neuroscience
      Amsterdamo, North Holland, Netherlands
    • Erasmus Universiteit Rotterdam
      Rotterdam, South Holland, Netherlands
    • University of North Carolina at Chapel Hill
      • Department of Psychiatry
      North Carolina, United States
    • Netherlands Institute for Space Research, Utrecht
      Utrecht, Utrecht, Netherlands
  • 2011
    • Academisch Medisch Centrum Universiteit van Amsterdam
      • Department of Psychiatry
      Amsterdam, North Holland, Netherlands
  • 2010
    • VU University Amsterdam
      Amsterdamo, North Holland, Netherlands
    • Canisius-Wilhelmina Ziekenhuis
      Nymegen, Gelderland, Netherlands
  • 2002–2010
    • University of Groningen
      • • Department of Psychiatry
      • • Department of Internal Medicine
      Groningen, Groningen, Netherlands
  • 2009
    • University of Cape Town
      • Department of Human Biology
      Cape Town, Province of the Western Cape, South Africa
    • Duke University
      Durham, North Carolina, United States
  • 2008
    • University of Barcelona
      Barcino, Catalonia, Spain
  • 2007
    • University of Amsterdam
      Amsterdamo, North Holland, Netherlands
  • 2004
    • Vincent van Gogh voor Geestelijke Gezondheidszorg
      Venraai, Limburg, Netherlands
  • 2001
    • Maastricht University
      Maestricht, Limburg, Netherlands
  • 1998
    • Université Victor Segalen Bordeaux 2
      Burdeos, Aquitaine, France
  • 1991–1994
    • Icahn School of Medicine at Mount Sinai
      • Department of Psychiatry
      Borough of Manhattan, New York, United States
    • Mount Sinai Medical Center
      New York City, New York, United States
    • Mount Sinai Hospital
      New York, New York, United States
    • Minneapolis Veterans Affairs Hospital
      Minneapolis, Minnesota, United States
  • 1984–1992
    • Albert Einstein College of Medicine
      • Department of Psychiatry & Behavioral Sciences
      New York City, New York, United States
  • 1990
    • Montefiore Medical Center
      New York, New York, United States