J.L. Frijling
VU University Medical Center
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Featured researches published by J.L. Frijling.
Biological Psychiatry | 2017
Mirjam van Zuiden; J.L. Frijling; L. Nawijn; Saskia B.J. Koch; J. Carel Goslings; J. S. K. Luitse; Tessa H. Biesheuvel; Adriaan Honig; Dick J. Veltman; M. Olff
BACKGROUNDnThere are currently few preventive interventions available for posttraumatic stress disorder (PTSD). Intranasal oxytocin administration early after trauma may prevent PTSD, because oxytocin administration was previously found to beneficially impact PTSD vulnerability factors, including neural fear responsiveness, peripheral stress reactivity, and socioemotional functioning. Therefore, we investigated the effects of intranasal oxytocin administration early after trauma on subsequent clinician-rated PTSD symptoms. We then assessed whether baseline characteristics moderated the interventions effects.nnnMETHODSnWe performed a multicenter, randomized, double-blind, placebo-controlled clinical trial. Adult emergency department patients with moderate to severe acute distress (n = 120; 85% accident victims) were randomized to intranasal oxytocin (8 days/40 IU twice daily) or placebo (8 days/10 puffs twice daily), initiated within 12 days posttrauma. The Clinician-Administered PTSD Scale (CAPS) was administered at baseline (within 10 days posttrauma) and at 1.5, 3, and 6 months posttrauma. The intention-to-treat sample included 107 participants (oxytocin: n = 53; placebo: n = 54).nnnRESULTSnWe did not observe a significant group difference in CAPS total score at 1.5 months posttrauma (primary outcome) or across follow-up (secondary outcome). Secondary analyses showed that participants with high baseline CAPS scores receiving oxytocin had significantly lower CAPS scores across follow-up than participants with high baseline CAPS scores receiving placebo.nnnCONCLUSIONSnOxytocin administration early after trauma did not attenuate clinician-rated PTSD symptoms in all trauma-exposed participants with acute distress. However, participants with high acute clinician-rated PTSD symptom severity did show beneficial effects of oxytocin. Although replication is warranted, these findings suggest that oxytocin administration is a promising preventive intervention for PTSD for individuals with high acute PTSD symptoms.
Journal of Neuroendocrinology | 2015
J.L. Frijling; M. van Zuiden; L. Nawijn; S.B.J. Koch; Inga D. Neumann; D.J. Veltman; M. Olff
Post‐traumatic stress disorder (PTSD) is characterised by symptoms associated with maladaptive fear and stress responses, as well as with social detachment. The neuropeptides oxytocin (OT) and arginine vasopressin (AVP) have been associated with both regulating fear and neuroendocrine stress responsiveness and social behaviour. However, there is only limited evidence for dysregulated peripheral OT and AVP levels in PTSD patients. The present study aimed to investigate basal salivary OT and AVP levels in trauma‐exposed male and female police officers with and without PTSD. Saliva samples were collected during rest and OT and AVP levels were determined using a radioimmunoassay. Men and women were analysed separately, having adjusted for differences in trauma history, and for hormonal contraception use in women. The results showed that male PTSD patients had lower basal salivary OT levels, and did not differ in AVP levels compared to male trauma‐exposed healthy controls after adjusting for childhood emotional abuse. There were no significant differences in basal salivary OT and AVP levels in women. Our findings indicate potential dysfunctioning of the OT system in male PTSD patients. Future studies are needed to replicate these findings and to further unravel the relationship between the OT and AVP systems, sex, trauma history and PTSD.
Biological Psychiatry | 2018
Mark W. Logue; Sanne J.H. van Rooij; Emily L. Dennis; Sarah L. Davis; Jasmeet P. Hayes; Jennifer S. Stevens; Maria Densmore; Courtney C. Haswell; Jonathan Ipser; Saskia Koch; Mayuresh S. Korgaonkar; Lauren A. M. Lebois; Matthew Peverill; Justin T. Baker; Premika S.W. Boedhoe; J.L. Frijling; Staci A. Gruber; Ilan Harpaz-Rotem; Neda Jahanshad; Sheri Koopowitz; Ifat Levy; L. Nawijn; Lauren O’Connor; Miranda Olff; David H. Salat; Margaret A. Sheridan; Jeffrey M. Spielberg; Mirjam van Zuiden; Sherry R. Winternitz; Jonathan Wolff
BACKGROUNDnMany studies report smaller hippocampal and amygdala volumes in posttraumatic stress disorder (PTSD), but findings have not always been consistent. Here, we present the results of a large-scale neuroimaging consortium study on PTSD conducted by the Psychiatric Genomics Consortium (PGC)-Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) PTSD Working Group.nnnMETHODSnWe analyzed neuroimaging and clinical data from 1868 subjects (794 PTSD patients) contributed by 16 cohorts, representing the largest neuroimaging study of PTSD to date. We assessed the volumes of eight subcortical structures (nucleus accumbens, amygdala, caudate, hippocampus, pallidum, putamen, thalamus, and lateral ventricle). We used a standardized image-analysis and quality-control pipeline established by the ENIGMA consortium.nnnRESULTSnIn a meta-analysis of all samples, we found significantly smaller hippocampi in subjects with current PTSD compared with trauma-exposed control subjects (Cohens dxa0=xa0-0.17, pxa0= .00054), and smaller amygdalae (dxa0=xa0-0.11, pxa0= .025), although the amygdala finding did not survive a significance level that was Bonferroni corrected for multiple subcortical region comparisons (p < .0063).nnnCONCLUSIONSnOur study is not subject to the biases of meta-analyses of published data, and it represents an important milestone in an ongoing collaborative effort to examine the neurobiological underpinnings of PTSD and the brains response to trauma.
European Neuropsychopharmacology | 2015
S.B.J. Koch; M. Van Zuiden; L. Nawijn; J.L. Frijling; D.J. Veltman; M. Olff
European Neuropsychopharmacology | 2017
M. Olff; M. Van Zuiden; L. Nawijn; S.B.J. Koch; J.L. Frijling; D.J. Veltman
European Neuropsychopharmacology | 2017
L. Nawijn; I. Krzyzewska; M. Van Zuiden; Peter Henneman; S.B.J. Koch; Adri Mul; J.L. Frijling; D.J. Veltman; Marcel Mannens; M. Olff
European Neuropsychopharmacology | 2016
L. Nawijn; M. Van Zuiden; S.B.J. Koch; J.L. Frijling; D.J. Veltman; M. Olff
European Neuropsychopharmacology | 2016
J.L. Frijling; M. Van Zuiden; L. Nawijn; S.B.J. Koch; D.J. Veltman; M. Olff
European Neuropsychopharmacology | 2015
L. Nawijn; M. Van Zuiden; S.B.J. Koch; J.L. Frijling; D.J. Veltman; M. Olff
European Neuropsychopharmacology | 2015
J.L. Frijling; M. Van Zuiden; S.B.J. Koch; L. Nawijn; D.J. Veltman; M. Olff