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7. Sense of coherence and psychological well-being; improvement with age

Author

Nilsson, K.W., Leppert, J., Simonsson, B., and Starrin, B.

Subjects
Quality of life -- Psychological aspects, Quality of life -- Health aspects, Quality of life -- Research, Quality of life -- Demographic aspects, Mental health -- Demographic aspects, Mental health -- Research, Health, Social sciences
Published
2010

9. Maltreatment, the oxytocin receptor gene, and conduct problems among male and female teenagers

Author

Andreou, D. Comasco, E. Åslund, C. Nilsson, K.W. Hodgins, S.

Abstract

The oxytocin receptor gene (OXTR) influences human behavior. The G allele of OXTR rs53576 has been associated with both prosocial and maladaptive behaviors but few studies have taken account of environmental factors. The present study determined whether the association of childhood maltreatment with conduct problems was modified by OXTR rs53576 genotypes. In a general population sample of 1591 teenagers, conduct problems as well as maltreatment were measured by self-report. DNA was extracted from saliva samples. In males, there was a significant positive association between maltreatment and conduct problems independent of the genotype. In females, among G allele carriers, the level of conduct problems was significantly higher among those who had been maltreated as compared to those not maltreated. By contrast, among female AA carriers, conduct problems did not vary between those who were, and who were not, maltreated. The results indicate that OXTR rs53576 plays a role in antisocial behavior in females such that the G allele confers vulnerability for antisocial behavior if they experience maltreatment, whereas the A allele has a protective effect. © 2018 Andreou, Comasco, Åslund, Nilsson and Hodgins.

Published
2018

10. Collaborative meta-Analysis finds no evidence of a strong interaction between stress and 5-HTTLPR genotype contributing to the development of depression

Author

Culverhouse, R.C. Saccone, N.L. Horton, A.C. Ma, Y. Anstey, K.J. Banaschewski, T. Burmeister, M. Cohen-Woods, S. Etain, B. Fisher, H.L. Goldman, N. Guillaume, S. Horwood, J. Juhasz, G. Lester, K.J. Mandelli, L. Middeldorp, C.M. Olié, E. Villafuerte, S. Air, T.M. Araya, R. Bowes, L. Burns, R. Byrne, E.M. Coffey, C. Coventry, W.L. Gawronski, K.A.B. Glei, D. Hatzimanolis, A. Hottenga, J.-J. Jaussent, I. Jawahar, C. Jennen-Steinmetz, C. Kramer, J.R. Lajnef, M. Little, K. Zu Schwabedissen, H.M. Nauck, M. Nederhof, E. Petschner, P. Peyrot, W.J. Schwahn, C. Sinnamon, G. Stacey, D. Tian, Y. Toben, C. Van Der Auwera, S. Wainwright, N. Wang, J.-C. Willemsen, G. Anderson, I.M. Arolt, V. Aslund, C. Bagdy, G. Baune, B.T. Bellivier, F. Boomsma, D.I. Courtet, P. Dannlowski, U. De Geus, E.J.C. Deakin, J.F.W. Easteal, S. Eley, T. Fergusson, D.M. Goate, A.M. Gonda, X. Grabe, H.J. Holzman, C. Johnson, E.O. Kennedy, M. Laucht, M. Martin, N.G. Munafò, M.R. Nilsson, K.W. Oldehinkel, A.J. Olsson, C.A. Ormel, J. Otte, C. Patton, G.C. Penninx, B.W.J.H. Ritchie, K. Sarchiapone, M. Scheid, J.M. Serretti, A. Smit, J.H. Stefanis, N.C. Surtees, P.G. Völzke, H. Weinstein, M. Whooley, M. Nurnberger, J.I., Jr. Breslau, N. Bierut, L.J.

Abstract

The hypothesis that the S allele of the 5-HTTLPR serotonin transporter promoter region is associated with increased risk of depression, but only in individuals exposed to stressful situations, has generated much interest, research and controversy since first proposed in 2003. Multiple meta-Analyses combining results from heterogeneous analyses have not settled the issue. To determine the magnitude of the interaction and the conditions under which it might be observed, we performed new analyses on 31 data sets containing 38 802 European ancestry subjects genotyped for 5-HTTLPR and assessed for depression and childhood maltreatment or other stressful life events, and meta-Analysed the results. Analyses targeted two stressors (narrow, broad) and two depression outcomes (current, lifetime). All groups that published on this topic prior to the initiation of our study and met the assessment and sample size criteria were invited to participate. Additional groups, identified by consortium members or self-identified in response to our protocol (published prior to the start of analysis) with qualifying unpublished data, were also invited to participate. A uniform data analysis script implementing the protocol was executed by each of the consortium members. Our findings do not support the interaction hypothesis. We found no subgroups or variable definitions for which an interaction between stress and 5-HTTLPR genotype was statistically significant. In contrast, our findings for the main effects of life stressors (strong risk factor) and 5-HTTLPR genotype (no impact on risk) are strikingly consistent across our contributing studies, the original study reporting the interaction and subsequent meta-Analyses. Our conclusion is that if an interaction exists in which the S allele of 5-HTTLPR increases risk of depression only in stressed individuals, then it is not broadly generalisable, but must be of modest effect size and only observable in limited situations. © 2018 Macmillan Publishers Limited, part of Springer Nature. All rights reserved.

Published
2018

11. Collaborative meta-analysis finds no evidence of a strong interaction between stress and 5-HTTLPR genotype contributing to the development of depression

Author

Culverhouse, R C, Saccone, N.L., Horton, A C, Ma, Y, Anstey, K J, Banaschewski, T., Burmeister, M., Cohen-Woods, Sarah, Etain, B., Fisher, H L, Goldman, N, Guillaume, S, Horwood, J., Juhasz, G, Lester, K J, Mandelli, L, Middeldorp, C M, Olié, E, Villafuerte, S., Air, T M, Araya, R., Bowes, L, Burns, M.R., Byrne, Enda M, Coffey, J.C., Coventry, W.L., Gawronski, K A B, Glei, D, Hatzimanolis, A, Hottenga, J-J, Jaussent, I, Jawahar, C, Jennen-Steinmetz, C, Kramer, J R, Lajnef, M, Little, K, Meyer zu Schwabedissen, H., Nauck, M., Nederhof, E., Petschner, P, Peyrot, Wouter J, Schwahn, C, Sinnamon, G, Stacey, D., Tian, Y, Toben, C, Van der Auwera, Sandra, Wainwright, N.W., Wang, J-C, Willemsen, G, Anderson, I M, Arolt, V., Åslund, C, Bagdy, G, Baune, Bernard T, Bellivier, F., Boomsma, D I, Courtet, P, Dannlowski, Udo, de Geus, E J C, Deakin, J F W, Easteal, S, Eley, T.C., Fergusson, D.M., Goate, A.M., Gonda, X, Grabe, Hans J, Holzman, C, Johnson, E.O., Kennedy, D.M., Laucht, M, Martin, Nicholas G, Munafò, Marcus R, Nilsson, K.W., Oldehinkel, Albertine J, Olsson, C A, Ormel, J., Otte, C., Patton, G C, Penninx, B W J H, Ritchie, K, Sarchiapone, M., Scheid, J M, Serretti, A, Smit, J H, Stefanis, N C, Surtees, P G, Völzke, H., Weinstein, M, Whooley, M.A., Nurnberger, J.I., Breslau, N., Bierut, L.J., Culverhouse, R C, Saccone, N.L., Horton, A C, Ma, Y, Anstey, K J, Banaschewski, T., Burmeister, M., Cohen-Woods, Sarah, Etain, B., Fisher, H L, Goldman, N, Guillaume, S, Horwood, J., Juhasz, G, Lester, K J, Mandelli, L, Middeldorp, C M, Olié, E, Villafuerte, S., Air, T M, Araya, R., Bowes, L, Burns, M.R., Byrne, Enda M, Coffey, J.C., Coventry, W.L., Gawronski, K A B, Glei, D, Hatzimanolis, A, Hottenga, J-J, Jaussent, I, Jawahar, C, Jennen-Steinmetz, C, Kramer, J R, Lajnef, M, Little, K, Meyer zu Schwabedissen, H., Nauck, M., Nederhof, E., Petschner, P, Peyrot, Wouter J, Schwahn, C, Sinnamon, G, Stacey, D., Tian, Y, Toben, C, Van der Auwera, Sandra, Wainwright, N.W., Wang, J-C, Willemsen, G, Anderson, I M, Arolt, V., Åslund, C, Bagdy, G, Baune, Bernard T, Bellivier, F., Boomsma, D I, Courtet, P, Dannlowski, Udo, de Geus, E J C, Deakin, J F W, Easteal, S, Eley, T.C., Fergusson, D.M., Goate, A.M., Gonda, X, Grabe, Hans J, Holzman, C, Johnson, E.O., Kennedy, D.M., Laucht, M, Martin, Nicholas G, Munafò, Marcus R, Nilsson, K.W., Oldehinkel, Albertine J, Olsson, C A, Ormel, J., Otte, C., Patton, G C, Penninx, B W J H, Ritchie, K, Sarchiapone, M., Scheid, J M, Serretti, A, Smit, J H, Stefanis, N C, Surtees, P G, Völzke, H., Weinstein, M, Whooley, M.A., Nurnberger, J.I., Breslau, N., and Bierut, L.J.

Abstract

The hypothesis that the S allele of the 5-HTTLPR serotonin transporter promoter region is associated with increased risk of depression, but only in individuals exposed to stressful situations, has generated much interest, research and controversy since first proposed in 2003. Multiple meta-analyses combining results from heterogeneous analyses have not settled the issue. To determine the magnitude of the interaction and the conditions under which it might be observed, we performed new analyses on 31 data sets containing 38 802 European ancestry subjects genotyped for 5-HTTLPR and assessed for depression and childhood maltreatment or other stressful life events, and meta-analysed the results. Analyses targeted two stressors (narrow, broad) and two depression outcomes (current, lifetime). All groups that published on this topic prior to the initiation of our study and met the assessment and sample size criteria were invited to participate. Additional groups, identified by consortium members or self-identified in response to our protocol (published prior to the start of analysis) with qualifying unpublished data, were also invited to participate. A uniform data analysis script implementing the protocol was executed by each of the consortium members. Our findings do not support the interaction hypothesis. We found no subgroups or variable definitions for which an interaction between stress and 5-HTTLPR genotype was statistically significant. In contrast, our findings for the main effects of life stressors (strong risk factor) and 5-HTTLPR genotype (no impact on risk) are strikingly consistent across our contributing studies, the original study reporting the interaction and subsequent meta-analyses. Our conclusion is that if an interaction exists in which the S allele of 5-HTTLPR increases risk of depression only in stressed individuals, then it is not broadly generalisable, but must be of modest effect size and only observable in limited situations.Molecular Psychiat

Published
2018
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13. Adolescent alcohol consumption: Biomarkers PEth and FAEE in relation to interview and questionnaire data

Author

Comasco, E., Nordquist, N., Leppert, J., Oreland, L., Kronstrand, Robert, Alling, C., Nilsson, K.W., Comasco, E., Nordquist, N., Leppert, J., Oreland, L., Kronstrand, Robert, Alling, C., and Nilsson, K.W.

Abstract

Objective: The aim of this study was to investigate the congruence of biomarkers, questionnaires, and interviews as instruments to assess adolescent alcohol consumption. Method: The methodology used was a cross-sectional study with a randomized sample. Four different methods were used to estimate high adolescent alcohol consumption. The concordance of the results was investigated. Surveys were performed, and biological specimens were collected at all schools in the county of Västmanland, Sweden, in 2001. Eighty-one boys and 119 girls from a population of 16- and 19-year-old adolescents were randomly selected from quartiles of volunteers representing various degrees of psychosocial risk behaviors. Using a questionnaire (for a 1-hour session) and in-depth interviews, subjects were assessed regarding their alcohol-use habits. Blood and hair samples were analyzed for phosphatidylethanol (PEth) and fatty acid ethyl esters (FAEEs), respectively. Results: High alcohol consumption was underreported in the questionnaire compared with the interviews. PEth and FAEE analyses weakly confirmed the self-reports, and the results of the two biochemical tests did not overlap. The PEth blood test was the most specific but the least sensitive, whereas the FAEE hair test revealed low specificity and an overrepresentation of positive results in girls. Conclusions: The expected higher self-report of high alcohol consumption by interview rather than by questionnaire was confirmed partly because of the infl uence of a bogus pipeline procedure. The absence of overlap between PEth and FAEE results and their poor agreement with self-reports suggested that biomarkers are unsuitable as screening tools for alcohol consumption in adolescents.

Published
2009

16. Collaborative meta-analysis finds no evidence of a strong interaction between stress and 5-HTTLPR genotype contributing to the development of depression

Author

Lucy Bowes, Richard Burns, Alex Hatzimanolis, Gonneke Willemsen, Martin A. Kennedy, Kathryn J. Lester, Katerina A.B. Gawronski, Udo Dannlowski, Alison Goate, Carolyn Coffey, Matthias Nauck, David Stacey, Ricardo Araya, Frank Bellivier, Cecilia Åslund, Catherine Toben, Catharine Jawahar, Karen Ritchie, Emilie Olié, Gyorgy Bagdy, Nicholas G. Martin, Robert Culverhouse, Isabelle Jaussent, Peter Petschner, Eric O. Johnson, Nancy L. Saccone, Sandra Villafuerte, Mohamed Lajnef, John I. Nurnberger, Volker Arolt, Laura Mandelli, Philippe Courtet, Henry Völzke, Yinjiao Ma, Craig A. Olsson, Y. Tian, Bernhard T. Baune, Keriann Little, Wouter J. Peyrot, Nicholas W.J. Wainwright, Helen L. Fisher, Brenda W.J.H. Penninx, Manfred Laucht, E.J.C. de Geus, Jan Smit, Sébastien Guillaume, J. M. Scheid, S Van der Auwera, Christian Schwahn, Hans-Jörgen Grabe, Kent W. Nilsson, Xenia Gonda, Dana A. Glei, Gabriella Juhasz, Bruno Etain, C. Holzman, Maxine Weinstein, Thalia C. Eley, Kaarin J. Anstey, Marco Sarchiapone, John Francis William Deakin, Naomi Breslau, P. G. Surtees, John Kramer, J-J Hottenga, Enda M. Byrne, Marcus R. Munafò, Christine Jennen-Steinmetz, Laura J. Bierut, Albertine J. Oldehinkel, Noreen Goldman, Dorret I. Boomsma, Simon Easteal, Margit Burmeister, John Horwood, George C Patton, Tobias Banaschewski, David M. Fergusson, Amy C. Horton, Mary A. Whooley, J. C. Wang, Esther Nederhof, H. M. Zu Schwabedissen, Grant C.B. Sinnamon, Christian Otte, Sarah Cohen-Woods, Ian M. Anderson, William L. Coventry, Tracy Air, Christel M. Middeldorp, Nicholas C. Stefanis, Alessandro Serretti, Johan Ormel, Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Biological Psychology, Amsterdam Neuroscience - Mood, Anxiety, Psychosis, Stress & Sleep, APH - Personalized Medicine, APH - Health Behaviors & Chronic Diseases, APH - Mental Health, APH - Methodology, roussel, pascale, Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Variabilité de réponse aux Psychotropes (VariaPsy - U1144), Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Montpellier (UM), Neuropsychiatrie : recherche épidémiologique et clinique (PSNREC), Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Département de psychiatrie adulte, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Hôpital La Colombière, Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Fondation FondaMental [Créteil], Hopital Saint-Louis [AP-HP] (AP-HP), Culverhouse, R.C., Saccone, N.L., Horton, A.C., Ma, Y., Anstey, K.J., Banaschewski, T., Burmeister, M., Cohen-Woods, S., Etain, B., Fisher, H.L., Goldman, N., Guillaume, S., Horwood, J., Juhasz, G., Lester, K.J., Mandelli, L., Middeldorp, C.M., Olié, E., Villafuerte, S., Air, T.M., Araya, R., Bowes, L., Burns, R., Byrne, E.M., Coffey, C., Coventry, W.L., Gawronski, K.A.B., Glei, D., Hatzimanolis, A., Hottenga, J.-J., Jaussent, I., Jawahar, C., Jennen-Steinmetz, C., Kramer, J.R., Lajnef, M., Little, K., Zu Schwabedissen, H.M., Nauck, M., Nederhof, E., Petschner, P., Peyrot, W.J., Schwahn, C., Sinnamon, G., Stacey, D., Tian, Y., Toben, C., Van Der Auwera, S., Wainwright, N., Wang, J.-C., Willemsen, G., Anderson, I.M., Arolt, V., Aslund, C., Bagdy, G., Baune, B.T., Bellivier, F., Boomsma, D.I., Courtet, P., Dannlowski, U., De Geus, E.J.C., Deakin, J.F.W., Easteal, S., Eley, T., Fergusson, D.M., Goate, A.M., Gonda, X., Grabe, H.J., Holzman, C., Johnson, E.O., Kennedy, M., Laucht, M., Martin, N.G., Munafò, M.R., Nilsson, K.W., Oldehinkel, A.J., Olsson, C.A., Ormel, J., Otte, C., Patton, G.C., Penninx, B.W.J.H., Ritchie, K., Sarchiapone, M., Scheid, J.M., Serretti, A., Smit, J.H., Stefanis, N.C., Surtees, P.G., Völzke, H., Weinstein, M., Whooley, M., Nurnberger, J.I., Breslau, N., Bierut, L.J., Université Montpellier 1 (UM1)-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM), Département d'Etudes des Combustibles (DEC), CEA-Direction des Energies (ex-Direction de l'Energie Nucléaire) (CEA-DES (ex-DEN)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Medical Faculty [Mannheim], Universität Heidelberg [Heidelberg], Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-IFR10, China Jiliang University (CJLU), Psychiatry, and APH - Digital Health

Subjects
DISORDER, Netherlands Twin Register (NTR), SAMPLE, [SDV]Life Sciences [q-bio], Brain and Behaviour, 0302 clinical medicine, Cooperative Behavior, Gene–environment interaction, Depression (differential diagnoses), Serotonin Plasma Membrane Transport Proteins, RISK, Depression, Tobacco and Alcohol, Interaction hypothesis, Life Change Event, Justice and Strong Institutions, 3. Good health, [SDV] Life Sciences [q-bio], ENVIRONMENT INTERACTION, Psychiatry and Mental health, Meta-analysis, Psychology, Serotonin Plasma Membrane Transport Protein, Molecular Biology, Cellular and Molecular Neuroscience, Psychiatry and Mental Health, Human, Clinical psychology, SDG 16 - Peace, LIFE EVENTS, Genotype, POLYMORPHISM 5-HTTLPR, Stress, Article, CHILDHOOD MALTREATMENT, Life Change Events, 03 medical and health sciences, Journal Article, Humans, Genetic Predisposition to Disease, Risk factor, Depressive Disorder, SEROTONIN TRANSPORTER GENE, Stressor, SDG 16 - Peace, Justice and Strong Institutions, MAJOR DEPRESSION, 030227 psychiatry, 5-HTTLPR, Behavioral medicine, COHORT PROFILE, Psychological, Gene-Environment Interaction, Stress, Psychological, 030217 neurology & neurosurgery
Abstract

The hypothesis that the S allele of the 5-HTTLPR serotonin transporter promoter region is associated with increased risk of depression, but only in individuals exposed to stressful situations, has generated much interest, research and controversy since first proposed in 2003. Multiple meta-analyses combining results from heterogeneous analyses have not settled the issue. To determine the magnitude of the interaction and the conditions under which it might be observed, we performed new analyses on 31 data sets containing 38 802 European ancestry subjects genotyped for 5-HTTLPR and assessed for depression and childhood maltreatment or other stressful life events, and meta-analysed the results. Analyses targeted two stressors (narrow, broad) and two depression outcomes (current, lifetime). All groups that published on this topic prior to the initiation of our study and met the assessment and sample size criteria were invited to participate. Additional groups, identified by consortium members or self-identified in response to our protocol (published prior to the start of analysis) with qualifying unpublished data, were also invited to participate. A uniform data analysis script implementing the protocol was executed by each of the consortium members. Our findings do not support the interaction hypothesis. We found no subgroups or variable definitions for which an interaction between stress and 5-HTTLPR genotype was statistically significant. In contrast, our findings for the main effects of life stressors (strong risk factor) and 5-HTTLPR genotype (no impact on risk) are strikingly consistent across our contributing studies, the original study reporting the interaction and subsequent meta-analyses. Our conclusion is that if an interaction exists in which the S allele of 5-HTTLPR increases risk of depression only in stressed individuals, then it is not broadly generalisable, but must be of modest effect size and only observable in limited situations.Molecular Psychiatry advance online publication, 4 April 2017; doi:10.1038/mp.2017.44.

Published
2018
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