Approaches for strengthening causal inference regarding prenatal risk factors for childhood behavioural and psychiatric disorders / Sarah J. LEWIS in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1095-1108 Titre : Approaches for strengthening causal inference regarding prenatal risk factors for childhood behavioural and psychiatric disorders Type de document : Texte imprimé et/ou numérique Auteurs : Sarah J. LEWIS, Auteur ; Caroline RELTON, Auteur ; Stanley ZAMMIT, Auteur ; George DAVEY SMITH, Auteur Article en page(s) : p.1095-1108 Langues : Anglais (eng) Mots-clés : Mendelian randomisation  causal inference  childhood behaviour  psychiatric disorders  instrumental variable analysis Index. décimale : PER Périodiques Résumé : Background The risk of childhood behavioural and psychiatric diseases could be substantially reduced if modifiable risk factors for these disorders were identified. The critical period for many of these exposures is likely to be in utero as this is the time when brain development is most rapid. However, due to confounding and other limitations of traditional epidemiological studies, identification of causal risk factors has proved challenging and on the whole research in this area has not been fruitful. Scope In this review, we highlight several alternative approaches including; comparisons across settings, the use of negative controls and natural experiments, which includes migration studies, studies of individuals conceived using in vitro fertilisation and not least Mendelian randomisation. We have illustrated these approaches using examples of behavioural and psychiatric disorders. Conclusion By having these approaches outlined together in one review, researchers can consider which of these methods would be most suitable for their study question. We have particularly focussed on Mendelian randomisation, as this is a relatively novel concept, in doing so, we have illustrated the concept and discused the implementation and the limitations of this approach. En ligne : http://dx.doi.org/10.1111/jcpp.12127 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Approaches for strengthening causal inference regarding prenatal risk factors for childhood behavioural and psychiatric disorders [Texte imprimé et/ou numérique] / Sarah J. LEWIS, Auteur ; Caroline RELTON, Auteur ; Stanley ZAMMIT, Auteur ; George DAVEY SMITH, Auteur . - p.1095-1108. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1095-1108 Mots-clés : Mendelian randomisation  causal inference  childhood behaviour  psychiatric disorders  instrumental variable analysis Index. décimale : PER Périodiques Résumé : Background The risk of childhood behavioural and psychiatric diseases could be substantially reduced if modifiable risk factors for these disorders were identified. The critical period for many of these exposures is likely to be in utero as this is the time when brain development is most rapid. However, due to confounding and other limitations of traditional epidemiological studies, identification of causal risk factors has proved challenging and on the whole research in this area has not been fruitful. Scope In this review, we highlight several alternative approaches including; comparisons across settings, the use of negative controls and natural experiments, which includes migration studies, studies of individuals conceived using in vitro fertilisation and not least Mendelian randomisation. We have illustrated these approaches using examples of behavioural and psychiatric disorders. Conclusion By having these approaches outlined together in one review, researchers can consider which of these methods would be most suitable for their study question. We have particularly focussed on Mendelian randomisation, as this is a relatively novel concept, in doing so, we have illustrated the concept and discused the implementation and the limitations of this approach. En ligne : http://dx.doi.org/10.1111/jcpp.12127 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Commentary: Response to commentary by Rutter on Munafo et al. (2014) / Marcus R. MUNAFO in Journal of Child Psychology and Psychiatry, 55-10 (October 2014)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 55-10 (October 2014) . - p.1105-1106 Titre : Commentary: Response to commentary by Rutter on Munafo et al. (2014) Type de document : Texte imprimé et/ou numérique Auteurs : Marcus R. MUNAFO, Auteur ; Stanley ZAMMIT, Auteur ; Jonathan FLINT, Auteur Article en page(s) : p.1105-1106 Langues : Anglais (eng) Mots-clés : Gene–environment (G×E) interactions, locus-specific  genome wide  psychiatric phenotypes Index. décimale : PER Périodiques Résumé : Rutter's commentary (Rutter, 2014) on our article (Munafò et al., 2014) provides us the opportunity to clarify some issues that he (and therefore, we suspect, others) may have misunderstood. En ligne : http://dx.doi.org/10.1111/jcpp.12308 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=239 [article] Commentary: Response to commentary by Rutter on Munafo et al. (2014) [Texte imprimé et/ou numérique] / Marcus R. MUNAFO, Auteur ; Stanley ZAMMIT, Auteur ; Jonathan FLINT, Auteur . - p.1105-1106. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 55-10 (October 2014) . - p.1105-1106 Mots-clés : Gene–environment (G×E) interactions, locus-specific  genome wide  psychiatric phenotypes Index. décimale : PER Périodiques Résumé : Rutter's commentary (Rutter, 2014) on our article (Munafò et al., 2014) provides us the opportunity to clarify some issues that he (and therefore, we suspect, others) may have misunderstood. En ligne : http://dx.doi.org/10.1111/jcpp.12308 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=239

Practitioner Review: A critical perspective on gene–environment interaction models – what impact should they have on clinical perceptions and practice? / Marcus R. MUNAFO in Journal of Child Psychology and Psychiatry, 55-10 (October 2014)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 55-10 (October 2014) . - p.1092-1101 Titre : Practitioner Review: A critical perspective on gene–environment interaction models – what impact should they have on clinical perceptions and practice? Type de document : Texte imprimé et/ou numérique Auteurs : Marcus R. MUNAFO, Auteur ; Stanley ZAMMIT, Auteur ; Jonathan FLINT, Auteur Article en page(s) : p.1092-1101 Langues : Anglais (eng) Mots-clés : Genetics  genome-wide association studies  heritability  gene × environment interaction  psychiatric disorder Index. décimale : PER Périodiques Résumé : Background Psychiatric disorders run in families, and early twin, family and adoption studies confirmed that this was due in part to shared genetic inheritance. While candidate gene studies largely failed to reliably identify genetic variants associated with psychiatric disorders, genome-wide association studies are beginning to do so. However, the proportion of phenotypic variance explained remains well below what would be expected from previous heritability estimates. Scope We review possible reasons for this ‘missing heritability’, and whether incorporating gene by environment interactions into our models will substantially improve our understanding of the aetiology of psychiatric disorders, and inform clinical perceptions and practice. Findings We discuss potential limitations of the gene by environment interaction approach. In particular, we discuss whether these are likely to be a major contributor to psychiatric disorders at the level of the specific interaction (as opposed to at an aggregate level). Conclusions Gene by environment interaction studies offered initial promise that a far greater proportion of phenotypic variance could be explained by incorporating measures of environmental exposures into genetic studies. However, in our opinion, there are few (if any) clear examples of gene by environment interactions in psychiatry, and their scope for informing either our understanding of disease pathology or clinical practice remains limited at present. En ligne : http://dx.doi.org/10.1111/jcpp.12261 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=238 [article] Practitioner Review: A critical perspective on gene–environment interaction models – what impact should they have on clinical perceptions and practice? [Texte imprimé et/ou numérique] / Marcus R. MUNAFO, Auteur ; Stanley ZAMMIT, Auteur ; Jonathan FLINT, Auteur . - p.1092-1101. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 55-10 (October 2014) . - p.1092-1101 Mots-clés : Genetics  genome-wide association studies  heritability  gene × environment interaction  psychiatric disorder Index. décimale : PER Périodiques Résumé : Background Psychiatric disorders run in families, and early twin, family and adoption studies confirmed that this was due in part to shared genetic inheritance. While candidate gene studies largely failed to reliably identify genetic variants associated with psychiatric disorders, genome-wide association studies are beginning to do so. However, the proportion of phenotypic variance explained remains well below what would be expected from previous heritability estimates. Scope We review possible reasons for this ‘missing heritability’, and whether incorporating gene by environment interactions into our models will substantially improve our understanding of the aetiology of psychiatric disorders, and inform clinical perceptions and practice. Findings We discuss potential limitations of the gene by environment interaction approach. In particular, we discuss whether these are likely to be a major contributor to psychiatric disorders at the level of the specific interaction (as opposed to at an aggregate level). Conclusions Gene by environment interaction studies offered initial promise that a far greater proportion of phenotypic variance could be explained by incorporating measures of environmental exposures into genetic studies. However, in our opinion, there are few (if any) clear examples of gene by environment interactions in psychiatry, and their scope for informing either our understanding of disease pathology or clinical practice remains limited at present. En ligne : http://dx.doi.org/10.1111/jcpp.12261 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=238

The association of serum 25-hydroxyvitamin D3 and D2 with depressive symptoms in childhood – a prospective cohort study / Anna-Maija TOLPPANEN in Journal of Child Psychology and Psychiatry, 53-7 (July 2012)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 53-7 (July 2012) . - p.757-766 Titre : The association of serum 25-hydroxyvitamin D3 and D2 with depressive symptoms in childhood – a prospective cohort study Type de document : Texte imprimé et/ou numérique Auteurs : Anna-Maija TOLPPANEN, Auteur ; Adrian SAYERS, Auteur ; William D. FRASER, Auteur ; Glyn LEWIS, Auteur ; Stanley ZAMMIT, Auteur ; Debbie A. LAWLOR, Auteur Année de publication : 2012 Article en page(s) : p.757-766 Langues : Anglais (eng) Mots-clés : 25-Hydroxyvitamin D  calcium  parathyroid hormone  child  depression  ALSPAC Index. décimale : PER Périodiques Résumé : Background:  Depression in adolescence is common and early onset predicts worse outcome in adulthood. Studies in adults have suggested a link between higher total 25-hydroxyvitamin D [25(OH)D] concentrations and lower risk of depression. Objectives:  To investigate (a) the association between serum 25(OH)D2 and 25(OH)D3 concentrations and depressive symptoms in children, and (b) whether the associations of 25(OH)D2 and 25(OH)D3 are different from, and independent of, each other. Methods:  Prospective cohort study with serum 25(OH)D2 and 25(OH)D3 concentrations measured at mean age of 9.8 years and depressive symptoms assessed with the Mood and Feelings Questionnaire by a trained interviewer at the mean ages of 10.6 years (n = 2,759) and 13.8 years (n = 2,752). Results:  Higher concentrations of 25(OH)D3 assessed at mean age 9.8 years were associated with lower levels of depressive symptoms at age 13.8 years [adjusted risk ratio (RR; 95% confidence interval (CI)): 0.90 (0.86–0.95)], but not at age 10.6 years [adjusted RR (95% CI): 0.98 (0.93–1.03)] and with increased odds of decreasing symptoms between age 10.6 and 13.8 years [adjusted RR (95% CI): 1.08 (1.01–1.16)]. Serum 25(OH)D2 concentrations were not associated with depressive symptoms. Conclusions:  This is the first study in children to suggest that the association between 25(OH)D3 concentrations and depression emerges in childhood. The association is independent of a wide range of potential confounding factors, and appears to be stronger with greater time separation between assessment of 25(OH)D3 and assessment of depressive symptoms. Confirmation of our findings in large prospective studies and trials would be valuable. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2011.02518.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=166 [article] The association of serum 25-hydroxyvitamin D3 and D2 with depressive symptoms in childhood – a prospective cohort study [Texte imprimé et/ou numérique] / Anna-Maija TOLPPANEN, Auteur ; Adrian SAYERS, Auteur ; William D. FRASER, Auteur ; Glyn LEWIS, Auteur ; Stanley ZAMMIT, Auteur ; Debbie A. LAWLOR, Auteur . - 2012 . - p.757-766. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 53-7 (July 2012) . - p.757-766 Mots-clés : 25-Hydroxyvitamin D  calcium  parathyroid hormone  child  depression  ALSPAC Index. décimale : PER Périodiques Résumé : Background:  Depression in adolescence is common and early onset predicts worse outcome in adulthood. Studies in adults have suggested a link between higher total 25-hydroxyvitamin D [25(OH)D] concentrations and lower risk of depression. Objectives:  To investigate (a) the association between serum 25(OH)D2 and 25(OH)D3 concentrations and depressive symptoms in children, and (b) whether the associations of 25(OH)D2 and 25(OH)D3 are different from, and independent of, each other. Methods:  Prospective cohort study with serum 25(OH)D2 and 25(OH)D3 concentrations measured at mean age of 9.8 years and depressive symptoms assessed with the Mood and Feelings Questionnaire by a trained interviewer at the mean ages of 10.6 years (n = 2,759) and 13.8 years (n = 2,752). Results:  Higher concentrations of 25(OH)D3 assessed at mean age 9.8 years were associated with lower levels of depressive symptoms at age 13.8 years [adjusted risk ratio (RR; 95% confidence interval (CI)): 0.90 (0.86–0.95)], but not at age 10.6 years [adjusted RR (95% CI): 0.98 (0.93–1.03)] and with increased odds of decreasing symptoms between age 10.6 and 13.8 years [adjusted RR (95% CI): 1.08 (1.01–1.16)]. Serum 25(OH)D2 concentrations were not associated with depressive symptoms. Conclusions:  This is the first study in children to suggest that the association between 25(OH)D3 concentrations and depression emerges in childhood. The association is independent of a wide range of potential confounding factors, and appears to be stronger with greater time separation between assessment of 25(OH)D3 and assessment of depressive symptoms. Confirmation of our findings in large prospective studies and trials would be valuable. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2011.02518.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=166

---

1 (1 - 4 / 4)