Pub Date : 2025-02-10DOI: 10.1038/s44220-025-00392-9
Alongside mental health, the term wellbeing is often included to describe influences that bear on a person’s quality of life, such as social or economic factors, or to a person’s subjective assessment of satisfaction or fulfillment. Competing concepts have proliferated, providing an important area in which increased clarity may help refine mental health research that includes wellbeing.
{"title":"Wellbeing: more than being well","authors":"","doi":"10.1038/s44220-025-00392-9","DOIUrl":"10.1038/s44220-025-00392-9","url":null,"abstract":"Alongside mental health, the term wellbeing is often included to describe influences that bear on a person’s quality of life, such as social or economic factors, or to a person’s subjective assessment of satisfaction or fulfillment. Competing concepts have proliferated, providing an important area in which increased clarity may help refine mental health research that includes wellbeing.","PeriodicalId":74247,"journal":{"name":"Nature mental health","volume":"3 2","pages":"159-159"},"PeriodicalIF":0.0,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s44220-025-00392-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-10DOI: 10.1038/s44220-024-00381-4
Fallon R. Goodman
People with higher well-being fare better on important life outcomes from financial stability to mortality risk. Enhancing well-being is important to patients and clinicians, and changes in well-being during and after a treatment may indicate meaningful improvement. Despite strong incentives for well-being measurement, well-being remains understudied in scientific literature on the course and treatment of psychopathology. To catalyze new inquiry, this Perspective illustrates ways that assessing well-being can enhance observational and treatment studies of psychopathology and provides recommendations to address measurement challenges that researchers face when targeting well-being. This Perspective equips researchers to test critical questions concerning resilience and recovery, optimize clinical interventions and enhance population mental health. This Perspective discusses methodological and theoretical challenges for measuring well-being in clinical research and the importance of including well-being measures in clinical studies.
{"title":"Assessing well-being in clinical research and treatment","authors":"Fallon R. Goodman","doi":"10.1038/s44220-024-00381-4","DOIUrl":"10.1038/s44220-024-00381-4","url":null,"abstract":"People with higher well-being fare better on important life outcomes from financial stability to mortality risk. Enhancing well-being is important to patients and clinicians, and changes in well-being during and after a treatment may indicate meaningful improvement. Despite strong incentives for well-being measurement, well-being remains understudied in scientific literature on the course and treatment of psychopathology. To catalyze new inquiry, this Perspective illustrates ways that assessing well-being can enhance observational and treatment studies of psychopathology and provides recommendations to address measurement challenges that researchers face when targeting well-being. This Perspective equips researchers to test critical questions concerning resilience and recovery, optimize clinical interventions and enhance population mental health. This Perspective discusses methodological and theoretical challenges for measuring well-being in clinical research and the importance of including well-being measures in clinical studies.","PeriodicalId":74247,"journal":{"name":"Nature mental health","volume":"3 2","pages":"167-174"},"PeriodicalIF":0.0,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-30DOI: 10.1038/s44220-024-00382-3
Brendan E. Walsh, Jonathan Rottenberg, Robert C. Schlauch
An immense corpus of work documents deleterious effects of loneliness on physical health, cognition, psychological symptoms, and wellbeing. In this Review, we argue that the widespread assumption that loneliness is unidimensional may lead to imprecise interpretations of findings and hamper intervention efforts. We critically revisit a longstanding multidimensional loneliness framework that posits two distinct dimensions: emotional loneliness (perceived lack of intimate connections) and social loneliness (perceived deficits in social networks). We demonstrate how distinguishing loneliness dimensions may provide a clearer picture of the nature of loneliness and its correlates, risk factors and consequences. For instance, emotional loneliness appears to be a more severe typology that overlaps greatly with pathology, whereas social loneliness is more reflective of deficits in social connectedness and social support. We additionally evaluate the utility of this multidimensional framework in the domains of clinical practice and public health and provide suggestions to stimulate further research. This Review discusses the multidimensional conceptualization of loneliness and the utility of this framework for clinical practice and public health.
{"title":"Why loneliness requires a multidimensional approach: a critical narrative review","authors":"Brendan E. Walsh, Jonathan Rottenberg, Robert C. Schlauch","doi":"10.1038/s44220-024-00382-3","DOIUrl":"10.1038/s44220-024-00382-3","url":null,"abstract":"An immense corpus of work documents deleterious effects of loneliness on physical health, cognition, psychological symptoms, and wellbeing. In this Review, we argue that the widespread assumption that loneliness is unidimensional may lead to imprecise interpretations of findings and hamper intervention efforts. We critically revisit a longstanding multidimensional loneliness framework that posits two distinct dimensions: emotional loneliness (perceived lack of intimate connections) and social loneliness (perceived deficits in social networks). We demonstrate how distinguishing loneliness dimensions may provide a clearer picture of the nature of loneliness and its correlates, risk factors and consequences. For instance, emotional loneliness appears to be a more severe typology that overlaps greatly with pathology, whereas social loneliness is more reflective of deficits in social connectedness and social support. We additionally evaluate the utility of this multidimensional framework in the domains of clinical practice and public health and provide suggestions to stimulate further research. This Review discusses the multidimensional conceptualization of loneliness and the utility of this framework for clinical practice and public health.","PeriodicalId":74247,"journal":{"name":"Nature mental health","volume":"3 2","pages":"175-184"},"PeriodicalIF":0.0,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-22DOI: 10.1038/s44220-024-00378-z
Eric L. Garland
Developing a robust approach to mitigating the current opioid crisis in the USA will require translating novel evidence-based, neuroscience-informed treatments into clinical care and public policy.
{"title":"Recovering wellbeing from the diseases of despair: integrating neuroscience, evidence-based practice and policy to heal the opioid crisis","authors":"Eric L. Garland","doi":"10.1038/s44220-024-00378-z","DOIUrl":"10.1038/s44220-024-00378-z","url":null,"abstract":"Developing a robust approach to mitigating the current opioid crisis in the USA will require translating novel evidence-based, neuroscience-informed treatments into clinical care and public policy.","PeriodicalId":74247,"journal":{"name":"Nature mental health","volume":"3 2","pages":"162-163"},"PeriodicalIF":0.0,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-20DOI: 10.1038/s44220-024-00377-0
Mohammad S. E. Sendi, Zening Fu, Nathaniel G. Harnett, Sanne J. H. van Rooij, Victor Vergara, Diego A. Pizzagalli, Nikolaos P. Daskalakis, Stacey L. House, Francesca L. Beaudoin, Xinming An, Thomas C. Neylan, Gari D. Clifford, Tanja Jovanovic, Sarah D. Linnstaedt, Laura T. Germine, Kenneth A. Bollen, Scott L. Rauch, John P. Haran, Alan B. Storrow, Christopher Lewandowski, Paul I. Musey Jr., Phyllis L. Hendry, Sophia Sheikh, Christopher W. Jones, Brittany E. Punches, Robert A. Swor, Nina T. Gentile, Vishnu P. Murty, Lauren A. Hudak, Jose L. Pascual, Mark J. Seamon, Erica Harris, Anna M. Chang, Claire Pearson, David A. Peak, Roland C. Merchant, Robert M. Domeier, Niels K. Rathlev, Brian J. O’Neil, Paulina Sergot, Leon D. Sanchez, Steven E. Bruce, John F. Sheridan, Steven E. Harte, Ronald C. Kessler, Karestan C. Koenen, Samuel A. McLean, Jennifer S. Stevens, Vince D. Calhoun, Kerry J. Ressler
Post-traumatic stress (PTS) encompasses a range of psychological responses following trauma, which may lead to more severe outcomes such as post-traumatic-stress disorder (PTSD). Identifying early neuroimaging biomarkers that link brain function to PTS outcomes is critical for understanding PTSD risk. This longitudinal study examines the association between brain dynamic functional network connectivity and current/future PTS symptom severity, and the impact of sex on this relationship. By analyzing 275 participants’ dynamic functional network connectivity data obtained ~2 weeks after trauma exposure, we noted that brain dynamics of an inter-network brain state link negatively with current (r = −0.197, Pcorrected = 0.0079) and future (r = –0.176, Pcorrected = 0.0176) PTS symptom severity. In addition, dynamics of an intra-network brain state correlated with future symptom intensity (r = 0.205, Pcorrected = 0.0079). We additionally observed that the association between the network dynamics of the inter-network and intra-network brain state with symptom severity is more pronounced in the female group. Our findings highlight a potential link between brain network dynamics in the aftermath of trauma with current and future PTSD outcomes, with a stronger effect in the female group, underscoring the importance of sex differences. This multisite study detects a link between brain dynamic functional network connectivity and current and future post-traumatic stress symptom severity with a stronger effect in the female group.
{"title":"Brain dynamics reflecting an intra-network brain state are associated with increased post-traumatic stress symptoms in the early aftermath of trauma","authors":"Mohammad S. E. Sendi, Zening Fu, Nathaniel G. Harnett, Sanne J. H. van Rooij, Victor Vergara, Diego A. Pizzagalli, Nikolaos P. Daskalakis, Stacey L. House, Francesca L. Beaudoin, Xinming An, Thomas C. Neylan, Gari D. Clifford, Tanja Jovanovic, Sarah D. Linnstaedt, Laura T. Germine, Kenneth A. Bollen, Scott L. Rauch, John P. Haran, Alan B. Storrow, Christopher Lewandowski, Paul I. Musey Jr., Phyllis L. Hendry, Sophia Sheikh, Christopher W. Jones, Brittany E. Punches, Robert A. Swor, Nina T. Gentile, Vishnu P. Murty, Lauren A. Hudak, Jose L. Pascual, Mark J. Seamon, Erica Harris, Anna M. Chang, Claire Pearson, David A. Peak, Roland C. Merchant, Robert M. Domeier, Niels K. Rathlev, Brian J. O’Neil, Paulina Sergot, Leon D. Sanchez, Steven E. Bruce, John F. Sheridan, Steven E. Harte, Ronald C. Kessler, Karestan C. Koenen, Samuel A. McLean, Jennifer S. Stevens, Vince D. Calhoun, Kerry J. Ressler","doi":"10.1038/s44220-024-00377-0","DOIUrl":"10.1038/s44220-024-00377-0","url":null,"abstract":"Post-traumatic stress (PTS) encompasses a range of psychological responses following trauma, which may lead to more severe outcomes such as post-traumatic-stress disorder (PTSD). Identifying early neuroimaging biomarkers that link brain function to PTS outcomes is critical for understanding PTSD risk. This longitudinal study examines the association between brain dynamic functional network connectivity and current/future PTS symptom severity, and the impact of sex on this relationship. By analyzing 275 participants’ dynamic functional network connectivity data obtained ~2 weeks after trauma exposure, we noted that brain dynamics of an inter-network brain state link negatively with current (r = −0.197, Pcorrected = 0.0079) and future (r = –0.176, Pcorrected = 0.0176) PTS symptom severity. In addition, dynamics of an intra-network brain state correlated with future symptom intensity (r = 0.205, Pcorrected = 0.0079). We additionally observed that the association between the network dynamics of the inter-network and intra-network brain state with symptom severity is more pronounced in the female group. Our findings highlight a potential link between brain network dynamics in the aftermath of trauma with current and future PTSD outcomes, with a stronger effect in the female group, underscoring the importance of sex differences. This multisite study detects a link between brain dynamic functional network connectivity and current and future post-traumatic stress symptom severity with a stronger effect in the female group.","PeriodicalId":74247,"journal":{"name":"Nature mental health","volume":"3 2","pages":"185-198"},"PeriodicalIF":0.0,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-15DOI: 10.1038/s44220-024-00369-0
Lachlan Gilchrist, Thomas P. Spargo, Rebecca E. Green, Jonathan R. I. Coleman, David M. Howard, Jackson G. Thorp, Brett N. Adey, Jodie Lord, Helena L. Davies, Jessica Mundy, Abigail R. ter Kuile, Molly R. Davies, Christopher Hübel, Shannon Bristow, Sang Hyuck Lee, Henry Rogers, Charles Curtis, Saakshi Kakar, Chelsea M. Malouf, Gursharan Kalsi, Ryan Arathimos, Anne Corbett, Clive Ballard, Helen Brooker, Byron Creese, Dag Aarsland, Adam Hampshire, Latha Velayudhan, Thalia C. Eley, Gerome Breen, Alfredo Iacoangeli, Sulev Kõks, Cathryn M. Lewis, Petroula Proitsi
Depression is a risk factor for the later development of Alzheimer’s disease (AD), but evidence for the genetic relationship is mixed. Assessing depression symptom-specific genetic associations may better clarify this relationship. To address this, we conducted genome-wide meta-analysis (a genome-wide association study, GWAS) of the nine depression symptom items, plus their sum score, on the Patient Health Questionnaire (PHQ-9) (GWAS-equivalent N: 224,535–308,421) using data from UK Biobank, the GLAD study and PROTECT, identifying 37 genomic risk loci. Using six AD GWASs with varying proportions of clinical and proxy (family history) case ascertainment, we identified 20 significant genetic correlations with depression/depression symptoms. However, only one of these was identified with a clinical AD GWAS. Local genetic correlations were detected in 14 regions. No statistical colocalization was identified in these regions. However, the region of the transmembrane protein 106B gene (TMEM106B) showed colocalization between multiple depression phenotypes and both clinical-only and clinical + proxy AD. Mendelian randomization and polygenic risk score analyses did not yield significant results after multiple testing correction in either direction. Our findings do not demonstrate a causal role of depression/depression symptoms on AD and suggest that previous evidence of genetic overlap between depression and AD may be driven by the inclusion of family history-based proxy cases/controls. However, colocalization at TMEM106B warrants further investigation. Using genome-wide meta-analyses of clinical measures of depression and biobank data, the authors investigate symptom-specific genetic associations between depression and subsequent risk for Alzheimer’s disease, finding an absence of a putative genetic overlap between disorders.
{"title":"Depression symptom-specific genetic associations in clinically diagnosed and proxy case Alzheimer’s disease","authors":"Lachlan Gilchrist, Thomas P. Spargo, Rebecca E. Green, Jonathan R. I. Coleman, David M. Howard, Jackson G. Thorp, Brett N. Adey, Jodie Lord, Helena L. Davies, Jessica Mundy, Abigail R. ter Kuile, Molly R. Davies, Christopher Hübel, Shannon Bristow, Sang Hyuck Lee, Henry Rogers, Charles Curtis, Saakshi Kakar, Chelsea M. Malouf, Gursharan Kalsi, Ryan Arathimos, Anne Corbett, Clive Ballard, Helen Brooker, Byron Creese, Dag Aarsland, Adam Hampshire, Latha Velayudhan, Thalia C. Eley, Gerome Breen, Alfredo Iacoangeli, Sulev Kõks, Cathryn M. Lewis, Petroula Proitsi","doi":"10.1038/s44220-024-00369-0","DOIUrl":"10.1038/s44220-024-00369-0","url":null,"abstract":"Depression is a risk factor for the later development of Alzheimer’s disease (AD), but evidence for the genetic relationship is mixed. Assessing depression symptom-specific genetic associations may better clarify this relationship. To address this, we conducted genome-wide meta-analysis (a genome-wide association study, GWAS) of the nine depression symptom items, plus their sum score, on the Patient Health Questionnaire (PHQ-9) (GWAS-equivalent N: 224,535–308,421) using data from UK Biobank, the GLAD study and PROTECT, identifying 37 genomic risk loci. Using six AD GWASs with varying proportions of clinical and proxy (family history) case ascertainment, we identified 20 significant genetic correlations with depression/depression symptoms. However, only one of these was identified with a clinical AD GWAS. Local genetic correlations were detected in 14 regions. No statistical colocalization was identified in these regions. However, the region of the transmembrane protein 106B gene (TMEM106B) showed colocalization between multiple depression phenotypes and both clinical-only and clinical + proxy AD. Mendelian randomization and polygenic risk score analyses did not yield significant results after multiple testing correction in either direction. Our findings do not demonstrate a causal role of depression/depression symptoms on AD and suggest that previous evidence of genetic overlap between depression and AD may be driven by the inclusion of family history-based proxy cases/controls. However, colocalization at TMEM106B warrants further investigation. Using genome-wide meta-analyses of clinical measures of depression and biobank data, the authors investigate symptom-specific genetic associations between depression and subsequent risk for Alzheimer’s disease, finding an absence of a putative genetic overlap between disorders.","PeriodicalId":74247,"journal":{"name":"Nature mental health","volume":"3 2","pages":"212-228"},"PeriodicalIF":0.0,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s44220-024-00369-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-15DOI: 10.1038/s44220-024-00379-y
Elnaz Moghimi, N. Zoe Hilton
Engaging survivors of intimate partner violence in research brings valuable perspectives that can drive meaningful improvements in mental health services.
{"title":"Transforming women’s mental health services through co-research with survivors of intimate partner violence","authors":"Elnaz Moghimi, N. Zoe Hilton","doi":"10.1038/s44220-024-00379-y","DOIUrl":"10.1038/s44220-024-00379-y","url":null,"abstract":"Engaging survivors of intimate partner violence in research brings valuable perspectives that can drive meaningful improvements in mental health services.","PeriodicalId":74247,"journal":{"name":"Nature mental health","volume":"3 2","pages":"164-166"},"PeriodicalIF":0.0,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-15DOI: 10.1038/s44220-024-00374-3
Rebecca Cooney
We speak to Eric Garland, an endowed professor in Health Sciences at the T. Denny Sanford Institute for Empathy and Compassion, professor in the Department of Psychiatry at the University of California San Diego, director of UCSD ONEMIND (optimized neuroscience-enhanced mindfulness intervention design) and the developer of mindfulness-oriented recovery enhancement (MORE), an evidence-based mind–body therapy for addiction, emotion dysregulation and chronic pain.
{"title":"What is MORE? Enhancing recovery with mindfulness","authors":"Rebecca Cooney","doi":"10.1038/s44220-024-00374-3","DOIUrl":"10.1038/s44220-024-00374-3","url":null,"abstract":"We speak to Eric Garland, an endowed professor in Health Sciences at the T. Denny Sanford Institute for Empathy and Compassion, professor in the Department of Psychiatry at the University of California San Diego, director of UCSD ONEMIND (optimized neuroscience-enhanced mindfulness intervention design) and the developer of mindfulness-oriented recovery enhancement (MORE), an evidence-based mind–body therapy for addiction, emotion dysregulation and chronic pain.","PeriodicalId":74247,"journal":{"name":"Nature mental health","volume":"3 2","pages":"160-161"},"PeriodicalIF":0.0,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-10DOI: 10.1038/s44220-024-00383-2
Machine learning for mental health and psychiatry research has emerged as a powerful set of tools for harnessing increased computing power to analyze relationships in massive and complex datasets. These findings are ultimately poised to help inform research directions, the diagnosis and prediction of psychopathology, and clinical recommendations for treating mental health disorders.
{"title":"Machine learning in mental health — getting better all the time","authors":"","doi":"10.1038/s44220-024-00383-2","DOIUrl":"10.1038/s44220-024-00383-2","url":null,"abstract":"Machine learning for mental health and psychiatry research has emerged as a powerful set of tools for harnessing increased computing power to analyze relationships in massive and complex datasets. These findings are ultimately poised to help inform research directions, the diagnosis and prediction of psychopathology, and clinical recommendations for treating mental health disorders.","PeriodicalId":74247,"journal":{"name":"Nature mental health","volume":"3 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s44220-024-00383-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142941344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-10DOI: 10.1038/s44220-024-00354-7
Xinyang Yu, Zuo Zhang, Moritz Herle, Tobias Banaschewski, Gareth J. Barker, Arun L. W. Bokde, Herta Flor, Antoine Grigis, Hugh Garavan, Penny Gowland, Andreas Heinz, Rüdiger Brühl, Jean-Luc Martinot, Marie-Laure Paillère Martinot, Eric Artiges, Frauke Nees, Dimitri Papadopoulos Orfanos, Hervé Lemaître, Tomáš Paus, Luise Poustka, Sarah Hohmann, Nathalie Holz, Christian Bäuchl, Michael N. Smolka, Nilakshi Vaidya, Henrik Walter, Robert Whelan, Ulrike Schmidt, Gunter Schumann, Sylvane Desrivières, on behalf of the IMAGEN consortium
Unhealthy eating, a risk factor for eating disorders (EDs) and obesity, often coexists with emotional and behavioral problems; however, the underlying neurobiological mechanisms are poorly understood. Analyzing data from the longitudinal IMAGEN adolescent cohort, we investigated associations between eating behaviors, genetic predispositions for high body mass index (BMI) using polygenic scores (PGSs), and trajectories (ages 14–23 years) of ED-related psychopathology and brain maturation. Clustering analyses at age 23 years (N = 996) identified 3 eating groups: restrictive, emotional/uncontrolled and healthy eaters. BMI PGS, trajectories of ED symptoms, internalizing and externalizing problems, and brain maturation distinguished these groups. Decreasing volumes and thickness in several brain regions were less pronounced in restrictive and emotional/uncontrolled eaters. Smaller cerebellar volume reductions uniquely mediated the effects of BMI PGS on restrictive eating, whereas smaller volumetric reductions across multiple brain regions mediated the relationship between elevated externalizing problems and emotional/uncontrolled eating, independently of BMI. These findings shed light on distinct contributions of genetic risk, protracted brain maturation and behaviors in ED symptomatology. This study identifies distinct eating behavior profiles and links them to eating disorder symptoms, genetic predispositions for high body mass index and brain maturation during adolescence.
{"title":"Relationships of eating behaviors with psychopathology, brain maturation and genetic risk for obesity in an adolescent cohort study","authors":"Xinyang Yu, Zuo Zhang, Moritz Herle, Tobias Banaschewski, Gareth J. Barker, Arun L. W. Bokde, Herta Flor, Antoine Grigis, Hugh Garavan, Penny Gowland, Andreas Heinz, Rüdiger Brühl, Jean-Luc Martinot, Marie-Laure Paillère Martinot, Eric Artiges, Frauke Nees, Dimitri Papadopoulos Orfanos, Hervé Lemaître, Tomáš Paus, Luise Poustka, Sarah Hohmann, Nathalie Holz, Christian Bäuchl, Michael N. Smolka, Nilakshi Vaidya, Henrik Walter, Robert Whelan, Ulrike Schmidt, Gunter Schumann, Sylvane Desrivières, on behalf of the IMAGEN consortium","doi":"10.1038/s44220-024-00354-7","DOIUrl":"10.1038/s44220-024-00354-7","url":null,"abstract":"Unhealthy eating, a risk factor for eating disorders (EDs) and obesity, often coexists with emotional and behavioral problems; however, the underlying neurobiological mechanisms are poorly understood. Analyzing data from the longitudinal IMAGEN adolescent cohort, we investigated associations between eating behaviors, genetic predispositions for high body mass index (BMI) using polygenic scores (PGSs), and trajectories (ages 14–23 years) of ED-related psychopathology and brain maturation. Clustering analyses at age 23 years (N = 996) identified 3 eating groups: restrictive, emotional/uncontrolled and healthy eaters. BMI PGS, trajectories of ED symptoms, internalizing and externalizing problems, and brain maturation distinguished these groups. Decreasing volumes and thickness in several brain regions were less pronounced in restrictive and emotional/uncontrolled eaters. Smaller cerebellar volume reductions uniquely mediated the effects of BMI PGS on restrictive eating, whereas smaller volumetric reductions across multiple brain regions mediated the relationship between elevated externalizing problems and emotional/uncontrolled eating, independently of BMI. These findings shed light on distinct contributions of genetic risk, protracted brain maturation and behaviors in ED symptomatology. This study identifies distinct eating behavior profiles and links them to eating disorder symptoms, genetic predispositions for high body mass index and brain maturation during adolescence.","PeriodicalId":74247,"journal":{"name":"Nature mental health","volume":"3 1","pages":"58-70"},"PeriodicalIF":0.0,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s44220-024-00354-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142941331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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