Psychological Medicine最新文献

{"title":"Adolescent resilience in the face of COVID-19 stressors: the role of trauma and protective factors.","authors":"Lu Zhang, Vanessa L Cropley, Sarah Whittle, Divyangana Rakesh","doi":"10.1017/S0033291724001806","DOIUrl":"10.1017/S0033291724001806","url":null,"abstract":"<p><strong>Background: </strong>The COVID-19 pandemic introduced unique stressors that posed significant threats to adolescent mental health. However, limited research has examined the impact of trauma exposure on vulnerability to subsequent stressor-related mental health outcomes in adolescents. Furthermore, it is unclear whether there are protective factors that promote resilience against the negative impacts of COVID-19 stressors in adolescents with prior trauma exposure. This preregistered study aimed to investigate the impact of trauma on COVID-19 stressor-related mental health difficulties in adolescents, in addition to the role of protective factors.</p><p><strong>Methods: </strong>Aims were investigated in a sample of 9696 adolescents (mean age 12.85 ± 0.88 years) from the Adolescent Brain Cognitive Development Study. Linear mixed-effects models were employed to examine (a) the associations of early trauma exposure (exposed <i>v.</i> non-exposed), COVID-19 stressors, and perceived stress, sadness, and positive affect levels during the pandemic period in the US, and (b) the role of protective factors (physical activity, parental support, and improvements in family and peer relationships) in these associations.</p><p><strong>Results: </strong>There was a positive association between COVID-19 stressors and sadness, which was enhanced in trauma-exposed adolescents. Improvements in family and peer relationships mitigated the association between COVID-19 stressors and poor mental health outcomes, regardless of prior traumatic experience.</p><p><strong>Conclusions: </strong>These findings support the hypothesis that prior trauma elevates risk of mental health difficulties in the face of future stressors. Results underscore the protective role of enhanced social relationships as targets for early prevention and intervention in those experiencing acute stressors, regardless of prior traumatic experiences.</p>","PeriodicalId":20891,"journal":{"name":"Psychological Medicine","volume":" ","pages":"1-11"},"PeriodicalIF":5.9,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11536143/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142473318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of benzodiazepine use with cognitive ability and age-related cognitive decline.","authors":"Merete Osler, Maarten Pieter Rozing, Ida Kim Wium-Andersen, Martin Balslev Jørgensen, Erik Lykke Mortensen, Gunhild Tidemann Okholm","doi":"10.1017/S0033291724002046","DOIUrl":"10.1017/S0033291724002046","url":null,"abstract":"<p><strong>Background: </strong>It remains uncertain whether long-term use of benzodiazepines is associated with age-related cognitive decline, and if cognitive ability in early life is the driver of any association. This study examines the association of cognitive ability in young adulthood with later use of benzodiazepines and explores whether the use of benzodiazepines during adult life is associated with cognitive decline in late midlife.</p><p><strong>Methods: </strong>The study samples include cognitive tests on the Børge Priens Prøve (BPP) from the conscription board examination (age 19 years) from 335 513 men born 1949-1961 and data from re-examinations of 5183 men 44 years later. Cognitive decline was defined as the difference between scores at the conscription board and the re-examination. Information on purchases of benzodiazepines was obtained from the Danish National Prescription Registry, 1995-2022. Associations were analysed using Cox proportional hazards and linear regression.</p><p><strong>Results: </strong>In total, 120 911 (36%) men purchased benzodiazepines during a follow-up of 20 years. Lower cognitive scores in young adulthood were associated with a higher risk of initiating benzodiazepines (hazard ratio [95% CI] = 0.71[0.68-0.75]). Men with the highest cumulative use of benzodiazepines had larger cognitive decline (<i>β</i>-coefficient [95% CI] = -1.66 [-2.09 to -1.23] BPP scores) compared with never users. Current benzodiazepine users showed a larger cognitive decline than never users (<i>β</i>-coefficient [95% CI] = -2.42[-3.18 to -1.66] BPP scores) and this partially explained the above association. These estimates for cognitive decline were relatively small and may lack clinical relevance.</p><p><strong>Conclusion: </strong>Low cognitive ability increases the risk of benzodiazepine use in adulthood and cognitive decline is more pronounced in those with the highest benzodiazepine use compared with never-use, but the difference lacks clinical significance.</p>","PeriodicalId":20891,"journal":{"name":"Psychological Medicine","volume":" ","pages":"1-8"},"PeriodicalIF":5.9,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11536101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142473319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impulsivity in first-degree relatives at risk of psychosis and mania: a systematic review and meta-analysis.","authors":"Jess Kerr-Gaffney, Yahufu Nuerzati, Emma I Kopra, Allan H Young","doi":"10.1017/S0033291724001752","DOIUrl":"10.1017/S0033291724001752","url":null,"abstract":"<p><p>Impulsivity is elevated in psychosis and during mania in bipolar disorder. Studies in unaffected relatives may help establish whether impulsivity is a heritable, state independent endophenotype. The aim of this systematic review and meta-analysis was to examine whether impulsivity is elevated in unaffected relatives of those with bipolar disorder, schizophrenia, and schizoaffective disorder, compared to controls. Databases were systematically searched up until March 2023 for articles reporting data on a behavioral or self-report measure of impulsivity in first-degree relatives and controls. Nineteen studies were included. Behavioral (10 studies, <i>d</i> = 0.35, <i>p</i> < 0.001) and self-reported impulsivity was significantly elevated in bipolar disorder relatives compared to controls (5 studies, <i>d</i> = 0.46, <i>p</i> < 0.001), with small effect sizes. Relatives of those with schizophrenia did not show significantly elevated impulsivity compared to controls on behavioral measures (6 studies, <i>d</i> = 0.42, <i>p</i> = 0.102). There were not enough studies to conduct a meta-analysis on self-report data in schizophrenia relatives or schizoaffective disorder relatives (self-report or behavioral). Study quality was good, however there was moderate to high heterogeneity in behavioral meta-analyses. Results suggest elevated impulsivity may be an endophenotype for bipolar disorder, present in an attenuated state before and after the illness and in at-risk individuals. This trait, amongst other behavioral and psychological indices, could be used to identify those who are at risk of developing bipolar disorder. Future research should refine measurement across studies and establish which components of impulsivity are affected in those at risk of psychotic and bipolar disorders.</p>","PeriodicalId":20891,"journal":{"name":"Psychological Medicine","volume":" ","pages":"1-9"},"PeriodicalIF":5.9,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11536112/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142473323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Longitudinal association between depressive symptoms and cognitive function: the neurological mechanism of psychological and physical disturbances on memory.","authors":"Xiangwei Dai, Sihan Liu, Xin Li, Kewei Chen, Shudan Gao, Jun Wang, Dag Aarsland, Zhuo Rachel Han, Zhanjun Zhang","doi":"10.1017/S0033291724001612","DOIUrl":"10.1017/S0033291724001612","url":null,"abstract":"<p><strong>Background: </strong>The neural correlates underlying late-life depressive symptoms and cognitive deterioration are largely unclear, and little is known about the role of chronic physical conditions in such association. This research explores both concurrent and longitudinal associations between late-life depressive symptoms and cognitive functions, with examining the neural substrate and chronic vascular diseases (CVDs) in these associations.</p><p><strong>Methods: </strong>A total of 4109 participants (mean age = 65.4, 63.0% females) were evaluated for cognitive functions through various neuropsychological assessments. Depressive symptoms were assessed by the Geriatric Depression Scale and CVDs were self-reported. T1-weighted magnetic resonance imaging (MRI), diffusion tensor imaging, and functional MRI (fMRI) data were acquired in a subsample (<i>n</i> = 791).</p><p><strong>Results: </strong>Cognitively, higher depressive symptoms were correlated with poor performance across all cognitive domains, with the strongest association with episodic memory (<i>r</i> = ‒0.138, <i>p</i> < 0.001). Regarding brain structure, depressive symptoms were negatively correlated with thalamic volume and white matter integrity. Further, white matter integrity was found to mediate the longitudinal association between depressive symptoms and episodic memory (<i>indirect effect</i> = -0.017, 95% CI -0.045 to -0.002) and this mediation was only significant for those with severe CVDs (<i>β</i> = -0.177, <i>p</i> = 0.008).</p><p><strong>Conclusions: </strong>This study is one of the first to provide neural evidence elucidating the longitudinal associations between late-life depressive symptoms and cognitive dysfunction. Additionally, the severity of CVDs strengthened these associations, which enlightens the potential of managing CVDs as an intervention target for preventing depressive symptoms-related cognitive decline.</p>","PeriodicalId":20891,"journal":{"name":"Psychological Medicine","volume":" ","pages":"1-10"},"PeriodicalIF":5.9,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11536121/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142473325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SARS-CoV-2 infection and the risk of depressive symptoms: a retrospective longitudinal study from the population-based CONSTANCES cohort.","authors":"Baptiste Pignon, Emmanuel Wiernik, Brigitte Ranque, Olivier Robineau, Fabrice Carrat, Gianluca Severi, Mathilde Touvier, Clément Gouraud, Charles Ouazana Vedrines, Victor Pitron, Nicolas Hoertel, Sofiane Kab, Sarah Tebeka, Marcel Goldberg, Marie Zins, Cédric Lemogne","doi":"10.1017/S0033291724002435","DOIUrl":"10.1017/S0033291724002435","url":null,"abstract":"<p><strong>Background: </strong>Should COVID-19 have a direct impact on the risk of depression, it would suggest specific pathways for prevention and treatment. In this retrospective population-based study, we aimed to examine the association of prior SARS-CoV-2 infection with depressive symptoms, distinguishing self-reported <i>v</i>. biologically confirmed COVID-19.</p><p><strong>Methods: </strong>32 007 participants from the SAPRIS survey nested in the French CONSTANCES cohort were included. COVID-19 was measured as followed: <i>ad hoc</i> serologic testing, self-reported PCR or serology positive test results, and self-reported COVID-19. Depressive symptoms were measured with the Center of Epidemiologic Studies-Depression Scale (CES-D). Outcomes were depressive symptoms (total CES-D score, its four dimensions, and clinically significant depressive symptoms) and exposure was prior COVID-19 (no COVID-19/self-reported unconfirmed COVID-19/biologically confirmed COVID-19).</p><p><strong>Results: </strong>In comparison to participants without COVID-19, participants with self-reported unconfirmed COVID-19 and biologically confirmed COVID-19 had higher CES-D scores (<i>β</i> for one interquartile range increase [95% CI]: 0.15 [0.08-0.22] and 0.09 [0.05-0.13], respectively) and somatic complaints dimension scores (0.15 [0.09-0.21] and 0.10 [0.07-0.13]). Only those with self-reported but unconfirmed COVID-19 had higher depressed affect dimension scores (0.08 [0.01-0.14]). Accounting for <i>ad hoc</i> serologic testing only, the CES-D score and the somatic complaints dimension were only associated with the combination of self-reported COVID-19 and negative serology test results.</p><p><strong>Conclusions: </strong>The association between COVID-19 and depressive symptoms was merely driven by somatic symptoms of depression and did not follow a gradient consistent with the hypothesis of a direct impact of SARS-CoV-2 infection on the risk of depression.</p>","PeriodicalId":20891,"journal":{"name":"Psychological Medicine","volume":" ","pages":"1-10"},"PeriodicalIF":5.9,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11578902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142473331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Patterns of abnormal activations in severe mental disorders a transdiagnostic data-driven meta-analysis of task-based fMRI studies.","authors":"Mélanie Boisvert, Jules R Dugré, Stéphane Potvin","doi":"10.1017/S003329172400165X","DOIUrl":"10.1017/S003329172400165X","url":null,"abstract":"<p><strong>Background: </strong>Studies suggest severe mental disorders (SMDs), such as schizophrenia, major depressive disorder and bipolar disorder, are associated with common alterations in brain activity, albeit with a graded level of impairment. However, discrepancies between study findings likely to results from both small sample sizes and the use of different functional magnetic resonance imaging (fMRI) tasks. To address these issues, data-driven meta-analytic approach designed to identify homogeneous brain co-activity patterns across tasks was conducted to better characterize the common and distinct alterations between these disorders.</p><p><strong>Methods: </strong>A hierarchical clustering analysis was conducted to identify groups of studies reporting similar neuroimaging results, independent of task type and psychiatric diagnosis. A traditional meta-analysis (activation likelihood estimation) was then performed within each of these groups of studies to extract their aberrant activation maps.</p><p><strong>Results: </strong>A total of 762 fMRI study contrasts were targeted, comprising 13 991 patients with SMDs. Hierarchical clustering analysis identified 5 groups of studies (meta-analytic groupings; MAGs) being characterized by distinct aberrant activation patterns across SMDs: (1) emotion processing; (2) cognitive processing; (3) motor processes, (4) reward processing, and (5) visual processing. While MAG1 was mostly commonly impaired, MAG2 was more impaired in schizophrenia, while MAG3 and MAG5 revealed no differences between disorder. MAG4 showed the strongest between-diagnoses differences, particularly in the striatum, posterior cingulate cortex, and ventromedial prefrontal cortex.</p><p><strong>Conclusions: </strong>SMDs are characterized mostly by common deficits in brain networks, although differences between disorders are also present. This study highlights the importance of studying SMDs simultaneously rather than independently.</p>","PeriodicalId":20891,"journal":{"name":"Psychological Medicine","volume":" ","pages":"1-12"},"PeriodicalIF":5.9,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11536122/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142473329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Finding the balance between lumping and splitting. A response to Martin et al.","authors":"Miriam K Forbes, Bryan Neo, Omid Mohamed Nezami, Eiko I Fried, Katherine Faure, Brier Michelsen, Maddison Twose, Mark Dras","doi":"10.1017/S0033291724002137","DOIUrl":"10.1017/S0033291724002137","url":null,"abstract":"","PeriodicalId":20891,"journal":{"name":"Psychological Medicine","volume":" ","pages":"1-2"},"PeriodicalIF":5.9,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11536098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142473322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cumulative stressor exposure predicts menstrual cycle affective changes in a transdiagnostic outpatient sample with past-month suicidal ideation.","authors":"Anisha Nagpal, Jordan C Barone, Hafsah Tauseef, Jaclyn Ross, Zach J Gray, Katja M Schmalenberger, Grant Shields, George M Slavich, Tory Eisenlohr-Moul","doi":"10.1017/S0033291724001661","DOIUrl":"10.1017/S0033291724001661","url":null,"abstract":"<p><strong>Background: </strong>Affective responses to the menstrual cycle vary widely. Some individuals experience severe symptoms like those with premenstrual dysphoric disorder, while others have minimal changes. The reasons for these differences are unclear, but prior studies suggest stressor exposure may play a role. However, research in at-risk psychiatric samples is lacking.</p><p><strong>Methods: </strong>In a large clinical sample, we conducted a prospective study of how lifetime stressors relate to degree of affective change across the cycle. 114 outpatients with past-month suicidal ideation (SI) provided daily ratings (<i>n</i> = 6187) of negative affect and SI across 1-3 menstrual cycles. Participants completed the Stress and Adversity Inventory (STRAIN), which measures different stressor exposures (i.e. interpersonal loss, physical danger) throughout the life course, including before and after menarche. Multilevel polynomial growth models tested the relationship between menstrual cycle time and symptoms, moderated by stressor exposure.</p><p><strong>Results: </strong>Greater lifetime stressor exposure predicted a more pronounced perimenstrual increase in active SI, along with marginally significant similar patterns for negative affect and passive SI. Additionally, pre-menarche stressors significantly increased the cyclicity of active SI compared to post-menarche stressors. Exposure to more interpersonal loss stressors predicted greater perimenstrual symptom change of negative affect, passive SI and active SI. Exploratory item-level analyses showed that lifetime stressors moderated a more severe perimenstrual symptom trajectory for mood swings, anger/irritability, rejection sensitivity, and interpersonal conflict.</p><p><strong>Conclusion: </strong>These findings suggest that greater lifetime stressor exposure may lead to heightened emotional reactivity to ovarian hormone fluctuations, elevating the risk of psychopathology.</p>","PeriodicalId":20891,"journal":{"name":"Psychological Medicine","volume":" ","pages":"1-12"},"PeriodicalIF":5.9,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11536118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142473320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mendelian randomization analysis of maternal coffee consumption during pregnancy on offspring neurodevelopmental difficulties in the Norwegian Mother, Father and Child Cohort Study (MoBa).","authors":"Shannon D'Urso, Robyn E Wootton, Helga Ask, Caroline Brito Nunes, Ole A Andreassen, Liang-Dar Hwang, Gunn-Helen Moen, David M Evans, Alexandra Havdahl","doi":"10.1017/S0033291724002216","DOIUrl":"10.1017/S0033291724002216","url":null,"abstract":"<p><strong>Background: </strong>Previous observational epidemiological studies have suggested that coffee consumption during pregnancy may affect fetal neurodevelopment. However, results are inconsistent and may represent correlational rather than causal relationships. The present study investigated whether maternal coffee consumption was observationally associated and causally related to offspring childhood neurodevelopmental difficulties (NDs) in the Norwegian Mother, Father and Child Cohort Study.</p><p><strong>Methods: </strong>The observational relationships between maternal/paternal coffee consumption (before and during pregnancy) and offspring NDs were assessed using linear regression analyses (<i>N</i> = 58694 mother-child duos; <i>N</i> = 22 576 father-child duos). To investigate potential causal relationships, individual-level (<i>N</i> = 46 245 mother-child duos) and two-sample Mendelian randomization (MR) analyses were conducted using genetic variants previously associated with coffee consumption as instrumental variables.</p><p><strong>Results: </strong>We observed positive associations between maternal coffee consumption and offspring difficulties with social-communication/behavioral flexibility, and inattention/hyperactive-impulsive behavior (multiple testing corrected <i>p</i> < 0.005). Paternal coffee consumption (negative control) was not observationally associated with the outcomes. After adjusting for potential confounders (smoking, alcohol, education and income), the maternal associations attenuated to the null. MR analyses suggested that increased maternal coffee consumption was causally associated with social-communication difficulties (individual-level: beta = 0.128, se = 0.043, <i>p</i> = 0.003; two-sample: beta = 0.348, se = 0.141, <i>p</i> = 0.010). However, individual-level MR analyses that modelled potential pleiotropic pathways found the effect diminished (beta = 0.088, se = 0.049, <i>p</i> = 0.071). Individual-level MR analyses yielded similar estimates (heterogeneity <i>p</i> = 0.619) for the causal effect of coffee consumption on social communication difficulties in maternal coffee consumers (beta = 0.153, se = 0.071, <i>p</i> = 0.032) and non-consumers (beta = 0.107, se = 0.134, <i>p</i> = 0.424).</p><p><strong>Conclusions: </strong>Together, our results provide little evidence for a causal effect of maternal coffee consumption on offspring NDs.</p>","PeriodicalId":20891,"journal":{"name":"Psychological Medicine","volume":" ","pages":"1-14"},"PeriodicalIF":5.9,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11496242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142392796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lagged effects of childhood depressive symptoms on adult epigenetic aging.","authors":"Laura K M Han, Moji Aghajani, Brenda W J H Penninx, William E Copeland, Karolina A Aberg, Edwin J C G van den Oord","doi":"10.1017/S0033291724001570","DOIUrl":"10.1017/S0033291724001570","url":null,"abstract":"<p><strong>Background: </strong>Cross-sectional studies have identified health risks associated with epigenetic aging. However, it is unclear whether these risks make epigenetic clocks 'tick faster' (i.e. accelerate biological aging). The current study examines concurrent and lagged within-person changes of a variety of health risks associated with epigenetic aging.</p><p><strong>Methods: </strong>Individuals from the Great Smoky Mountains Study were followed from age 9 to 35 years. DNA methylation profiles were assessed from blood, at multiple timepoints (i.e. waves) for each individual. Health risks were psychiatric, lifestyle, and adversity factors. Concurrent (<i>N</i> = 539 individuals; 1029 assessments) and lagged (<i>N</i> = 380 individuals; 760 assessments) analyses were used to determine the link between health risks and epigenetic aging.</p><p><strong>Results: </strong>Concurrent models showed that BMI (<i>r</i> = 0.15, <i>P</i>_FDR < 0.01) was significantly correlated to epigenetic aging at the subject-level but not wave-level. Lagged models demonstrated that depressive symptoms (<i>b</i> = 1.67 months per symptom, <i>P</i>_FDR = 0.02) in adolescence accelerated epigenetic aging in adulthood, also when models were fully adjusted for BMI, smoking, and cannabis and alcohol use.</p><p><strong>Conclusions: </strong>Within-persons, changes in health risks were unaccompanied by concurrent changes in epigenetic aging, suggesting that it is unlikely for risks to immediately 'accelerate' epigenetic aging. However, time lagged analyses indicated that depressive symptoms in childhood/adolescence predicted epigenetic aging in adulthood. Together, findings suggest that age-related biological embedding of depressive symptoms is not instant but provides prognostic opportunities. Repeated measurements and longer follow-up times are needed to examine stable and dynamic contributions of childhood experiences to epigenetic aging across the lifespan.</p>","PeriodicalId":20891,"journal":{"name":"Psychological Medicine","volume":" ","pages":"1-9"},"PeriodicalIF":5.9,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11496221/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142381496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}