首页 > 最新文献

Psychosomatic Medicine最新文献

英文 中文
Parental Preconception Posttraumatic Stress Symptoms and Maternal Prenatal Inflammation Prospectively Predict Shorter Telomere Length in Children. 父母孕前创伤后应激症状和母亲产前炎症可前瞻性地预测儿童端粒长度的缩短。
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2024-06-01 Epub Date: 2023-08-21 DOI: 10.1097/PSY.0000000000001241
Gabrielle R Rinne, Judith E Carroll, Christine M Guardino, Madeleine U Shalowitz, Sharon Landesman Ramey, Christine Dunkel Schetter

Objective: Parental trauma exposure and trauma-related distress can increase the risk of adverse health outcomes in offspring, but the pathways implicated in intergenerational transmission are not fully explicated. Accelerated biological aging may be one mechanism underlying less favorable health in trauma-exposed individuals and their offspring. This study examines the associations of preconception maternal and paternal posttraumatic stress disorder (PTSD) symptoms with child telomere length, and maternal prenatal C-reactive protein (CRP) as a biological mechanism.

Methods: Mothers ( n = 127) and a subset of the fathers ( n = 84) reported on PTSD symptoms before conception. Mothers provided blood spots in the second and third trimesters that were assayed for CRP. At age 4 years, children provided buccal cells for measurement of telomere length. Models adjusted for parental age, socioeconomic status, maternal prepregnancy body mass index, child biological sex, and child age.

Results: Mothers' PTSD symptoms were significantly associated with shorter child telomere length ( β = -0.22, SE = 0.10, p = .023). Fathers' PTSD symptoms were also inversely associated with child telomere length ( β = -0.21, SE = 0.11), although nonsignificant ( p = .065). There was no significant indirect effect of mothers' PTSD symptoms on child telomere length through CRP in pregnancy, but higher second-trimester CRP was significantly associated with shorter child telomere length ( β = -0.35, SE = 0.18, p = .048).

Conclusions: Maternal symptoms of PTSD before conception and second-trimester inflammation were associated with shorter telomere length in offspring in early childhood, independent of covariates. Findings indicate that intergenerational transmission of parental trauma may occur in part through accelerated biological aging processes and provide further evidence that prenatal proinflammatory processes program child telomere length.Open Science Framework Preregistration:https://osf.io/7c2d5/?view_only=cd0fb81f48db4b8f9c59fc8bb7b0ef97 .

目的:父母遭受创伤和与创伤相关的痛苦会增加后代出现不良健康后果的风险,但代际传播的途径尚未完全阐明。加速生物衰老可能是创伤暴露者及其后代健康状况较差的一个潜在机制。本研究探讨了孕前母亲和父亲创伤后应激障碍(PTSD)症状与儿童端粒长度的关系,以及作为生物机制的母亲产前C反应蛋白(CRP):母亲(n = 127)和一部分父亲(n = 84)报告了受孕前的创伤后应激障碍症状。母亲在怀孕的第二和第三个月提供血样,对血样进行 CRP 检测。4岁时,儿童提供口腔细胞以测量端粒长度。模型调整了父母年龄、社会经济地位、母亲孕前体重指数、儿童生理性别和儿童年龄:结果:母亲的创伤后应激障碍症状与较短的儿童端粒长度显著相关(β = -0.22, SE = 0.10, p = .023)。父亲的创伤后应激障碍症状也与儿童端粒长度成反比(β = -0.21,SE = 0.11),但不显著(p = 0.065)。母亲的创伤后应激障碍症状通过孕期CRP对儿童端粒长度没有明显的间接影响,但孕期后三个月较高的CRP与较短的儿童端粒长度显著相关(β = -0.35, SE = 0.18, p = .048):结论:母体在受孕前的创伤后应激障碍症状和孕期后三个月的炎症与幼儿期后代端粒长度的缩短有关,这与协变量无关。研究结果表明,父母创伤的代际传递可能部分是通过加速生物衰老过程发生的,并进一步证明了产前促炎症过程对儿童端粒长度的影响。开放科学框架预注册:https://osf.io/7c2d5/?view_only=cd0fb81f48db4b8f9c59fc8bb7b0ef97.
{"title":"Parental Preconception Posttraumatic Stress Symptoms and Maternal Prenatal Inflammation Prospectively Predict Shorter Telomere Length in Children.","authors":"Gabrielle R Rinne, Judith E Carroll, Christine M Guardino, Madeleine U Shalowitz, Sharon Landesman Ramey, Christine Dunkel Schetter","doi":"10.1097/PSY.0000000000001241","DOIUrl":"10.1097/PSY.0000000000001241","url":null,"abstract":"<p><strong>Objective: </strong>Parental trauma exposure and trauma-related distress can increase the risk of adverse health outcomes in offspring, but the pathways implicated in intergenerational transmission are not fully explicated. Accelerated biological aging may be one mechanism underlying less favorable health in trauma-exposed individuals and their offspring. This study examines the associations of preconception maternal and paternal posttraumatic stress disorder (PTSD) symptoms with child telomere length, and maternal prenatal C-reactive protein (CRP) as a biological mechanism.</p><p><strong>Methods: </strong>Mothers ( n = 127) and a subset of the fathers ( n = 84) reported on PTSD symptoms before conception. Mothers provided blood spots in the second and third trimesters that were assayed for CRP. At age 4 years, children provided buccal cells for measurement of telomere length. Models adjusted for parental age, socioeconomic status, maternal prepregnancy body mass index, child biological sex, and child age.</p><p><strong>Results: </strong>Mothers' PTSD symptoms were significantly associated with shorter child telomere length ( β = -0.22, SE = 0.10, p = .023). Fathers' PTSD symptoms were also inversely associated with child telomere length ( β = -0.21, SE = 0.11), although nonsignificant ( p = .065). There was no significant indirect effect of mothers' PTSD symptoms on child telomere length through CRP in pregnancy, but higher second-trimester CRP was significantly associated with shorter child telomere length ( β = -0.35, SE = 0.18, p = .048).</p><p><strong>Conclusions: </strong>Maternal symptoms of PTSD before conception and second-trimester inflammation were associated with shorter telomere length in offspring in early childhood, independent of covariates. Findings indicate that intergenerational transmission of parental trauma may occur in part through accelerated biological aging processes and provide further evidence that prenatal proinflammatory processes program child telomere length.Open Science Framework Preregistration:https://osf.io/7c2d5/?view_only=cd0fb81f48db4b8f9c59fc8bb7b0ef97 .</p>","PeriodicalId":20918,"journal":{"name":"Psychosomatic Medicine","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10879462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10024146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Chronic Social and Psychological Stress Impact Select Neuropathologies in the PS19 Mouse Model of Tauopathy. 慢性社会和心理压力影响选择神经病PS19小鼠tau病模型。
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2024-06-01 Epub Date: 2023-10-03 DOI: 10.1097/PSY.0000000000001256
Carey E Lyons, Sara I Graves, Maria Razzoli, Karthik Jeganathan, Rachel P Mansk, Seth McGonigle, Nivedita Sabarinathan, Jan M van Deursen, Darren J Baker, Alessandro Bartolomucci

Objective: Despite advances toward understanding the etiology of Alzheimer's disease (AD), it remains unclear which aspects of this disease are affected by environmental factors. Chronic life stress increases the risk of aging-related diseases including AD. The impact of stress on tauopathies remains understudied. We examined the effects of stress elicited by social (chronic subordination stress [CSS]) or psychological/physical (chronic restraint stress [CRS]) factors on the PS19 mouse model of tauopathy.

Methods: Male PS19 mice (average age, 6.3 months) were randomized to receive CSS or CRS, or to remain as singly housed controls. Behavioral tests were used to assess anxiety-like behaviors and cognitive functions. Immunofluorescence staining and Western blotting analysis were used to measure levels of astrogliosis, microgliosis, and tau burden. Immunohistochemistry was used to assess glucocorticoid receptor expression.

Results: PS19 mice exhibit neuroinflammation (glial fibrillary acidic protein, t tests: p = .0297; allograft inflammatory factor 1, t tests: p = .006) and tau hyperphosphorylation ( t test, p = .0446) in the hippocampus, reduced anxiety (post hoc, p = .046), and cognitive deficits, when compared with wild-type mice. Surprisingly, CRS reduced hippocampal levels of both total tau and phospho-tau S404 ( t test, p = .0116), and attenuated some aspects of both astrogliosis and microgliosis in PS19 mice ( t tests, p = .068-.0003); however, this was not associated with significant changes in neurodegeneration or cognitive function. Anxiety-like behaviors were increased by CRS (post hoc, p = .046). Conversely, CSS impaired spatial learning in Barnes maze without impacting tau phosphorylation or neurodegeneration and having a minimal impact on gliosis.

Conclusions: Our results demonstrate that social or psychological stress can differentially impact anxiety-like behavior, select cognitive functions, and some aspects of tau-dependent pathology in PS19 male mice, providing entry points for the development of experimental approaches designed to slow AD progression.

目的:尽管在了解阿尔茨海默病(AD)病因方面取得了进展,但尚不清楚这种疾病的哪些方面受到环境因素的影响。慢性生活压力会增加患包括AD在内的衰老相关疾病的风险。压力对tau病的影响尚不清楚。我们研究了社会(慢性从属压力,CSS)或心理/生理(慢性约束压力,CRS)因素引发的压力对PS19小鼠tau病模型的影响。方法:雄性PS19小鼠(平均年龄6.3个月)随机接受CSS、CRS或作为单独饲养的对照。行为测试用于评估类似焦虑的行为和认知功能。免疫荧光染色和蛋白质印迹分析用于测量星形胶质细胞增生、小胶质细胞增生和tau负荷的水平。免疫组织化学用于评估糖皮质激素受体的表达。结果:与野生型小鼠相比,PS19小鼠在海马中表现出神经炎症(GFAP,t检验;p=0.0297;Iba1,t检验,p=0.006)和tau过度磷酸化(t检验,p=0.046),焦虑减少(post-hoc,p=0.046)和认知缺陷。令人惊讶的是,CRS降低了PS19小鼠海马总tau和磷酸化tauS404的水平(t检验,p=0.0116),并减轻了星形胶质细胞增生和小胶质细胞增生的某些方面(t检验:p=0.068至p=0.0003);然而,这与神经退行性变或认知功能的显著变化无关。CRS增加了焦虑样行为(post-hoc,p=0.046)。相反,CSS损害了Barnes Maze的空间学习,而不影响tau磷酸化或神经退行性变,对胶质细胞增生的影响最小。结论:我们的研究结果表明,社会或心理压力可以不同地影响PS19雄性小鼠的焦虑样行为、选择认知功能和tau依赖性病理的某些方面,为开发旨在减缓AD进展的实验方法提供了切入点。
{"title":"Chronic Social and Psychological Stress Impact Select Neuropathologies in the PS19 Mouse Model of Tauopathy.","authors":"Carey E Lyons, Sara I Graves, Maria Razzoli, Karthik Jeganathan, Rachel P Mansk, Seth McGonigle, Nivedita Sabarinathan, Jan M van Deursen, Darren J Baker, Alessandro Bartolomucci","doi":"10.1097/PSY.0000000000001256","DOIUrl":"10.1097/PSY.0000000000001256","url":null,"abstract":"<p><strong>Objective: </strong>Despite advances toward understanding the etiology of Alzheimer's disease (AD), it remains unclear which aspects of this disease are affected by environmental factors. Chronic life stress increases the risk of aging-related diseases including AD. The impact of stress on tauopathies remains understudied. We examined the effects of stress elicited by social (chronic subordination stress [CSS]) or psychological/physical (chronic restraint stress [CRS]) factors on the PS19 mouse model of tauopathy.</p><p><strong>Methods: </strong>Male PS19 mice (average age, 6.3 months) were randomized to receive CSS or CRS, or to remain as singly housed controls. Behavioral tests were used to assess anxiety-like behaviors and cognitive functions. Immunofluorescence staining and Western blotting analysis were used to measure levels of astrogliosis, microgliosis, and tau burden. Immunohistochemistry was used to assess glucocorticoid receptor expression.</p><p><strong>Results: </strong>PS19 mice exhibit neuroinflammation (glial fibrillary acidic protein, t tests: p = .0297; allograft inflammatory factor 1, t tests: p = .006) and tau hyperphosphorylation ( t test, p = .0446) in the hippocampus, reduced anxiety (post hoc, p = .046), and cognitive deficits, when compared with wild-type mice. Surprisingly, CRS reduced hippocampal levels of both total tau and phospho-tau S404 ( t test, p = .0116), and attenuated some aspects of both astrogliosis and microgliosis in PS19 mice ( t tests, p = .068-.0003); however, this was not associated with significant changes in neurodegeneration or cognitive function. Anxiety-like behaviors were increased by CRS (post hoc, p = .046). Conversely, CSS impaired spatial learning in Barnes maze without impacting tau phosphorylation or neurodegeneration and having a minimal impact on gliosis.</p><p><strong>Conclusions: </strong>Our results demonstrate that social or psychological stress can differentially impact anxiety-like behavior, select cognitive functions, and some aspects of tau-dependent pathology in PS19 male mice, providing entry points for the development of experimental approaches designed to slow AD progression.</p>","PeriodicalId":20918,"journal":{"name":"Psychosomatic Medicine","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10987396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71426312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Article Summaries for June 2024 Psychosomatic Medicine, Volume 86, Issue 5. 2024 年 6 月文章摘要 《心身医学》第 86 卷第 5 期。
IF 3.3 3区 医学 Q2 Medicine Pub Date : 2024-06-01 DOI: 10.1097/PSY.0000000000001325
{"title":"Article Summaries for June 2024 Psychosomatic Medicine, Volume 86, Issue 5.","authors":"","doi":"10.1097/PSY.0000000000001325","DOIUrl":"https://doi.org/10.1097/PSY.0000000000001325","url":null,"abstract":"","PeriodicalId":20918,"journal":{"name":"Psychosomatic Medicine","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141184542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
All Issue Ads. 所有发行广告。
IF 3.3 3区 医学 Q2 Medicine Pub Date : 2024-06-01 DOI: 10.1097/01.psy.0001024868.45605.81
{"title":"All Issue Ads.","authors":"","doi":"10.1097/01.psy.0001024868.45605.81","DOIUrl":"https://doi.org/10.1097/01.psy.0001024868.45605.81","url":null,"abstract":"","PeriodicalId":20918,"journal":{"name":"Psychosomatic Medicine","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141238073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Financial Hardship and Age-Related Decrements in Kidney Function Among Black and White Adults in the Midlife in the United States Study. 美国黑人和白人中年成年人的经济困难和年龄相关的肾功能下降(MIDUS)研究。
IF 2.9 3区 医学 Q2 PSYCHIATRY Pub Date : 2024-06-01 Epub Date: 2023-11-10 DOI: 10.1097/PSY.0000000000001263
Agus Surachman, Meera Harhay, Alexis R Santos, Jonathan Daw, Lacy M Alexander, David M Almeida, Christopher L Coe

Objective: This analysis examined if financial hardship was associated with age-related decrements in kidney function using a material-psychosocial-behavioral framework. We also tested if this association was mediated by comorbidity of cardiometabolic risk factors (obesity, elevated blood pressure, and insulin resistance).

Methods: Data from 1361 non-Hispanic Black and White adults (ages 26-94 years; non-Hispanic Black = 258) were obtained from the Wave 3 and Refresher phases of the Midlife in the United States project. Kidney function was based on serum creatinine-based estimated glomerular filtration rate (eGFR; Chronic Kidney Disease Epidemiology Collaboration formula without race adjustment). Financial hardship was evaluated in three domains: material (income to poverty line ratio, health insurance coverage, and public/government financial assistance), psychological (perceived financial status, control over financial status, and perceived financial strains), and behavioral responses (financial adjustment/coping such as sold possessions and cutting back on spending).

Results: More severe financial hardship (overall score and in each domain) was associated with age-related decrements in eGFR, even after adjusting for sociodemographic, education, and health-related covariates. The association between financial hardship and age-related decrements in eGFR was conditional on sex but not race. Finally, cardiometabolic risk factors mediated the association between financial hardship and age-related decrements in eGFR.

Conclusions: These findings affirm the negative effects of financial hardship on age-related decrements in renal clearance. In addition to incorporating traditionally used indicators of SES, such as education and income, future research on social hallmarks of aging should also consider the role of financial hardship on the aging process and age-related diseases.

目的:本分析使用物质-心理-社会-行为框架检查经济困难是否与年龄相关的肾功能下降有关。我们还测试了这种关联是否由心血管代谢危险因素(肥胖、血压升高和胰岛素抵抗)的共病介导。方法:1361名非西班牙裔(NH)黑人和白人成年人(26-94岁;NH Black = 258)均来自美国MIDUS项目的Wave 3和Refresher阶段。肾功能以血清肌酐为基础估计肾小球滤过率(CKD-EPI公式,无种族调整)。经济困难在三个方面进行了评估:物质(收入与贫困线之比、健康保险覆盖率和公共/政府财政援助)、心理(感知的财务状况、对财务状况的控制和感知的财务压力)和行为反应(财务调整/应对,如变卖财产和削减支出)。结果:更严重的经济困难(总分和每个领域)与年龄相关的eGFR下降相关,即使在调整了社会人口统计学、教育和健康相关协变量后也是如此。经济困难与年龄相关的eGFR下降之间的联系与性别有关,而与种族无关。最后,心脏代谢危险因素介导了经济困难与年龄相关的eGFR下降之间的关联。结论:这些发现证实了经济困难对年龄相关性肾清除率下降的负面影响。除了纳入教育和收入等传统上使用的社会经济地位指标外,未来关于老龄化的社会特征的研究还应考虑经济困难对老龄化进程和与年龄有关的疾病的作用。
{"title":"Financial Hardship and Age-Related Decrements in Kidney Function Among Black and White Adults in the Midlife in the United States Study.","authors":"Agus Surachman, Meera Harhay, Alexis R Santos, Jonathan Daw, Lacy M Alexander, David M Almeida, Christopher L Coe","doi":"10.1097/PSY.0000000000001263","DOIUrl":"10.1097/PSY.0000000000001263","url":null,"abstract":"<p><strong>Objective: </strong>This analysis examined if financial hardship was associated with age-related decrements in kidney function using a material-psychosocial-behavioral framework. We also tested if this association was mediated by comorbidity of cardiometabolic risk factors (obesity, elevated blood pressure, and insulin resistance).</p><p><strong>Methods: </strong>Data from 1361 non-Hispanic Black and White adults (ages 26-94 years; non-Hispanic Black = 258) were obtained from the Wave 3 and Refresher phases of the Midlife in the United States project. Kidney function was based on serum creatinine-based estimated glomerular filtration rate (eGFR; Chronic Kidney Disease Epidemiology Collaboration formula without race adjustment). Financial hardship was evaluated in three domains: material (income to poverty line ratio, health insurance coverage, and public/government financial assistance), psychological (perceived financial status, control over financial status, and perceived financial strains), and behavioral responses (financial adjustment/coping such as sold possessions and cutting back on spending).</p><p><strong>Results: </strong>More severe financial hardship (overall score and in each domain) was associated with age-related decrements in eGFR, even after adjusting for sociodemographic, education, and health-related covariates. The association between financial hardship and age-related decrements in eGFR was conditional on sex but not race. Finally, cardiometabolic risk factors mediated the association between financial hardship and age-related decrements in eGFR.</p><p><strong>Conclusions: </strong>These findings affirm the negative effects of financial hardship on age-related decrements in renal clearance. In addition to incorporating traditionally used indicators of SES, such as education and income, future research on social hallmarks of aging should also consider the role of financial hardship on the aging process and age-related diseases.</p>","PeriodicalId":20918,"journal":{"name":"Psychosomatic Medicine","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11082066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138047860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Short Sleep and Insomnia Are Associated With Accelerated Epigenetic Age. 睡眠不足和失眠与表观遗传年龄的加快有关。
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2024-06-01 Epub Date: 2023-08-21 DOI: 10.1097/PSY.0000000000001243
Cynthia D J Kusters, Eric T Klopack, Eileen M Crimmins, Teresa E Seeman, Steve Cole, Judith E Carroll

Objective: Short sleep and insomnia are each associated with a greater risk of age-related disease, which suggests that insufficient sleep may accelerate biological aging. We examine whether short sleep and insomnia alone or together relates to epigenetic age among older adults.

Methods: A total of 3795 men (46.3%) and women aged 56 to 100 years from the Health and Retirement Study were included. Insomnia was defined as reporting at least one insomnia symptom (difficulty falling asleep, waking up at night, or waking up too early in the morning) and feeling unrested when waking up most of the time. Those reporting <6 hours of bedtime were categorized as short sleepers. Three second- or third-generation epigenetic age acceleration clocks were derived from the 2016 Health and Retirement Study Venous Blood Study. The linear regression analysis was adjusted for age, sex, race/ethnicity, education, and obesity status.

Results: Insomnia and short sleep were associated with acceleration of GrimAge of 0.49 (95% confidence interval [CI] = 0.03-0.94 years; p = .04) and 1.29 (95% CI = 0.52-2.07 years; p = .002) years, respectively, as well as a faster pace of aging (DunedinPACE; 0.018 [95% CI = 0.004-0.033; p = .02] and 0.022 [95% CI = -0.004 to 0.048; p = .11]). Compared with healthy sleepers, individuals with the combination of short sleep and insomnia had an accelerated GrimAge (0.97 years; 95% CI = 0.07-1.87 years, p = .04) and a greater DunedinPACE (0.032; 95% CI = 0.003-0.060, p = .04).

Conclusions: Our findings indicate that short sleep, insomnia, and the combination of the two are linked to epigenetic age acceleration, suggesting that these individuals have an older biological age that may contribute to risk of comorbidity and mortality.

目的:睡眠不足和失眠都与更大的年龄相关疾病风险有关,这表明睡眠不足可能会加速生物衰老。我们研究了睡眠不足和失眠是否单独或共同与老年人的表观遗传年龄有关。方法:纳入健康与退休研究中年龄在56-100岁的3795名男性(46.3%)和女性。失眠被定义为报告至少一种失眠症状(入睡困难、夜间醒来或早上起得太早),并且在大部分时间醒来时感觉没有得到回报。报告结果:失眠和睡眠时间短分别与GrimAge加速0.49年(95%CI:0.03-0.94;P=0.04)和1.29年(95%CI:0.52-0.07;P=0.002)以及衰老速度加快有关(DunedinPACE;0.018(95%CI:0004-0.033;P=0.02);0.022(95%可信区间:-0.004-0.048;P:0.11)。与健康睡眠者相比,睡眠不足和失眠相结合的个体的GrimAge加速(0.97岁;95%可信区间0.07-1.87;P:0.04)和DunedinPACE更大(0.032;95%置信区间0.003-0.060;P:0.04.)。结论:我们的研究结果表明,睡眠不足、失眠以及两者的结合与表观遗传学年龄加速有关,这表明这些人的生理年龄较大,可能会增加合并症和死亡率的风险。
{"title":"Short Sleep and Insomnia Are Associated With Accelerated Epigenetic Age.","authors":"Cynthia D J Kusters, Eric T Klopack, Eileen M Crimmins, Teresa E Seeman, Steve Cole, Judith E Carroll","doi":"10.1097/PSY.0000000000001243","DOIUrl":"10.1097/PSY.0000000000001243","url":null,"abstract":"<p><strong>Objective: </strong>Short sleep and insomnia are each associated with a greater risk of age-related disease, which suggests that insufficient sleep may accelerate biological aging. We examine whether short sleep and insomnia alone or together relates to epigenetic age among older adults.</p><p><strong>Methods: </strong>A total of 3795 men (46.3%) and women aged 56 to 100 years from the Health and Retirement Study were included. Insomnia was defined as reporting at least one insomnia symptom (difficulty falling asleep, waking up at night, or waking up too early in the morning) and feeling unrested when waking up most of the time. Those reporting <6 hours of bedtime were categorized as short sleepers. Three second- or third-generation epigenetic age acceleration clocks were derived from the 2016 Health and Retirement Study Venous Blood Study. The linear regression analysis was adjusted for age, sex, race/ethnicity, education, and obesity status.</p><p><strong>Results: </strong>Insomnia and short sleep were associated with acceleration of GrimAge of 0.49 (95% confidence interval [CI] = 0.03-0.94 years; p = .04) and 1.29 (95% CI = 0.52-2.07 years; p = .002) years, respectively, as well as a faster pace of aging (DunedinPACE; 0.018 [95% CI = 0.004-0.033; p = .02] and 0.022 [95% CI = -0.004 to 0.048; p = .11]). Compared with healthy sleepers, individuals with the combination of short sleep and insomnia had an accelerated GrimAge (0.97 years; 95% CI = 0.07-1.87 years, p = .04) and a greater DunedinPACE (0.032; 95% CI = 0.003-0.060, p = .04).</p><p><strong>Conclusions: </strong>Our findings indicate that short sleep, insomnia, and the combination of the two are linked to epigenetic age acceleration, suggesting that these individuals have an older biological age that may contribute to risk of comorbidity and mortality.</p>","PeriodicalId":20918,"journal":{"name":"Psychosomatic Medicine","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10879461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10555791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
All Issue Ads. 所有发行广告。
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2024-06-01 DOI: 10.1097/01.psy.0001024868.45605.81
{"title":"All Issue Ads.","authors":"","doi":"10.1097/01.psy.0001024868.45605.81","DOIUrl":"https://doi.org/10.1097/01.psy.0001024868.45605.81","url":null,"abstract":"","PeriodicalId":20918,"journal":{"name":"Psychosomatic Medicine","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141446900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
81st Annual Scientific Meeting Biopsychosocial Health in Context March 20-23, 2024, Brighton, UK 第 81 届科学年会 生物心理社会背景下的健康 2024 年 3 月 20-23 日,英国布莱顿
IF 3.3 3区 医学 Q2 Medicine Pub Date : 2024-06-01 DOI: 10.1097/psy.0000000000001324
{"title":"81st Annual Scientific Meeting Biopsychosocial Health in Context March 20-23, 2024, Brighton, UK","authors":"","doi":"10.1097/psy.0000000000001324","DOIUrl":"https://doi.org/10.1097/psy.0000000000001324","url":null,"abstract":"","PeriodicalId":20918,"journal":{"name":"Psychosomatic Medicine","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141234127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Sleep Disturbance as a Mediator of Lung Cancer Stigma on Psychological Distress and Physical Symptom Burden. 睡眠障碍是肺癌耻辱感对心理压力和身体症状负担的中介作用。
IF 2.9 3区 医学 Q2 PSYCHIATRY Pub Date : 2024-05-01 Epub Date: 2024-02-27 DOI: 10.1097/PSY.0000000000001299
Timothy J Williamson, Edward B Garon, Michael R Irwin, Alyssa K Choi, Jonathan W Goldman, Annette L Stanton

Objective: This study tested sleep disturbance as a mediator through which stigma and discrimination predict psychological distress and physical symptom burden in adults with lung cancer.

Methods: Lung cancer patients on active oncological treatment ( N = 108; 74.1% stage IV) completed questionnaires on lung cancer stigma, sleep, distress, and physical symptoms at study entry and at 6- and 12-week follow-up. Mediation analyses were conducted to investigate whether stigma and discrimination predicted distress and physical symptoms at study entry and across 12 weeks through disrupted sleep.

Results: Higher discrimination ( b = 5.52, 95% confidence interval [CI] = 2.10-8.94) and constrained disclosure ( b = 0.45, 95% CI = 0.05-0.85) were associated significantly with higher sleep disruption at study entry. Sleep disruption, in turn, was associated with higher distress ( b = 0.19, 95% CI = 0.09-0.29) and physical symptoms ( b = 0.28, 95% CI = 0.17-0.40) at study entry. Sleep disruption significantly mediated relationships between higher discrimination and the outcomes of distress (indirect effect = 1.04, 95% CI = 0.13-1.96) and physical symptoms (indirect effect = 1.58, 95% CI = 0.37-2.79) at study entry. Sleep disruption also mediated relationships between constrained disclosure and the outcomes of distress (indirect effect = 0.85, 95% CI = < 0.01-0.17) and physical symptoms (indirect effect = 0.13, 95% CI = 0.01-0.25).

Conclusions: Lung cancer patients evidenced pronounced sleep disruption, which mediated relationships between indicators of lung cancer stigma and distress and physical symptoms at study entry. Research is needed to test additional mechanisms through which lung cancer stigma predicts these outcomes longitudinally.

研究目的本研究测试了睡眠障碍作为一种中介因素对成年肺癌患者心理压力和身体症状负担的影响:正在接受积极肿瘤治疗的肺癌患者(108人;74.1%为IV期患者)在入组时、6周和12周随访时填写了有关肺癌耻辱感、睡眠、痛苦和身体症状的问卷。研究人员进行了中介分析,以调查污名化和歧视是否会通过扰乱睡眠来预测研究开始时和12周后的痛苦和身体症状:在研究开始时,较高的歧视(b = 5.52,95% CI [2.10,8.94])和限制性披露(b = 0.45,95% CI [0.05,0.85])与较高的睡眠中断显著相关。睡眠中断反过来又与研究开始时较高的痛苦(b = 0.19,95% CI [0.09,0.29])和身体症状(b = 0.28,95% CI [0.17,0.40])相关。在研究开始时,睡眠中断在较高的歧视与痛苦(间接效应 = 1.04,95% CI [0.13,1.96])和身体症状(间接效应 = 1.58,95% CI [0.37,2.79])结果之间存在明显的中介关系。睡眠障碍也是限制性披露与痛苦结果之间关系的中介(间接效应 = 0.85,95% CI [结论:肺癌患者有明显的睡眠障碍,这在研究开始时对肺癌污名化指标与痛苦和身体症状之间的关系起到了中介作用。还需要开展研究,对肺癌蔑视预测这些结果的其他机制进行纵向测试。
{"title":"Sleep Disturbance as a Mediator of Lung Cancer Stigma on Psychological Distress and Physical Symptom Burden.","authors":"Timothy J Williamson, Edward B Garon, Michael R Irwin, Alyssa K Choi, Jonathan W Goldman, Annette L Stanton","doi":"10.1097/PSY.0000000000001299","DOIUrl":"10.1097/PSY.0000000000001299","url":null,"abstract":"<p><strong>Objective: </strong>This study tested sleep disturbance as a mediator through which stigma and discrimination predict psychological distress and physical symptom burden in adults with lung cancer.</p><p><strong>Methods: </strong>Lung cancer patients on active oncological treatment ( N = 108; 74.1% stage IV) completed questionnaires on lung cancer stigma, sleep, distress, and physical symptoms at study entry and at 6- and 12-week follow-up. Mediation analyses were conducted to investigate whether stigma and discrimination predicted distress and physical symptoms at study entry and across 12 weeks through disrupted sleep.</p><p><strong>Results: </strong>Higher discrimination ( b = 5.52, 95% confidence interval [CI] = 2.10-8.94) and constrained disclosure ( b = 0.45, 95% CI = 0.05-0.85) were associated significantly with higher sleep disruption at study entry. Sleep disruption, in turn, was associated with higher distress ( b = 0.19, 95% CI = 0.09-0.29) and physical symptoms ( b = 0.28, 95% CI = 0.17-0.40) at study entry. Sleep disruption significantly mediated relationships between higher discrimination and the outcomes of distress (indirect effect = 1.04, 95% CI = 0.13-1.96) and physical symptoms (indirect effect = 1.58, 95% CI = 0.37-2.79) at study entry. Sleep disruption also mediated relationships between constrained disclosure and the outcomes of distress (indirect effect = 0.85, 95% CI = < 0.01-0.17) and physical symptoms (indirect effect = 0.13, 95% CI = 0.01-0.25).</p><p><strong>Conclusions: </strong>Lung cancer patients evidenced pronounced sleep disruption, which mediated relationships between indicators of lung cancer stigma and distress and physical symptoms at study entry. Research is needed to test additional mechanisms through which lung cancer stigma predicts these outcomes longitudinally.</p>","PeriodicalId":20918,"journal":{"name":"Psychosomatic Medicine","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11081853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140022490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Dyadic Investigation of Posttraumatic Stress Symptoms and Daily Sleep Health in Patients With Cancer and Their Caregivers. 对癌症患者及其护理人员的创伤后应激症状和日常睡眠健康的双向调查。
IF 3.3 3区 医学 Q2 Medicine Pub Date : 2024-05-01 Epub Date: 2024-01-11 DOI: 10.1097/PSY.0000000000001283
Thomas C Tsai, Hannah-Rose Mitchell, Jamie Zeitzer, Amanda Ting, Jean-Philippe Laurenceau, David Spiegel, Youngmee Kim

Objective: Cancer can be a traumatic experience affecting multidimensional aspects of sleep among patients and caregivers. This study examined the differential associations of cancer-related posttraumatic stress symptoms (PTSS) with various sleep markers in this population.

Methods: Patients newly diagnosed with colorectal cancer ( n = 138, mean age = 56.93 years, 31.88% female, 60.14% Hispanic, 6.53 months after diagnosis) and their sleep-partner caregivers ( n = 138, mean age = 55.32 years, 68.12% female, 57.97% Hispanic) completed questionnaires assessing the four PTSS clusters (intrusion, avoidance, alterations in arousal and reactivity, negative alterations in cognitions and mood). Participants also completed daily sleep diaries for 14 consecutive days, from which sleep onset latency (SOL), wake after sleep onset (WASO), and sleep duration were derived.

Results: Actor-partner interdependence model revealed that caregivers' greater alterations in arousal and reactivity were associated with their own longer SOL ( b = 15.59, p < .001) and their patients' longer sleep duration ( b = 0.61, p = .014), whereas patients' arousal and reactivity were associated with their caregivers' shorter SOL ( b = -8.47, p = .050). Patients' and caregivers' greater negative alterations in cognitions and mood were associated with patients' longer SOL ( b = 9.15, p = .014) and shorter sleep duration ( b = -0.41, p = .050), respectively. Caregivers' greater intrusion was related to their own shorter SOL ( b = -10.14, p = .004).

Conclusions: The four PTSS clusters, particularly arousal and reactivity and negative cognitions and mood, have distinct associations with sleep markers individually and dyadically in patients and caregivers affected by cancer. Investigations of psychosocial and biobehavioral pathways underlying these relations are warranted. Tailored trauma treatments and sleep interventions may improve the well-being of this population.

目的癌症可能是一种创伤性经历,会对患者和护理人员的睡眠产生多方面的影响。本研究探讨了癌症相关创伤后应激症状(PTSS)与该人群中各种睡眠指标的不同关联:新诊断为结肠直肠癌的患者(138 人,平均年龄 56.93 岁,31.88% 为女性,60.14% 为西班牙裔,诊断后 6.53 个月)及其睡眠伴侣照顾者(138 人,平均年龄 55.32 岁,68.12% 为女性,57.97% 为西班牙裔)填写了评估四组 PTSS 的问卷(入侵、回避、唤醒和反应性改变、认知和情绪的负面改变)。参与者还填写了连续 14 天的每日睡眠日记,并从中得出睡眠开始潜伏期(SOL)、睡眠开始后唤醒(WASO)和睡眠持续时间:行为者-伙伴相互依存模型显示,护理者的唤醒和反应性改变较大,这与他们自己较长的SOL(b = 14.54,p < .001)和患者较长的睡眠持续时间(b = 0.47,p = .040)有关,而患者的唤醒和反应性与护理者较短的SOL(b = -8.34,p = .047)和WASO(b = -8.12,p = .019)有关。患者和护理人员在认知和情绪方面的更大负面改变分别与患者更长的SOL(b = 8.89,p = .016)和更短的睡眠时间(b = -0.40,p = .038)相关。护理人员的更大侵扰与他们自身更短的SOL有关(b = -10.92,p = .002):结论:四个PTSS群组,尤其是唤醒和反应性以及负性认知和情绪,与癌症患者和护理人员的个人睡眠指标和夫妻睡眠指标有明显的关联。有必要对这些关系背后的心理社会和生物行为途径进行研究。量身定制的创伤治疗和睡眠干预措施可能会改善这类人群的福祉。
{"title":"Dyadic Investigation of Posttraumatic Stress Symptoms and Daily Sleep Health in Patients With Cancer and Their Caregivers.","authors":"Thomas C Tsai, Hannah-Rose Mitchell, Jamie Zeitzer, Amanda Ting, Jean-Philippe Laurenceau, David Spiegel, Youngmee Kim","doi":"10.1097/PSY.0000000000001283","DOIUrl":"10.1097/PSY.0000000000001283","url":null,"abstract":"<p><strong>Objective: </strong>Cancer can be a traumatic experience affecting multidimensional aspects of sleep among patients and caregivers. This study examined the differential associations of cancer-related posttraumatic stress symptoms (PTSS) with various sleep markers in this population.</p><p><strong>Methods: </strong>Patients newly diagnosed with colorectal cancer ( n = 138, mean age = 56.93 years, 31.88% female, 60.14% Hispanic, 6.53 months after diagnosis) and their sleep-partner caregivers ( n = 138, mean age = 55.32 years, 68.12% female, 57.97% Hispanic) completed questionnaires assessing the four PTSS clusters (intrusion, avoidance, alterations in arousal and reactivity, negative alterations in cognitions and mood). Participants also completed daily sleep diaries for 14 consecutive days, from which sleep onset latency (SOL), wake after sleep onset (WASO), and sleep duration were derived.</p><p><strong>Results: </strong>Actor-partner interdependence model revealed that caregivers' greater alterations in arousal and reactivity were associated with their own longer SOL ( b = 15.59, p < .001) and their patients' longer sleep duration ( b = 0.61, p = .014), whereas patients' arousal and reactivity were associated with their caregivers' shorter SOL ( b = -8.47, p = .050). Patients' and caregivers' greater negative alterations in cognitions and mood were associated with patients' longer SOL ( b = 9.15, p = .014) and shorter sleep duration ( b = -0.41, p = .050), respectively. Caregivers' greater intrusion was related to their own shorter SOL ( b = -10.14, p = .004).</p><p><strong>Conclusions: </strong>The four PTSS clusters, particularly arousal and reactivity and negative cognitions and mood, have distinct associations with sleep markers individually and dyadically in patients and caregivers affected by cancer. Investigations of psychosocial and biobehavioral pathways underlying these relations are warranted. Tailored trauma treatments and sleep interventions may improve the well-being of this population.</p>","PeriodicalId":20918,"journal":{"name":"Psychosomatic Medicine","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11081839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139723864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Psychosomatic Medicine
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1