Pub Date : 2025-01-01Epub Date: 2024-11-25DOI: 10.1097/EDE.0000000000001803
Karynsa Kilpatrick, Katherine Cahill, Urmila Chandran, Daniel Riskin
Background: Asthma is a phenotypically complex disease requiring nuanced data to generate clinically and scientifically robust real-world evidence. A quantitative measure of data quality is important for variables key to the research questions at hand. Using electronic health record (EHR) data, this study compared accuracy for asthma features between traditional real-world evidence approaches using structured data and advanced approaches applying artificial intelligence technologies to unstructured clinical data.
Methods: We extracted 18 protocol-defined features from 6037 healthcare encounters among 3481 patients. Features included asthma severity subtypes, comorbidities, symptoms, findings, and procedures. We created a manual reference standard through chart abstraction, with two annotators reviewing each record. We assessed interrater reliability using Cohen's kappa score and accuracy against the reference standard as an F1-score.
Results: In the traditional study arm, average recall was 40.8%, precision 72.5%, and F1-score across features was 52.2%. In the advanced study arm, average recall was 95.7%, precision 93.8%, and F1-score was 94.7%. There was an absolute increase of 42.5% and a relative increase of 81.4% in the F1-score between traditional and advanced approaches. Cohen's kappa score indicated 0.80 inter-rater reliability, reflecting a credible reference standard.
Conclusions: Use of advanced approaches can enable high-quality real-world data sets in asthma, including granular clinical features such as disease subtypes and symptomatic outcomes. Data quality can be measured and, when high, can support generation of high-validity real-world evidence using routinely collected healthcare data.
背景:哮喘是一种表型复杂的疾病,需要细致入微的数据来生成临床和科学上可靠的真实世界证据。数据质量的定量测量对于手头研究问题的关键变量非常重要。本研究使用电子健康记录(EHR)数据,比较了使用结构化数据的传统真实世界证据方法和将人工智能技术应用于非结构化临床数据的先进方法对哮喘特征的准确性:我们从 3481 名患者的 6037 次医疗保健会诊中提取了 18 个协议定义的特征。特征包括哮喘严重程度亚型、合并症、症状、检查结果和治疗过程。我们通过病历摘要创建了一个人工参考标准,由两名注释者审查每份记录。我们用 Cohen's kappa 分数评估了研究者之间的可靠性,并用 F1 分数评估了对照参考标准的准确性:传统研究组的平均召回率为 40.8%,精确率为 72.5%,各特征的 F1 分数为 52.2%。在高级研究组中,平均召回率为 95.7%,精确率为 93.8%,F1 分数为 94.7%。传统方法和先进方法的 F1 分数绝对值提高了 42.5%,相对值提高了 81.4%。科恩卡帕(Cohen's kappa)评分显示评分者之间的可靠性为 0.80,反映出参考标准是可信的:结论:使用先进的方法可以获得高质量的真实世界哮喘数据集,包括细粒度的临床特征,如疾病亚型和症状结果。数据质量是可以衡量的,如果数据质量较高,则可以支持利用常规收集的医疗保健数据生成高效力的真实世界证据。
{"title":"Advanced Approaches to Generating High-validity Real-world Evidence in Asthma.","authors":"Karynsa Kilpatrick, Katherine Cahill, Urmila Chandran, Daniel Riskin","doi":"10.1097/EDE.0000000000001803","DOIUrl":"10.1097/EDE.0000000000001803","url":null,"abstract":"<p><strong>Background: </strong>Asthma is a phenotypically complex disease requiring nuanced data to generate clinically and scientifically robust real-world evidence. A quantitative measure of data quality is important for variables key to the research questions at hand. Using electronic health record (EHR) data, this study compared accuracy for asthma features between traditional real-world evidence approaches using structured data and advanced approaches applying artificial intelligence technologies to unstructured clinical data.</p><p><strong>Methods: </strong>We extracted 18 protocol-defined features from 6037 healthcare encounters among 3481 patients. Features included asthma severity subtypes, comorbidities, symptoms, findings, and procedures. We created a manual reference standard through chart abstraction, with two annotators reviewing each record. We assessed interrater reliability using Cohen's kappa score and accuracy against the reference standard as an F1-score.</p><p><strong>Results: </strong>In the traditional study arm, average recall was 40.8%, precision 72.5%, and F1-score across features was 52.2%. In the advanced study arm, average recall was 95.7%, precision 93.8%, and F1-score was 94.7%. There was an absolute increase of 42.5% and a relative increase of 81.4% in the F1-score between traditional and advanced approaches. Cohen's kappa score indicated 0.80 inter-rater reliability, reflecting a credible reference standard.</p><p><strong>Conclusions: </strong>Use of advanced approaches can enable high-quality real-world data sets in asthma, including granular clinical features such as disease subtypes and symptomatic outcomes. Data quality can be measured and, when high, can support generation of high-validity real-world evidence using routinely collected healthcare data.</p>","PeriodicalId":11779,"journal":{"name":"Epidemiology","volume":"36 1","pages":"20-27"},"PeriodicalIF":4.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11594548/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715624","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}
Pub Date : 2025-01-01Epub Date: 2024-09-24DOI: 10.1097/EDE.0000000000001795
Claire E Thomas, Yi Lin, Michelle Kim, Eric S Kawaguchi, Conghui Qu, Caroline Y Um, Brigid M Lynch, Bethany Van Guelpen, Kostas Tsilidis, Robert Carreras-Torres, Franzel J B van Duijnhoven, Lori C Sakoda, Peter T Campbell, Yu Tian, Jenny Chang-Claude, Stéphane Bézieau, Arif Budiarto, Julie R Palmer, Polly A Newcomb, Graham Casey, Loic Le Marchandz, Marios Giannakis, Christopher I Li, Andrea Gsur, Christina Newton, Mireia Obón-Santacana, Victor Moreno, Pavel Vodicka, Hermann Brenner, Michael Hoffmeister, Andrew J Pellatt, Robert E Schoen, Niki Dimou, Neil Murphy, Marc J Gunter, Sergi Castellví-Bel, Jane C Figueiredo, Andrew T Chan, Mingyang Song, Li Li, D Timothy Bishop, Stephen B Gruber, James W Baurley, Stephanie A Bien, David V Conti, Jeroen R Huyghe, Anshul Kundaje, Yu-Ru Su, Jun Wang, Temitope O Keku, Michael O Woods, Sonja I Berndt, Stephen J Chanock, Catherine M Tangen, Alicja Wolk, Andrea Burnett-Hartman, Anna H Wu, Emily White, Matthew A Devall, Virginia Díez-Obrero, David A Drew, Edward Giovannucci, Akihisa Hidaka, Andre E Kim, Juan Pablo Lewinger, John Morrison, Jennifer Ose, Nikos Papadimitriou, Bens Pardamean, Anita R Peoples, Edward A Ruiz-Narvaez, Anna Shcherbina, Mariana C Stern, Xuechen Chen, Duncan C Thomas, Elizabeth A Platz, W James Gauderman, Ulrike Peters, Li Hsu
Background: Colorectal cancer (CRC) is a common, fatal cancer. Identifying subgroups who may benefit more from intervention is of critical public health importance. Previous studies have assessed multiplicative interaction between genetic risk scores and environmental factors, but few have assessed additive interaction, the relevant public health measure.
Methods: Using resources from CRC consortia, including 45,247 CRC cases and 52,671 controls, we assessed multiplicative and additive interaction (relative excess risk due to interaction, RERI) using logistic regression between 13 harmonized environmental factors and genetic risk score, including 141 variants associated with CRC risk.
Results: There was no evidence of multiplicative interaction between environmental factors and genetic risk score. There was additive interaction where, for individuals with high genetic susceptibility, either heavy drinking (RERI = 0.24, 95% confidence interval [CI] = 0.13, 0.36), ever smoking (0.11 [0.05, 0.16]), high body mass index (female 0.09 [0.05, 0.13], male 0.10 [0.05, 0.14]), or high red meat intake (highest versus lowest quartile 0.18 [0.09, 0.27]) was associated with excess CRC risk greater than that for individuals with average genetic susceptibility. Conversely, we estimate those with high genetic susceptibility may benefit more from reducing CRC risk with aspirin/nonsteroidal anti-inflammatory drugs use (-0.16 [-0.20, -0.11]) or higher intake of fruit, fiber, or calcium (highest quartile versus lowest quartile -0.12 [-0.18, -0.050]; -0.16 [-0.23, -0.09]; -0.11 [-0.18, -0.05], respectively) than those with average genetic susceptibility.
Conclusions: Additive interaction is important to assess for identifying subgroups who may benefit from intervention. The subgroups identified in this study may help inform precision CRC prevention.
{"title":"Characterization of Additive Gene-environment Interactions For Colorectal Cancer Risk.","authors":"Claire E Thomas, Yi Lin, Michelle Kim, Eric S Kawaguchi, Conghui Qu, Caroline Y Um, Brigid M Lynch, Bethany Van Guelpen, Kostas Tsilidis, Robert Carreras-Torres, Franzel J B van Duijnhoven, Lori C Sakoda, Peter T Campbell, Yu Tian, Jenny Chang-Claude, Stéphane Bézieau, Arif Budiarto, Julie R Palmer, Polly A Newcomb, Graham Casey, Loic Le Marchandz, Marios Giannakis, Christopher I Li, Andrea Gsur, Christina Newton, Mireia Obón-Santacana, Victor Moreno, Pavel Vodicka, Hermann Brenner, Michael Hoffmeister, Andrew J Pellatt, Robert E Schoen, Niki Dimou, Neil Murphy, Marc J Gunter, Sergi Castellví-Bel, Jane C Figueiredo, Andrew T Chan, Mingyang Song, Li Li, D Timothy Bishop, Stephen B Gruber, James W Baurley, Stephanie A Bien, David V Conti, Jeroen R Huyghe, Anshul Kundaje, Yu-Ru Su, Jun Wang, Temitope O Keku, Michael O Woods, Sonja I Berndt, Stephen J Chanock, Catherine M Tangen, Alicja Wolk, Andrea Burnett-Hartman, Anna H Wu, Emily White, Matthew A Devall, Virginia Díez-Obrero, David A Drew, Edward Giovannucci, Akihisa Hidaka, Andre E Kim, Juan Pablo Lewinger, John Morrison, Jennifer Ose, Nikos Papadimitriou, Bens Pardamean, Anita R Peoples, Edward A Ruiz-Narvaez, Anna Shcherbina, Mariana C Stern, Xuechen Chen, Duncan C Thomas, Elizabeth A Platz, W James Gauderman, Ulrike Peters, Li Hsu","doi":"10.1097/EDE.0000000000001795","DOIUrl":"10.1097/EDE.0000000000001795","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is a common, fatal cancer. Identifying subgroups who may benefit more from intervention is of critical public health importance. Previous studies have assessed multiplicative interaction between genetic risk scores and environmental factors, but few have assessed additive interaction, the relevant public health measure.</p><p><strong>Methods: </strong>Using resources from CRC consortia, including 45,247 CRC cases and 52,671 controls, we assessed multiplicative and additive interaction (relative excess risk due to interaction, RERI) using logistic regression between 13 harmonized environmental factors and genetic risk score, including 141 variants associated with CRC risk.</p><p><strong>Results: </strong>There was no evidence of multiplicative interaction between environmental factors and genetic risk score. There was additive interaction where, for individuals with high genetic susceptibility, either heavy drinking (RERI = 0.24, 95% confidence interval [CI] = 0.13, 0.36), ever smoking (0.11 [0.05, 0.16]), high body mass index (female 0.09 [0.05, 0.13], male 0.10 [0.05, 0.14]), or high red meat intake (highest versus lowest quartile 0.18 [0.09, 0.27]) was associated with excess CRC risk greater than that for individuals with average genetic susceptibility. Conversely, we estimate those with high genetic susceptibility may benefit more from reducing CRC risk with aspirin/nonsteroidal anti-inflammatory drugs use (-0.16 [-0.20, -0.11]) or higher intake of fruit, fiber, or calcium (highest quartile versus lowest quartile -0.12 [-0.18, -0.050]; -0.16 [-0.23, -0.09]; -0.11 [-0.18, -0.05], respectively) than those with average genetic susceptibility.</p><p><strong>Conclusions: </strong>Additive interaction is important to assess for identifying subgroups who may benefit from intervention. The subgroups identified in this study may help inform precision CRC prevention.</p>","PeriodicalId":11779,"journal":{"name":"Epidemiology","volume":" ","pages":"126-138"},"PeriodicalIF":4.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-10-01DOI: 10.1097/EDE.0000000000001800
Futu Chen, Beau MacDonald, Yan Xu, Wilma Franco, Alberto Campos, Lawrence A Palinkas, Jill Johnston, Sandrah P Eckel, Erika Garcia
Background: To our knowledge, no agreed-upon best practices exist for joining U.S. Census ZIP Code Tabulation Areas (ZCTAs) and U.S. Postal Service ZIP Codes (ZIPs). One-to-one linkage using 5-digit ZCTA identifiers excludes ZIPs without direct matches. "Crosswalk" linkage may match a ZCTA to multiple ZIPs, avoiding losses.
Methods: We compared noncrosswalk and crosswalk linkages nationally and for mortality and health insurance in California. To elucidate selection implications, generalized additive models related sociodemographics to whether ZCTAs contained nonmatching ZIPs.
Results: Nationwide, 15% of ZCTAs had nonmatching ZIPs, i.e., ZIPs dropped under noncrosswalk linkage. ZCTAs with nonmatching ZIPs were positively associated with metropolitan core location, lower socioeconomics, and non-White population. In California, 34% of ZIPs in the mortality and 25% in the health insurance data had ZCTAs with nonmatching ZIPs; however, these ZIPs constitute only 0.03% of total mortality and 0.44% of total insurance enrollees.
Conclusions: Our study findings support the use of crosswalk linkages and ZCTAs as a unit of analysis. One-to-one linkage may cause bias by differentially excluding ZIPs with more disadvantaged populations, although affected population sizes seem small.
{"title":"ZIP Code and ZIP Code Tabulation Area Linkage: Implications for Bias in Epidemiologic Research.","authors":"Futu Chen, Beau MacDonald, Yan Xu, Wilma Franco, Alberto Campos, Lawrence A Palinkas, Jill Johnston, Sandrah P Eckel, Erika Garcia","doi":"10.1097/EDE.0000000000001800","DOIUrl":"10.1097/EDE.0000000000001800","url":null,"abstract":"<p><strong>Background: </strong>To our knowledge, no agreed-upon best practices exist for joining U.S. Census ZIP Code Tabulation Areas (ZCTAs) and U.S. Postal Service ZIP Codes (ZIPs). One-to-one linkage using 5-digit ZCTA identifiers excludes ZIPs without direct matches. \"Crosswalk\" linkage may match a ZCTA to multiple ZIPs, avoiding losses.</p><p><strong>Methods: </strong>We compared noncrosswalk and crosswalk linkages nationally and for mortality and health insurance in California. To elucidate selection implications, generalized additive models related sociodemographics to whether ZCTAs contained nonmatching ZIPs.</p><p><strong>Results: </strong>Nationwide, 15% of ZCTAs had nonmatching ZIPs, i.e., ZIPs dropped under noncrosswalk linkage. ZCTAs with nonmatching ZIPs were positively associated with metropolitan core location, lower socioeconomics, and non-White population. In California, 34% of ZIPs in the mortality and 25% in the health insurance data had ZCTAs with nonmatching ZIPs; however, these ZIPs constitute only 0.03% of total mortality and 0.44% of total insurance enrollees.</p><p><strong>Conclusions: </strong>Our study findings support the use of crosswalk linkages and ZCTAs as a unit of analysis. One-to-one linkage may cause bias by differentially excluding ZIPs with more disadvantaged populations, although affected population sizes seem small.</p>","PeriodicalId":11779,"journal":{"name":"Epidemiology","volume":" ","pages":"115-118"},"PeriodicalIF":4.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-10-22DOI: 10.1097/EDE.0000000000001796
Jacopo Vanoli, Arturo de la Cruz Libardi, Francesco Sera, Massimo Stafoggia, Pierre Masselot, Malcolm N Mistry, Sanjay Rajagopalan, Jennifer K Quint, Chris Fook Sheng Ng, Lina Madaniyazi, Antonio Gasparrini
Background: Evidence for long-term mortality risks of PM 2.5 comes mostly from large administrative studies with incomplete individual information and limited exposure definitions. Here we assess PM 2.5 -mortality associations in the UK Biobank cohort using detailed information on confounders and exposure.
Methods: We reconstructed detailed exposure histories for 498,090 subjects by linking residential data with high-resolution PM 2.5 concentrations from spatiotemporal machine-learning models. We split the time-to-event data and assigned yearly exposures over a lag window of 8 years. We fitted Cox proportional hazard models with time-varying exposure controlling for contextual- and individual-level factors, as well as trends. In secondary analyses, we inspected the lag structure using distributed lag models and compared results with alternative exposure sources and definitions.
Results: In fully adjusted models, an increase of 10 μg/m³ in PM 2.5 was associated with hazard ratios of 1.27 (95% confidence interval: 1.06, 1.53) for all-cause, 1.24 (1.03, 1.50) for nonaccidental, 2.07 (1.04, 4.10) for respiratory, and 1.66 (0.86, 3.19) for lung cancer mortality. We found no evidence of association with cardiovascular deaths (hazard ratio = 0.88, 95% confidence interval: 0.59, 1.31). We identified strong confounding by both contextual- and individual-level lifestyle factors. The distributed lag analysis suggested differences in relevant exposure windows across mortality causes. Using more informative exposure summaries and sources resulted in higher risk estimates.
Conclusions: We found associations of long-term PM 2.5 exposure with all-cause, nonaccidental, respiratory, and lung cancer mortality, but not with cardiovascular mortality. This study benefits from finely reconstructed time-varying exposures and extensive control for confounding, further supporting a plausible causal link between long-term PM 2.5 and mortality.
{"title":"Long-term Associations Between Time-varying Exposure to Ambient PM 2.5 and Mortality: An Analysis of the UK Biobank.","authors":"Jacopo Vanoli, Arturo de la Cruz Libardi, Francesco Sera, Massimo Stafoggia, Pierre Masselot, Malcolm N Mistry, Sanjay Rajagopalan, Jennifer K Quint, Chris Fook Sheng Ng, Lina Madaniyazi, Antonio Gasparrini","doi":"10.1097/EDE.0000000000001796","DOIUrl":"10.1097/EDE.0000000000001796","url":null,"abstract":"<p><strong>Background: </strong>Evidence for long-term mortality risks of PM 2.5 comes mostly from large administrative studies with incomplete individual information and limited exposure definitions. Here we assess PM 2.5 -mortality associations in the UK Biobank cohort using detailed information on confounders and exposure.</p><p><strong>Methods: </strong>We reconstructed detailed exposure histories for 498,090 subjects by linking residential data with high-resolution PM 2.5 concentrations from spatiotemporal machine-learning models. We split the time-to-event data and assigned yearly exposures over a lag window of 8 years. We fitted Cox proportional hazard models with time-varying exposure controlling for contextual- and individual-level factors, as well as trends. In secondary analyses, we inspected the lag structure using distributed lag models and compared results with alternative exposure sources and definitions.</p><p><strong>Results: </strong>In fully adjusted models, an increase of 10 μg/m³ in PM 2.5 was associated with hazard ratios of 1.27 (95% confidence interval: 1.06, 1.53) for all-cause, 1.24 (1.03, 1.50) for nonaccidental, 2.07 (1.04, 4.10) for respiratory, and 1.66 (0.86, 3.19) for lung cancer mortality. We found no evidence of association with cardiovascular deaths (hazard ratio = 0.88, 95% confidence interval: 0.59, 1.31). We identified strong confounding by both contextual- and individual-level lifestyle factors. The distributed lag analysis suggested differences in relevant exposure windows across mortality causes. Using more informative exposure summaries and sources resulted in higher risk estimates.</p><p><strong>Conclusions: </strong>We found associations of long-term PM 2.5 exposure with all-cause, nonaccidental, respiratory, and lung cancer mortality, but not with cardiovascular mortality. This study benefits from finely reconstructed time-varying exposures and extensive control for confounding, further supporting a plausible causal link between long-term PM 2.5 and mortality.</p>","PeriodicalId":11779,"journal":{"name":"Epidemiology","volume":" ","pages":"1-10"},"PeriodicalIF":4.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142460874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-10-22DOI: 10.1097/EDE.0000000000001798
Meredith O'Connor, Craig A Olsson, Katherine Lange, Marnie Downes, Margarita Moreno-Betancur, Lisa Mundy, Russell M Viner, Sharon Goldfeld, George Patton, Susan M Sawyer, Steven Hope
Purpose: "Positive epidemiology" emphasizes strengths and assets that protect the health of populations. Positive mental health refers to a range of social and emotional capabilities that may support adaptation to challenging circumstances. We examine the role of positive mental health in promoting adolescent health during the crisis phase of the COVID-19 pandemic.
Methods: We used four long-running Australian and UK longitudinal cohorts: Childhood to Adolescence Transition Study (CATS; analyzed N = 809; Australia); Longitudinal Study of Australian Children (LSAC) - Baby (analyzed N =1,534) and Kindergarten (analyzed N = 1,300) cohorts; Millennium Cohort Study (MCS; analyzed N = 2,490; United Kingdom). Measures included prepandemic exposure: positive mental health (parent reported, 13-15 years) including regulating emotions, interacting well with peers, and caring for others; and pandemic outcomes: psychological distress, life satisfaction, and sleep and alcohol use outside of recommendations (16-21 years; 2020). We used a two-stage meta-analysis to estimate associations between positive mental health and outcomes across cohorts, accounting for potential confounders.
Results: Estimates suggest meaningful effects of positive mental health on psychosocial outcomes during the pandemic, including lower risk of psychological distress (risk ratio [RR] = 0.83, 95% confidence interval [CI] = 0.71, 0.97) and higher life satisfaction (RR = 1.1, 95% CI = 1.0, 1.2). The estimated effects for health behaviors were smaller in magnitude (sleep: RR = 0.95, 95% CI = 0.86, 1.1; alcohol use: RR = 0.97, 95% CI = 0.85, 1.1).
Conclusions: Our results are consistent with the hypothesis that adolescents' positive mental health supports better psychosocial outcomes during challenges such as the COVID-19 pandemic, but the relevance for health behaviors is less clear. These findings reinforce the value of extending evidence to include positive health states and assets.
{"title":"Progressing \"Positive Epidemiology\": A Cross-national Analysis of Adolescents' Positive Mental Health and Outcomes During the COVID-19 Pandemic.","authors":"Meredith O'Connor, Craig A Olsson, Katherine Lange, Marnie Downes, Margarita Moreno-Betancur, Lisa Mundy, Russell M Viner, Sharon Goldfeld, George Patton, Susan M Sawyer, Steven Hope","doi":"10.1097/EDE.0000000000001798","DOIUrl":"10.1097/EDE.0000000000001798","url":null,"abstract":"<p><strong>Purpose: </strong>\"Positive epidemiology\" emphasizes strengths and assets that protect the health of populations. Positive mental health refers to a range of social and emotional capabilities that may support adaptation to challenging circumstances. We examine the role of positive mental health in promoting adolescent health during the crisis phase of the COVID-19 pandemic.</p><p><strong>Methods: </strong>We used four long-running Australian and UK longitudinal cohorts: Childhood to Adolescence Transition Study (CATS; analyzed N = 809; Australia); Longitudinal Study of Australian Children (LSAC) - Baby (analyzed N =1,534) and Kindergarten (analyzed N = 1,300) cohorts; Millennium Cohort Study (MCS; analyzed N = 2,490; United Kingdom). Measures included prepandemic exposure: positive mental health (parent reported, 13-15 years) including regulating emotions, interacting well with peers, and caring for others; and pandemic outcomes: psychological distress, life satisfaction, and sleep and alcohol use outside of recommendations (16-21 years; 2020). We used a two-stage meta-analysis to estimate associations between positive mental health and outcomes across cohorts, accounting for potential confounders.</p><p><strong>Results: </strong>Estimates suggest meaningful effects of positive mental health on psychosocial outcomes during the pandemic, including lower risk of psychological distress (risk ratio [RR] = 0.83, 95% confidence interval [CI] = 0.71, 0.97) and higher life satisfaction (RR = 1.1, 95% CI = 1.0, 1.2). The estimated effects for health behaviors were smaller in magnitude (sleep: RR = 0.95, 95% CI = 0.86, 1.1; alcohol use: RR = 0.97, 95% CI = 0.85, 1.1).</p><p><strong>Conclusions: </strong>Our results are consistent with the hypothesis that adolescents' positive mental health supports better psychosocial outcomes during challenges such as the COVID-19 pandemic, but the relevance for health behaviors is less clear. These findings reinforce the value of extending evidence to include positive health states and assets.</p>","PeriodicalId":11779,"journal":{"name":"Epidemiology","volume":" ","pages":"28-39"},"PeriodicalIF":4.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142460885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-09-27DOI: 10.1097/EDE.0000000000001799
Min Hee Kim, Sze Yan Liu, Willa D Brenowitz, Audrey R Murchland, Thu T Nguyen, Jennifer J Manly, Virginia J Howard, Marilyn D Thomas, Tanisha Hill-Jarrett, Michael Crowe, Charles F Murchison, M Maria Glymour
Background: Education is strongly associated with cognitive outcomes at older ages, yet the extent to which these associations reflect causal effects remains uncertain due to potential confounding.
Methods: Leveraging changes in historical measures of state-level education policies as natural experiments, we estimated the effects of educational attainment on cognitive performance over 10 years in 20,248 non-Hispanic Black and non-Hispanic White participants, aged 45+ in the Reasons for Geographic and Racial Disparities in Stroke cohort (2003-2020) by (1) using state- and year-specific compulsory schooling laws, school-term length, attendance rate, and student-teacher ratio policies to predict educational attainment for US Census microsample data from 1980 and 1990, and (2) applying policy-predicted years of education (PPYEd) to predict memory, verbal fluency, and a cognitive composite. We estimated overall and race- and sex-specific effects of PPYEd on level and change in each cognitive outcome using random intercept and slope models, adjusting for age, year of first cognitive assessment, and indicators for state of residence at age 6.
Results: Each year of PPYEd was associated with higher baseline cognition (0.11 standard deviation [SD] increase in composite measure for each year of PPYEd, 95% confidence interval [CI] = 0.07, 0.15). Subanalyses focusing on individual cognitive domains estimate the largest effects of PPYEd on memory. PPYEd was not associated with the rate of change in cognitive scores. Estimates were similar across Black and White participants and across sex.
Conclusions: Historical policies shaping educational attainment are associated with better later-life memory, a major determinant of dementia risk.
{"title":"State Schooling Policies and Cognitive Performance Trajectories: A Natural Experiment in a National US Cohort of Black and White Adults.","authors":"Min Hee Kim, Sze Yan Liu, Willa D Brenowitz, Audrey R Murchland, Thu T Nguyen, Jennifer J Manly, Virginia J Howard, Marilyn D Thomas, Tanisha Hill-Jarrett, Michael Crowe, Charles F Murchison, M Maria Glymour","doi":"10.1097/EDE.0000000000001799","DOIUrl":"10.1097/EDE.0000000000001799","url":null,"abstract":"<p><strong>Background: </strong>Education is strongly associated with cognitive outcomes at older ages, yet the extent to which these associations reflect causal effects remains uncertain due to potential confounding.</p><p><strong>Methods: </strong>Leveraging changes in historical measures of state-level education policies as natural experiments, we estimated the effects of educational attainment on cognitive performance over 10 years in 20,248 non-Hispanic Black and non-Hispanic White participants, aged 45+ in the Reasons for Geographic and Racial Disparities in Stroke cohort (2003-2020) by (1) using state- and year-specific compulsory schooling laws, school-term length, attendance rate, and student-teacher ratio policies to predict educational attainment for US Census microsample data from 1980 and 1990, and (2) applying policy-predicted years of education (PPYEd) to predict memory, verbal fluency, and a cognitive composite. We estimated overall and race- and sex-specific effects of PPYEd on level and change in each cognitive outcome using random intercept and slope models, adjusting for age, year of first cognitive assessment, and indicators for state of residence at age 6.</p><p><strong>Results: </strong>Each year of PPYEd was associated with higher baseline cognition (0.11 standard deviation [SD] increase in composite measure for each year of PPYEd, 95% confidence interval [CI] = 0.07, 0.15). Subanalyses focusing on individual cognitive domains estimate the largest effects of PPYEd on memory. PPYEd was not associated with the rate of change in cognitive scores. Estimates were similar across Black and White participants and across sex.</p><p><strong>Conclusions: </strong>Historical policies shaping educational attainment are associated with better later-life memory, a major determinant of dementia risk.</p>","PeriodicalId":11779,"journal":{"name":"Epidemiology","volume":" ","pages":"79-87"},"PeriodicalIF":4.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11598670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343965","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}
Pub Date : 2025-01-01Epub Date: 2024-10-08DOI: 10.1097/EDE.0000000000001804
Christiane Didden, Matthias Egger, Naomi Folb, Gary Maartens, Eliane Rohner, Reshma Kassanjee, Cristina Mesa-Vieira, Ayesha Kriel, Soraya Seedat, Andreas D Haas
Background: The increased prevalence of physical diseases among individuals with mental illness contributes to their increased risk of mortality. However, the mediating role of specific diseases in the effect of mental illness on mortality is not well understood.
Method: We conducted a longitudinal causal mediation analysis using data from beneficiaries of a South African medical insurance scheme from 2011 to 2020. We estimated the overall effect of major depressive disorder (MDD) on mortality and evaluated reductions in this overall effect through hypothetical interventions on the risks of mediating physical diseases using an interventional effects approach. Monte Carlo simulation-based g-computation was used for estimation.
Results: Among 981,540 individuals, 143,314 (14.6%) were diagnosed with MDD. Mortality risk after 8 years was 6.5% under MDD, and 5.3% under no MDD (risk ratio 1.23, 95% CI = 1.19, 1.26). Overall, 43.4% of this disparity could be attributed to higher rates of physical comorbidities due to MDD. Cardiovascular diseases accounted for 17.8%, followed by chronic respiratory diseases (8.6%), cancers (7.5%), diabetes and chronic kidney disease (5.8%), tuberculosis (4.3%), and HIV (2.7%).
Conclusion: Within the privately insured population of South Africa, MDD is associated with increased mortality. We found that noncommunicable diseases, rather than infectious diseases, are important mediators of the effect of MDD on mortality.
背景:精神疾病患者躯体疾病的发病率增加是导致其死亡风险增加的原因之一。然而,人们对特定疾病在精神病对死亡率的影响中所起的中介作用还不甚了解:我们利用 2011 年至 2020 年南非医疗保险计划受益人的数据进行了纵向因果中介分析。我们估算了重度抑郁障碍(MDD)对死亡率的总体影响,并采用干预效应法评估了通过对介导性躯体疾病风险进行假设干预而降低总体影响的情况。估算采用了基于蒙特卡罗模拟的 g 计算方法:在 981,540 人中,143,314 人(14.6%)被诊断患有 MDD。多发性硬化症患者 8 年后的死亡率为 6.5%,无多发性硬化症患者为 5.3%(风险比 1.23,95% CI = 1.19,1.26)。总体而言,43.4%的差异可归因于多发性硬化症导致的更高的身体合并症发病率。心血管疾病占 17.8%,其次是慢性呼吸系统疾病(8.6%)、癌症(7.5%)、糖尿病和慢性肾病(5.8%)、肺结核(4.3%)和艾滋病(2.7%):结论:在南非的私人投保人群中,多发性硬化症与死亡率的增加有关。我们发现,非传染性疾病而非传染性疾病是多发性硬化症对死亡率影响的重要媒介。
{"title":"The Contribution of Noncommunicable and Infectious Diseases to the Effect of Depression on Mortality: A Longitudinal Causal Mediation Analysis.","authors":"Christiane Didden, Matthias Egger, Naomi Folb, Gary Maartens, Eliane Rohner, Reshma Kassanjee, Cristina Mesa-Vieira, Ayesha Kriel, Soraya Seedat, Andreas D Haas","doi":"10.1097/EDE.0000000000001804","DOIUrl":"10.1097/EDE.0000000000001804","url":null,"abstract":"<p><strong>Background: </strong>The increased prevalence of physical diseases among individuals with mental illness contributes to their increased risk of mortality. However, the mediating role of specific diseases in the effect of mental illness on mortality is not well understood.</p><p><strong>Method: </strong>We conducted a longitudinal causal mediation analysis using data from beneficiaries of a South African medical insurance scheme from 2011 to 2020. We estimated the overall effect of major depressive disorder (MDD) on mortality and evaluated reductions in this overall effect through hypothetical interventions on the risks of mediating physical diseases using an interventional effects approach. Monte Carlo simulation-based g-computation was used for estimation.</p><p><strong>Results: </strong>Among 981,540 individuals, 143,314 (14.6%) were diagnosed with MDD. Mortality risk after 8 years was 6.5% under MDD, and 5.3% under no MDD (risk ratio 1.23, 95% CI = 1.19, 1.26). Overall, 43.4% of this disparity could be attributed to higher rates of physical comorbidities due to MDD. Cardiovascular diseases accounted for 17.8%, followed by chronic respiratory diseases (8.6%), cancers (7.5%), diabetes and chronic kidney disease (5.8%), tuberculosis (4.3%), and HIV (2.7%).</p><p><strong>Conclusion: </strong>Within the privately insured population of South Africa, MDD is associated with increased mortality. We found that noncommunicable diseases, rather than infectious diseases, are important mediators of the effect of MDD on mortality.</p>","PeriodicalId":11779,"journal":{"name":"Epidemiology","volume":"36 1","pages":"88-98"},"PeriodicalIF":4.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11594557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715634","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}
Pub Date : 2025-01-01Epub Date: 2024-09-20DOI: 10.1097/EDE.0000000000001791
Ziqing Wang, Baoyi Shi, Cécile Proust-Lima, Hélène Jacqmin-Gadda, Linda Valeri
{"title":"Multistate approach for stochastic interventions on a time-to-event mediator in the presence of competing risks: A new R command within the CMAverse R package.","authors":"Ziqing Wang, Baoyi Shi, Cécile Proust-Lima, Hélène Jacqmin-Gadda, Linda Valeri","doi":"10.1097/EDE.0000000000001791","DOIUrl":"10.1097/EDE.0000000000001791","url":null,"abstract":"","PeriodicalId":11779,"journal":{"name":"Epidemiology","volume":"36 1","pages":"139-140"},"PeriodicalIF":4.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-09-24DOI: 10.1097/EDE.0000000000001789
Salina Tewolde, Ashley Scott, Alianna Higgins, Jasmine Blake, Amy Michals, Matthew P Fox, Yorghos Tripodis, Eric Rubenstein
Background: Intersectionality, or the multidimensional influence of social identity and systems of power, may drive increased morbidity and mortality for adults of color with Down syndrome. We documented racial and ethnic differences in death and hospitalizations among Medicaid-enrolled adults with Down syndrome and assessed the interaction of racial-ethnic group and Down syndrome.
Methods: Our sample consisted of 119,325 adults with Down syndrome and >3.2 million adults without intellectual disability enrolled in Medicare at any point from 2011 to 2019. We calculated age-adjusted mortality and hospitalization rates by racial-ethnic group among those with Down syndrome. We examined the additive interaction between Down syndrome and racial and ethnic group on mortality and hospitalization rates.
Results: Among those with Down syndrome, age-adjusted mortality rate did not differ between Black and White racial groups (rate ratio: 0.96, 95% confidence interval [CI] = 0.92, 1.01), while the mortality rate was lower for Pacific Islanders (0.80), Asian (0.71), Native (0.77), and mixed-race groups (0.50). Hospitalization rates were higher for all marginalized groups compared to the White group. When assessing the interaction between racial-ethnic group and Down syndrome, Black, Native Americans, and mixed-race groups exhibited a negative additive interaction for mortality rate, and all groups except Native Americans exhibited positive additive interaction for hospitalization.
Conclusions: Increased hospitalization rates for adults with Down syndrome from marginalized racial and ethnic groups suggest worse health and healthcare. Similar mortality rates across racial and ethnic groups may result from an increased infant mortality rate in marginalized groups with Down syndrome, leading to reduced mortality among those surviving to adulthood.
{"title":"Doubly Marginalized: The Interplay of Racism and Disability in Outcomes for Minoritized People With Down Syndrome.","authors":"Salina Tewolde, Ashley Scott, Alianna Higgins, Jasmine Blake, Amy Michals, Matthew P Fox, Yorghos Tripodis, Eric Rubenstein","doi":"10.1097/EDE.0000000000001789","DOIUrl":"10.1097/EDE.0000000000001789","url":null,"abstract":"<p><strong>Background: </strong>Intersectionality, or the multidimensional influence of social identity and systems of power, may drive increased morbidity and mortality for adults of color with Down syndrome. We documented racial and ethnic differences in death and hospitalizations among Medicaid-enrolled adults with Down syndrome and assessed the interaction of racial-ethnic group and Down syndrome.</p><p><strong>Methods: </strong>Our sample consisted of 119,325 adults with Down syndrome and >3.2 million adults without intellectual disability enrolled in Medicare at any point from 2011 to 2019. We calculated age-adjusted mortality and hospitalization rates by racial-ethnic group among those with Down syndrome. We examined the additive interaction between Down syndrome and racial and ethnic group on mortality and hospitalization rates.</p><p><strong>Results: </strong>Among those with Down syndrome, age-adjusted mortality rate did not differ between Black and White racial groups (rate ratio: 0.96, 95% confidence interval [CI] = 0.92, 1.01), while the mortality rate was lower for Pacific Islanders (0.80), Asian (0.71), Native (0.77), and mixed-race groups (0.50). Hospitalization rates were higher for all marginalized groups compared to the White group. When assessing the interaction between racial-ethnic group and Down syndrome, Black, Native Americans, and mixed-race groups exhibited a negative additive interaction for mortality rate, and all groups except Native Americans exhibited positive additive interaction for hospitalization.</p><p><strong>Conclusions: </strong>Increased hospitalization rates for adults with Down syndrome from marginalized racial and ethnic groups suggest worse health and healthcare. Similar mortality rates across racial and ethnic groups may result from an increased infant mortality rate in marginalized groups with Down syndrome, leading to reduced mortality among those surviving to adulthood.</p>","PeriodicalId":11779,"journal":{"name":"Epidemiology","volume":" ","pages":"66-75"},"PeriodicalIF":4.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-10-01DOI: 10.1097/EDE.0000000000001802
Erin E Bennett, Chelsea Liu, Emma K Stapp, Kan Z Gianattasio, Scott C Zimmerman, Jingkai Wei, Michael E Griswold, Annette L Fitzpatrick, Rebecca F Gottesman, Lenore J Launer, B Gwen Windham, Deborah A Levine, Alison E Fohner, M Maria Glymour, Melinda C Power
Background: Observational studies link high midlife systolic blood pressure to increased dementia risk. However, the synthesis of evidence from randomized controlled trials has not definitively demonstrated that antihypertensive medication use reduces dementia risk. Here, we emulate target trials of antihypertensive medication initiation on incident dementia using three cohort studies, with attention to potential violations of necessary assumptions.
Methods: We emulated trials of antihypertensive medication initiation on incident dementia using data from the Atherosclerosis Risk in Communities study, Cardiovascular Health Study, and Health and Retirement Study. We used data-driven methods to restrict participants to initiators and noninitiators with overlap in propensity scores and positive control outcomes to look for violations of positivity and exchangeability assumptions.
Results: Analyses were limited by the small number of cohort participants who met eligibility criteria. Associations between antihypertensive medication initiation and incident dementia were inconsistent and imprecise (Atherosclerosis Risk in Communities: HR = 0.30 [0.05, 1.93]; Cardiovascular Health Study: HR = 0.66 [0.27, 1.64]; Health and Retirement Study: HR = 1.09 [0.75, 1.59]). More stringent propensity score restrictions had little effect on findings. Sensitivity analyses using a positive control outcome unexpectedly suggested antihypertensive medication initiation increased the risk of coronary heart disease in all three samples.
Conclusions: Positive control outcome analyses suggested substantial residual confounding in effect estimates from our target trials, precluding conclusions about the impact of antihypertensive medication initiation on dementia risk through target trial emulation. Formalized processes for identifying violations of necessary assumptions will strengthen confidence in target trial emulation and avoid inappropriate confidence in emulated trial results.
{"title":"Target Trial Emulation Using Cohort Studies: Estimating the Effect of Antihypertensive Medication Initiation on Incident Dementia.","authors":"Erin E Bennett, Chelsea Liu, Emma K Stapp, Kan Z Gianattasio, Scott C Zimmerman, Jingkai Wei, Michael E Griswold, Annette L Fitzpatrick, Rebecca F Gottesman, Lenore J Launer, B Gwen Windham, Deborah A Levine, Alison E Fohner, M Maria Glymour, Melinda C Power","doi":"10.1097/EDE.0000000000001802","DOIUrl":"10.1097/EDE.0000000000001802","url":null,"abstract":"<p><strong>Background: </strong>Observational studies link high midlife systolic blood pressure to increased dementia risk. However, the synthesis of evidence from randomized controlled trials has not definitively demonstrated that antihypertensive medication use reduces dementia risk. Here, we emulate target trials of antihypertensive medication initiation on incident dementia using three cohort studies, with attention to potential violations of necessary assumptions.</p><p><strong>Methods: </strong>We emulated trials of antihypertensive medication initiation on incident dementia using data from the Atherosclerosis Risk in Communities study, Cardiovascular Health Study, and Health and Retirement Study. We used data-driven methods to restrict participants to initiators and noninitiators with overlap in propensity scores and positive control outcomes to look for violations of positivity and exchangeability assumptions.</p><p><strong>Results: </strong>Analyses were limited by the small number of cohort participants who met eligibility criteria. Associations between antihypertensive medication initiation and incident dementia were inconsistent and imprecise (Atherosclerosis Risk in Communities: HR = 0.30 [0.05, 1.93]; Cardiovascular Health Study: HR = 0.66 [0.27, 1.64]; Health and Retirement Study: HR = 1.09 [0.75, 1.59]). More stringent propensity score restrictions had little effect on findings. Sensitivity analyses using a positive control outcome unexpectedly suggested antihypertensive medication initiation increased the risk of coronary heart disease in all three samples.</p><p><strong>Conclusions: </strong>Positive control outcome analyses suggested substantial residual confounding in effect estimates from our target trials, precluding conclusions about the impact of antihypertensive medication initiation on dementia risk through target trial emulation. Formalized processes for identifying violations of necessary assumptions will strengthen confidence in target trial emulation and avoid inappropriate confidence in emulated trial results.</p>","PeriodicalId":11779,"journal":{"name":"Epidemiology","volume":" ","pages":"48-59"},"PeriodicalIF":4.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11598662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364901","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}