About

Liying Luo is an Associate Professor of Sociology and Demography and the Associate Director of the Center for Social Data Analytics at Penn State. She obtained her Ph.D. in Sociology in 2015 and an M.S. in Biostatistics in 2011 from the University of Minnesota, Twin Cities. Prior to joining Penn State, she served as an Assistant of Sociology at the University of Delaware. Her research focuses on how social change and population processes interact with social institutions such as schools and family to produce inequality and health disparities over the life course. She examines distinct patterns and trends in social, demographic, and health outcomes among sociodemographic groups, including gender and racial/ethnic groups. Methodologically, Luo has developed a novel model for determining age, time periods, and cohort patterns in various outcomes such as cognitive functioning, health behaviors, mortality, and substance use. Supported by the National Institutes of Health, she recently designed a new intergenerational mobility model and a multigenerational approach for estimating the effect of cumulative exposure to socioeconomic and contextual disadvantages across multiple generations in a family on health disparities.

Research topics

• Medicine
• Sociology
• Clinical psychology
• Psychiatry
• Psychology
• Gerontology
• Biology
• Demography
• Pathology
• Neuroscience
• Environmental health
• Social psychology

Selected publications

• Association and mediating pathways between intergenerational educational mobility and depressive symptoms: findings from high- and middle-income countries

  BMC Medicine · 2026-04-02

  articleOpen access

  BACKGROUND: Education is an important determinant of health throughout the life course. However, less is understood about whether and how intergenerational educational mobility-comparing an individual's own and their parents' education-is associated with depressive symptoms among aging populations across diverse settings. This study examines this association and its mediating pathways. METHODS: Using data from six harmonized longitudinal aging studies: the US Health and Retirement Study (HRS) and its partner studies in England, European countries, South Korea, Mexico, and China, we conducted cross-sectional (n = 94,655) and longitudinal analyses (n = 56,817) to first establish the association across diverse populations, and then strengthen causal inference by examining whether educational mobility relates to depressive symptoms over time. Educational mobility was categorized as stably low, downwardly mobile, stably middle, upwardly mobile, and stably high group based on country- and cohort-specific percentiles. Depressive symptoms were assessed using the Euro-D or CES-D. We also examined the moderating role of gender in these associations. Mediating pathways through household wealth, social activeness, and multimorbidity were also explored. RESULTS: Longitudinal analyses revealed consistent gradient associations across countries. Compared to the stably low group, downwardly mobile (OR: 0.84, 95% CI: 0.76-0.93), stably middle (OR: 0.78, 95% CI: 0.72-0.84), upwardly mobile (OR: 0.74, 95% CI: 0.67-0.83), and stably high (OR: 0.65, 95% CI: 0.53-0.80) showed lower odds of depressive symptoms. Gender differences emerged in European countries and South Korea, where women had lower odds than men in downwardly mobile and stably high groups. Cross-sectional results showed similar but stronger patterns. Household wealth was the most consistent mediator, explaining 24-34% of the association in the USA and comparable proportions elsewhere except for South Korea. Social activeness and multimorbidity also showed important but varying mediating proportions across countries. CONCLUSIONS: Advantaged educational mobility is associated with reduced depressive symptoms in mid- and later-life. Household wealth, social activeness, and multimorbidity contribute as important mediators. Future policies are needed to promote intergenerational educational equity and implement integrated strategies to reduce mental health disparities.

  PublisherDOI

• Examining the Unequal Decline in Race-Specific Youth Offending: A Decomposition Analysis 

  Journal of Quantitative Criminology · 2026-04-01

  articleOpen accessSenior author

  The current study examines offending patterns among Black and White youth across cohorts between 1988 and 2019 in the U.S. Specifically, we investigate how changes in adolescents’ exposure to social control, access to crime opportunities, and motivation for crime are linked to the unequal decline in offending among Black and White youth. We apply the Blinder-Oaxaca (BO) three-fold decomposition method to analyze Monitoring the Future (MTF) 12th Grade data from 1988 to 2019. This approach allows us to disentangle the contributions of endowment changes and coefficient changes across all independent variables to the race-specific decline in violent and property offending. We find that the declines in unstructured socializing and alcohol use account for most of the reduction in offending among White youth, but such changes did not yield comparable declines in offending among Black youth. This disparity reflects countervailing endowment and coefficient changes uniquely experienced by Black adolescents, including sharper declines in school attachment, modest increases in sensation seeking, and a strengthening of the criminogenic effects of unstructured socializing, as well as potential changes in unobserved factors not captured in the analysis. The processes underlying between-cohort changes in offending are different for Black youth compared to their White counterparts. Broader social changes associated with crime reduction among youth in recent decades might have had limited or delayed protective effects in specific population subgroups. Our findings suggest that understanding temporal changes in youth behavior requires a race-specific perspective and a clear differentiation between endowment and coefficient changes.

  PublisherOA PDFDOI

• Demographic and biosocial determinants of beneficial trends in older adult cognition in the USA and England: the role of cohort succession

  International Journal of Epidemiology · 2026-02-18

  articleOpen accessSenior author

  BACKGROUND: Concerns about the consequences of rapid population aging in the USA and England often neglect the key demographic processes of cohort succession and its influence on population health. In this study, we quantify the extent to which trends between 2004 and 2018 in older US and English adults' cognition functioning are related to population composition changes in three areas: (i) age distribution, (ii) socioeconomic factors, and (iii) chronic disease prevalence. METHODS: Using data from the USA-based Health and Retirement Study (n = 17 305 person-years) and the English Longitudinal Study of Aging (n = 7557 person-years), we apply the Kitagawa-Oaxaca-Blinder two-fold decomposition to estimate the contributions of changes in each country's population composition to changes in overall cognitive functioning between 2004 and 2018. RESULTS: For both men and women, improvements in cognitive functioning were largely driven by cohort succession increasing the average educational attainment of the two populations. Increases in the proportions of the youngest old adults counteracted the negative contributions of increased proportions of the oldest adults. However, increases in the prevalence of psychological conditions (for US men, US women, and English women) and the prevalence of diabetes and divorce (for US women) emerge as specific risk factors that are detrimental to continued gains in cognitive functioning. CONCLUSION: Population aging may not necessarily portend an increasing burden of cognitive diseases when cohorts bring different socioeconomic and health protective and risk factors with them into older adulthood.

  PublisherOA PDFDOI

• TEA domain transcription factor 3 suppresses aortic and left ventricular remodeling via transcriptional activation of PDZ domain containing 1

  Biochemical Pharmacology · 2025-09-11

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  PublisherDOI

• Cohort profile: the Guangzhou older longitudinal dynamic health (GOLD-Health) cohort

  European Journal of Epidemiology · 2025-06-23 · 5 citations

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  PublisherDOI

• Associations between insulin resistance indices and cardiovascular disease in older adults with cardiovascular-kidney-metabolic syndrome stage 0–3: The GOLD-Health cohort

  Diabetes Research and Clinical Practice · 2025-06-13 · 9 citations

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  PublisherDOI

• Effects of Apigenin on the Apoptosis Index of Atherosclerosis

  Journal of Cardiovascular Pharmacology · 2025-08-07

  article

  ABSTRACT: Recently, apigenin has been widely studied for its antiatherosclerosis properties, but its mechanism remains to be further elucidated. This study aims to evaluate the expression of LOX-1, Bcl-2, and Bax in apigenin-treated atherosclerotic rats and to explore whether apigenin affect the expression of apoptotic genes. We analyzed the relationship between these 3 genes and atherosclerosis based on bioinformatics methods and conducted animal experiments on them. We used a fully automatic analyzer to analyze blood lipid levels and found that apigenin had a good effect on lowering blood lipids. Western blot was used to detect LOX-1 protein, and RT-qPCR was used to detect Bcl-2 and Bax mRNA.The fruit showed that apigenin treatment reduced LOX-1 gene expression while increasing the Bcl-2/Bax ratio. These studies provide an experimental basis for the development of apigenin as a new drug for the treatment of atherosclerosis.

  PublisherDOI

• <scp>PDZK1</scp> Regulates the Stability and Function of <scp>ADRB2</scp> to Prevent Vascular Remodelling in Hypertension

  Clinical and Experimental Pharmacology and Physiology · 2025-10-26

  articleOpen access

  In this study, we found that PDZK1, a scaffold protein, interacts with the β₂-adrenergic receptor (ADRB2) through its PDZ domains, stabilising ADRB2 by inhibiting its ubiquitination and proteasomal degradation. This study explored the PDZK1-ADRB2 interaction and its role in hypertension-induced vascular remodelling. Using PDZK1 knockout mice infused with angiotensin II, we found that PDZK1 deficiency further exacerbates angiotensin II-induced hypertension, vascular dysfunction, and vascular remodelling. Mechanistically, PDZK1 stabilises ADRB2 protein by preventing its ubiquitination and proteasomal degradation, thereby maintaining ADRB2-mediated vasodilation. Additionally, PDZK1 prevents ADRB2 internalisation and its interaction with β-arrestin, thereby inhibiting β-arrestin-mediated ERK activation and suppressing vascular smooth muscle cell (VSMC) phenotypic switching. This mechanism contributes to vascular protection under hypertensive conditions. Targeting the PDZK1/ADRB2 interaction may provide a novel therapeutic strategy for hypertension-related vascular complications.

  PublisherOA PDFDOI

• Intergenerational occupational mobility and health in the United States

  Social Science & Medicine · 2025-05-28

  articleOpen access
  PublisherOA PDFDOI

• Ambient PM _2.5 and Its Components Associated with Dynamic Progression from Different Blood Pressure States to Cardiovascular Diseases and Mortality: The GOLD-Health Cohort

  Environment & Health · 2025-12-09

  articleOpen access

  The relationships between fine particulate matter (PM2.5) and the risk of hypertension (HTN) and cardiovascular disease (CVD) have been well documented. However, the associations between specific chemical constituents of PM2.5 and the dynamic progression of hypertensive CVD remain unclear. Using multistate models and mediation analyses in a cohort of 316,087 individuals, we investigated the associations between PM2.5, PM2.5 chemical components (sulfate [SO42–], nitrate [NO3–], ammonium [NH4+], organic matter [OM], and black carbon [BC]), and the dynamic progression from different blood pressure states to incident CVD and mortality. Our findings revealed that PM2.5 and its constituents were positively associated with the dynamic HTN progression. For example, with each interquartile range (IQR) increase, PM2.5, SO42–, NO3–, NH4+, OM, and BC were significantly associated with the disease transition from prehypertension (pre-HTN) to HTN, with hazard ratios (HRs) of 1.116 (95% confidence interval [CI]: 1.104–1.128), 1.186 (95% CI: 1.171–1.202), 1.179 (95% CI: 1.166–1.193), 1.171 (95% CI: 1.159–1.184), 1.155 (95% CI: 1.141–1.169), and 1.147 (95% CI: 1.133–1.161), respectively. Mediation analysis demonstrated that pre-HTN and HTN significantly mediated the relationships between PM2.5, PM2.5 components, and the increased risk of CVD and cardiovascular mortality. This study provides evidence that ambient PM2.5 and its chemical constituents may be important determinants in the dynamic progression of HTN. Controlling exposure to PM2.5 and its components, particularly during the pre-HTN phase, could be an effective strategy to curb the development of hypertensive CVD and alleviate its public health impact.

  PublisherDOI

Recent grants

• Heterogeneous Effects of Education on Alzheimers Disease and Related Dementia among Demographic Groups: A Multigenerational and Multilevel Study

  NIH · $1.1M · 2022–2028

• Cohort Differences in Cognitive Impairment and Alzheimer Disease and Related Dementias: Education Effects and Sex Differences

  NIH · $321k · 2021–2024

Frequent coauthors

• Zhiyuan Guan

  35 shared

• Kun Tao

  Tongji Hospital

  19 shared

• Shengfu Liu

  Shanghai Tenth People's Hospital

  18 shared

• Zhiqiang Guan

  Xuzhou Medical College

  15 shared

• Jiahui Wu

  13 shared

• Xiao Jin

  Lishui Central Hospital

  12 shared

• Yanyun Jiang

  Tongren Hospital

  12 shared

• Qinggang Zhang

  Shandong Normal University

  10 shared