Losing Years Doing Time: Incarceration Exposure and Accelerated Biological Aging among African American Adults

2021 ◽  
pp. 002214652110525
Author(s):  
Mark T. Berg ◽  
Ethan M. Rogers ◽  
Man-Kit Lei ◽  
Ronald L. Simons

Research suggests that incarceration exposure increases the prevalence of morbidity and premature mortality. This work is only beginning to examine whether the stressors of the incarceration experience become biologically embedded in ways that affect physiological deterioration. Using data from a longitudinal sample of 410 African American adults in the Family and Community Health Study and an epigenetic index of aging, this study tests the extent to which incarceration accelerates epigenetic aging and whether experiences with violence moderate this association. Results from models that adjust for selection effects suggest that incarceration exposure predicted accelerated aging, leaving formerly incarcerated African American individuals biologically older than their calendar age. Direct experiences with violence also exacerbated the effects of incarceration. These findings suggest that incarceration possibly triggers a stress response that affects a biological signature of physiological deterioration.

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S735-S735
Author(s):  
Luigi Ferrucci ◽  
Shabnam Salimi ◽  
Luigi Ferrucci

Abstract Any stimulus that endangers body integrity (stressor) results in an adaptive response to resolve stressful state and determine adaptive or and maladaptive responses. Both chronic extrinsic and intrinsic stressors can produce long-lasting, epigenetic changes in various organs that can eventually result in accelerated changes in bio-physio-pathology. There is initial evidence that stress response involves mechanisms of the epigenetic basis of adaptation and stress response to biological aging and chronic diseases. With aging, homeostasis stability declines causing augmented vulnerability to the external and internal stress. Individuals in whom vulnerability trespass a certain threshold experience accelerated aging and deterioration of health and/ or “secondary aging” phenomena such as premature mortality. Because of substantial heterogeneity of the rate of decline in homeostatic stability, there is inter-individual variability in the age of appearance of chronic diseases and the increased risk of disability and mortality. Thus, tools for the quantification of a stress response would be clinically valuable. Therefore, this symposium suggests approaches to study the epigenetic basis of molecular adaptations across various age, organs’ health-span, and life-span.


2019 ◽  
Author(s):  
Anil P.S. Ori ◽  
Loes M. Olde Loohuis ◽  
Jerry Guintivano ◽  
Eilis Hannon ◽  
Emma Dempster ◽  
...  

AbstractSchizophrenia (SCZ) is a severe mental illness that is associated with an increased prevalence of age-related disability and morbidity compared to the general population. An accelerated aging process has therefore been hypothesized as a component of the SCZ disease trajectory. Here, we investigated differential aging using three DNA methylation (DNAm) clocks (i.e. Hannum, Horvath, Levine) in a multi-cohort SCZ whole blood sample consisting of 1,100 SCZ cases and 1,200 controls. It is known that all three DNAm clocks are highly predictive of chronological age and capture different features of biological aging. We found that blood-based DNAm aging is significantly altered in SCZ with age- and sexspecific effects that differ between clocks and map to distinct chronological age windows. Most notably, the predicted phenotypic age (Levine clock) in female cases, starting at age 36 and beyond, is 3.21 years older compared to matching control subjects (95% CI: 1.92-4.50, P=1.3e-06) explaining 7.7% of the variance in disease status. Female cases with high SCZ polygenic risk scores present the highest age acceleration in this age group with +7.03 years (95% CI: 3.87-10.18, P=1.7E-05). Since increased phenotypic age is associated with increased risk of all-cause mortality, our findings suggests that specific and identifiable patient groups are at increased mortality risk as measured by the Levine clock. These results provide new biological insights into the aging landscape of SCZ with age- and sexspecific effects and warrant further investigations into the potential of DNAm clocks as clinical biomarkers that may help with disease management in schizophrenia.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 304-304
Author(s):  
Bridget Farmer ◽  
Jennifer Johnson ◽  
Rodlescia Sneed

Abstract Strong social relationships and social engagement are crucial for both successful aging and successful community re-entry after incarceration. Here, we utilized a mixed methods approach to understand the impact of incarceration on social relationships and social engagement among formerly incarcerated community-dwelling African-American adults aged >50. Participants in the 2012 or 2014 waves of the Health and Retirement Study answered questions regarding prior incarceration, social relationships, and participation in social activities. Additionally, we utilized key informant interviews to further explore how incarceration might impact relationships and social engagement. This presentation will describe quantitative associations between prior incarceration and social relationship structure & function. Further, we will use our qualitative interview data to further explore possible explanations for our findings. Finally, we will describe how MCUAAAR Scientist/Faculty interactions facilitated this work.


2021 ◽  
Vol 62 (3) ◽  
pp. 436-453
Author(s):  
Ronald L. Simons ◽  
Man-Kit Lei ◽  
Eric Klopach ◽  
Mark Berg ◽  
Yue Zhang ◽  
...  

Research on biological embedding of the social environment has been expedited by increased availability of biomarkers. Recently, this arsenal of measures has been expanded to include epigenetic clocks that indicate in years the extent to which an individual is older or younger than their chronological age. These measures of biological aging, especially GrimAge, are robust predictors of both illness and time to death. Importantly for sociologists, several studies have linked social conditions to these indices of aging. The present study extends this research using longitudinal data from a sample of 223 black women participating in the Family and Community Health Study. We find that changes in income and living arrangements over an 11-year period predict changes in speed of biological aging. These results provide further support for the idea that epigenetic aging is a mechanism whereby social conditions become biologically embedded. The utility of epigenetic clocks for sociological studies of health are discussed.


2005 ◽  
Vol 76 (3) ◽  
pp. 463-477 ◽  
Author(s):  
Alexander P. Reiner ◽  
Elad Ziv ◽  
Denise L. Lind ◽  
Caroline M. Nievergelt ◽  
Nicholas J. Schork ◽  
...  

2019 ◽  
Author(s):  
Zuyun Liu ◽  
Diana Leung ◽  
Morgan Levine

AbstractTo date, a number of epigenetic clocks have been developed using DNA methylation data, aimed at approximating biological aging in multiple tissues/cells. However, despite the assumption that these clocks are meant to capture the same phenomenon-aging, their correlations with each other are weak, and there is a lack of consistency in their associations with outcomes of aging. Therefore, the goal of this study was to compare and contrast the molecular characteristics and functional associations of 11 existing epigenetic clocks, using data from diverse human tissue and cell types. Results suggest that the CpGs comprised in the various clocks differ in regards to the consistency of their age correlations across tissues/cells. Using microarray expression data from purified CD14+ monocytes, we found that six clocks—Yang, Hannum, Lin, Levine, Horvath1, and Horvath2—has relatively similar transcriptional profiles. Network analysis revealed nine co-expression modules, most of which display robust correlations across various clocks. One significant module—turquoise is involved in mitochondrial translation, gene expression, respiratory chain complex assembly, and oxidative phosphorylation. Finally, using data from 143B cells with chronically depleted mtDNA (rho0) and 143B controls, we found that rho0 cells have more than a three-standard deviation increase in epigenetic age for Levine (p=0.006), Lin (p=0.012), and Yang (p=0.013). In summary, these results demonstrate the shared and contrasting features of existing epigenetic clocks, in regards to the CpG characteristic, tissue specificity, and co-regulatory gene network signatures, and suggesting a link between two hallmarks of aging—epigenetic alterations and mitochondrial dysfunction.


2021 ◽  
Author(s):  
Laura Etzel ◽  
Waylon J. Hastings ◽  
Molly A. Hall ◽  
Christine Heim ◽  
Michael J. Meaney ◽  
...  

Background: New insights into mechanisms linking obesity to poor health outcomes suggest a role for cellular aging pathways, casting obesity as a disease of accelerated biological aging. Although obesity has been linked to accelerated epigenetic aging in middle-aged adults, the impact during childhood remains unclear. We tested the association between body mass index (BMI) and accelerated epigenetic aging in a cohort of high-risk children. Participants were children (N=273, aged 8 to 14 years, 82% investigated for maltreatment) recruited to the Child Health Study, an ongoing prospective study of youth investigated for maltreatment and a comparison youth. BMI was measured as a continuous variable. Accelerated epigenetic aging of blood leukocytes was defined as the age-adjusted residuals of several established epigenetic aging clocks (Horvath, Hannum, GrimAge, PhenoAge) along with a newer algorithm, the DunedinPoAm, developed to quantify the pace-of-aging. Hypotheses were tested with generalized linear models. Results: Higher BMI was significantly correlated with older chronological age, maltreatment status, household income, blood cell counts, and three of the accelerated epigenetic aging measures: GrimAge (r=0.29, P<.0001), PhenoAge (r=0.25, P<.0001), and DunedinPoAm (r=0.37, P<.0001). In fully adjusted models, GrimAge (b=.06; P=.007) and DunedinPoAm (b=.0017; P<.0001) remained significantly associated with higher BMI. Maltreatment-status was not independently associated with accelerated epigenetic aging after accounting for other factors. Conclusion: In a high-risk cohort of children, higher BMI predicted epigenetic aging as assessed by two epigenetic aging clocks. These results suggest the association between obesity and accelerated epigenetic aging begins in early life, with implications for future morbidity and mortality risk.


2020 ◽  
Author(s):  
Chantel L. Martin ◽  
Cavin K. Ward-Caviness ◽  
Radhika Dhingra ◽  
Tarek M. Zikry ◽  
Sandro Galea ◽  
...  

ABSTRACTLiving in adverse neighborhood environments have been linked to increased risk of aging-related diseases and mortality; however, the biological mechanisms explaining this observation remain poorly understood. DNA methylation (DNAm), a proposed biomarker of biological aging responsive to environmental stressors, offers promising insight into molecular pathways. We examined associations of three measures of neighborhood conditions (poverty, quality, and social cohesion) with three different epigenetic clocks (Horvath, Hannum, and Levine) using data from the Detroit Neighborhood Health Study (n=158). Using linear regression models, we evaluated associations in the total sample and stratified by gender and social cohesion. Differential effects by gender were found between men and women. Neighborhood poverty was associated with PhenoAge acceleration among women, but not among men (women: β = 1.4; 95% CI: −0.4, 3.3 vs. men: β = −0.3; 95% CI: −2.2, 1.5) in fully adjusted models. In models stratified on social cohesion, association of neighborhood poverty and quality with accelerated DNAm aging remained elevated for residents living in neighborhoods with lower social cohesion, but were null for those living in neighborhoods with higher social cohesion. Our study suggests that living in adverse neighborhood conditions can speed up epigenetic aging, while positive neighborhood characteristics may buffer effects.


Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Steven Nguyen ◽  
Weihua Guan ◽  
Jan Bressler ◽  
Megan Grove ◽  
Rui Xia ◽  
...  

Introduction: Individuals with obesity are thought to be protected against some chronic disease as long as they do not incur metabolic health (MH) conditions. A new epigenetic biomarker of accelerated biological aging and health span, PhenoAge, was developed using DNA methylation (DNAm) markers. We hypothesized that obesity would be associated with higher PhenoAge than normal weight and overweight individuals only in the presence of MH conditions. Methods: DNAm was measured in leukocyte DNA for 2,454 African American participants (mean age=56.4 years) and used to calculate PhenoAge. BMI status was categorized as normal weight, overweight, and obese and MH was categorized by 0, 1, or at least 2 of the following: coronary heart disease, stroke, hypertension, type-2 diabetes, and hyperlipidemia. Linear regression tested the cross-sectional association of PhenoAge with BMI and MH, adjusting for sociodemographic variables, smoking, and technical variables. Stratified analyses by MH status were conducted to illustrate the statistical effects of BMI status in adults with and without MH conditions. Results: Participants with obesity had approximately 8 months higher PhenoAge compared to normal weight (β=0.68, 95% CI=0.21, 1.14, p=4.1E-3), and those with one (β=0.55, 95% CI=0.15, 0.94, p=6.4E-3) or at least 2 (β=0.81, 95% CI=0.38, 1.25, p=2E-4) MH conditions also had higher PhenoAge compared to those with 0 conditions. Figure 1 shows increments in PhenoAge with increments in number of MH conditions regardless of BMI. PhenoAge was significantly higher for obese compared to overweight for 0 and 1 MH conditions, but not compared to normal weight. Conclusions: In African American adults, both obesity status and presence of MH conditions were associated with a higher PhenoAge, suggesting metabolically healthy obesity is not entirely benign. Further phenotyping of the “metabolic health” obese condition is warranted to understand its relevance for healthspan.


2018 ◽  
Vol 65 (3) ◽  
pp. 322-351 ◽  
Author(s):  
Sara Z. Evans ◽  
Frances P. Abderhalden ◽  
Leslie G. Simons ◽  
Ronald L. Simons

Using data from the Family and Community Health Survey, the current study explores developmental pathways from age 11 to 24 of African American males and females. This study describes the number and type of trajectories of offending for male and female African Americans, as much research in the past on trajectories has focused on White and/or male samples. We also investigate predictors of offending for the females both between and within trajectory groups. Results indicated that females who experienced higher levels of racial discrimination and greater parental hostility were more likely to be in a late bloomer group, compared with the low-level group. In addition, higher levels of racial discrimination and deviant peer affiliation were predictive of more offending.


Sign in / Sign up

Export Citation Format

Share Document