Man Kit Lei

University of Georgia United States
{{numberWithCommas(64)}} Publications

The Effect of Tobacco Smoking Differs across Indices of DNA Methylation-Based Aging in an African American Sample: DNA Methylation-Based Indices of Smoking Capture These Effects

Smoking is one of the leading preventable causes of morbidity and mortality worldwide, prompting interest in its association with DNA methylation-based measures of biological aging. Considerable progress has been made in developing DNA methylation-based measures that correspond to self-reported smoking status. In addition, assessment of DNA methylation-based aging has been expanded to better capture individual differences in risk for morbidity and mortality. Untested to date, however, is whether smoking is similarly related to older and newer indices of DNA methylation-based aging, and whether DNA methylation-based indices of smoking can be used in lieu of self-reported smoking to examine effects on DNA methylation-based aging measures. In the current investigation we examine mediation of the impact of self-reported cigarette consumption on accelerated, intrinsic DNA methylation-based aging using indices designed to predict chronological aging, phenotypic aging, and mortality risk, as well as a newly developed DNA methylation-based measure of telomere length. Using a sample of 500 African American middle aged smokers and non-smokers, we found that a) self-reported cigarette consumption was associated with accelerated intrinsic DNA methylation-based aging on some but not all DNA methylation-based aging indices, b) for those aging outcomes associated with self-reported cigarette consumption, DNA methylation-based indicators of smoking typically accounted for greater variance than did self-reported cigarette consumption, and c) self-reported cigarette consumption effects on DNA methylation-based aging indices typically were fully mediated by DNA methylation-based indicators of smoking (e.g., PACKYRS from GrimAge; or cg05575921 CpG site). Results suggest that when DNA methylation-based indices of smoking are substituted for self-reported assessments of smoking, they will typically fully reflect the varied impact of cigarette smoking on intrinsic, accelerated DNA methylation-based aging.

Childhood adversity and cardiovascular disease risk: An appraisal of recall methods with a FOCUS ON stress-buffering processes in childhood and adulthood

Abstract

Introduction: Associations between childhood/adolescent adversity and poor adult physical health have been reported in past work. Much of this work has relied on either retrospective or prospective measures of childhood experiences. However, the effect of different assessment methods on potential stress buffering processes remains largely unknown.


Objective: We first examined the extent to which long-term cardiovascular disease risk (CVD) was predicted by reports obtained from 10-year old youth regarding adversity experienced in the prior year and those obtained from the same individuals as adults (age 29) regarding their experience of childhood adversity from ages 0-10, focusing in each case on similar types of adversity. To test stress buffering perspectives, we examined the effects of parental emotional support on the association between each measure of childhood adversities and cardiovascular health.


Methods: We used data from a longitudinal sample of 454 African Americans enrolled in the Family and Community Health Study. The outcome variable was a 30-year CVD risk score computed from the Framingham algorithm. The hypotheses were tested with beta regression models.   


Results: The findings revealed a link between childhood adversity and adult CVD risk at age 29, for both measures of adversity. Consistent with the stress-buffering hypothesis, prospectively assessed parental emotional support in adolescence, but not adulthood, buffered effects on cardiovascular risk for each type of assessment of childhood adversity.


Conclusions: Prospective and retrospective measures correlated in a manner similar to prior reports (i.e. significantly, but poorly). Further, in line with stress-buffering hypothesis, parental emotional support received at age 10 yielded different buffering effects than parental emotional support received at age 29. The study’s findings suggest that theoretically consistent patterns of stress-buffering are detectable using either type of assessment of childhood adversity and provide useful information in the prediction of adult CVD risk. 

Testing Life Course Models Whereby Juvenile and Adult Adversity Combine to Influence Speed of Biological Aging

The present study extends prior research on the links between social adversity and aging by employing more comprehensive measures of adversity and a new gene expression index of aging. Hierarchical regression and 20 years of data from a sample of 381 black Americans were used to test models regarding the impact of social adversity on speed of aging. Consistent with the early life sensitivity model, early adversity continued to predict accelerated aging after controlling for adult adversity. Contrary to the pathway model, adult adversity was not related to aging following controls for early adversity. The cumulative stress model received partial support as high adversity during adulthood amplified the effect of early adversity on aging. Finally, consonant with the social change model, low adversity during adulthood buffered the effect of early adversity on aging. These findings held after controlling for health behaviors such as smoking, diet, and exercise.

Socially Demoralizing Environments and the Development of the Street Code from Childhood to Emerging Adulthood

Abstract

Objectives

This study examines hypotheses regarding patterns of developmental change in street code commitment from childhood through emerging adulthood. It tests whether street code commitment demonstrates developmental stability or if it fluctuates in response to evolving socially demoralizing conditions.

Methods

Latent growth curve and parallel process models are applied to longitudinal data from an African American sample. Confirmatory factor analysis tests the degree to which neighborhood violence, peer processes, and family hostilities combine to form a latent construct of socially demoralizing environments. Analysis also tests measurement invariance across the study assessment periods.

Results

Street code commitment demonstrates a non-linear growth pattern across time. Commitment increases in childhood, peaks in late adolescence, and declines in emerging adulthood. Exposure to demoralizing social environments demonstrates a similar pattern of change characterized by a peak in adolescence followed by a gradual decline. Harsh childhood social environments affect the initial levels but not the growth of the street code. Street code commitment fluctuates in response to contemporaneous environmental conditions.

Conclusion

The street code is malleable from childhood through emerging adulthood. Commitment to the street code is not a stable product of socialization or early childhood social environmental exposures. The degree to which individuals embrace the code is largely a function of their current social environment.

{{numberWithCommas(vm.followersTotal)}} Followers
{{numberWithCommas(vm.followingTotal)}} Following