Cumulative Stress Across the Life Course and Biological Aging in Adulthood.

OBJECTIVE: Psychosocial stressors have been linked with accelerated biological aging in adults; however, few studies have examined stressors across the life course in relation to biological aging. METHODS: In 359 individuals (57% White, 34% Black) from the Child Health and Development Studies Disparities study, economic (income, education, financial strain), social (parent-child relations, caretaker responsibilities) and traumatic (death of a sibling or child, violence exposure) stressors were assessed at multiple time points (birth and ages 9, 15, and 50 years). Experiences of major discrimination were assessed at age 50. Life period stress scores were then assessed as childhood (birth-age 15 years) and adulthood (age 50 years). At age 50 years, participants provided blood samples, and DNA methylation was assessed with the EPIC BeadChip. Epigenetic age was estimated using six epigenetic clocks (Horvath, Hannum, Skin and Blood age, PhenoAge, GrimAge, Dunedin Pace of Aging). Age acceleration was determined using residuals from regressing chronologic age on each of the epigenetic age metrics. Telomere length was assessed using the quantitative polymerase chain reaction-based methods. RESULTS: In linear regression models adjusted for race and gender, total life stress, and childhood and adult stress independently predicted accelerated aging based on GrimAge and faster pace of aging based on the DunedinPace. Associations were attenuated after adjusting for smoking status. In sex-stratified analyses, greater childhood stress was associated with accelerated epigenetic aging among women but not men. No associations were noted with telomere length. CONCLUSIONS: We found that cumulative stressors across the life course were associated with accelerated epigenetic age, with differences by sex (e.g., accelerated among women). Further research of this association in large and diverse samples is needed.

Explaining the Black-white depression paradox: Interrogating the Environmental Affordances Model.

The Environmental Affordances (EA) model posits that Black Americans' engagement with unhealthy behaviors (i.e. smoking, alcohol use, eating calorie-dense foods) to cope with stressor exposure may simultaneously account for their observed greater risk of chronic physical illness, and their observed equal or lesser prevalence of depression, relative to white Americans - the so-called "Black-white depression paradox." However, the specific mechanisms through which such effects might arise have been theorized and analyzed inconsistently across studies, raising concerns regarding the appropriateness of existing empirical tests of the model as well as the validity of the conclusions. We specify the two mechanisms most consistent with the EA model - 'Mediation-only' and 'Mediation and Modification' - and derive a priori predictions based on each. We systematically test these pathways using a subset of 559 participants of the Child Health and Development Study who were included in an adult follow-up study between 2010 and 2012 and self-identified as Black or white. Results failed to support either of the two mechanisms derived from the EA model, challenging the validity and utility of the model for explaining racial differences in depression; efforts to develop alternative hypotheses to explain the paradox are needed.

Fundamental social causes of inequalities in colorectal cancer mortality: A study of behavioral and medical mechanisms.

BACKGROUND: Fundamental cause theory posits that social conditions strongly influence the risk of health risks. This study identifies risk mechanisms that social conditions associated with socioeconomic status (SES) and race/ethnicity shape in the production of colorectal cancer (CRC) mortality. METHODS: Two large datasets in the United States examining behavioral and medical preventive factors (N = 4.63-million people) were merged with population-level mortality data observing 761,100 CRC deaths among 3.31-billion person-years of observation to examine trends in CRC mortality from 1999-2012. Analyses examined the changing role of medical preventions and health behaviors in catalyzing SES and racial/ethnic inequalities in CRC mortality. RESULTS: Lower SES as well as Black, Hispanic, Asian/Pacific Islander, and Native American race/ethnicity were associated with decreased access to age-appropriate screening and/or increased prevalence of behavioral risk factors. Analyses further revealed that SES and racial/ethnic inequalities were partially determined by differences in engagement in two preventive factors: use of colonoscopy, and participation in physical activity. DISCUSSION: Social inequalities were not completely determined by behavioral risk factors. Nevertheless, a more equitable distribution of preventive medicines has the potential to reduce both the risk of, and social inequalities in, CRC mortality.

Racial differences in alcohol and tobacco use in adolescence and mid-adulthood in a community-based sample.

PURPOSE: Smoking and alcohol use have been posited as possible contributors to racial health disparities, despite higher smoking and alcohol use among non-Hispanic White youth and young adults compared to Blacks. To further investigate this claim, we aim to assess variation in alcohol and cigarette use across two distinct points of the life course. METHOD: Data are from a subset of 559 (279 male, 280 female) self-identified Black and White participants of the Child Health and Development study. Self-report alcohol and cigarette use were collected between age 15-17 and at mean age 50. Logistic regressions were estimated; supplementary analyses adjusted for maternal age, prenatal smoking, household income, childhood SES, and education. RESULTS: White participants were more likely to drink regularly (Odds ratio (OR) 2.2; 95%CI 1.2, 4.0) and be intoxicated (OR 2.0; 95%CI 1.2, 3.2) in adolescence compared with Blacks. In mid-adulthood, Whites remained more likely to currently drink (OR 2.3; 95%CI 1.6, 3.4) but among drinkers, less likely to binge drink (OR 0.4; 95%CI 0.2, 0.8). White participants were less likely to smoke in mid-adulthood (OR 0.4; 95%CI 0.3, 0.6), but among smokers, were more likely to smoke ≥ ½ a pack per day (OR 3.4; 95%CI 1.5, 7.8). CONCLUSIONS: Blacks were less likely to engage in drinking across the life course, but, among drinkers, more likely to binge drink in mid-adulthood. Blacks were more likely to smoke in mid-adulthood, but smoked infrequently compared with Whites. These patterns suggest that a reframing of disparities mechanisms to focus on broader structural and social factors may benefit progress in understanding and ameliorating inequities.

Fundamental causes of accelerated declines in colorectal cancer mortality: Modeling multiple ways that disadvantage influences mortality risk.

BACKGROUND: Improvements in colorectal cancer (CRC) mortality reflect the distribution of effective preventions. Social inequalities often generate unequal diffusion of medical interventions, resulting in disparate outcomes while preventions are being disseminated throughout the population. This study used a novel method to examine whether Race (Black versus White) and SES influenced when rates of CRC mortality started to decline, and how rapidly they did so. METHOD: Mortality counts from 1968-2010 were derived from death certificates of U.S. residents aged 25 + years. Individuals' race, age, county of residence, and sex were collected from death certificates. County-level SES was measured using the decennial U.S. census. Layered joinpoint regression was used to model CRC mortality trends over time. Acceleration in rates of historical decline were used to indicate preventability within counties. RESULTS: Black race was associated with a 4.1-year delay in colonoscopy-attributable declines in CRC mortality and each standard deviation unit change in SES with a 5.7-year delay in such mortality. Following the onset of a decline, colonoscopy-attributable mortality change was slower by 0.5% among Blacks, and 2.0%/standard deviation in SES. Modifying the rapidity of colonoscopy uptake could have averted 12-14,000 and 83-86,000 deaths among Blacks and residents of lower SES counties, respectively. CONCLUSIONS: Successful interventions do not uniformly benefit the U.S. POPULATION: This study highlighted the notable impact that substantial delays in the provision of interventions, and in the relative rapidity of dissemination, and estimated the extent to which there was a preventable loss of life concentrated amongst the most disadvantaged. A more egalitarian delivery of life-saving interventions could drastically reduce mortality by improving effectiveness of interventions while also addressing inequalities in health.

Age at cancer diagnosis, amenability to medical interventions, and racial/ethnic disparities in cancer mortality.

PURPOSE: Racial disparities in cancer mortality may be greater for cancers that are amenable to available early detection and treatment (amenability level). We investigated whether these patterns vary by age at cancer diagnosis. METHODS: Using 5-year relative survival rates (5Y-RSR), we classified 51 cancer sites into least amenable, partly amenable, and mostly amenable cancers (<40%, 40-69%, ≥70% 5-YRS, respectively). We examined whether racial disparities in mortality rates (African-Americans, Asian/Pacific Islanders, Hispanics, whites), as estimated through Cox regression models, were modified by age at diagnosis and amenability level in 516,939 cancer cases diagnosed in 1995-1999. RESULTS: As compared with whites, all racial minority groups experienced higher cancer mortality rates in the youngest age group of 20-34 years. African-Americans and Hispanics diagnosed with partly and mostly amenable cancers had higher mortality rates relative to whites with cancers of the same amenability levels; further, these differences decreased in magnitude or reversed in direction with increasing age. In contrast, the racial differences in mortality were smaller and remained fairly constant across age groups for least amenable cancers. For example, in the youngest (20-34) and oldest (80-99) age groups, the adjusted hazard ratios (HRs) for African-Americans versus whites with least amenable cancers were, respectively, 1.26 (95% CI 1.02, 1.55) and 0.90 (95% CI 0.85, 0.96), while the HRs for African-Americans versus whites with mostly amenable cancers were 2.77 (95% CI 2.38, 3.22) and 1.07 (95% CI 0.98, 1.17). CONCLUSIONS: Cancer survival disadvantage for racial minorities is larger in younger age groups for cancers that are more amenable to medical interventions.

Why the Neighborhood Social Environment Is Critical in Obesity Prevention.

The continuing obesity epidemic in the USA calls for the examination of antecedents to the well-known risk factors of physical activity and diet. The neighborhood built environment has been extensively studied in relation to obesity noting an increased risk of development and prevalence of obesity in relation to numerous built environment characteristics (lack of green spaces, higher number of fast food restaurants, low walkability indices). The neighborhood social environment, however, has been less extensively studied but is perhaps an equally important component of the neighborhood environment. The neighborhood social environment, particularly constructs of social capital, collective efficacy, and crime, is associated with obesity among both adults and children. Several studies have identified physical activity as a potential pathway of the neighborhood social environment and obesity association. Further work on social networks and norms and residential segregation, as well as the examination of dietary behaviors and mental health as potential mediating pathways, is necessary. Given the existing evidence, intervening on the neighborhood social environment may prove to be an effective target for the prevention on obesity. Intervention studies that promote healthy behaviors and prevent obesity while addressing aspects of the neighborhood social environment are necessary to better identify targets for obesity prevention.

Association between an Internet-Based Measure of Area Racism and Black Mortality.

Racial disparities in health are well-documented and represent a significant public health concern in the US. Racism-related factors contribute to poorer health and higher mortality rates among Blacks compared to other racial groups. However, methods to measure racism and monitor its associations with health at the population-level have remained elusive. In this study, we investigated the utility of a previously developed Internet search-based proxy of area racism as a predictor of Black mortality rates. Area racism was the proportion of Google searches containing the "N-word" in 196 designated market areas (DMAs). Negative binomial regression models were specified taking into account individual age, sex, year of death, and Census region and adjusted to the 2000 US standard population to examine the association between area racism and Black mortality rates, which were derived from death certificates and mid-year population counts collated by the National Center for Health Statistics (2004-2009). DMAs characterized by a one standard deviation greater level of area racism were associated with an 8.2% increase in the all-cause Black mortality rate, equivalent to over 30,000 deaths annually. The magnitude of this effect was attenuated to 5.7% after adjustment for DMA-level demographic and Black socioeconomic covariates. A model controlling for the White mortality rate was used to further adjust for unmeasured confounders that influence mortality overall in a geographic area, and to examine Black-White disparities in the mortality rate. Area racism remained significantly associated with the all-cause Black mortality rate (mortality rate ratio = 1.036; 95% confidence interval = 1.015, 1.057; p = 0.001). Models further examining cause-specific Black mortality rates revealed significant associations with heart disease, cancer, and stroke. These findings are congruent with studies documenting the deleterious impact of racism on health among Blacks. Our study contributes to evidence that racism shapes patterns in mortality and generates racial disparities in health.

A fundamental cause approach to the study of disparities in lung cancer and pancreatic cancer mortality in the United States.

This study examines how associations between socioeconomic status (SES) and lung and pancreatic cancer mortality have changed over time in the U.S. The fundamental cause hypothesis predicts as diseases become more preventable due to innovation in medical knowledge or technology, individuals with greater access to resources will disproportionately benefit, triggering the formation or worsening of health disparities along social cleavages. We examine socioeconomic disparities in mortality due to lung cancer, a disease that became increasingly preventable with the development and dissemination of knowledge of the causal link between smoking cigarettes and lung cancer, and compare it to that of pancreatic cancer, a disease for which there have been no major prevention or treatment innovations. County-level disease-specific mortality rates for those ≥45 years, adjusted for sex, race, and age during 1968-2009 are derived from death certificate and population data from the National Center for Health Statistics. SES is measured using five county-level variables from four decennial censuses, interpolating values for intercensal years. Negative binomial regression was used to model mortality. Results suggest the impact of SES on lung cancer mortality increases 0.5% per year during this period. Although lung cancer mortality rates are initially higher in higher SES counties, by 1980 persons in lower SES counties are at greater risk and by 2009 the difference in mortality between counties with SES one SD above compared to one SD below average was 33 people per 100,000. In contrast, we find a small but significant reverse SES gradient in pancreatic cancer mortality that does not change over time. These data support the fundamental cause hypothesis: social conditions influencing access to resources more greatly impact mortality when preventative knowledge exists. Public health interventions and policies should facilitate more equitable distribution of new health-enhancing knowledge and faster uptake and utilization among lower SES groups.

Fundamental causes of colorectal cancer mortality in the United States: understanding the importance of socioeconomic status in creating inequality in mortality.

OBJECTIVES: We used the fundamental cause hypothesis as a framework for understanding the creation of health disparities in colorectal cancer mortality in the United States from 1968 to 2005. METHODS: We used negative binomial regression to analyze trends in county-level gender-, race-, and age-adjusted colorectal cancer mortality rates among individuals aged 35 years or older. RESULTS: Prior to 1980, there was a stable gradient in colorectal cancer mortality, with people living in counties of higher socioeconomic status (SES) being at greater risk than people living in lower SES counties. Beginning in 1980, this gradient began to narrow and then reversed as people living in higher SES counties experienced greater reductions in colorectal cancer mortality than those in lower SES counties. CONCLUSIONS: Our findings support the fundamental cause hypothesis: once knowledge about prevention and treatment of colorectal cancer became available, social and economic resources became increasingly important in influencing mortality rates.

Do socio-economic gradients in smoking emerge differently across time by gender? Implications for the tobacco epidemic from a pregnancy cohort in California, USA.

Understanding current patterns of population smoking by socioeconomic position (SEP) can be substantially enhanced by research that follows birth cohorts over long periods of time, yet such data in the US are rare. Information from birth cohorts followed during critical time periods when the health consequences of smoking became widely known can inform the ways in which current smoking prevalence has been shaped by the historical processes that preceded it. The present study utilizes data from a substudy of the Child Health and Development Study pregnancy cohort (N = 1612). Women were queried about smoking status in 1959-1962, 1971-1972 and 1977-1980. Women were divided into three cohorts based on date of birth. Offspring represented another birth cohort assessed for smoking in 1977-1980. Results indicated that the overall prevalence of smoking exhibited cohort-specific patterns that persisted across time. Notably, the youngest maternal cohort (born 1937-1946) had high smoking prevalence throughout and showed no appreciable decrease (44.7%, 41.4%, 40.1% for 1959-1962, 1971-1972, and 1977-1980). Results also indicated that the relation of smoking to SEP exhibited cohort-specific patterns over time. Among the oldest birth cohort (born 1914-1930), no inverse relation of SEP to smoking was observed at any time; in contrast, an inverse relation emerged by 1959-1962 among the youngest cohort of mothers. Among the adolescent offspring, there was a strong SEP gradient (OR = 2.0, 95% CI = 1.4-3.0) that was stronger than in any maternal birth cohort at any assessment (ß = 0.40, SE = 0.1, p<0.01). We conclude that SEP gradients in smoking emerge across birth cohorts rather than time alone, with increasingly strong gradients across time especially among younger cohorts.

Fundamental causes of colorectal cancer mortality: the implications of informational diffusion.

CONTEXT: Colorectal cancer is a major cause of mortality in the United States, with 52,857 deaths estimated in 2012. To explore further the social inequalities in colorectal cancer mortality, we used fundamental cause theory to consider the role of societal diffusion of information and socioeconomic status. METHODS: We used the number of deaths from colorectal cancer in U.S. counties between 1968 and 2008. Through geographical mapping, we examined disparities in colorectal cancer mortality as a function of socioeconomic status and the rate of diffusion of information. In addition to providing year-specific trends in colorectal cancer mortality rates, we analyzed these data using negative binomial regression. FINDINGS: The impact of socioeconomic status (SES) on colorectal cancer mortality is substantial, and its protective impact increases over time. Equally important is the impact of informational diffusion on colorectal cancer mortality over time. However, while the impact of SES remains significant when concurrently considering the role of diffusion of information, the propensity for faster diffusion moderates its effect on colorectal cancer mortality. CONCLUSIONS: The faster diffusion of information reduces both colorectal cancer mortality and inequalities in colorectal cancer mortality, although it was not sufficient to eliminate SES inequalities. These findings have important long-term implications for policymakers looking to reduce social inequalities in colorectal cancer mortality and other, related, preventable diseases.

Medical advances and racial/ethnic disparities in cancer survival.

BACKGROUND: Although advances in early detection and treatment of cancer improve overall population survival, these advances may not benefit all population groups equally and may heighten racial/ethnic differences in survival. METHODS: We identified cancer cases in the Surveillance, Epidemiology and End Results program, who were ages > or = 20 years and diagnosed with one invasive cancer in 1995 to 1999 (n = 580,225). We used 5-year relative survival rates to measure the degree to which mortality from each cancer is amenable to medical interventions (amenability index). We used Kaplan-Meier methods and Cox proportional hazards regression to estimate survival differences between each racial/ethnic minority group relative to Whites, by the overall amenability index, and three levels of amenability (nonamenable, partly amenable, and mostly amenable cancers, corresponding to cancers with 5-year relative survival rate < 40%, 40-69%, and > or = 70%, respectively), adjusting for gender, age, disease stage, and county-level poverty concentration. RESULTS: As amenability increased, racial/ethnic differences in cancer survival increased for African Americans, American Indians/Native Alaskans, and Hispanics relative to Whites. For example, the hazard ratios (95% confidence intervals) for African Americans versus Whites from nonamenable, partly amenable, and mostly amenable cancers were 1.05 (1.03-1.07), 1.38 (1.34-1.41), and 1.41 (1.37-1.46), respectively. Asians/Pacific Islanders had similar or longer survival relative to Whites across amenability levels; however, several subgroups experienced increasingly poorer survival with increasing amenability. CONCLUSIONS: Cancer survival disparities for most racial/ethnic minority populations widen as cancers become more amenable to medical interventions. Efforts in developing cancer control measures must be coupled with specific strategies for reducing the expected disparities.

The social shaping of health and smoking.

When major disease processes move from processes that humans cannot control to processes we do understand and do control at least to some extent a social shaping of health disparities occurs. When humans control, it is their policies, their knowledge, and their behaviors that shape the consequences of biomedical knowledge and technology to achieve a powerful social shaping of extant patterns of disease and death. Evidence to support this approach is garnered from data showing dramatic improvements in population health and in the uneven distribution of those improvements across persons, places and times. Health improvements suggest that humans have gained control of disease whereas the uneven and very slow spread of such improvements underscores the critical importance of social factors. Smoking beliefs and behaviors gathered in surveys conducted over the past 50 years conform to this social shaping notion providing insights into the current distribution of beliefs and behaviors.

Smoking and the emergence of a stigmatized social status.

An increase in the social unacceptability of smoking has dramatically decreased tobacco use in the USA. However, how policies (e.g., smoke free air laws) and social factors (e.g., social norms) drive the social unacceptability of tobacco use are not well understood. New research suggests that the stigmatization of smokers is an unrecognized force in the tobacco epidemic and could be one such mechanism. Thus, it is important to investigate the sources of smoker-related stigmatization as perceived by current and former smokers. In this study, we draw on the broader literature about stigma formation in the context of the tobacco epidemic and examine the role of attribution, fear, tobacco control policies, power and social norms in the formation of smoker-related stigma. We test hypotheses about the determinants of stigma using a population-based sample of 816 current and former smokers in New York City. The results show that perceptions of individual attributions for smoking behavior and fear about the health consequences of second hand smoke are important influences on smoker-related stigmatization. Structural forms of discrimination perpetrated against smokers and former smokers (e.g., company policies against hiring smokers) are also related to smoker-related stigma. Respondents with more education perceive more smoker-related stigma than respondents with less education and, Black and Latino respondents perceive less smoker-related stigma than White respondents. Social norms, specifically family and friends' expressed disapproval of smoking, contribute to the formation of smoker-related stigma. These findings suggest important points of leverage to harness the powerful role of stigma in the smoking epidemic and raise concerns about the possible role of stigma in the production of smoking disparities.

Epidemiological sociology and the social shaping of population health.

When biomedical knowledge and technology create the capacity for humans to avoid disease and circumvent early death, sociological factors become more, not less important for population health. The transformation of disease causation from cruel fate, accident, and bad luck to circumstances that are under some degree of human control facilitates a powerful social shaping of disease and death. When humans have control, it is their policies, their knowledge, and their behaviors that shape the consequences of biomedical accomplishments, and thereby extant patterns of disease and death. I propose a "social shaping approach" that can frame our understanding of these processes and allow us to take action to optimize population health. Support for this approach is garnered from evidence of dramatic improvements in population health and in the uneven distribution of those improvements across persons, places, and times. Health improvements suggest that humans have gained control of disease whereas the uneven and very slow spread of such improvements underscores the critical importance of social factors. But the evidence presented represents a stick figure at best, one that needs to be filled in by a well-supported "epidemiological sociology" that uses a wide range of sociological concepts and theories to elucidate the social shaping of disease and death. Absent a robust societal investment in epidemiological sociology, population health will reside below its optimal level and the maldistribution of health-enhancing innovations will continue to create health disparities.