Associations of acculturation and socioeconomic status with subclinical cardiovascular disease in the multi-ethnic study of atherosclerosis

Objectives. We assessed whether markers of acculturation (birthplace and number of US generations) and socioeconomic status (SES) are associated with markers of subclinical cardiovascular disease—carotid artery plaque, internal carotid intima-media thickness, and albuminuria—in 4 racial/ethnic groups.Methods. With data from the Multi-Ethnic Study of Atherosclerosis (n = 6716 participants aged 45–84 years) and race-specific binomial regression models, we computed prevalence ratios adjusted for demographics and traditional cardiovascular risk factors.Results. The adjusted US- to foreign-born prevalence ratio for carotid plaque was 1.20 (99% confidence interval [CI] = 0.97, 1.39) among Whites, 1.91 (99% CI = 0.94, 2.94) among Chinese, 1.62 (99% CI = 1.28, 2.06) among Blacks, and 1.23 (99% CI = 1.15, 1.31) among Hispanics. Greater carotid plaque prevalence was found among Whites, Blacks, and Hispanics with a greater number of generations with US residence (P < .001) and among Whites with less education and among Blacks with lower incomes. Similar associations were observed with intima-media thickness. There was also evidence of an inverse association between albuminuria and SES among Whites and Hispanics.Conclusions. Greater US acculturation and lower SES were associated with a higher prevalence of carotid plaque and greater intima-media thickness but not with albuminuria. Maintenance of healthful habits among recent immigrants should be encouraged.Beginning with the Ni-Hon-San study,^1,2 which was initiated in the 1960s, research has associated increased acculturation to Western lifestyles with more-adverse cardiovascular disease (CVD) risk factor profiles and with increased CVD morbidity and mortality. Specifically, greater Western acculturation has frequently been linked to increased body mass index (BMI; weight in kilograms divided by height in meters squared),^3–5 waist circumference and abdominal obesity,^6,7 hypertension,^7–9 type II diabetes,^10,11 and CVD morbidity and mortality.^1,12,13 However, little research has explored associations between acculturation and subclinical CVD.^14,15Abundant research also exists that links low socioeconomic status (SES) to increased levels of CVD risk factors, morbidity, and mortality.^14,16–18 In general, SES has been found to be inversely related to subclinical measures of CVD, including coronary artery calcification (CAC),^14,19–22 carotid artery plaque, and intima-media thickness^20,23–26 and albuminuria.²⁷ Relations with peripheral artery disease have been inconsistent.^28–30 The extent to which these associations vary by race/ethnicity has been examined infrequently. There is, however, some evidence that the relation between SES and disease may differ across racial/ethnic groups.^14,31,32 Specifically, in the Multi-Ethnic Study of Atherosclerosis (MESA) there was a higher prevalence of CAC among Whites with low education than among those with more education, whereas the reverse was true for Hispanics.¹⁴We investigated whether acculturation and SES were associated with other measures of subclinical disease, specifically with carotid plaque and albuminuria. The relation of acculturation and SES to CAC has been described in MESA.¹⁴ Although CAC, carotid plaque, and albuminuria are all subclinical measures of CVD and are related to adverse clinical outcomes, these measures represent different aspects of the disease process and have relatively weak intercorrelations.³³ Thus, they may be differentially related to our exposures of interest.The investigation of these patterns is important from a public health perspective and may yield clues regarding the etiology of atherosclerosis. On the basis of previous work,¹⁴ we hypothesized that increased Western acculturation, as assessed by place of birth, migration history, and duration of US residence, is associated with increased carotid plaque, intima-media thickness, and albuminuria. Additionally, we expected there to be an interaction between race/ethnicity and SES with respect to their associations with subclinical CVD. Specifically, we expected Whites and Blacks at lower SES to have more-adverse subclinical CVD profiles than those at higher SES, whereas for Hispanics and Chinese, we expected the reverse to be true.     

Racial/Ethnic and Socioeconomic Differences in Short-Term Breast Cancer Survival Among Women in an Integrated Health System

Objectives. We examined the combined influence of race/ethnicity and neighborhood socioeconomic status (SES) on short-term survival among women with uniform access to health care and treatment.Methods. Using electronic medical records data from Kaiser Permanente Northern California linked to data from the California Cancer Registry, we included 6262 women newly diagnosed with invasive breast cancer. We analyzed survival using multivariable Cox proportional hazards regression with follow-up through 2010.Results. After consideration of tumor stage, subtype, comorbidity, and type of treatment received, non-Hispanic White women living in low-SES neighborhoods (hazard ratio [HR] = 1.28; 95% confidence interval [CI] = 1.07, 1.52) and African Americans regardless of neighborhood SES (high SES: HR = 1.44; 95% CI = 1.01, 2.07; low SES: HR = 1.88; 95% CI = 1.42, 2.50) had worse overall survival than did non-Hispanic White women living in high-SES neighborhoods. Results were similar for breast cancer–specific survival, except that African Americans and non-Hispanic Whites living in high-SES neighborhoods had similar survival.Conclusions. Strategies to address the underlying factors that may influence treatment intensity and adherence, such as comorbidities and logistical barriers, should be targeted at low-SES non-Hispanic White and all African American patients.Breast cancer is the most common cancer among women in the United States, and it is the second leading cause of cancer death.1 Despite significant improvements in breast cancer survival from 1992 to 2009,1,2 racial/ethnic and socioeconomic survival disparities have persisted.3,4 African American women have consistently been found to have worse survival after breast cancer,3,5–11 Hispanic women have worse or similar survival,3,9,11,12 and Asian women as an aggregated group have better or similar survival3,9,11,12 than do non-Hispanic White women. Underlying factors thought to contribute to these racial/ethnic disparities include differences in stage at diagnosis,8,12,13 distributions of breast cancer subtypes,14–16 comorbidities,12,13,17 access to and utilization of quality care,13,18 and treatment.12,13Numerous studies also have found poorer survival after breast cancer diagnosis among women residing in neighborhoods of lower socioeconomic status (SES).6,9,19,20 Research has shown that inadequate use of cancer screening services, and consequent late stage diagnosis and decreased survival, contribute to the SES disparities.21,22 Similar to racial/ethnic disparities, SES disparities have been attributed to inadequate treatment and follow-up care and comorbidities.18 Previous population-based studies have continued to observe racial/ethnic survival disparities after adjusting for neighborhood SES, but these studies have not considered the combined influence of neighborhood SES and race/ethnicity.3,9,11,12,23 These disparities may remain because information on individual-level SES, health insurance coverage, comorbidities, quality of care, and detailed treatment regimens have typically not been available.3,8,9,11,13 Even among studies using national Surveillance Epidemiology and End Results–Medicare linked data, in which more detailed information on treatment and comorbidities are available among some patients aged 65 years and older, survival disparities have remained.12,23,24 However, not all data on medical conditions and health care services are captured in Medicare claims, including data on Medicare beneficiaries enrolled in HMOs (health maintenance organizations).25,26Using electronic medical records data from Kaiser Permanente Northern California (KPNC) linked to data from the population-based California Cancer Registry (CCR), we recently reported that chemotherapy use followed practice guidelines but varied by race/ethnicity and neighborhood SES in this integrated health system.27 Therefore, to overcome the limitations of previous studies and address simultaneously the multiple social28 and clinical factors affecting survival after breast cancer diagnosis, we used the linked KPNC–CCR database to determine whether racial/ethnic and socioeconomic differences in short-term overall and breast cancer–specific survival persist in women in a membership-based health system. Our study is the first, to our knowledge, to consider the combined influence of neighborhood SES and race/ethnicity and numerous prognostic factors, including breast cancer subtypes and comorbidities, thought to underlie these long-standing survival disparities among women with uniform access to health care and treatment.     

Racial/Ethnic Disparities in Hypertension Prevalence: Reconsidering the Role of Chronic Stress

Objectives. We investigated the association between anticipatory stress, also known as racism-related vigilance, and hypertension prevalence in Black, Hispanic, and White adults.Methods. We used data from the Chicago Community Adult Health Study, a population-representative sample of adults (n = 3105) surveyed in 2001 to 2003, to regress hypertension prevalence on the interaction between race/ethnicity and vigilance in logit models.Results. Blacks reported the highest vigilance levels. For Blacks, each unit increase in vigilance (range = 0–12) was associated with a 4% increase in the odds of hypertension (odds ratio [OR] = 1.04; 95% confidence interval [CI] = 1.00, 1.09). Hispanics showed a similar but nonsignificant association (OR = 1.05; 95% CI = 0.99, 1.12), and Whites showed no association (OR = 0.95; 95% CI = 0.87, 1.03).Conclusions. Vigilance may represent an important and unique source of chronic stress that contributes to the well-documented higher prevalence of hypertension among Blacks than Whites; it is a possible contributor to hypertension among Hispanics but not Whites.Racial and ethnic disparities in hypertension are some of the most widely studied and consequential sources of social disparities in health in the United States.1–3 For example, recent prevalence estimates show that roughly 40% of Black adults but only 30% of White adults have hypertension.4 In addition, the incidence of hypertension occurs at younger ages for Blacks than Whites.1 These disparities are reflected in the larger burden of hypertension-related health and economic costs carried by non-White than White Americans. For example, mortality rates attributable to hypertension are roughly 15 deaths per 100 000 people for White men and women; the mortality rate for Black women is 40 per 100 000 and more than 50 per 100 000 for Black men.5 Among all health conditions, hypertension accounts for the greatest portion of disparities in years of lost life.6 Economically speaking, if Black Americans had the hypertension prevalence of White Americans, about $400 million would be saved in out-of-pocket health care expenses, about $2 billion would be saved in private insurance costs, and $375 million would be saved from Medicare and Medicaid—per year.7Despite the tremendous amount of research devoted to clarifying the factors that generate these disparities, most studies find that they persist after adjustment for a wide range of socioeconomic, behavioral, and biomedical risk factors.8 In fact, although disparities exist for several of these risk factors (e.g., socioeconomic status), numerous studies have shown no disparities in many others (e.g., smoking, obesity for men, lipid profile).2 Despite substantial investment in interventions to eliminate hypertension disparities, evidence suggests that these disparities have actually grown over the past few decades,9 suggesting that numerous unknown factors drive disparities in hypertension.3     

Community Poverty and Trends in Racial/Ethnic Survival Disparities Among People Diagnosed With AIDS in Florida, 1993–2004

Objectives. We described the racial/ethnic disparities in survival among people diagnosed with AIDS in Florida from 1993 to 2004, as the availability of highly active antiretroviral therapy (HAART) became widespread. We determined whether these disparities decreased after controlling for measures of community-level socioeconomic status.Methods. We compared survival from all causes between non-Hispanic Blacks and non-Hispanic Whites vis-a-vis survival curves and Cox proportional hazards models controlling for demographic, clinical, and area-level poverty factors.Results. Racial/ethnic disparities in survival peaked for those diagnosed during the early implementation of HAART (1996–1998) with a Black-to-White hazard ratio (HR) of 1.72 (95% confidence interval [CI] = 1.62, 1.83) for males and 1.40 (95% CI = 1.24, 1.59) for females. These HRs declined significantly to 1.48 (95% CI = 1.35, 1.64) for males and nonsignificantly to 1.25 (95% CI = 1.05, 1.48) for females in the 2002 to 2004 diagnosis cohort. Disparities decreased significantly for males but not females when controlling for baseline demographic factors and CD4 count and percentage, and became nonsignificant in the 2002 to 2004 cohort after controlling for area poverty.Conclusions. Area poverty appears to play a role in racial/ethnic disparities even after controlling for demographic factors and CD4 count and percentage.The HIV/AIDS epidemic has disproportionately affected the non-Hispanic Black population in the United States. In 2008, an estimated 545 000 non-Hispanic Blacks were living with HIV/AIDS.1 The estimated prevalence of HIV infection for 2008 among non-Hispanic Blacks was 18.2 per 1000 population, more than 7 times higher than the estimated rate for non-Hispanic Whites (non-Hispanic Whites; 2.4 per 1000).1 Non-Hispanic Blacks as a group not only have a higher prevalence of HIV/AIDS, but once infected also have a lower survival rate. The 3-year survival rate in the United States for people diagnosed with AIDS between 2001 and 2005 was 80% among non-Hispanic Blacks compared with 84% for non-Hispanic Whites, 83% for Hispanics, and 88% for Asians,2 further contributing to the disparities in the HIV mortality rate of 16.8 per 100 000 among non-Hispanic Blacks compared with 1.6 per 100 000 among non-Hispanic Whites during 2007.3 Race/ethnicity is a fundamentally social as opposed to a biological construct,4,5 and survival disparities between non-Hispanic Blacks and non-Hispanic Whites have not generally been seen in settings with universal health care access such as in the Veterans Administration health care system,6 the military health care system,7 or a health maintenance organization.8 Therefore, potentially modifiable social explanations for the observed racial/ethnic disparities in survival should be examined.A most remarkable advance in medical treatment in the past century was the development of highly active antiretroviral therapy (HAART). It led to a significant improvement in survival from HIV/AIDS, 9–12 but racial/ethnic disparities in HIV/AIDS survival remain2, 13–16 and in New York City appeared to widen.17 Despite these well-recognized health disparities, there is a critical gap in the knowledge about why the disparity exists. Two population-based studies, both in San Francisco, California (a city that has provided free HIV care for those who cannot afford it), found that Black race was no longer associated with survival between 1996 and 2001 after controlling for neighborhood socioeconomic status (SES), and that this SES effect seemed to be related to HAART use.18,19 However, in a study using HIV surveillance data from 33 states, racial/ethnic disparities in 5-year survival after HIV diagnosis between 1996 and 2003 persisted after adjusting for county-level SES and other factors.20 The objective of this study was to describe the racial/ethnic disparities in AIDS survival in Florida among people diagnosed with AIDS between 1993 and 2004 (a period spanning the time before and during the widespread availability of HAART) and to determine if these disparities decrease after controlling for community-level SES.     

Health status, neighborhood socioeconomic context, and premature mortality in the United States: The National Institutes of Health-AARP Diet and Health Study

Objectives. We examined whether the risk of premature mortality associated with living in socioeconomically deprived neighborhoods varies according to the health status of individuals.Methods. Community-dwelling adults (n = 566 402; age = 50–71 years) in 6 US states and 2 metropolitan areas participated in the ongoing prospective National Institutes of Health–AARP Diet and Health Study, which began in 1995. We used baseline data for 565 679 participants on health behaviors, self-rated health status, and medical history, collected by mailed questionnaires. Participants were linked to 2000 census data for an index of census tract socioeconomic deprivation. The main outcome was all-cause mortality ascertained through 2006.Results. In adjusted survival analyses of persons in good-to-excellent health at baseline, risk of mortality increased with increasing levels of census tract socioeconomic deprivation. Neighborhood socioeconomic mortality disparities among persons in fair-to-poor health were not statistically significant after adjustment for demographic characteristics, educational achievement, lifestyle, and medical conditions.Conclusions. Neighborhood socioeconomic inequalities lead to large disparities in risk of premature mortality among healthy US adults but not among those in poor health.Research dating back to at least the 1920s has shown that the United States has experienced persistent and widening socioeconomic disparities in premature mortality over time.^1–5 However, it has been unclear whether socioeconomic inequalities affect the longevity of persons in good and poor health equally. Socioeconomic status (SES) and health status are interrelated,^6–8 and both are strong independent predictors of mortality.⁹ Low SES is associated with greater risk of ill health and premature death,^{1–5,8,10–13} partly attributable to disproportionately high prevalence of unhealthful lifestyle practices^10,14,15 and physical and mental health conditions.^13,16 Correspondingly, risk of premature mortality is higher in poor than in more affluent areas.^16,17 Although the association between neighborhood poverty and mortality is independent of individual-level SES,^17,18 aggregation of low-SES populations in poor areas may contribute to variations in health outcomes across neighborhoods. Conversely, economic hardships resulting from ill health may lead persons in poor physical or mental health to move to poor neighborhoods.¹⁹ This interrelatedness may create spurious associations between neighborhood poverty and mortality.Although previous studies have found that the risk of premature death associated with poor health status varies according to individuals'' SES,^20,21 no published studies have examined whether the relative risks for premature mortality associated with living in neighborhoods with higher levels of socioeconomic deprivation vary by health status of individuals. Clarifying these relationships will inform social and public health policies and programs that aim to mitigate the health consequences of neighborhood poverty.^22,23We used data from a large prospective study to examine whether the risk of premature mortality associated with neighborhood socioeconomic context differs according to health status at baseline and remains after adjustment for person-level risk factors for mortality, such as SES, lifestyle practices, and chronic medical illnesses.     

Income Inequality,Alcohol Use,and Alcohol-Related Problems

Objectives. We examined the relationship between state-level income inequality and alcohol outcomes and sought to determine whether associations of inequality with alcohol consumption and problems would be more evident with between-race inequality measures than with the Gini coefficient. We also sought to determine whether inequality would be most detrimental for disadvantaged individuals.Methods. Data from 2 nationally representative samples of adults (n = 13 997) from the 2000 and 2005 National Alcohol Surveys were merged with state-level inequality and neighborhood disadvantage indicators from the 2000 US Census. We measured income inequality using the Gini coefficient and between-race poverty ratios (Black–White and Hispanic–White). Multilevel models accounted for clustering of respondents within states.Results. Inequality measured by poverty ratios was positively associated with light and heavy drinking. Associations between poverty ratios and alcohol problems were strongest for Blacks and Hispanics compared with Whites. Household poverty did not moderate associations with income inequality.Conclusions. Poverty ratios were associated with alcohol use and problems, whereas overall income inequality was not. Higher levels of alcohol problems in high-inequality states may be partly due to social context.A growing literature examines the impact of area-level income inequality on health. Inequality, or the size of the difference in income between rich and poor, is distinct from absolute income or socioeconomic status (SES).1 Recent systematic reviews have found associations between income inequality and health.2–6 Theoretical3,7 and empirical work suggests that income inequality may affect health through psychosocial pathways, whereby people compare themselves with those who are better (or worse) off,4,8–10 and neomaterial pathways, whereby inequality leads to limited public investment in social goods such as education, health services, and welfare that directly affect health.3,11,12 (The term “neomaterial” is used to acknowledge the fact that material conditions relevant to present-day health outcomes differ from those material conditions that influenced infectious diseases in the 19th century.3)Most research on income inequality and health has focused broadly on health status and mortality,2 but a few studies focus on specific health outcomes and health behaviors.2,13,14 Among these is a small literature on alcohol that suggests that income inequality is associated with increased frequency of alcohol consumption,13 volume of alcohol consumed,14,15 drinking to drunkenness,14 and death from chronic alcohol-attributable illnesses.16 Results are not unequivocal, however. Findings for alcoholic cirrhosis are mixed, with one study finding a positive association for men but not women15 and others finding no association.17,18 Another study documented a curvilinear relationship with alcohol-related hospitalization, suggesting an initial decline in hospitalizations followed by a rapid rise as inequality increases.16 Finally, one study found that state-level income inequality was negatively associated with women’s alcohol dependence, but not after adjustment for state beer taxes.19To date, this literature on income inequality and alcohol has not examined whether income inequality affects alcohol consumption and related problems equally across SES and race/ethnicity. Furthermore, it has primarily measured income inequality using the Gini coefficient, a measure that captures the difference between an observed income distribution and a condition of complete equality.1 We have expanded on the existing literature by examining SES and race/ethnicity as moderators of associations between income inequality and alcohol outcomes, and by examining race-based measures of income inequality in addition to the Gini coefficient.Income inequality may not affect everyone in the same way.2,20 Affluent individuals may benefit from2 or be immune to the negative effects of²¹ living in unequal areas, whereas poorer people and Black and Hispanic people may suffer a “double jeopardy” in unequal areas.20,21 This double jeopardy hypothesis, however, may be specific to certain health and social outcomes.18 For example, compared with more egalitarian areas, areas with more unequal income distribution have stronger inverse associations between individual SES and adolescent literacy21 as well as mortality from alcoholic liver disease.18 These studies indicate that there is an interaction of individual SES and income inequality for certain outcomes. By contrast, some evidence suggests largely uniform (rather than differential) effects of income inequality on poor self-rated health22; however, most alcohol studies have not examined possible moderators of effects of income inequality.Income inequality can be measured overall or by comparing the status of 2 groups. Overall measures incorporate the range and distribution of incomes with the extent of inequality. The most commonly used overall measure is the Gini coefficient.1 By contrast, relative measures emphasize income or poverty differences between groups based on demographic characteristics. For example, between-race income inequality measures summarize differentials in income between various racial/ethnic groups living in the same area and have been used in the criminology literature.23,24 In the United States, there are stark differences in income and poverty status between Whites, Blacks, and Hispanics. In 2000, the ratio of per capita income of Whites to Blacks was 1.66 and of Whites to Hispanics was 1.97, with 15% of Whites, almost 30% of Blacks, and more than 20% of Hispanics having family incomes below the federal poverty threshold.25 Use of these relative measures seems especially relevant given our interest in examining whether race/ethnicity moderates the associations between income inequality and alcohol outcomes.We examined whether income inequality, measured by the Gini coefficient and 2 between-race measures, is associated with light to moderate alcohol consumption, heavy alcohol consumption, alcohol-related consequences, and alcohol dependence. Although not tested explicitly here, heavy (but not light) alcohol consumption may be linked to income inequality primarily through the psychosocial pathway (such as drinking to cope with stress), whereas alcohol problems additionally may be influenced by neomaterial effects of inequality (such as increased policing24 or decreased funding for alcohol treatment services). We also investigated whether associations with inequality were most detrimental for disadvantaged individuals (people in poor neighborhoods, with low household income, or racial/ethnic minority status), which also may suggest neomaterial effects of inequality.3     

Race,Ethnicity, and Self-Reported Hypertension: Analysis of Data From the National Health Interview Survey, 1997–2005

Objective. I estimated the association between race and self-reported hypertension among Hispanics and non-Hispanics and determined whether this association was stronger among non-Hispanics.Methods. With data from the 1997–2005 National Health Interview Survey, I used logistic regression to estimate the strength of the association between race/ethnicity and self-reported hypertension among US adults.Results. The overall prevalence of self-reported hypertension was 24.5%, with lower prevalence among Hispanics (16.7%) than among non-Hispanics (25.2%; P < .01). Blacks, regardless of ethnicity, had the highest prevalence. Compared with non-Hispanic Whites, non-Hispanic Blacks had 48% (odds ratio [OR] = 1.48; 95% confidence interval [CI] = 1.41, 1.55) greater odds of reporting hypertension; Hispanic Whites had 23% (OR = 0.81; 95% CI = 0.76, 0.88) lower odds. There was no difference in the strength of the association between race and self-reported hypertension observed among non-Hispanics (OR for Blacks = 1.47) and among Hispanics (OR for Blacks = 1.20; for interaction, P = 0.43).Conclusions. The previously reported hypertension advantage of Hispanics holds for Hispanic Whites only. As Hispanics continue their rapid growth in the United States, race may have important implications on their disease burden, because most US health disparities are driven by race and its socially patterned experiences.Hypertension affects more than 65 million US adults¹ and is a major risk factor for cardiovascular disease (CVD).^2,3 The prevalence of hypertension in the US population increased by 30% between the third National Health and Nutrition Examination Survey (NHANES III, 1988–1994) and NHANES 1999–2000.¹ Previous studies have consistently reported that, compared with non-Hispanic Whites, Hispanics have a lower prevalence of hypertension and that non-Hispanic Blacks have a higher prevalence of hypertension.^1,2,4–7 However, these studies focused mostly on Mexican Americans, ignoring the heterogeneity of the Hispanic population. For example, because of their colonization patterns, Hispanics can be of any race (i.e., White, Black, or some other race).⁸ Despite the impact of race on health in US society^9–11 and the projected growth of the Hispanic population,^12–14 there is a dearth of knowledge addressing the relationship between race and health among Hispanics. However, the evidence that does exist parallels findings observed among non-Hispanics: Hispanic Blacks experience worse health outcomes than do Hispanic Whites.^15–18 Thus, the investigation of race and health outcomes in Hispanics is imperative.Hypertension has been attributed to obesity, sodium and potassium intake, physical inactivity, alcohol consumption, smoking, and psychosocial stress.³ Of these, only psychosocial stress has been shown to be unequally distributed across racial/ethnic groups. Research suggests that racial discrimination—a trigger of psychosocial stress—is common in the everyday life of non-Hispanic Blacks and may lead to CVD.^19–26 Given this, and consistent with the historical pattern of disadvantage among non-Hispanic Blacks,^9,11,27,28 it is possible that Hispanic Blacks could be exposed to the same deleterious experiences of racial discrimination and racism as non-Hispanic Blacks because of the salience and social visibility associated with their race or dark skin color. These experiences may lead to disadvantaged life chances, which then translate into poorer health.The availability of 9 years of data from the National Health Interview Survey (NHIS, 1997–2005) afforded the opportunity to investigate the association between race and self-reported hypertension in Hispanics and non-Hispanics before and after adjustment for selected characteristics and known risk factors and to compare the strength of this association in Hispanics and non-Hispanics. If race as a social construct channels Hispanic Blacks to exposures detrimental to health as it does for non-Hispanic Blacks, the lower odds of hypertension for Hispanics observed in previous studies would apply only to Hispanic Whites whereas Hispanic Blacks would have odds of hypertension similar to those of non-Hispanic Whites or intermediate between non-Hispanic Whites and non-Hispanic Blacks. However, the magnitude of the association between race and hypertension would be stronger among non-Hispanics than among Hispanics.     

Geographic Residency Status and Census Tract Socioeconomic Status as Determinants of Colorectal Cancer Outcomes

Objectives. We examined the impact of geographic residency status and census tract (CT)-level socioeconomic status (SES) on colorectal cancer (CRC) outcomes.Methods. This was a retrospective cohort study of patients diagnosed with CRC in Georgia for the years 2000 through 2007. Study outcomes were late-stage disease at diagnosis, receipt of treatment, and survival.Results. For colon cancer, residents of lower-middle-SES and low-SES census tracts had decreased odds of receiving surgery. Rural, lower-middle-SES, and low-SES residents had decreased odds of receiving chemotherapy. For patients with rectal cancer, suburban residents had increased odds of receiving radiotherapy, but low SES resulted in decreased odds of surgery. For survival, rural residents experienced a partially adjusted 14% (hazard ratio [HR] = 1.14; 95% confidence interval [CI] = 1.07, 1.22) increased risk of death following diagnosis of CRC that was somewhat explained by treatment differences and completely explained by CT-level SES. Lower-middle- and low-SES participants had an adjusted increased risk of death following diagnosis for CRC (lower-middle: HR = 1.16; 95% CI = 1.10, 1.22; low: HR = 1.24; 95% CI = 1.16, 1.32).Conclusions. Future efforts should focus on developing interventions and policies that target rural residents and lower SES areas to eliminate disparities in CRC-related outcomes.For men and women in the United States, colorectal cancer (CRC) ranks third in incidence and mortality among cancers, with an estimated 142 820 new cases and 50 830 deaths in 2013.1 Reflecting the US population distribution according to geography2 and evidence of similar incidence rates3,4 for rural residents, approximately 20% of incident CRC cases are expected to occur in rural populations. Although CRC incidence is equivalent for rural and urban residents, CRC mortality is higher in rural populations,5 and the causes of rural versus urban disparities in CRC mortality are not well understood. Compared with their suburban and urban counterparts, rural citizens are more likely to be older, live in poverty, have less education, lack health insurance, and have no regular health care provider.6–9 These facets of rural living pose challenges to accessing health promotional messages and high-quality primary care, not to mention treatment of cancer.10,11Those of lower socioeconomic status (SES) have worse health-related outcomes than their more affluent counterparts, and SES often has a gradient effect on health.12 A challenge in studying the association between rurality and health is being able to disentangle the confounding effect of SES associated with geographic residency.13 As we previously demonstrated for a sample of urban and rural residents of Georgia with CRC, rural residence was associated with an increased risk of death following diagnosis.14 A limitation of that study was an inability to account for SES differences between urban and rural populations. If adjustment for SES explains the poorer survival that is associated with rural residence, this explanation provides an opportunity to investigate mediators of the SES effect as potential avenues for intervention.15 Identification of these mediating factors will facilitate the development of focused interventions with the goal of eliminating rural CRC-related disparities.16,17Building on our previous work,14 we evaluated the independent and combined effects of rurality and area-level SES on CRC outcomes. In our previous study, (1) we were unable to evaluate the independent and potential confounding effect of SES on rurality,2 (2) our study population was a sample of the Georgia CRC population, and (3) residents were classified as urban or rural at the county level, which may have resulted in misclassification. In the present study, the exposures of interest were geographic residency status (rural, suburban, or urban) and area-level SES, both at the census tract (CT) level. In addition, the study population represents the entire state of Georgia rather than a sample. The primary study outcome was overall survival. Secondarily, we wanted to evaluate the effect of SES and geography adjusted for SES on the odds of late-stage disease at diagnosis and receipt of first-course treatment.The findings of this study are meant to bring importance to a highly relevant area of public health research: disparities related to rural versus urban cancer outcomes, and specifically to rural CRC outcomes. As a result, interventions may be designed and policies developed to address the difficulties of accessing and providing high-quality cancer care in rural areas of the United States.11 It is through the combination of applying what is learned from epidemiological findings to community-level interventions and policymaking that the elimination of health disparities will occur.18     

Posttraumatic Stress Disorder and Incident Heart Failure Among a Community-Based Sample of US Veterans

Objectives. We investigated the association between posttraumatic stress disorder (PTSD) and incident heart failure in a community-based sample of veterans.Methods. We examined Veterans Affairs Pacific Islands Health Care System outpatient medical records for 8248 veterans between 2005 and 2012. We used multivariable Cox regression to estimate hazard ratios and 95% confidence intervals for the development of heart failure by PTSD status.Results. Over a mean follow-up of 7.2 years, veterans with PTSD were at increased risk for developing heart failure (hazard ratio [HR] = 1.47; 95% confidence interval [CI] = 1.13, 1.92) compared with veterans without PTSD after adjustment for age, gender, diabetes, hyperlipidemia, hypertension, body mass index, combat service, and military service period. Additional predictors for heart failure included age (HR = 1.05; 95% CI = 1.03, 1.07), diabetes (HR = 2.54; 95% CI = 2.02, 3.20), hypertension (HR = 1.87; 95% CI = 1.42, 2.46), overweight (HR = 1.72; 95% CI = 1.25, 2.36), obesity (HR = 3.43; 95% CI = 2.50, 4.70), and combat service (HR = 4.99; 95% CI = 1.29, 19.38).Conclusions. Ours is the first large-scale longitudinal study to report an association between PTSD and incident heart failure in an outpatient sample of US veterans. Prevention and treatment efforts for heart failure and its associated risk factors should be expanded among US veterans with PTSD.Posttraumatic stress disorder (PTSD) is a psychiatric illness that affects approximately 7.7 million Americans aged older than 18 years.1 PTSD typically results after the experience of severe trauma, and veterans are at elevated risk for the disorder. The National Vietnam Veterans Readjustment Study reported the prevalence of PTSD among veterans who served in Vietnam as 15.2% among men and 8.1% among women.2 In fiscal year 2009, nearly 446 045 Veterans Administration (VA) patients had a primary diagnosis of PTSD, a threefold increase since 1999.3 PTSD is of growing clinical concern as evidence continues to link psychiatric illnesses to conditions such as arthritis,4 liver disease,5 digestive disease,6 and cancer.6 When the postwar health status of Vietnam veterans was examined, those with PTSD had higher rates of diseases of the circulatory, nervous, digestive, musculoskeletal, and respiratory systems.7The evidence linking PTSD to coronary heart disease (CHD) is substantial.8–10 Veterans with PTSD are significantly more likely to have abnormal electrocardiograph results, myocardial infarctions, and atrioventricular conduction deficits than are veterans without PTSD.11 In a study of 605 male veterans of World War II and the Korean War, CHD was more common among veterans with PTSD than among those without PTSD.12 Worldwide, adults exposed to the disaster at Chernobyl experienced increased rates of CHD up to 10 years after the event,13 and studies of stressors resulting from the civil war in Lebanon found elevated CHD mortality.14,15Although the exact biological mechanism by which PTSD contributes to CHD remains unclear, several hypotheses have been suggested, including autonomic nervous system dysfunction,16 inflammation,17 hypercoagulability,18 cardiac hyperreactivity,19 altered neurochemistry,20 and co-occurring metabolic syndrome.16 One of the hallmark symptoms of PTSD is hyperarousal,21 and the neurobiological changes brought on from sustained sympathetic nervous system activation affect the release of neurotransmitters and endocrine function.22 These changes have negative effects on the cardiovascular system, including increased blood pressure, heart rate, and cardiac output.22,23Most extant literature to date examining cardiovascular sequelae has shown a positive association between PTSD and coronary artery disease.8–10 Coronary artery disease is well documented as one of the most significant risk factors for future development of heart failure.24 Despite burgeoning evidence for the role of PTSD in the development of coronary artery disease, there are few studies specifically exploring the relationship between PTSD and heart failure. Limited data suggest that PTSD imparts roughly a threefold increase in the odds of developing heart failure in both the general population5 and in a sample of the elderly.25 These investigations, however, have been limited by cross-sectional study design, a small proportion of participants with PTSD, and reliance on self-reported measures for both PTSD and heart failure.5,25 Heart failure is a uniquely large public health issue, as nearly 5 million patients in the United States are affected and there are approximately 500 000 new cases each year.26 Identifying predictors of heart failure can aid in early detection efforts while simultaneously increasing understanding of the mechanism behind development of heart failure.To mitigate the limitations of previous investigations, we undertook a large-scale prospective study to further elucidate the role of prevalent PTSD and development of incident heart failure among veterans, while controlling for service-related and clinical covariates. Many studies investigating heart failure have relied on inpatient records; we leveraged outpatient records to more accurately reflect the community burden of disease.     

Trust,Medication Adherence,and Hypertension Control in Southern African American Men

We examined the relationship between trust in the medical system, medication adherence, and hypertension control in Southern African American men. The sample included 235 African American men aged 18 years and older with hypertension. African American men with higher general trust in the medical system were more likely to report better medication adherence (odds ratio [OR] = 1.06), and those with higher self-efficacy were more likely to report better medication adherence and hypertension control (OR = 1.08 and OR = 1.06, respectively).Trust remains an important issue with African Americans (AAs), particularly in the South where its history of mistreatment and racial discrimination at times were highly prevalent.1 Racial and ethnic minorities are more prone than are Whites to distrust the health care establishment, and historically, minority men have had less access to culturally competent providers.2–4 Southern AAs are more likely than are Whites to report perceived racial barriers to care,5 and AA men are more likely than are AA women to report perceived discrimination.6–10 Perceived discrimination and mistreatment are associated with poorer medical adherence and delays in seeking health care.11–14 In addition, higher levels of trust in the health care system are associated with better adherence to recommended care, greater patient satisfaction, and better outcomes.15–18 This has significant implications considering that AA men develop hypertension (HTN) at an earlier age, have higher rates of advanced (stage 3) HTN, are more likely to experience HTN complications, and are less likely to achieve HTN-control compared with White men.19–21 The rates of HTN are even higher in the South for AA men, accounting, in part, for higher stroke (80% higher) and cardiovascular mortality (50% higher) in this subpopulation compared with other groups in other regions.21–23The goal of this brief study was to assess the relationship between trust in the medical, medication adherence,24 and HTN control25 among Southern AA men. Other covariates were perceived discrimination, perceived racism, self-efficacy, and participation in medical decision-making. This study is based on the Race and Health Outcomes Model developed by Williams et al.26     

The Effect of a “Maintain,Don’t Gain” Approach to Weight Management on Depression Among Black Women: Results From a Randomized Controlled Trial

Objectives. We evaluated the effect of a weight gain prevention intervention (Shape Program) on depression among socioeconomically disadvantaged overweight and obese Black women.Methods. Between 2009 and 2012, we conducted a randomized trial comparing a 12-month electronic health–based weight gain prevention intervention to usual primary care at 5 central North Carolina community health centers. We assessed depression with the Patient Health Questionnaire (PHQ-8). We analyzed change in depression score from baseline to 12- and 18-month follow-up across groups with mixed models. We used generalized estimating equation models to analyze group differences in the proportion above the clinical threshold for depression (PHQ-8 score ≥ 10).Results. At baseline, 20% of participants reported depression. Twelve-month change in depression scores was larger for intervention participants (mean difference = −1.85; 95% confidence interval = −3.08, −0.61; P = .004). There was a significant reduction in the proportion of intervention participants with depression at 12 months with no change in the usual-care group (11% vs 19%; P = .035). All effects persisted after we controlled for weight change and medication use. We saw similar findings at 18 months.Conclusions. The Shape Program, which includes no mention of mood, improved depression among socioeconomically disadvantaged Black women.Depression is one of the most common and disabling, yet treatable, mental health conditions in the United States.1,2 Women are twice as likely as men to be affected,3 and more than 1 in 7 (14.9%) Black women will experience major depression in their lifetime.4 Observational evidence suggests that, although the prevalence of major depression is lower among Blacks than Whites, its severity is greater for Blacks.5 This is likely a result of racial disparities in access to depression treatment.6 Indeed, compared with their White counterparts, Black adults with depression are less likely to receive treatment for depression (39.7% vs 54.0%).6 Of those who do seek treatment, Blacks are less likely than Whites to receive care that corresponds to clinical practice guidelines.6,7 These racial disparities are magnified by socioeconomic disadvantage.8 Depression is 3 times more common for those with incomes below the federal poverty level, compared with those with higher incomes.9 As a consequence, the challenge remains how to effectively treat socioeconomically disadvantaged Black women with depression.Obesity is also disproportionately prevalent among Black women relative to other racial/ethnic groups.10 The high burden of obesity among Black women not only indicates a higher prevalence of obesity-related chronic diseases (e.g., diabetes, heart disease),11 but it may also have an impact on psychosocial outcomes such as depression.12 As such, interventions focusing on behavioral weight control may present a useful opportunity to address both obesity and depression.Behavioral weight loss interventions typically include frequent contact with a weight loss counselor; self-monitoring of diet, exercise, and weight; and lessons that cover various topics such as problem solving, relapse prevention, and stress management. Indeed, across numerous studies, behavioral weight loss interventions have been shown to promote reductions in depression.13,14 Such findings are generally believed to be related to weight loss15 and mediated by improvements in body satisfaction; that is, for many, weight loss might enhance body satisfaction and, thus, improve depression outcomes.16,17 However, this finding has most frequently been demonstrated in predominantly socioeconomically advantaged White women, who tend to exhibit strong relations between body size and mood.16,18 In contrast, Black women have greater social acceptance of overweight, less body weight dissatisfaction, and higher body weight ideals compared with White women.19–22 Thus, it is unclear whether Black women would experience a similar reduction in depression as a result of obesity treatment.Although weight loss is indicated for those with obesity, promoting clinically meaningful weight change among Black women has been a major challenge.23 Across various studies, Black women achieve less weight loss relative to White women.24–26 The reason for this racial disparity in weight loss outcomes is unclear, but may be influenced in part by differences in sociocultural norms related to weight, diet, and physical activity.27 As a result, interventions that focus on preventing weight gain may be a useful alternative treatment approach among overweight and obese Black women.27We recently conducted a study titled the Shape Program, a 12-month randomized controlled trial with follow-up at 18 months, evaluating an electronic health weight gain prevention intervention among Black women compared with usual care in the primary care setting.27 The Shape intervention was found to be effective in staving off weight gain at 12 and 18 months.28 It is unclear whether a weight gain prevention approach, as was tested in Shape, would be helpful for treating depression among Black women. As such, we sought to examine the potential spillover benefits produced by this “maintain, don’t gain” approach on depression, compared with usual care.     

Community Socioeconomic Disadvantage and the Survival of Infants With Congenital Heart Defects

Objectives. We examined the association between survival of infants with severe congenital heart defects (CHDs) and community-level indicators of socioeconomic status.Methods. We identified infants born to residents of Arizona, New Jersey, New York, and Texas between 1999 and 2007 with selected CHDs from 4 population-based, statewide birth defect surveillance programs. We linked data to the 2000 US Census to obtain 11 census tract–level socioeconomic indicators. We estimated survival probabilities and hazard ratios adjusted for individual characteristics.Results. We observed differences in infant survival for 8 community socioeconomic indicators (P < .05). The greatest mortality risk was associated with residing in communities in the most disadvantaged deciles for poverty (adjusted hazard ratio [AHR] = 1.49; 95% confidence interval [CI]  = 1.11, 1.99), education (AHR = 1.51; 95% CI = 1.16, 1.96), and operator or laborer occupations (AHR = 1.54; 95% CI = 1.16, 1.96). Survival decreased with increasing numbers of indicators that were in the most disadvantaged decile. Community-level mortality risk persisted when we adjusted for individual-level characteristics.Conclusions. The increased mortality risk among infants with CHDs living in socioeconomically deprived communities might indicate barriers to quality and timely care at which public health interventions might be targeted.Advances in medical and surgical care for individuals born with congenital heart defects (CHDs) has improved survival in recent years, yet despite this progress, mortality due to CHDs remains a significant public health issue.1,2 CHDs are the most common type of birth defect and are the leading cause of death among those born with birth defects.3,4 CHDs necessitate medical and often surgical intervention early in life, and timely detection and quality care can improve health outcomes.5,6 Medical factors such as low birth weight, preterm birth, severity of the condition, and the presence of comorbidities are well-established risk factors for mortality, particularly during the neonatal period.7 Nonmedical factors (particularly race/ethnicity) also play an important role in the survival of infants with birth defects and potentially contribute significantly to unexplained survival differences.8 Several factors that influence access to and use of care have been examined among cohorts of infants born with CHDs, but these have been limited to race/ethnicity,2,9–16 medical insurance,9,16–20 and distance to specialty care.10,17,21,22 Assessment of the potential impact of socioeconomic status (SES) on survival has been challenging, largely because SES has been defined and measured in many ways and is often unavailable in large, population-based data sets. SES has been investigated as a risk factor for the occurrence of different types of birth defects,23–28 but few published population-based studies have included SES as a risk factor for CHD-related mortality.Community-level factors related to socioeconomic conditions have been associated with decreased access to pediatric subspecialty care and early mortality of infants with low birth weight,29,30 and they might provide evidence of contextual factors that could potentially influence the survival of infants with CHDs, who require timely medical intervention.31–33 In this population-based study, we estimated the association of census tract–level indicators of SES with the survival of infants born with CHDs and examined the potential impact of communities on observed racial/ethnic disparities in infant survival.     

Socioeconomic Status and Bullying: A Meta-Analysis

We examined whether socioeconomic status (SES) could be used to identify which schools or children are at greatest risk of bullying, which can adversely affect children’s health and life.We conducted a review of published literature on school bullying and SES. We identified 28 studies that reported an association between roles in school bullying (victim, bully, and bully-victim) and measures of SES. Random effects models showed SES was weakly related to bullying roles. Adjusting for publication bias, victims (odds ratio [OR] = 1.40; 95% confidence interval [CI] = 1.24, 1.58) and bully-victims (OR = 1.54; 95% CI = 1.36, 1.74) were more likely to come from low socioeconomic households. Bullies (OR = 0.98; 95% CI = 0.97, 0.99) and victims (OR = 0.95; 95% CI = 0.94, 0.97) were slightly less likely to come from high socioeconomic backgrounds.SES provides little guidance for targeted intervention, and all schools and children, not just those with more socioeconomic deprivation, should be targeted to reduce the adverse effects of bullying.Bullying is defined as repeated, harmful behavior, characterized by an imbalance of power between the victim and perpetrator(s).1 There is compelling evidence that school bullying affects children’s health and well being, with the effects lasting long into adulthood.2,3 Victims of school bullying are at greater risk of physical and mental health problems,4,5 including depression,6,7 anxiety,8,9 psychotic or borderline personality symptoms,10,11 and are more likely to self-harm and attempt suicide.12,13 A small proportion of victims are classified as bully-victims, children who are victimized by their peers, but who also bully other children. Bully-victims are at even greater risk for maladjustment,5 exhibiting attention and behavioral difficulties,4,14 displaying poor social skills,15,16 and reporting increased levels of depression and anxiety through adolescence and into adulthood.2 By contrast, the negative outcomes of bullying perpetration are less clear. Bullies have been found more likely to engage in delinquent or antisocial behavior17,18; however, once other family and childhood risk factors are taken into account, they do not appear to be at any greater risk for poorer health, criminal, or social outcomes in adulthood.3Up to one third of children are involved in bullying, as bully, victim, or bully-victim,19,20 and when considered alongside the damaging effects on physical and mental health, bullying can be seen as a major public health concern.21 Identifying risk factors for bullying aids potential efforts in targeting resources, which can prevent youths from becoming involved in bullying, but also limits the impact it has on their health and well being. Traditional risk factors, such as age and gender, show a clear association22,23; however, there are a range of other potential determinants whose relationship to bullying remain unclear. One such determinant is socioeconomic status (SES), which shows some links to bullying, but at present, research findings are inconsistent regarding roles (i.e., bully, victim, or bully-victim).SES is an aggregate concept comprising resource-based (i.e., material and social resources) and prestige-based (individual’s rank or status) indicators of socioeconomic position, which can be measured across societal levels (individual, household, and neighborhood) and at different periods in time.24 It can be assessed through individual measures, such as education, income, or occupation,25,26 but also through composite measures that combine or assign weights to different socioeconomic aspects to provide an overall index of socioeconomic level. There is no standard measure of SES; indicators are used to measure specific aspects of socioeconomic stratification.26 Accordingly, different measures of SES may show varying effects, which can result from differing causal pathways, or through interactions with other social characteristics, such as gender or race.27 The multifaceted nature of SES has resulted in a lack of consistency in how researchers measure its relationship to bullying, and although several studies provide individual assessments of this relationship, as yet there is no clear consensus over whether roles in bullying are associated with individual socioeconomic measures, or in general, with SES.Currently, the literature suggests some link between low SES and victims or bully-victims at school.28,29 Specifically, being a victim has been reported to be associated with poor parental education,30,31 low parental occupation,32 economic disadvantage,33,34 and poverty.35 In addition, several studies found that bully-victims are also more likely to come from low socioeconomic backgrounds,29,30 including low maternal education28 and maternal unemployment.36 However, others found little or no association between SES and victims or bully-victims.37–39 The type of bullying may matter in relation to SES. Victims of physical and relational bullying have been found to more often come from low affluence families, whereas victims of cyber bullying have not.40Compared with victimization, few studies have explored the link between SES and bullying others. Some studies found bullying others to be associated with low SES, including economic disadvantage,34 poverty,35 and low parental education.30 Additionally, where composite measures have been used, children from low socioeconomic backgrounds have been found to bully others slightly more often.29,41 By contrast, others found no association between bullying perpetration and measures of SES.38,39,42There is a small but growing body of literature that examines the relationship between bullying and SES, and although findings tend to suggest that victims, bully-victims, and bullies are more likely to come from low socioeconomic backgrounds, the results are far from conclusive. First, studies differ in their approach to measuring SES; some use composite measures, combining multiple indicators such as parental education, wealth, and occupation, whereas others concentrate on a single socioeconomic indicator, most often parental education, affluence, or occupation. How bullying relates to SES may differ according to which socioeconomic indicator is used; therefore, in interpreting results, one must consider not only how bullying relates to SES in general, but also which socioeconomic indicator was used, and how this may have influenced the result. Furthermore, although several studies indicate an association between bullying and low SES, the reported effect sizes vary greatly across studies, with some reporting weak and others moderate to strong associations. So far, the associations between bullying and SES have not been quantified across a range of studies in a systematic way. To address this gap in the literature, we conducted a systematic review and meta-analysis that aimed to determine more precisely the exact nature and strength of the relationship between SES and bullying. We systematically investigated the association between the role taken in school bullying (victim, bully, or bully-victim) and measures of SES.     

Mortality Patterns of Native Hawaiians Across Their Lifespan: 1990�C2000

Objectives. We examined mortality patterns across the lifespan of Native Hawaiians and compared mortality disparities across races.Methods. We determined the age-specific and age-adjusted mortality rates of Native Hawaiians from 1990 to 2000 by using national census and vital registration data.Results. Among Native Hawaiians aged younger than 1 year, expected deaths were 15% lower than for Blacks and 50% higher than for Whites. Among older adults, Native Hawaiians had higher rates of mortality compared with the general population, particularly in 1990 and 1995. Crude death rates for Native Hawaiians were similar to those for Blacks in 1990 and 1995 but were 20% lower than those for Blacks by 2000. Crude death rates for Native Hawaiians were 30% higher than for Whites in 1990 and 1995 and more than 40% higher than for Whites in 2000.Conclusions. Compared with Whites, Native Hawaiians and Blacks face similar challenges regarding infant and early-life mortality and increasing risks of mortality in mid-life and early old age. Our analyses document a need for renewed efforts to identify the determinants of ill health and commitment to address them.In 1997, the US Office of Management and Budget (OMB) implemented a new classification for identifying racial groups that, for the first time, designated “Native Hawaiians and Other Pacific Islanders” (NHPIs) as a distinct racial group, separate from Asians.^1,2 Traditionally, Pacific Islanders have been aggregated with Asian populations in statistical reports and public-use data sets under the “Asian/Pacific Islander” category. This Asian/Pacific Islander grouping has created ongoing measurement problems because of high levels of heterogeneity within the category.^3–5 The disaggregation of Asians from the category comprising NHPIs was a major first step in accurately characterizing these culturally, linguistically, demographically, and sociopolitically diverse populations.^6–10 Additionally, the OMB 1997 classification of race and ethnicity facilitated new opportunities for analysis of national-level data on NHPI health.^11–19The Native Hawaiian group represents the largest sector (46%) of the NHPI population²⁰ and is the only indigenous subpopulation within the NHPI designation. Thus, the Native Hawaiian population is similar sociopolitically to other indigenous populations such as American Indians and Alaska Natives, in that their indigenous status reflects a distinct relationship with the US federal government, which can have important implications for their health. Historically, Native Hawaiians were the first inhabitants of the Hawaiian archipelago. Their population was about 800 000 at the time of the first Western contact ²¹ in 1778, although by the early 1900s, the introduction of new diseases and cultures had reduced the native population by 85%.^22–29Little is known about the health of Native Hawaiians outside of the state of Hawaii, owing in large part to the sample limitation in most national-level surveys. An accurate assessment of morbidity and mortality among Native Hawaiians has also been hampered by their aggregation with Asians, which increased sample sizes but made it impossible to look at heterogeneity within this diverse population.^30,31 Still, reports of health outcomes among NHPIs have increased somewhat in recent years. These reports suggest that NHPIs face elevated risks for cardiovascular disease,¹⁹ poor health,^13,14,17,18 cancer,^15,16 obesity and diabetes,^32,33 and mortality across the life course.^11,12,34,35 However, baseline health statistics from larger national databases on specific health issues, which represent a vital element for informing policies on NHPI health and well-being, remain sparse.Because mortality represents a key outcome measure to inform policymakers and public health officials on the overall health of a population, we examined mortality patterns across the lifespan of Native Hawaiians. Using well-established demographic estimation techniques, we calculated age-specific and age-adjusted mortality for the period 1990 through 2000, allowing us to compare Native Hawaiian health disparities with those of Blacks and Whites.     

A Novel Look at Racial Health Disparities: The Interaction Between Social Disadvantage and Environmental Health

Objectives. We explored the notion that social disadvantage increases vulnerability to the health effects of environmental hazards. Specifically, we examined (1) whether race modifies the association between blood lead and blood pressure and (2) whether socioeconomic status (SES) plays a role in this modifying effect.Methods. Using the National Health and Nutrition Examination Survey (2001–2008) and linear regression, we estimated the association between blood lead and blood pressure. Using interactions among race, SES, and lead, we estimated this association by levels of social disadvantage.Results. Black men and women showed a 2.8 (P < .001) and 4.0 (P < .001) millimeters mercury increase in SBP, respectively, for each doubling of blood lead. White adults showed no association. This lead–SBP association exhibited by Blacks was primarily isolated to Blacks of low SES. For example, poor but not nonpoor Black men showed a 4.8 millimeters mercury (P < .001) increase in SBP for each doubling of blood lead.Conclusions. Our results suggest that social disadvantage exacerbates the deleterious health effects of lead. Our work provides evidence that social and environmental factors must be addressed together to eliminate health disparities.Black–White disparities in hypertension have been well-documented for decades.1–3 A 2010 American Heart Association report put nationwide prevalence estimates at roughly 33% for White adults but 43% for Black adults.4 Economically, if Black Americans had the hypertension rates of White Americans, about $400 million would have been saved in out-of-pocket health care expenses, about $2 billion would have been saved in private insurance costs, and $375 million would have been saved from Medicare and Medicaid—per year.5 More seriously, disparities are also seen in outcomes related to hypertension. For example, mortality rates because of hypertension are roughly 15 deaths per 100 000 people for White men and women; but 40 and more than 50 per 100 000 for Black men and women, respectively.4 Disparities in hypertension account for the greatest disparities in years of lost life compared with any other health condition.6A growing body of literature in different disciplines indicates that both social and environmental factors are important in the production and maintenance of hypertension disparities.7–10 There are racial disparities in numerous social factors, such as socioeconomic status (SES), that have a robust association with hypertension.2 For example, 2009 estimates put 26% of Blacks living in poverty compared with only 12% of Whites.11 Importantly, however, controlling for poverty does not attenuate the racial disparities in hypertension, indicating that there are complex mechanisms at work.12 There are also racial disparities in numerous environmental hazards, some of which are associated with hypertension. For example, lead is causally associated with a modest increase in blood pressure and risk of hypertension in a dose-dependent manner13–16 through several biological mechanisms, including increases in oxidative stress and alterations in control of the cardiovascular system.17 Furthermore, racial disparities in lead have been reported for decades.18,19In the environmental health literature, researchers have described the notion of differential vulnerability to the deleterious health effects of environmental hazards.20,21 Some have shown that psychosocial stress and social stressors potentiate the association between lead and blood pressure. For example, in 1 study, men who report high levels of perceived stress show an association between bone lead and blood pressure, whereas men who do not report high levels of stress do not reveal this association.22 Similarly, those adults who have higher allostatic load scores, a measure of stress-related wear and tear on the body, show a stronger association between blood lead and the odds of hypertension compared with adults with lower allostatic load scores.23,24It may be that this differential vulnerability, resulting from differential exposure to social factors, contributes to racial disparities in hypertension.25 In other words, it may be that the greater social stressors and psychosocial stress experienced by Black compared with White Americans may exacerbate the health effects of environmental hazards, including lead. In fact, researchers have reported that there is a modifying effect of race on the association between blood lead and blood pressure. Specifically, Black adults exhibit a roughly 1 millimeter mercury increase in systolic blood pressure for every 3 micrograms increase in blood lead.26 Yet, no such association is seen for Whites.19,26,27 It may be that, compared with White adults, Black adults show a stronger association between lead and blood pressure because they experience greater social stressors, such as higher levels of poverty.In the present study, we have updated and expanded on previous work by examining the notion that social disadvantage, as marked by race and SES, modifies the association between blood lead and blood pressure. Specifically, we first updated the literature on the modifying effect of race on the association between blood lead and blood pressure. The most recent work in this area is based on data from 1988 to 1991. Blood lead levels have continued to decline for both Blacks and Whites.19 Because there is a dose-dependent association between lead and blood pressure, it is not known whether blood lead and blood pressure are associated for Black adults using current data (2001 to 2008). Second, we examined the role of SES, specifically education and poverty, in the stronger association between blood lead and blood pressure seen in Black compared with White adults.     

Life-Course Socioeconomic Position and Incidence of Diabetes Mellitus Among Blacks and Whites: The Alameda County Study, 1965�C1999

Objectives. We examined associations between several life-course socioeconomic position (SEP) measures (childhood SEP, education, income, occupation) and diabetes incidence from 1965 to 1999 in a sample of 5422 diabetes-free Black and White participants in the Alameda County Study.Methods. Race-specific Cox proportional hazard models estimated diabetes risk associated with each SEP measure. Demographic confounders (age, gender, marital status) and potential pathway components (physical inactivity, body composition, smoking, alcohol consumption, hypertension, depression, access to health care) were included as covariates.Results. Diabetes incidence was twice as high for Blacks as for Whites. Diabetes risk factors independently increased risk, but effect sizes were greater among Whites. Low childhood SEP elevated risk for both racial groups. Protective effects were suggested for low education and blue-collar occupation among Blacks, but these factors increased risk for Whites. Income was protective for Whites but not Blacks. Covariate adjustment had negligible effects on associations between each SEP measure and diabetes incidence for both racial groups.Conclusions. These findings suggest an important role for life-course SEP measures in determining risk of diabetes, regardless of race and after adjustment for factors that may confound or mediate these associations.Diabetes mellitus is a major cause of morbidity and mortality in the United States.^1,2 Type 2 diabetes disproportionately affects Hispanics, as well as non-Hispanic Black Americans, American Indians/Alaska Natives, and some Asian/Pacific Islander groups. In the United States, members of racial and ethnic minority groups are almost twice as likely to develop or have type 2 diabetes than are non-Hispanic Whites.^2–5 Significant racial and ethnic differences also exist in the rates of diabetes-related preventive services, quality of care, and disease outcomes.^6–10Researchers have attempted to determine why, relative to Whites, members of racial and ethnic minority groups are disproportionately affected by diabetes. For example, compared with White Americans, Black Americans are presumed to have stronger genetic^5,11 or physiological^11–13 susceptibility to diabetes, or greater frequency or intensity of known diabetes risk factors, such as obesity, physical inactivity, and hypertension.^14–17Black Americans also are more likely than are White Americans to occupy lower socioeconomic positions.¹⁸ Low socioeconomic position (SEP) across the life course is known to influence the prevalence^19–24 and incidence^3,19,25–30 of type 2 diabetes. The risk of diabetes also is greater for people who are obese,^3,17,31 physically inactive,^3,32 or have hypertension,^33,34 all of which are conditions more common among people with lower SEP.^16,35–37Several studies have focused on the extent to which socioeconomic factors, body composition (i.e., weight, height, body mass index, and waist circumference), and behaviors explain the excess risk of diabetes attributed to race.^4,12,19,30 For example, 2 separate studies, one with data from the Health and Retirement Study¹⁹ and the other with data from the Atherosclerosis Risk in Communities Study,³⁰ used race to predict diabetes incidence. Attempting to separate the direct and indirect effects of race on diabetes,³⁸ these studies assessed, via statistical adjustment, which socioeconomic measures and diabetes-related risk factors, when adjusted, could account for the excess risk among Black participants relative to White participants.^19,30 Adjustment for education lessened the effect of Black race on diabetes incidence in the Atherosclerosis Risk in Communities Study.³⁰ In the Health and Retirement Study, excess risk attributed to Black race was not explained by early-life socioeconomic disadvantage, but it was reduced after adjustment for education and later-life economic resources.¹⁹ The validity of this analytic approach has been challenged, however, because the socioeconomic measures used were assumed to have the same meaning across all racial/ethnic groups, a questionable assumption³⁸ in the United States, especially in 1965.We sought to explore the predictive effects of several life-course socioeconomic factors on the incidence of diabetes among both Black and White Americans. We examined demographic confounders (age, gender, marital status) and diabetes risk factors (obesity, large waist circumference, physical inactivity, high blood pressure, depression, access to health care) as possible mediators of the observed associations between SEP and incident diabetes (i.e., the development of new cases of diabetes over time).     

Social Branding to Decrease Smoking Among Young Adults in Bars

Objectives. We evaluated a Social Branding antitobacco intervention for “hipster” young adults that was implemented between 2008 and 2011 in San Diego, California.Methods. We conducted repeated cross-sectional surveys of random samples of young adults going to bars at baseline and over a 3-year follow-up. We used multinomial logistic regression to evaluate changes in daily smoking, nondaily smoking, and binge drinking, controlling for demographic characteristics, alcohol use, advertising receptivity, trend sensitivity, and tobacco-related attitudes.Results. During the intervention, current (past 30 day) smoking decreased from 57% (baseline) to 48% (at follow-up 3; P = .002), and daily smoking decreased from 22% to 15% (P < .001). There were significant interactions between hipster affiliation and alcohol use on smoking. Among hipster binge drinkers, the odds of daily smoking (odds ratio [OR] = 0.44; 95% confidence interval [CI] = 0.30, 0.63) and nondaily smoking (OR = 0.57; 95% CI = 0.42, 0.77) decreased significantly at follow-up 3. Binge drinking also decreased significantly at follow-up 3 (OR = 0.64; 95% CI = 0.53, 0.78).Conclusions. Social Branding campaigns are a promising strategy to decrease smoking in young adult bar patrons.Tobacco companies1 and public health authorities2–5 recognize young adulthood as a critical time when experimenters either quit or transition to regular tobacco use. Young adults are also aspirational role models for youths.1,6,7 Tobacco companies devote considerable resources to reaching young adults to encourage tobacco use,1,8–11 and young adults have a high prevalence of smoking.12 In California in 2011, young adults had the highest smoking prevalence of any age group, and the Department of Health estimated that 32% of California smokers started smoking between the ages of 18 and 26 years.13 Although they are more likely to intend to quit and successfully quit than older adults,14–17 young adults are less likely to receive assistance with smoking cessation.18,19 Although there are few proven interventions to discourage young adult smoking,20 cessation before age 30 years avoids virtually all of the long-term adverse health effects of smoking.21Tobacco companies have a long history of using bars and nightclubs to reach young adults and to encourage smoking.1,6,9–11,22–24 Bar attendance and exposure to tobacco bar marketing is strongly associated with smoking.25 The 1998 Master Settlement Agreement and Food and Drug Administration regulations that limit tobacco advertising to youths, explicitly permit tobacco marketing in “adult only” venues, including bars and nightclubs.26,27Aggressive tobacco marketing may actually be more intensive in smoke-free bars: a 2010 study of college students attending bars found that students in the community with a smoke-free bar law were more likely to be approached by tobacco marketers, offered free gifts, and to take free gifts for themselves than in communities without a smoke-free bar law.28 Bars and nightclubs also attract young adults who are more likely to exhibit personality traits such as sensation seeking,29 increasing their risk30 independently of receptivity to tobacco advertising; tobacco promotional messages resonate with these personality traits.8,31 Tobacco marketing campaigns are tailored to specific segments of the population defined by psychographics (e.g., values, attitudes, shared interests, such as tastes in music and fashion, and friend groups) and demographic criteria, and they aim to create positive smoker images, identities, and social norms for smoking.1,8 Tobacco marketing campaigns also focus on young adult trendsetters to leverage peer influence to promote smoking.6,10In contrast to the tobacco companies’ efforts, most young adult health interventions take place in colleges or health centers rather than social environments.32–39 Bars and nightclub venues represent an opportunity to reach those at highest risk for long-term smoking morbidity and mortality.40 We evaluated the effectiveness of an intervention to decrease cigarette smoking by countering tobacco industry marketing strategies targeting young adults attending bars and nightclubs in the San Diego, California, “hipster” scene. Because tobacco and alcohol use are strongly linked,41,42 we also examined the effects of the intervention on alcohol use and among binge drinkers. We found a significant decrease in smoking in the community where the intervention took place, including significant decreases among nondaily smokers and binge drinkers, as well as a significant decrease in binge drinking.     

Meta-analysis of All-Cause Mortality According to Serum 25-Hydroxyvitamin D

We examined the relationship between serum 25-hydroxyvitamin D (25[OH]D) and all-cause mortality. We searched biomedical databases for articles that assessed 2 or more categories of 25(OH)D from January 1, 1966, to January 15, 2013. We identified 32 studies and pooled the data.The hazard ratio for all-cause mortality comparing the lowest (0–9 nanograms per milliliter [ng/mL]) to the highest (> 30 ng/mL) category of 25(OH)D was 1.9 (95% confidence interval = 1.6, 2.2; P < .001). Serum 25(OH)D concentrations less than or equal to 30 ng/mL were associated with higher all-cause mortality than concentrations greater than 30 ng/mL (P < .01).Our findings agree with a National Academy of Sciences report, except the cutoff point for all-cause mortality reduction in this analysis was greater than 30 ng/mL rather than greater than 20 ng/mL.An inverse association was proposed between solar irradiance and incidence of colon and breast cancer, based on a mechanism involving insufficient vitamin D. Individuals with lower serum 25-hydroxyvitamin D (25[OH]D) have higher risk of breast1–3 and colon cancer,4–6 other specific cancers,7 all invasive cancers combined,8 and coronary heart disease.9,10 Physiological mechanisms for the inverse association of 25(OH)D with cancer have been reported.11Despite research on the association between low vitamin D status and many diseases,12 no consensus has emerged on the optimal serum 25(OH)D concentration. The concern is whether it is safe to maintain serum 25(OH)D concentrations in the range high enough to prevent some types of cancers13–15 and coronary heart disease.9,10We decided to analyze the strength and consistency of the inverse association between levels of serum 25(OH)D and age-adjusted mortality hazard ratios in a rapidly expanding field of public health. A previous meta-analysis summarized 12 studies,16 another summarized 14,17 and another summarized a broader range.18We hypothesized that lower serum 25(OH)D was associated with higher all-cause mortality hazard ratios, and defined the age-adjusted hazard ratio for death from any cause as the outcome addressed by the meta-analysis. This analysis includes all studies of all-cause mortality hazard ratios by categories of serum 25(OH)D in healthy or general medical clinic cohorts that met the eligibility criteria. Twenty new studies of serum 25(OH)D and all-cause mortality entered the literature since the Zittermann et al. review,17 for a total of 32 in this review.19–50 Two studies in the review by Zittermann et al. did not meet the stringent inclusion criterion of the present study, and were not included.     

Clustering of Midlife Lifestyle Behaviors and Subsequent Cognitive Function: A Longitudinal Study

Objectives. We examined the association between individual and clustered lifestyle behaviors in middle age and later in cognitive functioning.Methods. Middle-aged participants (n = 2430) in the Supplémentation en Vitamines et Minéraux Antioxydant study self-reported their low physical activity, sedentary behavior, alcohol use, smoking, low fruit and vegetable consumption, and low fish consumption. We assessed cognition 13 years later via 6 neuropsychological tests. After standardization, we summed the scores for a composite cognitive measure. We estimated executive functioning and verbal memory scores using principal component analysis. We estimated the mean differences (95% confidence intervals [CIs]) in cognitive performance by the number of unhealthy behaviors using analysis of covariance. We identified latent unhealthy behavior factor via structural equation modeling.Results. Global cognitive function and verbal memory were linearly, negatively associated with the number of unhealthy behaviors: adjusted mean differences = −0.36 (95% CI = −0.69, −0.03) and −0.46 (95% CI = −0.80, −0.11), respectively, per unit increase in the number of unhealthy behaviors. The latent unhealthy behavior factor with low fruit and vegetable consumption and low physical activity as main contributors was associated with reduced verbal memory (RMSEA = 0.02; CFI = 0.96; P = .004). No association was found with executive functioning.Conclusions. Comprehensive public health strategies promoting healthy lifestyles might help deter cognitive aging.Noncommunicable diseases with notable lifestyle components are the leading causes of death worldwide.1,2 There is also growing evidence of the critical role of different midlife health and risk behaviors in cognitive aging.3–7 Because lifestyles are inherently modifiable and no treatment of cognitive decline is available, such findings argue for the paramount importance of prevention.8,9Current data support a deleterious effect of alcohol abstinence or abuse (compared with moderate alcohol consumption),10 smoking,7 low fruit and vegetable intake,11 low fish intake,12 and low physical activity (PA) levels13 on cognitive aging. However, it has been widely documented that lifestyle factors are strongly correlated with each other, forming a cluster of healthy or unhealthy behaviors.14 Traditionally, such interrelations have been accounted for by statistical adjustment; however, it is of major public health interest to consider the cumulative and combined effect of the various lifestyle behaviors on health by using multidimensional strategies.14Research that examines the combined effect of lifestyle factors on mortality is plentiful, and data have been colligated in a recent meta-analysis.15 These authors reported a 66% reduction in mortality risk by comparing adherence to 4 or more healthy lifestyle behaviors versus engagement in any number of unhealthy behaviors.The combined effect of lifestyle factors has also been explored in relation to cardiovascular diseases,16–18 cancer,18–22 diabetes,18,23 memory complaints,24 and dementia25–27; however, very few studies have reported findings regarding cognition.28,29 Despite heterogeneity in the definition of a healthy lifestyle, study design, and residual confounding, available, but scarce, data support a critical, protective role of healthy lifestyles in cognitive health through their beneficial properties via oxidative, inflammatory, vascular, and other neuroprotective pathways.30–33Our objectives in this study were to examine the association between individual and clustered lifestyle behaviors and later cognitive functioning. We employed traditional and innovative techniques (structural equation modeling) in our epidemiological pursuit.     

Racial Differences in Breast Cancer Stage at Diagnosis in the Mammography Era

Objectives. We assessed racial differences in breast cancer mortality by stage at diagnosis, since mammography became available.Methods. We calculated adjusted odds of distant (versus local or regional) tumors for 143 249 White and 13 571 Black women aged 50 to 69 years, diagnosed with breast cancer between 1982 and 2007 and living in a Surveillance, Epidemiology, and End Results region. We compared linear trends in stage at diagnosis before and after 1998.Results. Distant-stage cancer was diagnosed in 5.8% of White and 10.2% of Black participants. The Black–White disparity in distant tumors narrowed until 1998 (1998 adjusted difference = 0.65%), before increasing. Between 1982 and 1997, the proportion of distant tumors decreased for Blacks (adjusted odds ratio [AOR]/y = 0.973; 95% confidence interval [CI] = 0.960, 0.987) and Whites (AOR/y = 0.978; 95% CI = 0.973, 0.983), with no racial differences (P = .47). From 1998 to 2007, the odds of distant versus local or regional tumors increased for Blacks (AOR/y = 1.036; 95% CI = 1.013, 1.060) and Whites (AOR/y = 1.011; 95% CI = 1.002, 1.021); the rate of increase was greater for Blacks than Whites (P = .04).Conclusions. In the mammography era, racial disparities remain in stage at diagnosis.Despite a lower incidence of invasive breast cancer, Black women in the United States are more likely than are White women to die of the disease.1,2 Since 1992, although breast cancer deaths have declined in both White and Black women, the overall disparity in mortality has increased.3 Stage at diagnosis is the strongest predictor of survival in breast cancer,4–6 and Black women are more often diagnosed with advanced-stage disease than are White women.7–10Mammography is an important tool in the early detection of breast cancer.11–13 First introduced in the United States in the early 1980s,14 mammography was initially most prevalent among White women. Racial disparities in mammography rates narrowed by the mid-1990s,12,15 and Black women had rates equivalent to or greater than those of White women between 1996 and 2000.10,15,16 From 2000 to 2005, mammography use declined nationally in women aged 50 to 64 years (78.6% to 71.8%), with a slightly larger decrement for White (−4.0%) than Black (−3.3%) women.13The survival benefit of any screening program, including mammography, is related to its ability to detect tumors at earlier stages. Meta-analyses continue to find mortality benefit for mammography, although uncertainty remains regarding both the appropriate target population and the optimal screening interval.11,17,18 Consistent with the expected effect of screening, an observational cohort analysis found that improvements in screening rates for both Black and White women during the 1990s contributed to diagnosis at an earlier stage in both groups.10Nevertheless, despite generally equivalent rates of mammography for the past 15 years, the racial disparity in breast cancer mortality between Black and White women persists. Although previous meta-analyses suggested a mortality benefit for mammography, randomized controlled data regarding the efficacy of screening programs in minority populations are limited.18,19 Because stage at diagnosis is an important predictor of survival in breast cancer, we assessed temporal changes in the distribution of stage at diagnosis between 1982 and 2007, in both Black and White women, adjusting for covariates known to affect stage at diagnosis.