Showing papers by "Sandro Galea published in 2011"

Estimated deaths attributable to social factors in the United States

Abstract: Objectives. We estimated the number of deaths attributable to social factors in the United States. Methods. We conducted a MEDLINE search for all English-language articles published between 1980 and 2007 with estimates of the relation between social factors and adult all-cause mortality. We calculated summary relative risk estimates of mortality, and we obtained and used prevalence estimates for each social factor to calculate the population-attributable fraction for each factor. We then calculated the number of deaths attributable to each social factor in the United States in 2000. Results. Approximately 245000 deaths in the United States in 2000 were attributable to low education, 176000 to racial segregation, 162000 to low social support, 133000 to individual-level poverty, 119000 to income inequality, and 39000 to area-level poverty. Conclusions. The estimated number of deaths attributable to social factors in the United States is comparable to the number attributed to pathophysiological and behavioral causes. These findings argue for a broader public health conceptualization of the causes of mortality and an expansive policy approach that considers how social factors can be addressed to improve the health of populations. (Am J Public Health. Published online ahead of print June 16, 2011:e1-e10. doi:10.2105/AJPH.2010.300086).

Differences in the determinants of posttraumatic stress disorder and depression after a mass traumatic event

Abstract: Background: Hurricane Ike struck the Galveston Bay area of Texas on September 13, 2008, leaving substantial destruction and a number of deaths in its wake. We assessed differences in the determinants of posttraumatic stress disorder (PTSD) and depression after this event, including the particular hurricane experiences, including postevent nontraumatic stressors, that were associated with these pathologies. Methods: 658 adults who had been living in Galveston and Chambers counties, TX in the month before Hurricane Ike were interviewed 2-5 months after the hurricane. We collected information on experiences during and after Hurricane Ike, PTSD and depressive symptoms in the month before the interview, and socio-demographic characteristics. Results: The prevalence of past month hurricane-related PTSD and depression was 6.1 and 4.9%, respectively. Hurricane experiences, but not socio-demographic characteristics, were associated with Ike-related PTSD. By contrast, lower education and household income, and more lifetime stressors were associated with depression, as were hurricane exposures and hurricane-related stressors. When looking at specific hurricane-related stressors, loss or damage of sentimental possessions was associated with both PTSD and depression; however, health problems related to Ike were associated only with PTSD, whereas financial loss as a result of the hurricane was associated only with depression. Conclusions: PTSD is indeed a disorder of event exposure, whereas risk of depression is more clearly driven by personal vulnerability and exposure to stressors. The role of nontraumatic stressors in shaping risk of both pathologies suggests that alleviating stressors after disasters has clear potential to mitigate the psychological sequelae of these events. Depression and Anxiety 0:1-10, 2011. © 2011 Wiley-Liss, Inc. Language: en

Epigenetic and inflammatory marker profiles associated with depression in a community-based epidemiologic sample

Abstract: Background Recent work suggests that epigenetic differences may be associated with psychiatric disorders. Here we investigate, in a community-based sample, whether methylation profiles distinguish between individuals with and without lifetime depression. We also investigate the physiologic consequences that may be associated with these profiles. Method Using whole blood-derived genomic DNA from a subset of participants in the Detroit Neighborhood Health Study (DNHS), we applied methylation microarrays to assess genome-wide methylation profiles for over 14 000 genes in 33 persons who reported a lifetime history of depression and 67 non-depressed adults. Bioinformatic functional analyses were performed on the genes uniquely methylated and unmethylated in each group, and inflammatory biomarkers [interleukin (IL)-6 and C-reactive protein (CRP)] were measured to investigate the possible functional significance of the methylation profiles observed. Results Uniquely unmethylated gene sets distinguished between those with versus without lifetime depression. In particular, some processes (e.g. brain development, tryptophan metabolism) showed patterns suggestive of increased methylation among individuals with depression whereas others (e.g. lipoprotein) showed patterns suggestive of decreased methylation among individuals with depression. IL-6 and CRP levels were elevated among those with lifetime depression and, among those with depression only, IL-6 methylation showed an inverse correlation with circulating IL-6 and CRP. Conclusions Genome-wide methylation profiles distinguish individuals with versus without lifetime depression in a community-based setting, and show coordinated signals with pathophysiological mechanisms previously implicated in the etiology of this disorder. Examining epigenetic mechanisms in concert with other dynamic markers of physiologic functioning should improve our understanding of the neurobiology of depression.

Pervasive exposure to violence and posttraumatic stress disorder in a predominantly African American Urban Community: The Detroit neighborhood health study

Abstract: Exposure to traumatic events is common, particularly among economically disadvantaged, urban African Americans. There is, however, scant data on the psychological consequences of exposure to traumatic events in this group. We assessed experience with traumatic events and posttraumatic stress disorder (PTSD) among 1,306 randomly selected, African American residents of Detroit. Lifetime prevalence of exposure to at least 1 traumatic event was 87.2% (assault = 51.0%). African Americans from Detroit have a relatively high burden of PTSD; 17.1% of those who experienced a traumatic event met criteria for probable lifetime PTSD. Assaultive violence is pervasive and is more likely to be associated with subsequent PTSD than other types of events. Further efforts to prevent violence and increase access to mental health treatment could reduce the mental health burden in economically disadvantaged urban areas.

SLC6A4 methylation modifies the effect of the number of traumatic events on risk for posttraumatic stress disorder

Abstract: Background: Posttraumatic stress disorder (PTSD) is a common and debilitating mental disorder that occurs following exposure to a traumatic event. However, most individuals do not develop PTSD following even a severe trauma, leading to a search for new variables, such as genetic and other molecular variation, associated with vulnerability and resilience in the face of trauma exposure. Method: We examined whether serotonin transporter (SLC6A4) promoter genotype and methylation status modified the association between number of traumatic events experienced and PTSD in a subset of 100 individuals from the Detroit Neighborhood Health Study. Results: Number of traumatic events was strongly associated with risk of PTSD. Neither SLC6A4 genotype nor methylation status was associated with PTSD in main effects models. However, SLC6A4 methylation levels modified the effect of the number of traumatic events on PTSD after controlling for SLC6A4 genotype. Persons with more traumatic events were at increased risk for PTSD, but only at lower methylation levels. At higher methylation levels, individuals with more traumatic events were protected from this disorder. This interaction was observed whether the outcome was PTSD diagnosis, symptom severity, or number of symptoms. Conclusions: Gene-specific methylation patterns may offer potential molecular signatures of increased risk for and resilience to PTSD. Depression and Anxiety 28:639–647, 2011. r 2011 Wiley-Liss, Inc.

Long-term Posttraumatic Stress Symptoms Among 3,271 Civilian Survivors of the September 11, 2001, Terrorist Attacks on the World Trade Center

Abstract: Although the September 11, 2001, terrorist attacks were the largest human-made disaster in US history, there is little extant research documenting the attacks' consequences among those most directly affected, that is, persons who were in the World Trade Center towers. Data from a cross-sectional survey conducted 2-3 years after the attacks ascertained the prevalence of long-term, disaster-related posttraumatic stress symptoms and probable posttraumatic stress disorder (PTSD) in 3,271 civilians who evacuated World Trade Center towers 1 and 2. Overall, 95.6% of survivors reported at least 1 current posttraumatic stress symptom. The authors estimated the probable rate of PTSD at 15.0% by using the PTSD Checklist. Women and minorities were at an increased risk of PTSD. A strong inverse relation with annual income was observed. Five characteristics of direct exposure to the terrorist attacks independently predicted PTSD: being on a high floor in the towers, initiating evacuation late, being caught in the dust cloud that resulted from the tower collapses, personally witnessing horror, and sustaining an injury. Working for an employer that sustained fatalities also increased risk. Each addition of an experience of direct exposure resulted in a 2-fold increase in the risk of PTSD (odds ratio = 2.09, 95% confidence interval: 1.84, 2.36). Identification of these risk factors may be useful when screening survivors of large-scale terrorist events for long-term psychological sequelae.

Genetic Markers for PTSD Risk and Resilience Among Survivors of the World Trade Center Attacks

Abstract: We have previously reported the differential expression of 17 probe sets in survivors of the 9/11 attacks with current posttraumatic stress disorder (PTSD) compared to similarly exposed survivors with no lifetime PTSD. The current study presents an expanded analysis of these subjects, including genotype at FKBP5, a modulator of glucocorticoid receptor (GR) sensitivity. It includes data from additional subjects who developed PTSD following 9/11 but then recovered, distinguishing expression profiles associated with risk for developing PTSD, resilience, and symptom recovery. 40 Caucasians (20 with and 20 without PTSD, matched for exposure, age, and gender) were selected from a population-representative sample of persons exposed to the 9/11 attacks from which longitudinal data had been collected in four previous waves. Whole blood gene expression and cortisol levels were obtained and genome-wide gene expression was analyzed. 25 probe sets were differentially expressed in PTSD. Identified genes were generally involved in hypothalamic-pituitary-adrenal axis, signal transduction, or in brain and immune cell function. STAT5B, a direct inhibitor of GR, and nuclear factor I/A, both showed reduced expression in PTSD. Comparison of lifetime versus current PTSD identified overlapping genes with altered expression suggesting enduring markers, while some markers present only in current PTSD may reflect state measures. As a follow-up, direct comparisons of expression in current PTSD, lifetime-only PTSD, and control groups identified FKBP5 and MHC Class II as state markers, and also identified several trait markers. An analysis of indirect effects revealed that homozygosity for any of 4 PTSD risk-related polymorphisms at FKBP5 predicted FKBP5 expression, which mediated indirect effects of genotype on plasma cortisol and PTSD severity.

Accidental poisoning mortality among patients in the Department of Veterans Affairs Health System.

Abstract: BACKGROUND: Accidental poisoning mortality is an increasingly important concern, particularly for health systems, which distribute potentially poisoning medications and treat substance use disorders. OBJECTIVES: To describe the rate of accidental poisoning mortality in the Veterans Health Administration (VHA) during fiscal year 2005, assess differences with rates observed in the general US population, and describe the frequency with which specific drugs and medications were mentioned on the death records of accidental poisoning decedents. RESEARCH DESIGN: Cohort study. SUBJECTS: All 5,567,621 individuals aged 18+ who received VHA inpatient or outpatient services in fiscal year 2004 (October 1, 2003 to September 30, 2004) or fiscal year 2005 and were alive at the start of fiscal year 2005. MEASURES: The National Death Index indicated vital status and cause of death, the National Patient Care Database indicated who used VHA services and consequently was in the study cohort, and the Web-based Injury Statistics Query and Reporting System indicated poisoning mortality rates in the general US population. RESULTS: The crude rate of accidental poisoning mortality in the VHA for fiscal year 2005 was 19.85 deaths per 100,000 person-years. After accounting for gender and age distribution, VHA patients had nearly twice the rate of fatal accidental poisoning compared with adults in the general US population (standardized mortality ratio=1.96; 95% confidence interval: 1.83, 2.08). Opioid medications and cocaine were frequently mentioned as the agents causing poisoning on death records. CONCLUSIONS: The present work indicates that a substantial need exists for interventions to reduce the risk of accidental poisoning among VHA patients. Language: en

Economic downturns and population mental health: research findings, gaps, challenges and priorities

Abstract: Prior research suggests that the current global economic crisis may be negatively affecting population mental health. In that context, this paper has several goals: (1) to discuss theoretical and conceptual explanations for how and why economic downturns might negatively affect population mental health; (2) present an overview of the literature on the relationship between economic recessions and population mental health; (3) discuss the limitations of existing empirical work; and (4) highlight opportunities for improvements in both research and practice designed to mitigate any negative impact of economic declines on the mental health of populations. Research has consistently demonstrated that economic crises are negatively associated with population mental health. How economic downturns influence mental health should be considered in policies such as social protection programs that aim to promote recovery.

PTSD comorbidity and suicidal ideation associated with PTSD within the Ohio Army National Guard

Abstract: Objective To study the relation between posttraumatic stress disorder (PTSD) psychiatric comorbidity and suicidal ideation in a representative sample of Ohio Army National Guard soldiers. Method Using retrospective data collected on the telephone from a random sample of 2,616 National Guard soldiers who enrolled in a 10-year longitudinal study (baseline data collected November 2008-November 2009), we examined (1) the prevalence of other psychopathologies among those with DSM-IV-diagnosed PTSD compared to those without PTSD and (2) the association between PTSD comorbidity and suicidal ideation (reporting thoughts of being better off dead or hurting themselves). All analyses were carried out using logistic regression. Results Of guard members with PTSD in the last year, 61.7% had at least 1 other psychopathology; 20.2% had at least 2 other co-occurring conditions. The most common co-occurring psychopathology was depression. While those with PTSD overall were 5.4 (95% CI, 3.8-7.5) times more likely to report suicidality than those without PTSD, those who had at least 2 additional conditions along with PTSD were 7.5 (95% CI, 3.0-18.3) times more likely to report suicidal ideation at some point in their lifetime than those with PTSD alone. Conclusions Soldiers with PTSD were at increased risk for suicidality, and, among those with PTSD, those with at least 2 additional conditions were at the highest risk of suicidal ideation. Future research should address the mechanisms that contribute to multimorbidity in this population and the appropriate treatment methods for this high-risk group.

Life-Course Socioeconomic Position and Incidence of Dementia and Cognitive Impairment Without Dementia in Older Mexican Americans: Results From the Sacramento Area Latino Study on Aging

Abstract: There have been few investigations of the link between changes in life-course socioeconomic position (SEP) and cognitive decline or incidence of dementia. The authors examined the impact of changes in life-course SEP on incidence of dementia and cognitive impairment but not dementia (CIND) over a decade of follow-up. Participants of Mexican origin (n ¼ 1,789) were members of the Sacramento Area Latino Study on Aging cohort. Incidence of dementia/CIND was ascertained by using standard diagnostic criteria. SEP indicators at 3 life stages (childhood, adulthood, and midlife) were used to derive a measure of cumulative SEP (range, 0 to 8) and SEP mobility. Nearly 24% of the sample maintained a low SEP throughout life. Hazard ratios and 95% confidence intervals were computed from Cox proportional hazards regression models. In fully adjusted models, participants with a continuously high SEP had lower hazard ratios for dementia/CIND compared with those with a continuously low SEP at all 3 life stages (hazard ratio ¼ 0.49, 95% confidence interval: 0.24, 0.98; P ¼ 0.04). In age-adjusted models, participants experienced a 16% greater hazard of dementia/CIND with every 1-unit increase in cumulative SEP disadvantage across the life course (hazard ratio ¼ 1.16, 95% confidence interval: 1.01, 1.33; P ¼ 0.04). Early exposures to social disadvantage may increase the risk of late-life dementia.

The urban environment and mental disorders: Epigenetic links.

Abstract: For the first time in human history, more than half of the world’s population lives in urban areas and this is projected to increase to two-thirds by 2030. This increased urbanity of the world’s population has substantial public health implications. Nearly a century of research has shown higher risk of mental disorder among persons living in urban versus rural areas. Epidemiologic research has documented that associations between particular features of the urban environment, such as concentrated disadvantage, residential segregation and social norms, contribute to the risk of mental illness. We propose that changes in DNA methylation may be one potential mechanism through which features of the urban environment contribute to psychopathology. Recent advances in animal models and human correlation studies suggest DNA methylation as a promising mechanism that can explain how the environment “gets under the skin.” Aberrant DNA methylation signatures characterize mental disorders in community settings. Emergin...

Ethnic inequalities in obesity among children and adults in the UK: a systematic review of the literature.

Abstract: Ethnic minority groups are growing as a proportion of the British population. Although disparate, literature suggests inequalities in obesity risk within and among ethnic minority groups relative to Caucasians in the UK. We summarize and appraise the existing peer-reviewed literature about the prevalence and determinants of obesity among ethnic minority groups relative to Caucasians among children and adults in the UK. There was no consensus about obesity prevalence relative to Caucasians among South Asian or Black children or among South Asian adults relative to Caucasians. Black adults generally had higher risk for obesity than Caucasians. Both Chinese children and adults had lower risk for obesity than Caucasians. Few studies have considered differences in the aetiology of obesity by ethnicity. The lack of consensus regarding obesity risk among large ethnic minority groups relative to Caucasians in the UK, and the paucity of studies concerned with differences in obesity aetiology by ethnicity warrant further research in this area. Certain obesity metrics may bias obesity prevalence among particular ethnic groups relative to Caucasians. We summarize key methodological limitations to the current literature and suggest avenues for future research.

Research Review: Gene-environment interaction research in youth depression - A systematic review with recommendations for future research

Abstract: Background Depression is a major public health problem among youth, currently estimated to affect as many as 9% of US children and adolescents. The recognition that both genes (“nature”) and environments (“nurture”) are important for understanding the etiology of depression has led to rapid growth in research exploring gene–environment interactions (GxE). However, there has been no systematic review of GxE in youth depression to date.

Gene Expression and Methylation Signatures of MAN2C1 are Associated with PTSD

Abstract: As potential regulators of DNA accessibility and activity, epigenetic modifications offer a mechanism by which the environment can moderate the effects of genes. To date, however, there have been relatively few studies assessing epigenetic modifications associated with post-traumatic stress disorder (PTSD). Here we investigate PTSD-associated methylation differences in 33 genes previously shown to differ in whole blood-derived gene expression levels between those with vs. without the disorder. Drawing on DNA samples similarly obtained from whole blood in 100 individuals, 23 with and 77 without lifetime PTSD, we used methylation microarray data to assess whether these 33 candidate genes showed epigenetic signatures indicative of increased risk for, or resilience to, PTSD. Logistic regression analyses were performed to assess the main and interacting effects of candidate genes’ methylation values and number of potentially traumatic events (PTEs), adjusting for age and other covariates. Results revealed that only one candidate gene–MAN2C1–showed a significant methylation x PTE interaction, such that those with both higher MAN2C1 methylation and greater exposure to PTEs showed a marked increase in risk of lifetime PTSD (OR 4.35, 95% CI: 1.07, 17.77, p = 0.04). These results indicate that MAN2C1 methylation levels modify cumulative traumatic burden on risk of PTSD, and suggest that both gene expression and epigenetic changes at specific loci are associated with this disorder.

Effects of war exposure on air force personnel's mental health, job burnout and other organizational related outcomes

Abstract: Longitudinal data from a stratified representative sample of U.S. Air Force personnel (N = 1009) deployed to the wars in Iraq, Afghanistan, and other locations were analyzed in this study. Using structural equation models, we examined the effects of war exposure on traumatic experiences, Post Traumatic Stress (PTS) symptoms, resource loss, and on subsequent functioning, perceived health, and on job and organizationally relevant outcomes. The job and organizational outcomes included job burnout, job involvement, job strain, job satisfaction, work-family conflict, organizational commitment, deployment readiness, and intention to reenlist. We found that deployment to the theater of the war increased risk of exposure to trauma, which in turn, predicted elevated PTS symptoms and resource loss. PTS symptoms predicted later loss of resources and deterioration in perceived health and functioning. In turn, resource loss predicted negative job and organizational outcomes. Exposure to trauma fully mediated the effects of deployment to the theater of war on PTS symptoms and resource loss and had additional significant indirect effects on several job and organizational relevant outcomes. For returning veterans, deployment to the theater of war, exposure to trauma, PTS symptoms, and resource loss represents a "cascading" chain of events that over time results in a decline of health and functioning as well as in adverse job and organizationally relevant outcomes that may affect organizational effectiveness.

Major depressive disorder following terrorist attacks: A systematic review of prevalence, course and correlates

Abstract: Background: Terrorist attacks are traumatic events that may result in a wide range of psychological disorders for people exposed. This review aimed to systematically assess the current evidence on major depressive disorder (MDD) after terrorist attacks. Methods: A systematic review was performed. Studies included assessed the impact of human-made, intentional, terrorist attacks in direct victims and/or persons in general population and evaluated MDD based on diagnostic criteria. Results: A total of 567 reports were identified, 11 of which were eligible for this review: 6 carried out with direct victims, 4 with persons in general population, and 1 with victims and general population. The reviewed literature suggests that the risk of MDD ranges between 20 and 30% in direct victims and between 4 and 10% in the general population in the first few months after terrorist attacks. Characteristics that tend to increase risk of MDD after a terrorist attack are female gender, having experienced more stressful situations before or after the attack, peritraumatic reactions during the attack, loss of psychosocial resources, and low social support. The course of MDD after terrorist attacks is less clear due to the scarcity of longitudinal studies. Conclusions: Methodological limitations in the literature of this field are considered and potentially important areas for future research such as the assessment of the course of MDD, the study of correlates of MDD or the comorbidity between MDD and other mental health problems are discussed.

The Role of Genes in Defining a Molecular Biology of PTSD

Abstract: Because environmental exposure to trauma is the sine qua non for the development of Post Traumatic Stress Disorder (PTSD), the recent focus on genetic studies has been noteworthy. The main catalyst for such studies is the observation fr om epidemiological studies that not all trauma survivors develop this disorder. Furthermore, neuroendocrine findings su ggest pre- existing hormonal alterations that confer risk for PTSD. This paper presents the rationale for examining genetic facto rs in PTSD and trauma exposure, but suggests that studies of genotype may only present a limited picture of the molecular biology of this disorder. We describe the type of information that can be obtained from candidate gene and genomic studies that incorporate environmental factors in the design (i.e., gene - environment interaction and gene-environment correlation studies) and studies that capitalize on the idea that environment modifies gene ex pression, via epigenetic or other molecular mechanisms. The examination of epigenetic mechanisms in tandem with gene expression will help refine models that explain how PTSD risk, pathophysiology, and recovery is mediated by the environment. Since inherited genetic variation may also influence the extent of epigenetic or gene expression changes resulting from the environment, such studies should optimally be followed up by studies of genotype.

Longitudinal assessment of cognitive and psychosocial functioning after Hurricanes Katrina and Rita: Exploring disaster impact on middle-aged, older, and oldest-old adults

Abstract: The authors examined the effects of Hurricanes Katrina and Rita (HKR) on cognitive and psychosocial functioning in a lifespan sample of adults 6 to 14 months after the storms Participants were recruited from the Louisiana Healthy Aging Study (LHAS) Most were assessed during the immediate impact period and retested for this study Analyses of pre-and post-disaster cognitive data confirmed that storm-related decrements in working memory for middle-aged and older adults observed in the immediate impact period had returned to pre-hurricane levels in the post-disaster recovery period Middle-aged adults reported more storm-related stressors and greater levels of stress than the two older groups at both waves of testing These results are consistent with a burden perspective on post-disaster psychological reactions

Intimate partner violence perpetration and condom use-related factors: associations with heterosexual men's consistent condom use.

Abstract: Intimate partner violence victimization has been linked to sexual HIV risk behavior among heterosexual women. The unique role of perpetration of intimate partner violence (IPV) in sexual risk behavior among men has not been studied as well. Based on interviews with 518 heterosexual men recruited via street-intercept between 2005 and 2007 in New York City, we assessed the relationship between perpetration of IPV against a main female partner and inconsistent condom use with that same partner, while controlling for condom use-related factors. Multivariate logistic regression revealed that men who perpetrated physical IPV were half as likely to report consistent condom use as compared with men who did not use violence, while controlling for sociodemographic, condom use-related and other factors. Physical IPV perpetration by heterosexual men makes an independent contribution to consistent condom use. Designing interventions for heterosexual men that simultaneously address both IPV and sexual risk behaviors is critical.

Life-course exposure to early socioeconomic environment, education in relation to late-life cognitive function among older Mexicans and Mexican Americans.

Abstract: Objectives: To examine the associations between life-course education and late-life cognitive function along with the modifying role of migration history. Method: The combined sample includes 1,789 participants from the Sacramento Area Latino Study on Aging and 5,253 participants from the Mexican Health and Aging Study. Aged 60+ at baseline, participants were classified as Mexican residents, Mexicans–return migrants, Mexicans–immigrants to the United States, and Mexicans–U.S. born. Cognitive function was measured using standardized z scores of a short-term verbal recall test. Multivariate linear regression analysis was conducted. Results: Participants’ z scores were higher among those whose mother had more than elementary education (β = 0.28, p < .05). Participant’s education mediated this association. For 5-year difference in education, the cognitive z score increased by 0.3 points for a U.S. born. Results were similar with father’s education. Discussion: Adult educational attainment mediates the effect ...

Equity and the child health Millennium Development Goal: the role of pro-poor health policies

Abstract: Background There are substantial disparities in mortality between rich and poor children in developing countries. As a result, there is a call for explicitly pro-poor health programming in efforts to reach the child health Millennium Development Goals. Aim To estimate the contribution made by pro-poor health policy to reduction in wealth disparities in under-5 mortality. Methods An ecological, cross-sectional analysis was performed using Demographic and Health Survey data from 47 developing countries. Multivariate analysis was used to estimate the association between government health expenditure, the wealth distribution of two essential child health services (concentration indices of immunisation and treatment for acute respiratory infection) and aggregate under-5 mortality, as well as two measures of poor–rich equity in mortality outcomes—the quintile ratio and the concentration index of under-5 mortality—while confounders were controlled for. Results Lower concentration (more pro-poor) indices for immunisation and treatment for acute respiratory infection were found to be associated with a reduction in inequity in under-5 mortality to the benefit of the poor. Government health expenditures were associated with lower overall national mortality reductions but had no effect on equity of mortality outcomes. Conclusions Redistributive health policies that promote pro-poor distribution of health services may reduce the gap in under-5 mortality between rich and poor in low-income and middle-income countries. To ensure that the poor gain from the current efforts to reach the Millennium Development Goals, essential child health services should explicitly target the poor. Failing that, the gains from these services will tend to accrue to the wealthier children in countries, magnifying inequalities in mortality.

Ethnic Inequalities in Mortality: The Case of Arab-Americans

Abstract: Background Although nearly 112 million residents of the United States belong to a non-white ethnic group, the literature about differences in health indicators across ethnic groups is limited almost exclusively to Hispanics. Features of the social experience of many ethnic groups including immigration, discrimination, and acculturation may plausibly influence mortality risk. We explored life expectancy and age-adjusted mortality risk of Arab-Americans (AAs), relative to non-Arab and non-Hispanic Whites in Michigan, the state with the largest per capita population of AAs in the US.