Despite the many triumphs of biomedical research over infectious diseases, human pathogens continue to impact profoundly populations deprived of social resources. Correspondingly, health researchers have advocated a social determinants approach to the study and prevention of infectious diseases. However, it is unknown whether this call has resulted in an increase in the number of studies examining social determinants of infectious outcomes.
Research on social determinants of infectious diseases was systematically quantified by assessing temporal trends in the published literature using MEDLINE, PsycINFO and ISI Web of Science.
Results of the literature review spanning 1966–2005 show that socially related citations increased an annual average of 180.3 for neuropsychiatric conditions, 81.9 for chronic conditions, 44.7 for sexually transmitted diseases and 18.9 for non‐sexually transmitted infectious diseases (p<0.0001). Of the 279 publications found to employ the term “social epidemiology”, 15 (5.4%) investigated infectious outcomes.
The results of the literature review suggest a paucity of social research on infectious diseases. There is a need for increased dialogue and collaboration between infectious disease epidemiologists and social epidemiologists.
Helicobacter pylori seroprevalence levels in US adults participating in the continuous National Health and Nutrition Examination Survey (1999–2000) increased with age in all racial/ethnic groups, with significantly higher age-standardized levels in Mexican Americans (64.0%, 95% confidence interval (CI): 58.8, 69.2) and non-Hispanic blacks (52.0%, 95% CI: 48.3, 55.7) compared with non-Hispanic whites (21.2%, 95% CI: 19.1, 23.2). Although seroprevalence levels remained similar to those found in National Health and Nutrition Examination Surveys from 1988 to 1991 among non-Hispanic blacks and Mexican Americans, they were significantly lower in non-Hispanic whites, especially at older ages. The factors driving the decline in H. pylori seroprevalence appear to be acting preferentially on the non-Hispanic white population.
cohort effect; ethnic groups; health status disparities; Helicobacter pylori; nutrition surveys; seroepidemiologic studies
In 1 previous study, it was shown that neighborhood socioeconomic disadvantage is associated with cognitive decline among Latinos. No studies have explored whether and to what extent individual-level socioeconomic factors account for the relation between neighborhood disadvantage and cognitive decline. The purpose of the present study was to assess the influence of neighborhood socioeconomic position (SEP) on cognitive decline and examine how individual-level SEP factors (educational level, annual income, and occupation) influenced neighborhood associations over the course of 10 years. Participants (n = 1,789) were community-dwelling older Mexican Americans from the Sacramento Area Latino Study on Aging. Neighborhood SEP was derived by linking the participant's individual data to the 2000 decennial census. The authors assessed cognitive function with the Modified Mini-Mental State Examination. Analyses used 3-level hierarchical linear mixed models of time within individuals within neighborhoods. After adjustment for individual-level sociodemographic characteristics, higher neighborhood SEP was significantly associated with cognitive function (β = −0.033; P < 0.05) and rates of decline (β = −0.0009; P < 0.10). After adjustment for individual educational level, neighborhood SEP remained associated with baseline cognition but not with rates of decline. Differences in individual educational levels explained most of the intra- and interneighborhood variance. These results suggest that the effect of neighborhood SEP on cognitive decline among Latinos is primarily accounted for by education.
aging; cognition; education; Mexican Americans; residence characteristics
Biomarkers are an important aspect of research linking psychosocial stress and health. This paper aims to characterize the biological pathways that may mediate the relationship between socioeconomic position (SEP) and cardiovascular disease (CVD) and address opportunities for further research within the Panel Study for Income Dynamics (PSID), with a focus on psychosocial stressors related to SEP. We review the literature on CVD biomarkers, including adhesion and proinflammatory molecules (IL-6, other cytokines, C-reactive proteins, fibrinogen, etc.) and microbial pathogens. The impact of socioeconomic determinants and related psychosocial stressors on CVD biomarkers mediated by behavioral and central nervous system pathways are described. We also address measurement and feasibility issues including: specimen collection methods, processing and storage procedures, laboratory error, and within-person variability. In conclusion, we suggest that PSID consider adding important assessments of specific CVD biomarkers and mediating behavioral measures, health, and medications that will ultimately address many of the gaps in the literature regarding the relationship between socioeconomic position and cardiovascular health.
The objective of this study was to examine whether cytomegalovirus (CMV), herpes simplex virus type-1 (HSV-1), and C-reactive protein (CRP) are associated with functional impairment in older Latinos.
A cross-sectional analysis of a cohort study conducted with a community dwelling elderly population. The sample was a subset (N = 1507/1789) of participants in the Sacramento Area Latino Study on Aging (SALSA) ages 60–101 with available serum samples and functional impairment measures. Baseline serum samples were assayed for levels of immunoglobulin G antibodies to CMV and HSV-1 and for levels of CRP. Several measures were used to assess functional impairment, including activities of daily living (ADL), instrumental activities of daily living (IADL), and walking pace.
CMV and CRP showed statistically significant graded associations with ADL functional impairment, even after controlling for age and gender. The relationship between CMV and ADL was slightly attenuated, and the confidence interval contained the null value when adjusted for total number of health conditions, body mass index, and household income. Only high levels of CRP were significantly related to ADL and IADL impairment even after adjusting for all other covariates.
Inflammation is clearly linked to physical functioning among aging Latinos. This study also suggests a role for CMV infection in relation to ADL impairment. Further research examining the influence of infection, immune response, and inflammation on longitudinal trajectories of physical functioning is warranted.
Cytomegalovirus (CMV); CRP; Latinos; Physical function; Community
This study examined the relation between immune response to cytomegalovirus (CMV) and all-cause and cardiovascular disease (CVD) mortality, and possible mediating mechanisms. Data were derived from the Sacramento Area Latino Study on Aging, a population-based study of older Latinos (aged 60–101 years) in California followed in 1998–2008. CMV immunoglobulin G (IgG), tumor necrosis factor, and interleukin-6 were assayed from baseline blood draws. Data on all-cause and CVD mortality were abstracted from death certificates. Analyses included 1,468 of 1,789 participants. For individuals with CMV IgG antibody titers in the highest quartile compared with lower quartiles, fully adjusted models showed that all-cause mortality was 1.43 times (95% confidence interval: 1.14, 1.79) higher over 9 years. In fully adjusted models, the hazard of CVD mortality was also elevated (hazard ratio = 1.35, 95% confidence interval: 1.01, 1.80). A composite measure of tumor necrosis factor and interleukin-6 mediated a substantial proportion of the association between CMV and all-cause (18.9%, P < 0.001) and CVD (29.0%, P = 0.02) mortality. This study is the first known to show that high CMV IgG antibody levels are significantly related to mortality and that the relation is largely mediated by interleukin-6 and tumor necrosis factor. Further studies investigating methods for reducing IgG antibody response to CMV are warranted.
cardiovascular diseases; cytomegalovirus; immune system; infection; inflammation
Early life environmental and psychological influences are thought to play an important role in the development of the immune system. Antibody response to latent herpesviruses has been used as an indirect measure of cell-mediated immune function but has seldom been applied to younger age groups.
We used data from the 1999–2004 National Health and Nutrition Examination Survey (NHANES) to test for an association between family poverty and continuous antibody response to cytomegalovirus (CMV) in U.S. children aged 6–16 (N= 2,226) using OLS regression.
Poverty was significantly associated with increased antibody levels among seropositive individuals. The association between income and antibody levels exhibited a threshold effect, with additional income beyond the poverty line not associated with increased antibody titers.
Early life social factors such as family poverty could have detrimental impacts on the developing immune system, with potentially important consequences for later life health outcomes.
CMV; poverty; socioeconomic status; health disparities; NHANES; immunity
The pathophysiological mechanisms that underlie health disparities by socioeconomic status and race/ethnicity are poorly understood. Promising new research suggests that the burden of persistent infection may influence adult disease risk and mortality. This article examines how multiple persistent infections cluster within individuals and how this clustering varies by socioeconomic position and race/ethnicity in U.S. adults.
We analyze data from the National Health and Nutrition Examination Survey III (N = 19,275) for adults aged 17–90 years. The clustering of infections within individuals is studied using tetrachoric correlations. Multiple indicator multiple cause models are used to analyze the infection burden construct as measured by seropositivity to Helicobacter pylori, cytomegalovirus, herpes simplex virus-1, and hepatitis B, focusing on the burden's distribution by socioeconomic position and race/ethnicity. The results are corroborated using ordered logistic regression for a commonly used count index of individual infections.
Seroprevalence of individual persistent infections is positively correlated, suggesting common factors related to exposure or susceptibility. Education, income, and race/ethnicity are strong and significant independent predictors of infection burden in U.S. adults in all models.
The disproportionate burden of persistent infections among disadvantaged groups across all ages may be one biologic pathway by which low socioeconomic position is related to increased rates of morbidity and mortality in the United States.
Socioeconomic; Race; Ethnic; United states; Adults; Infection; Biomarkers
Chronic infections could be contributing to the socioeconomic gradient in chronic diseases. Although chronic infections have been associated with increased levels of inflammatory cytokines and cardiovascular disease, there is limited evidence on how infections affect risk of diabetes.
RESEARCH DESIGN AND METHODS
We examined the association between serological evidence of chronic viral and bacterial infections and incident diabetes in a prospective cohort of Latino elderly. We analyzed data on 782 individuals aged >60 years and diabetes-free in 1998–1999, whose blood was tested for antibodies to herpes simplex virus 1, varicella virus, cytomegalovirus, Helicobacter pylori, and Toxoplasma gondii and who were followed until June 2008. We used Cox proportional hazards regression to estimate the relative incidence rate of diabetes by serostatus, with adjustment for age, sex, education, cardiovascular disease, smoking, and cholesterol levels.
Individuals seropositive for herpes simplex virus 1, varicella virus, cytomegalovirus, and T. gondii did not show an increased rate of diabetes, whereas those who were seropositive for H. pylori at enrollment were 2.7 times more likely at any given time to develop diabetes than seronegative individuals (hazard ratio 2.69 [95% CI 1.10–6.60]). Controlling for insulin resistance, C-reactive protein and interleukin-6 did not attenuate the effect of H. pylori infection.
We demonstrated for the first time that H. pylori infection leads to an increased rate of incident diabetes in a prospective cohort study. Our findings implicate a potential role for antibiotic and gastrointestinal treatment in preventing diabetes.
Levels of antimicrobial drug resistance did not differ significantly between persons in households that used antibacterial cleaning and hygiene products and those that did not.
We examined whether household use of antibacterial cleaning and hygiene products is an emerging risk factor for carriage of antimicrobial drug–resistant bacteria on hands of household members. Households (N = 224) were randomized to use of antibacterial or nonantibacterial cleaning and hygiene products for 1 year. Logistic regression was used to assess the influence of antibacterial product use in homes. Antibacterial product use did not lead to a significant increase in antimicrobial drug resistance after 1 year (odds ratio 1.33, 95% confidence interval 0.74–2.41), nor did it have an effect on bacterial susceptibility to triclosan. However, more extensive and longer term use of triclosan might provide a suitable environment for emergence of resistant species. Further research on this issue is needed.
Antibacterial products; triclosan; antibiotic resistance; antimicrobial drug resistance; household; research
Alone among herpesviruses, persistent Cytomegalovirus (CMV) markedly alters the numbers and proportions of peripheral immune cells in infected-vs-uninfected people. Because the rate of CMV infection increases with age in most countries, it has been suggested that it drives or at least exacerbates “immunosenescence”. This contention remains controversial and was the primary subject of the Third International Workshop on CMV & Immunosenescence which was held in Cordoba, Spain, 15-16th March, 2012. Discussions focused on several main themes including the effects of CMV on adaptive immunity and immunosenescence, characterization of CMV-specific T cells, impact of CMV infection and ageing on innate immunity, and finally, most important, the clinical implications of immunosenescence and CMV infection. Here we summarize the major findings of this workshop.
Emerging work suggests that both environmental and genetic factors contribute to risk of depression in adolescents, and that these factors may differ between genders. We assessed whether features of the social environment (SE), measured at varying levels, and genetic factors jointly shape the risk of depression in adolescent males and females.
Using data from a national survey of U.S. adolescents, we applied cross-sectional, multilevel mixed models to assess the contribution of: (i) 5-HTTLPR genotype and respondent-level building conditions to depressive sympton score (DSS); and (ii) 5-HTTLPR genotype and neighborhood-level building conditions to DSS. Models testing potential gene-SE (G × SE) interactions were also conducted. All models were stratified by gender and adjusted for age, race/ethnicity, family structure, parental education and social support.
Among females, adjusted analyses indicated that sl genotype carriers enjoyed a marginally significant (p=0.07) protective effect against higher DSS in models assessing respondent-level building conditions. In contrast, among males, adjusted analyses predicted significantly higher DSS for residents of neighborhoods with relatively poor building conditions (p<0.01). No significant G X SE interactions were detected for either gender.
These results suggest that adverse, macro-level SE effects increase risk of depression to a greater extent in adolescent males than females. Intervention strategies designed to improve mental health in adolescent populations should consider a growing body of work suggesting that the contextual effects conferring increased risk of depression differ among males and females.
social epidemiology; genetics; mental health; gender
To examine the associations between life-course education and late-life cognitive function along with the modifying role of migration history.
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 US, and Mexicans-US-born. Cognitive function was measured using standardized z-scores of a short-term verbal recall test. Multivariate linear regression analysis was conducted.
Participants’ z-scores were higher among those whose mother had more than elementary education (β=0.28, p<0.05). Participant’s education mediated this association. For 5-year difference in education, the cognitive z-score increased by 0.3 points for a US-born. Results were similar with father’s education.
Adult educational attainment mediates the effect of childhood socioeconomic status on late-life cognition. Migration plays a role in shaping cognitive aging.
cognition; health; education; life course; old age; Mexican Americans
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.
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.
Number of traumatic events was strongly associated with risk of PTSD. Neither SLC6A4 genotype or nor methylation status were associated with PTSD in main effects models. However, SLC6A4 methylation levels modified the effect of 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.
Gene-specific methylation patterns may offer potential molecular signatures of increased risk for and resilience to PTSD.
posttraumatic stress disorder; epigenetic; methylation; SLC6A4; trauma
Early life circumstances influence health across the life span. Migration and ethnicity may modify the lifetime trajectory of socioeconomic status (SES) and lead to heterogeneity in cognitive aging in later life.
We examined the effects of both lifetime socioeconomic trajectory and cumulative disadvantage from childhood through adulthood on late life cognitive performance in a 9-year cohort of 1,789 Mexican Americans aged 60–100 years in 1998–1999.
Compared with those with low SES sustained over the life course, we found that those with more advantaged lifetime SES trajectories experienced fewer declines on a test of global cognitive function and a short-term verbal memory test. These associations are larger in first- and second-generation immigrant families.
Heterogeneity of cognitive aging among diverse race/ethnic groups may be influenced by intergenerational changes in SES, cultural norms, and behaviors and changes in health related to changes in the social and physical environment.
Acculturation; Cognition; Epidemiology; Life course and developmental change
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 = 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 = 0.49, 95% confidence interval: 0.24, 0.98; P = 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 = 1.16, 95% confidence interval: 1.01, 1.33; P = 0.04). Early exposures to social disadvantage may increase the risk of late-life dementia.
aged; dementia; longitudinal studies; Mexican Americans; social class; socioeconomic factors
There are few studies that have assessed factors influencing infection control practices among health care workers (HCW) in nursing homes. We conducted a cross-sectional survey of HCWs (N = 392) in 4 nursing homes to assess whether knowledge, beliefs, and perceptions influence reported hand hygiene habits. Positive perceptions and beliefs regarding effectiveness of infection control in nursing homes were associated with reported appropriate glove use and fingernail characteristics, respectively, among HCWs. Further research on hand hygiene interventions, including targeted educational in-services should be conducted in the nursing home setting.
Limited vaccine availability and the potential for resistance to antiviral medications have led to calls for establishing the efficacy of non-pharmaceutical measures for mitigating pandemic influenza. Our objective was to examine if the use of face masks and hand hygiene reduced rates of influenza-like illness (ILI) and laboratory-confirmed influenza in the natural setting. A cluster-randomized intervention trial was designed involving 1,178 young adults living in 37 residence houses in 5 university residence halls during the 2007–2008 influenza season. Participants were assigned to face mask and hand hygiene, face mask only, or control group during the study. Discrete-time survival models using generalized estimating equations to estimate intervention effects on ILI and confirmed influenza A/B infection over a 6-week study period were examined. A significant reduction in the rate of ILI was observed in weeks 3 through 6 of the study, with a maximum reduction of 75% during the final study week (rate ratio [RR] = 0.25, [95% CI, 0.07 to 0.87]). Both intervention groups compared to the control showed cumulative reductions in rates of influenza over the study period, although results did not reach statistical significance. Generalizability limited to similar settings and age groups. Face masks and hand hygiene combined may reduce the rate of ILI and confirmed influenza in community settings. These non-pharmaceutical measures should be recommended in crowded settings at the start of an influenza pandemic.
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 × 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.
epigenetics; psychiatric epidemiology; trauma; interaction; genomics
Little is known about the correlates of low-grade inflammation in U.S. children.
This study describes the factors associated with increased levels of C-Reactive Protein (CRP) in U.S. children and tests whether differences in CRP by socioeconomic factors emerge in childhood.
Data were analyzed in 2009 from 6004 children aged 3 to 16 years from the National Health and Nutrition Examination Survey, 1999–2004, a representative sample of the U.S. non-institutionalized population. Tobit regression models are used to evaluate associations between predictors including BMI-for-age, skinfold body fat measures, chronic infections, environmental tobacco exposure, low birth weight and sociodemographics and continuous high-sensitivity C-reactive protein (CRP) in mg/L.
CRP levels were higher in U.S. children with lower family income, and these differences are largely accounted for by differences in adiposity and recent illness. Mexican-American children had higher levels of CRP compared to both whites and blacks, but these differences were not explained by physical risk factors.
Increased adiposity is associated with higher CRP concentrations in U.S children aged 3–16 years, and both socioeconomic and race/ethnic differences exist in systemic inflammation in U.S. children. Increased childhood obesity and low-grade inflammation may contribute to later life chronic disease risk.
We introduce a method for estimating incidence curves of several co-circulating infectious pathogens, where each infection has its own probabilities of particular symptom profiles. Our deconvolution method utilizes weekly surveillance data on symptoms from a defined population as well as additional data on symptoms from a sample of virologically confirmed infectious episodes. We illustrate this method by numerical simulations and by using data from a survey conducted on the University of Michigan campus. Last, we describe the data needs to make such estimates accurate.