Parisa Tehranifar

Social Conditions as Fundamental Causes of Health Inequalities Theory, Evidence, and Policy Implications

Link and Phelan (1995) developed the theory of fundamental causes to explain why the association between socioeconomic status (SES) and mortality has persisted despite radical changes in the diseases and risk factors that are presumed to explain it. They proposed that the enduring association results because SES embodies an array of resources, such as money, knowledge, prestige, power, and beneficial social connections that protect health no matter what mechanisms are relevant at any given time. In this article, we explicate the theory, review key findings, discuss refinements and limits to the theory, and discuss implications for health policies that might reduce health inequalities. We advocate policies that encourage medical and other health-promoting advances while at the same time breaking or weakening the link between these advances and socioeconomic resources. This can be accomplished either by reducing disparities in socioeconomic resources themselves or by developing interventions that, by their nature, are more equally distributed across SES groups.

Genomic DNA Methylation among Women in a Multiethnic New York City Birth Cohort

One plausible mechanism for the environment to alter cancer susceptibility is through DNA methylation. Alterations in DNA methylation can lead to genomic instability and altered gene transcription. Genomic DNA methylation levels have been inversely associated with age, suggesting that factors throughout life may be associated with declines in DNA methylation. Using information from a multiethnic New York City birth cohort (born between 1959 and 1963), we examined whether genomic DNA methylation, measured in peripheral blood mononuclear cells, was associated with smoking exposure and other epidemiologic risk factors across the life course. Information on prenatal and childhood exposures was collected prospectively through 1971, and information on adult exposures and blood specimens were collected in adulthood from 2001 to 2007. Methylation levels of leukocyte DNA were determined using a [3H]-methyl acceptance assay where higher values of disintegrations per minute per microgram DNA indicate less DNA methylation. Genomic methylation of leukocyte DNA differed by ethnicity (66% of Blacks, 48% of Whites, and 29% of Hispanics were above the median level of disintegrations per minute per microgram DNA; P = 0.03). In multivariable modeling, DNA methylation was statistically significantly associated with maternal smoking during pregnancy, longer birth length, later age at menarche, nulliparity, and later age at first birth. These data, if replicated in larger samples, suggest that risk factors across the life course may be associated with DNA methylation in adulthood. Larger studies and studies that measure within-individual changes in DNA methylation over time are a necessary next step. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2306–10)

Birth Weight, Postnatal Growth, and Age at Menarche

Larger body size in childhood is correlated with earlier age at menarche; whether birth and infant body size changes are also associated with age at menarche is less clear. The authors contacted female participants enrolled in the New York site of the US National Collaborative Perinatal Project born between 1959 and 1963 (n = 262). This racially and ethnically diverse cohort (38% white, 40% African American, and 22% Puerto Rican) was used to investigate whether maternal (body size, pregnancy weight gain, age at menarche, smoking) and birth (birth weight, birth length, placental weight) variables and early infant body size changes were associated with age at menarche even after considering later childhood body size. Higher percentile change in weight from ages 4 months to 1 year was associated with earlier age at menarche even after adjustment for later childhood growth (beta = -0.15, 95% confidence interval: -0.27, -0.02 years per 10-percentile change in weight from ages 4 months to 1 year). The association was in the same direction for all 3 racial/ethnic groups but was largest for the white group. These New York Womens Birth Cohort Adult Follow-up data (2001-2006) suggest that infant weight gain, in addition to childhood weight gain, may be associated with earlier age at menarche.

Prenatal Smoke Exposure and Genomic DNA Methylation in a Multiethnic Birth Cohort

Background: Exposure to prenatal tobacco smoke (PTS) has been associated with a number of health outcomes in the offspring, including some childhood cancers. Lower levels of genomic DNA methylation have also been associated with several types of cancers. We investigated whether PTS was associated with global DNA methylation levels in the offspring. Methods: Our sample was drawn from a birth cohort of women born between 1959 and 1963 in New York City (n = 90). We measured methylation of repetitive elements (Sat2, Alu, LINE-1) from peripheral blood granulocytes. We combined prospectively collected data on PTS with adult epidemiologic data and blood samples collected in 2001 to 2007 (mean age, 43 years). We used linear regression to assess the association between PTS and repetitive element methylation. Results: Thirty-six percent of mothers smoked during pregnancy. We observed an inverse association between PTS and Sat2 methylation. This inverse association remained even after adjustment for potential mediators including child environmental tobacco smoke exposure, birth size, postnatal weight and height changes, and adult smoking status and alcohol intake (β = −0.22, 95% confidence interval = −0.40 to −0.03 for ever exposed to PTS vs. never exposed using models of log-transformed methylation levels). PTS exposure was not statistically significantly associated with LINE-1 or Alu methylation. Conclusions: PTS exposure, measured at the time of pregnancy and not retrospectively reported, was associated with a decrease in Sat2 methylation but not LINE-1 or Alu methylation. Impact: If replicated in larger studies, this study supports a persistent effect of PTS on DNA methylation levels, as measured by Sat2, in adulthood. Cancer Epidemiol Biomarkers Prev; 20(12); 2518–23. ©2011 AACR.

Medical Advances and Racial/ethnic Disparities in Cancer Survival

Background: Although advances in early detection and treatment of cancer improve overall population survival, these advances may not benefit all population groups equally and may heighten racial/ethnic differences in survival. Methods: We identified cancer cases in the Surveillance, Epidemiology and End Results program, who were ages ≥20 years and diagnosed with one invasive cancer in 1995 to 1999 (n = 580,225). We used 5-year relative survival rates to measure the degree to which mortality from each cancer is amenable to medical interventions (amenability index). We used Kaplan-Meier methods and Cox proportional hazards regression to estimate survival differences between each racial/ethnic minority group relative to Whites, by the overall amenability index, and three levels of amenability (nonamenable, partly amenable, and mostly amenable cancers, corresponding to cancers with 5-year relative survival rate <40%, 40-69%, and ≥70%, respectively), adjusting for gender, age, disease stage, and county-level poverty concentration. Results: As amenability increased, racial/ethnic differences in cancer survival increased for African Americans, American Indians/Native Alaskans, and Hispanics relative to Whites. For example, the hazard ratios (95% confidence intervals) for African Americans versus Whites from nonamenable, partly amenable, and mostly amenable cancers were 1.05 (1.03-1.07), 1.38 (1.34-1.41), and 1.41 (1.37-1.46), respectively. Asians/Pacific Islanders had similar or longer survival relative to Whites across amenability levels; however, several subgroups experienced increasingly poorer survival with increasing amenability. Conclusions: Cancer survival disparities for most racial/ethnic minority populations widen as cancers become more amenable to medical interventions. Efforts in developing cancer control measures must be coupled with specific strategies for reducing the expected disparities. (Cancer Epidemiol Biomarkers Prev 2009;18(10):2701–8)

Rethinking the Bystander Role in School Violence Prevention

Public concerns about school shootings and safety draw attention to the role bystanders can play in preventing school violence. Although school violence prevention plans are often required, there is little guidance about whether these should address the roles of bystanders and what actions bystanders should take in different circumstances, from more common instances of bullying and fighting to rare, but potentially lethal, threats and use of weapons. Literature pertaining to bystanders is reviewed and applied to the school setting. The definition of bystander is expanded, including parents, teachers, and other school staff as well as youths and those who have information about potential violence as well as those who witness its occurrence. Barriers preventing bystanders from taking positive actions are discussed. The authors call on health promotion researchers and practitioners to work with school communities to identify norms, attitudes, and outcome expectancies that shape bystander behaviors to inform prevention efforts.

The Impact of Socioeconomic Status across Early Life on Age at Menarche Among a Racially Diverse Population of Girls

PURPOSE We sought to evaluate the association between childhood socioeconomic status (SES) at two time points and age at menarche in a multiracial sample of U.S. girls. METHODS Our study population consisted of a cohort of female participants enrolled at birth at the New York site of the Collaborative Perinatal Project, who were born during the period 1959-1963 (n = 262). SES at birth, at age 7, and change between birth and age 7 were measured prospectively through an index score of family income, paternal occupation, and education. Data on age at menarche were collected retrospectively through adult self-report. We used multivariable linear regression to examine the association between SES and age at menarche after adjusting for childhood body mass index (BMI) and other covariates associated with age at menarche. RESULTS After adjustment, SES at age 7 was positively associated with age at menarche (beta: 0.015, 95% confidence interval [CI]: 0.003-0.024 per unit of SES index). Change in SES was significantly associated with age at menarche; a 20-unit decrease in SES was associated with a 4-month decrease in age at menarche. CONCLUSIONS Our results suggest that lower SES at 7 years and reductions in SES in early childhood are both associated with an earlier age at menarche.

Early life socioeconomic factors and genomic DNA methylation in mid-life

Epigenetic modifications may be one mechanism linking early life factors, including parental socioeconomic status (SES), to adult onset disease risk. However, SES influences on DNA methylation patterns remain largely unknown. In a US birth cohort of women, we examined whether indicators of early life and adult SES were associated with white blood cell methylation of repetitive elements (Sat2, Alu and LINE-1) in adulthood. Low family income at birth was associated with higher Sat2 methylation (β = 19.7, 95% CI: 0.4, 39.0 for lowest vs. highest income quartile) and single parent family was associated with higher Alu methylation (β = 23.5, 95% CI: 2.6, 44.4), after adjusting for other early life factors. Lower adult education was associated with lower Sat2 methylation (β = -16.7, 95% CI: -29.0, -4.5). There were no associations between early life SES and LINE-1 methylation. Overall, our preliminary results suggest possible influences of SES across the life-course on genomic DNA methylation in adult women. However, these preliminary associations need to be replicated in larger prospective studies.

Prenatal and childhood environmental tobacco smoke exposure and age at menarche

Previous studies have reported mixed results regarding the association between age at menarche and environmental tobacco smoke exposure, both prenatally and during early childhood; however, few studies have had data available during both time periods. The present study examined whether exposure to prenatal tobacco smoke (PTS) via maternal smoking during pregnancy or childhood environmental tobacco smoke (ETS) was associated with age at menarche in a multi-ethnic birth cohort. With the uniquely available prospectively collected data on body size and growth at birth and in early life, we further examined whether the association between PTS and ETS exposure and age at menarche was mediated by these variables. From 2001 to 2006, we recruited 262 women born between 1959 and 1963 who were enrolled previously in a New York City site of the National Collaborative Perinatal Project. Mothers who smoked during pregnancy vs. those who did not were more likely to be White, younger, have more education and have lower birthweight babies. Daughters with heavy PTS exposure (≥ 20 cigarettes per day) had a later age at menarche (>12 years vs. ≤ 12 years), odds ratio (OR) =2.1 [95% confidence interval (CI) 0.9, 5.0] compared with daughters with no PTS. Daughters exposed to only childhood ETS had a later age at menarche, OR=2.1 [95% CI 1.0, 4.3], and those exposed to PTS and ETS combined had a statistically significant later age at menarche, OR=2.2 [95% CI 1.1, 4.6] compared with daughters with no PTS and no ETS. These results did not change after further adjustment for birthweight and postnatal growth suggesting that exposure to PTS and ETS is associated with later age at menarche even after considering possible relationships with growth.

Alcohol intake over the life course and mammographic density

Alcohol intake is one of the few modifiable risk factors for breast cancer. Current alcohol intake has been associated with mammographic density, a strong intermediate marker of breast cancer risk, though few studies have examined the effect of both current and average lifetime alcohol intake. We interviewed 262 participants from a New York birth cohort (born 1959–1963) and obtained mammograms from 163 (71.5% of participants with a mammogram). We collected information on alcohol intake by beverage type separately for each decade of life. We used multivariable linear models to assess the associations between current and average lifetime alcohol intake and mammographic density using a quantitative measure of density from digitized images. Overall, current alcohol intake was more strongly associated with mammographic density than average lifetime alcohol intake; compared with nondrinkers, those with current intake of seven or more servings per week had on average 12.3% (95% CI: 4.3, 20.4) higher density, adjusted for average lifetime alcohol intake, age, and body mass index. We observed a consistent inverse association for red wine intake and mammographic density, suggesting that the positive association between mammographic density and overall alcohol intake was driven by other types of alcoholic beverages. Our findings support an association between current alcohol intake and increased mammographic density independent of the effect of average lifetime alcohol intake. If replicated, our study suggests that reducing current alcohol consumption, particularly beer and white wine intake, may be a means of reducing mammographic density regardless of intake earlier in life.