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.

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 multi-ethnic 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 lifecourse. Information on prenatal and childhood exposures was collected prospectively through 1971; and information on adult exposures and blood specimens were collected in adulthood from 2001-2007. Methylation levels of leukocyte DNA were determined using a [3H]-methyl acceptance assay where higher values of DPM/μg 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 DPM/μg 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 lifecourse 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.

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 Women's 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.

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 (R/E) differences in survival. METHODS We identified cancer cases in the Surveillance, Epidemiology, and End Results program, who were ≥ 20 years and diagnosed with one invasive cancer in 1995–1999 (n=580,225). We used 5-year relative survival rates (5Y-RSR) 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 R/E minority group relative to whites, by the overall amenability index, and three levels of amenability (non-amenable, partly and mostly amenable cancers, corresponding to cancers with 5Y-RSR <40%, 40–69% and ≥ 70%, respectively), adjusting for gender, age, disease stage and county-level poverty concentration. RESULTS As amenability increased, R/E differences in cancer survival increased for African Americans, American Indians/Native Alaskans and Hispanics relative to whites. For example, the hazard rate ratios (95% confidence intervals) for African Americans vs. whites from non-amenable, 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 R/E 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.