Page 1 Page 2 Page 3 Page 4 Page 5 Page 6 Page 7 Page 8 Page 9 Page 10 Page 11 Page 12 Page 13 Page 14 Page 15 Page 16 Page 17 Page 18 Page 19 Page 20 Page 21 Page 22 Page 23 Page 24 Page 25 Page 26 Page 27 Page 28 Page 29 Page 30 Page 31 Page 32 Page 33 Page 34 Page 35 Page 36 Page 37 Page 38 Page 39 Page 40 Page 41 Page 42 Page 43 Page 44 Page 45 Page 46 Page 47 Page 48 Page 49 Page 50 Page 51 Page 52 Page 53 Page 54 Page 55 Page 56 Page 57 Page 58 Page 59 Page 60 Page 61 Page 62 Page 63 Page 64 Page 65 Page 66 Page 67 Page 68 Page 69 Page 70 Page 71 Page 72 Page 73 Page 74 Page 75 Page 76 Page 77 Page 78 Page 79 Page 80 Page 81 Page 82 Page 83 Page 84 Page 85 Page 86 Page 87 Page 88 Page 89 Page 90 Page 91 Page 92 Page 93 Page 94 Page 95 Page 96 Page 97 Page 98 Page 99 Page 100 Page 101 Page 102 Page 103 Page 104 Page 105 Page 106 Page 107 Page 10881 CHAPTER 4 | CROSS-NATIONAL HEALTH DISPARITIES AND US DISADVANTAGE Bowen (2009) finds that Black parents of HRS participants had lower education than White parents, and Black fathers had lower occupational status. Accounting for relevant risks, these measures of childhood disadvantage explain part of the racial disparity in adult disabilities. Haas (2008) examines the impact of both childhood health and socioeconomic disadvantage on trajectories of change in functional limitations. Accounting for chronic diseases in adulthood and adult SES at the beginning of the study, greater childhood health problems and worse socioeconomic conditions in childhood predicts a faster decline in physical functioning. Because of the importance of childhood health on later life outcomes, the HRS is now expanding its measurement. Using data on biomarkers in the HRS, Lin et al. (2015) find a link between traumatic events in adulthood and inflammation, indicated by ele- vated levels of high sensitivity C-reactive protein. Bodily inflammation is an important biomarker indicating risk for a range of health conditions, especially heart disease. Those with childhood adversity are almost three times as likely to have experienced trauma as an adult. Childhood ad- versity and adulthood trauma are independently associated with elevated inflammation. Another study suggests a genetic mechanism. M. Levine et al. (2015) show that childhood trauma increases the expression of genes that determine inflam- mation. Having low SES in adulthood has the greatest effect on inflammatory gene expression for those who had traumatic events in childhood. Other studies evaluate effects on cognitive functioning. Examining the influence of psychi- atric history on cognitive functioning at older ages, Brown (2010) finds that childhood health influences later life cognition through its effect on later life health. Another study finds that adult SES affects the relationship between childhood SES and cognitive function. Those with higher cumulative SES have an advantage in cognitive function. Childhood SES and adult SES are both related to cognitive status and to cognitive changes at older ages (Lyu and Burr 2016). Other research examines the potential impact of the disease environment of HRS participants when they were children. Linking to census region-level information on mortality from typhoid, malaria, measles, influenza and diarrhea, Case and Paxson (2009) find evidence that those who grew up in regions of the country with higher disease-specif- ic and overall infant mortality have lower scores on cognitive tests in old age. Those who grew up in regions of the country with higher disease-specific and overall infant mortality have lower scores on cognitive tests in old age.