Parental education is related to C-reactive protein among female middle aged community volunteers

Abstract

Growing evidence suggests that socioeconomic attributes of both childhood and adulthood confer risk for cardiovascular morbidity and mortality. In this study, we examine the association of both parental and individual educational attainment with C-reactive protein (CRP), an inflammatory mediator relevant to cardiovascular pathophysiology, in a mid-life community sample. Subjects were 811 men and women (394 men/417 women; 87% European-American/13% African-American), 30–54 years of age. Plasma concentrations of CRP were determined from blood samples obtained at a single session following an overnight fast. Regression analyses adjusting for age and race showed both parental education and individual education to be associated inversely with CRP in women, but not men. The relationship of parental education with CRP in women persisted on multivariable adjustment for both lifestyle risk factors (smoking, alcohol consumption, sleep, exercise, body mass index) and individual SES. Independent of reported personal educational attainment, mid-life adult women whose parents achieved fewer years of educational attainment exhibit higher levels of circulating CRP than women with higher parental education. This association may help explain the increased risk of atherosclerotic cardiovascular morbidity and mortality conferred by low childhood socioeconomic status.

Introduction

Variation in socioeconomic status (SES) is inversely related to cardiovascular mortality (Salonen, 1982, Siegel et al., 1987, Keil et al., 1992), incident coronary heart disease (Rose and Marmot, 1981, Liu et al., 1982, Diez-Roux et al., 1995), and cardiovascular disease risk factors, including cigarette smoking (Zang and Wynder, 1998), generalized obesity (Sobal and Stunkard, 1989), and physical activity (Evenson et al., 2002). In general, these associations hold for both men and women, though the strength of the relationships may vary between sexes. Among women, stronger inverse associations between SES and incident coronary heart disease (Vogels et al., 1999, Thurston et al., 2005), coronary mortality (Chandola, 1998, Pekkanen et al., 1995), and obesity (Sobal and Stunkard, 1989, Langenberg et al., 2003, Zhang and Wang, 2004) have been documented in some, but not all (Marmot et al., 1997, Frank et al., 2003, Diez-Roux et al., 1995) investigations.

Although most literature has focused primarily on adult SES, growing evidence indicates that lower childhood SES, independently of adult social standing, is associated with increased risk of incident coronary heart disease (CHD) outcomes, including myocardial infarction (Notkola et al., 1985, Kaplan and Salonen, 1990, Gliksmen et al., 1995, Wannamathee et al., 1996, Wamala et al., 2001, Davey Smith et al., 2002), and several CHD risk factors (Poulton et al., 2002, Blane et al., 1996, Ebrahim et al., 2004). Here, also, sex differences have been documented, with childhood SES predicting serum triglycerides (Parker et al., 2003), HDL cholesterol (Brunner et al., 1999), and metabolic syndrome (Lehman et al., 2005) in women, but not men.

Inflammation is now recognized as a risk factor for the development and exacerbation of atherosclerotic cardiovascular disease (Ross, 1999). C-reactive protein (CRP) is a frequently cited inflammatory marker shown to predict future cardiovascular morbidity and mortality (Danesh et al., 2000, Danesh et al., 2004, Lagrand et al., 1999). Growing evidence also suggests that adult SES, whether indicated by occupation (Owen et al., 2003), employment status (employed/unemployed; Danesh et al., 1999), education (Panagiotakos et al., 2004, Wu et al., 2002); composites of income and education (Jousilahti et al., 2003), or community-level SES (Petersen et al., 2008) is inversely related to CRP.

Extending the literature on SES associations with inflammation, more recent attention has turned to the role of childhood influences on inflammatory processes in adulthood. In this regard, it is suggested that the early-childhood environment can regulate immune development in ways that influence health in adulthood, even when adult SES is taken into account (e.g., Lynch et al., 1997). Thus, early life variation in exposure to environmental factors that covary inversely with SES and modulate immune function, such as air pollutants, viral infections, maternal smoking, psychological stress, and allergen exposure (Donovan and Finn, 1999) may have far-reaching effects. Childhood SES may also affect adult inflammation through more proximal behavioral mechanisms. For example, lower SES families engage in poorer health practices, such as smoking, physical inactivity, poorer dietary choices (Marmot et al., 1991), that have been associated with higher systemic inflammation (Bruunsgaard, 2005, Frohlich et al., 2003). Lifestyle practices are often established early in life, with lower childhood SES predicting poorer health practices in adulthood (Politt et al., 2005). Thus, in examining possible associations between childhood SES and adult inflammation, it is important to determine whether contemporaneous factors such as adult lifestyle choices or remaining in one’s social class of childhood explain observed effects or whether there is something unique about childhood SES that influences later inflammatory processes.

To date, findings from the few studies examining childhood SES in relation to adult CRP levels have been mixed. One study showed a positive association between father’s occupation and CRP in men 45–59 years of age (Mendall et al., 2000), and similar findings obtained for a composite of father’s occupation and education in younger adults (Pollitt et al., 2007). A third investigation failed to find parental education associated with CRP (Gimeno et al., 2008), whereas a fourth (Taylor et al., 2006) found that parental education was indirectly associated with adult CRP levels through a pathway encompassing a history of familial adversity, later psychological functioning, and body mass. The model tested in that study did not adjust for adult subjects’ own educational attainments, however, and did not specifically address potential sex differences in the magnitude of association between early life SES and CRP. The purpose of the present study, then, was to further explore the relationship of parental education (as one frequently studied component of childhood SES) with CRP concentrations, adjusting for participants’ own education, among a diverse community sample of mid-life men and women, and to examine whether these relationships might vary by sex.