Pico de Orizaba

Pico de Orizaba
Taken from Huatusco, Veracruz, the closest town to Margarita's family's ranch.

Friday, March 20, 2015

Childhood Misfortune and Acute Myocardial Infarction in Adulthood (an excerpt)

As stated in cummulated inequality (CI) theory, childhood is a particularly vulnerable period of the life course since it comprises a significant portion of cognitive, neural, and biological maturation (Maggi, Irwin, Siddiqi, & Hertzman, 2010). Research has demonstrated how childhood insults, such as parental loss, can alter biological functioning and neurological response systems (Luecken, 1998). Many physical ailments in later life still bear the imprint of childhood misfortune, illustrating its far-reaching grasp. Childhood misfortune can later manifest as adult obesity (Greenfield & Marks, 2009), cancer (Morton, Schafer, & Ferraro, 2012), and lung disease (Blackwell et al., 2001). Among the diseases studied in relation to childhood misfortune, the most pervasive in the United States remains CVD.

Investigating how childhood misfortune raises the risk of CVD has generally taken two approaches: analyzing unique or cumulative effects of misfortune. Among the commonly examined types of misfortune, such as Socio-Economic Scale (SES), poor childhood health, and a harsh family environment, many studies treat these as individual CVD risk factors (e.g., Beebe-Dimmer et al., 2004; Blackwell et al., 2001; Luecken, 1998). Although many of these childhood insults have independent effects, the accumulation of childhood misfortune also presents a lasting threat to cardiovascular conditions. Additive measures of childhood misfortune that capture child maltreatment, family structure, and the psychos2ocial environment have displayed a doseresponse effect: as the number of adversities a child experiences increases, so does the risk of heart disease and CVD risk factors (Dong et al., 2004; Felitti et al., 1998; Loucks et al., 2011).

Although many studies link childhood misfortune and CVD, we identified only a few that focused on AMI. O’Rand and Hamil-Luker (2005) have found that adults who experienced poor health, family instability, and low SES during childhood were at increased risk for AMI, and they extended their findings to show that childhood misfortune was more consequential for women than for men (Hamil-Luker & O’Rand, 2007). Whereas O’Rand and Hamil-Luker’s research identified how different clusters of misfortune raise AMI risk, Hallqvist and associates’ (2004) research focused on SES; they found that the life course trajectory of low SES, rooted in childhood, raises AMI risk in adulthood. These three studies paint a compelling picture of the influence of childhood misfortune on the risk of heart attack, but we draw attention to two notable risk factors that have not yet been incorporated in research on the topic.

First, a risk factor that merits attention is family history of heart disease. Previous research shows that having just one first-degree family member with ischemic heart disease doubles the risk of AMI, and the risk elevates further with two or more relatives with heart disease (Bertuzzi, Negri, Tavani, & La Vecchia, 2003). We are unaware, however, of any studies on childhood misfortune and AMI that account for family history of AMI or any type of CVD, potentially leading to an overestimation of the effect of childhood misfortune on AMI. In addition to this confounding relationship, childhood misfortune could also moderate or mediate the relationship between family history of AMI and AMI risk. Regardless of the relationship, we build upon prior literature by incorporating family history of AMI into our analyses.

Second, a growing body of literature has revealed that child maltreatment raises the risk of multiple health problems in adulthood, from ulcers (Springer, 2009) to cancer (Morton et al., 2012). Childhood experiences such as household financial strain or living in a fatherless home may have lasting effects on health, but many studies also point to the long-term effects due to traumatic experiences. Child maltreatment is often a traumatic experience that activates a host of physiological, psychological, and social responses—from secretion of glucocorticoids to social withdrawal. Despite substantial literature suggesting that child maltreatment influences cardiac health, we found only one published study examining the link between child maltreatment and AMI (Fuller-Thomson, Bejan, Hunter, Grundland, & Brennenstuhl, 2012). The authors examined one type of maltreatment—sexual abuse—and reported that it raised the risk of AMI for men but not for women. Most studies of sexual

Morton et al. Page 4

Soc Sci Med. Author manuscript; available in PMC 2015 March 01.

NIH-PA Author ManuscriptNIH-PA Author ManuscriptNIH-PA Author Manuscript

abuse and CVD, however, report that women are at greater risk (e.g., Goodwin, & Stein, 2004). The current study does not include measurement of sexual abuse per se, but we are able to capitalize on an extensive battery of questions tapping both physical and emotional abuse. As such, we examine whether AMI risk is related to an overall measure of accumulated misfortune (including maltreatment) or maltreatment as a special type of early misfortune.

Mechanisms of childhood misfortune Many life course scholars contend that childhood misfortune triggers a chain of risks, where one event increases the likelihood of other negative events. Experiencing childhood misfortune may propel an individual toward risky lifestyles and behaviors that lead to poor health. Childhood misfortune has been shown to increase the risk of smoking, alcoholism, drug abuse, and obesity, each of which may mediate the relationship between childhood misfortune and adult health (Brown et al., 2010; Felitti et al., 1998; Greenfield & Marks, 2009).

Felitti and colleagues (1998) developed a conceptual model that includes both health behaviors and psychosocial factors as potential mediators of the childhood-adult health relationship. Applying this model to childhood misfortune and heart disease, Dong et al. (2004) found that both health behaviors and psychological risk factors mediated the relationship, with the latter, psychological risk factors, producing a stronger mediation effect. Therefore, the mechanisms linking childhood experiences to adult AMI may extend beyond the adult health behaviors, social support, and SES trajectories already identified by Hallqvist et al. (2004) and O’Rand and Hamil-Luker (2005). Prior research reveals that anxiety, locus of control, and family strain are potential mechanisms. Previous studies have reported associations between childhood misfortune and risk of anxiety, low locus of control, and familial relationship strain (Irving & Ferraro 2006; Kessler et al., 1997; Loucks et al., 2011). Anxiety, low locus of control, and family strain have also been associated with increased AMI risk (Kubzansky, Cole, Kawachi, Vokonas, & Sparrow, 2006; Rosengren et al., 2004). Bridging together this research, we investigate psychosocial factors of anxiety, locus of control, and family strain as potential mediators that may link childhood misfortune to adult AMI risk.1.

Selection issues Selection processes are also important for the study of AMI. Although AMI is often considered a disease of old age, many AMI studies also identify cases of early onset – as early as 25 years old (e.g., Fang, Alderman, Keenan, & Ayala, 2010). Moreover, a Swedish study of AMI survivors found that approximately one-fourth of adults who had an AMI between the ages of 25 and 55 died within 5 years (Isaksson et al., 2011). In the US, women under the age of 55 have the highest AMI mortality rates (Vaccarino et al., 2009). This type of mortality leads to a selection problem when studying the effects of childhood misfortune on AMI risk in adulthood (people die from an AMI or other causes before they are eligible

1We investigated anxiety instead of depression because Kubzansky et al. (2006) found that anxiety, but not depression, predicted AMI. Moreover, Davidson et al. (2005) contend that the effects of depression on CVD are more reliable when using clinical depression measures rather than self-reported depressive symptoms. The MIDUS only measures self-reported depressive symptoms.

Morton et al. Page 5

Soc Sci Med. Author manuscript; available in PMC 2015 March 01.

NIH-PA Author ManuscriptNIH-PA Author ManuscriptNIH-PA Author Manuscript

to be surveyed). This is an important consideration because previous studies of childhood misfortune and adult AMI rely on samples of adults aged 51 and older (Hallqvist et al., 2004; Hamil-Luker & O’Rand, 2007; O’Rand & Hamil-Luker, 2005). By restricting the sample to persons 51 years and older, existing AMI studies may be underestimating the effects of childhood misfortune, especially if those who were faced with early disadvantage and heart trouble did not survive until late middle age. As Vaccarino and colleagues note (1998), limiting samples to older populations can lead to underestimating the prevalence of AMI at younger ages as well as the potential effect of childhood misfortune on AMI risk. To account for those earlier heart attacks, we use an age-heterogeneous sample of adults.

To extend the literature, we propose three hypotheses:

H1 Childhood misfortune is associated with greater risk of AMI.

H2 Health lifestyle factors will mediate the relationship between childhood misfortune and AMI.

H3 Psychosocial factors will mediate the relationship between childhood misfortune and AMI.

No comments: