The period of adolescence is arguably the healthiest and most resilient of the entire life span. The typical adolescent enjoys peak performance in a number of physiologic indicators of health, including muscular strength, flexibility of joints, and increased resistance to colds. Yet, the overall morbidity and mortality rates increase as much as 200 % during middle childhood and adolescence. Moreover, adolescence is a time of biological and social transitions, with youth continuing to undergo a number of profound neurological, hormonal, and psychosocial changes that make them potentially vulnerable to factors such as poverty and low SES. As they mature, adolescents experience sustained growths in planning, reasoning abilities, problem-solving, and inhibitory control (Luna, Padmanabhan, & O’Hearn, 2010). These changes take place as the adolescent brain undergoes the second wave of overproduction of gray matter (Giedd et al., 1999), followed by synaptic pruning and increases in white matter (Gogtay & Thompson, 2010). With pubertal initiation of hormonal changes, adolescents exhibit greater risk-taking and novelty-seeking (Steinberg, 2008), an increase in emotional intensity, and an increased likelihood of being diagnosed with affective disorders (Pine, 2003). These changes point to adolescence as a time of considerable brain plasticity, with particular adolescence-limited vulnerabilities to psychosocial stress. In fact, research indicates that adolescents are more sensitive to the effects of stressors and negative life events than children or adults are (Walker, Sabuwalla, & Huot, 2004). Furthermore, socioeconomic disadvantage, a context associated with detriments in health among adults, may be even more harmful to adolescents, as it can set a stage for vulnerabilities that alter trajectories of health and health-associated behaviors throughout adulthood.

At the psychosocial level, adolescence is the time of increasing autonomy and self-determination. As parental influence gradually declines, youths begin to turn to their peers for social support, romantic involvements, and information relevant for identity and self (Steinberg & Silverberg, 1986). These changes may contribute to a decline in the importance of family context for adolescent adjustment and increasing roles of peer, school, and neighborhood contexts. However, the effects of parental SES continue to exert an influence on health, as it is an important determinant of access to good schools, safe neighborhood environments, and high-quality health care.

Understanding the effects of SES on youth health is critical, given the recent history of economic changes. Economic conditions have declined for many families in the USA, over the past decade. For the first time since the Great Depression, the housing prices have followed a sustained decline (Organisation for Economic Co-operation & Development, 2010). Combined with subprime mortgage practices, this trend has started an avalanche of mortgage foreclosures that has forced millions of families out of their homes. Although no official information is available on the number of completed foreclosures in the past years, some estimate that 2.5 million households have lost their home to foreclosure in the short period between January 2007 and the end of 2009 (Bocian, Li, Ernst, & Center for Responsible Lending, 2010). The housing crisis has, in turn, triggered a shortage of liquidity in the US banking system, leading to the wide-spread economic consequences. As a result, the unemployment rate among individuals aged 16 years and older increased from 3.9 % in 2000 to 10.5 % in 2010 (US Bureau of Labor Statistics, 2011). Similarly, the real median household income for full-time workers has declined by 4.2 % between 2007 and 2009, and approximately 31.6 % of the population has had at least one episode of poverty that lasted 2 or more months between 2004 and 2007 (DeNavas-Walt, Proctor, Smith, & US Census Bureau, 2010). The impact of the economic crisis has not been experienced to the same extend by some segments of the population. For example, the average household income has dropped for families with children, whereas families without children have experienced an increase in income (DeNavas-Walt et al., 2010). Most importantly, income inequalities have expanded over the past decade, with the 5 and 9 % declines in the real income among households in the 50th and 10th income percentiles, respectively. This drop in income corresponded to no significant changes in real income of households in the 90th percentile for income.

These trends are especially troubling given that the effects of SES go beyond the effects of severe poverty (e.g., a level of poverty where individuals are not able to meet basic nutritional or health care needs). In contrast, the effects of SES are monotone, with higher levels of SES providing extra health advantage at every level of the hierarchy (Adler et al., 1994; Backlund, Sorlie, & Johnson, 1996; Ecob & Davey Smith, 1999; Marmot et al., 1991). Thus, even relatively modest negative changes in the economic conditions of today’s youths can precipitate measurable declines in health.

There is a history of disagreements among social scientists regarding the precise definition of the SES (e.g., McLoyd, 1997). Most would agree that SES should embody the idea of capital, including financial capital (e.g., material resources and assets), human capital (e.g., education), and social capital (e.g., resources available through social networks) (Bradley & Corwyn, 2002). The core of the disagreement emerges from various strategies that are available to assess these aspects of capital. For example, financial capital is often measured by income. However, current earnings may not be the best indicator of financial resources available to an individual. Compared to this, a measure that includes income, occupational status, and financial assets (e.g., housing tenure) provides a better estimate of the financial resources and opportunities (Ostrove, Feldman, & Adler, 1999; Williams & Collins, 1995).

Notwithstanding this debate, social scientists often employ a composite measure of SES that comprises of income, social status (e.g., education), and occupational status (Adler et al., 1994). Whereas some researchers combine the three indicators into a single measure, others use one of these indicators as a measure of SES. This chapter considers the effects of both the broadly defined combined indicator SES and its specific facets.

Although there is an unequivocal link between SES and health among adults and children, this association is less unambiguous among adolescents. Goodman (1999) reports that SES is related to increased depression, greater obesity, and lower self-rated overall health. However, among adolescents, SES is not associated with asthma prevalence and is inconsistently related to suicide attempts (Goodman, 1999).

During the late 1980s and early 1990s, the existence of SES disparities in health during adolescence has been questioned by several investigators who observed a lack of the expected SES-to-health associations among youth. Most notably, West (West, 1988; West, Macintyre, Annandale, & Hunt, 1990) hypothesized that the effects of SES on health during adolescence should be evident within the domain of chronic illnesses, because chronic illnesses are likely to have been acquired as a consequence of childhood exposure to low SES conditions. In contrast, acute and adolescent-onset conditions should not be affected by SES because of the increasing influences of school, peer group, and youth culture during this period of life. His analysis of data for youth in the UK through mid-1990s revealed a pattern that is consistent with this theory (West, 1997). Since then, several other researchers (e.g., Pensola & Valkonen, 2000; Vuille & Schenkel, 2001; Williams, Currie, Wright, Elton, & Beattie, 1997) have found supporting evidence for West’s (1988, 1990) hypothesis. Thus, these researchers came to view adolescence as the time of equalization, when adolescent autonomy and youth culture has an equalizing effect on youth from families with different SES standings.

A more recent analysis of health inequalities in the UK, however, suggests that the attenuation in SES health disparities among adolescents is only evident when considering some measures of health but not others. For example, Spencer’s (2006) analysis of 15,756 children and adolescents from 8,541 British households found that there is an attenuation of SES differences for youth-reported health outcomes, but not parent-reported health outcomes of 12- to 14-year old adolescents. Furthermore, adolescents between the ages of 14 and 18 years old do not exhibit the hypothesized attenuation in SES-to-health differences. Likewise, Chen, Matthews, and Boyce (2002) reviewed seven large-scale studies of SES effects on children and adolescents, concluding that SES is linked to all-cause mortality and morbidity in a monotonic fashion in both of these age groups. More specifically, youths of lower SES were more likely to die from chronic conditions, such as asthma, cancers, congenital abnormalities, and heart disease, as well as from acute conditions, such as pneumonia or injuries. Similarly, youths of lower SES also had higher rates of chronic and acute conditions, and experienced greater impairment in association with their illnesses.

Historically, two major theories have been advanced to explain the association between SES and health—i.e., the social causation and the social selection theories. The social causation theory asserts that poverty is responsible for the environmental adversity and stress that are, in turn, implicated in the etiology of the physical and mental problems experienced by the low-SES youths (e.g., Conger & Conger, 2002; Haas, 2006). The social selection (also known as the drift) theory proposes that those with physical and mental disorders drift into lower SES or fail to rise out of low SES (e.g., McLeod & Kaiser, 2004; Wender, Rosenthal, Kety, Schulsinger, & Welner, 1973). According to this theory, positive psychological adjustment and good physical health are the adaptive qualities that allow an individual to better adjust to their environment and, consequently, be more successful in the social and economic realm. Both, socioeconomic advantage and these positive qualities could be further transmitted to the offspring generation, either via social (e.g., cultural transmission of the value of persistence in the face of adversity or of good health habits) or genetic modes of transmission.

Elements of both theories have been supported by research. Longitudinal studies provide support for the social causation theory, demonstrating that loss of income predicts deterioration in mental health (Catalano, Dooley, Wilson, & Hough, 1993; Dodge, Pettit, & Bates, 1994; Link & Phelan, 1995; Loeber, Green, Keenan, & Lahey, 1995; Shaw, Winslow, Owens, & Hood, 1998). On the other hand, there is also evidence for the social selection theory. It is known, for example, that psychiatric disorders predict poor educational and occupational outcomes (Miech, Caspi, Moffitt, Wright, & Silva, 1999). There is also evidence that childhood externalizing problems diminish youth chances of receiving a high school degree, and of subsequent college enrollment (McLeod & Kaiser, 2004). However, this model does not provide a complete picture of the SES–health association because SES shows prospective effects on health (Adler et al., 1994).

Thus, a more complete theory of SES-to-health association requires specification of both social causation and social selection patterns. Conger and Donnellan (2007) proposed the Interactionist Perspective, combining the social causation and social selection theories. This model suggests a reciprocal process by which childhood SES predicts children’s and adolescents’ personal characteristics that further influence their SES during adulthood. In support of the model, recent studies find that childhood family SES is predictive of mental and physical problems among youth, in turn predicting economic problem during young adulthood (Conger, Conger, & Martin, 2010). Similarly, Martin et al. (2010) report that parental SES predicts adolescent problem behaviors, which in turn are associated with subsequently lower SES and greater family stress when adolescents reach adulthood. The lower SES and higher family stress were further associated with the offspring antisocial behavior, providing a compelling picture of intergenerational transmission of the socioeconomic standing and antisocial behavior.

In a different attempt to reconciliate the social selection and social causation theories, each of the two patterns of association can be seen as better suited for explaining some disease processes than others. Indeed, Johnson, Cohen, Dohrenwend, Link, and Brook (1999) investigated multigenerational associations among SES and health measures in a sample 736 families. Their results provide some support for the social causation hypothesis, indicating that low parental SES is associated with higher likelihood of offspring anxiety, depression, disruptive disorders, and personality disorders, over and beyond the effects of parental psychopathology, single-parent status, and IQ. Offspring alcohol and marijuana abuse were not predicted by parental SES. The social selection hypothesis was also supported for some outcomes: adolescents who were diagnosed with disruptive disorders or substance abuse disorders were twice as likely to drop out of high school and almost four times more likely to discontinue education after completing high school than youth not diagnosed with these disorders. However, the social selection hypothesis was not supported for anxiety, depression, and personality disorders. Thus, the direction of association between SES and health can vary across different adolescent health outcomes. Further multigenerational investigations would be required to test the combined propositions of the social selection and social causation theories across different health outcomes.

Finally, the application of the social selection theory to adolescents requires a slight reconceptualization. Children’s and adolescents’ health is not likely to influence their SES. Thus, it is more reasonable to assume that illness on the part of the parents (or members of a prior generation) is responsible for the family drift in SES. Youth demonstrate a correlation between SES and illness because of the hereditary nature of the illnesses they have inherited from their parents. If propositions of the social selection theory are correct, we can expect a lower correspondence between the parental SES and youth health than between the parental SES and parental health. This proposition has not been empirically tested; however, the greater amount of inconsistencies in the SES disparities in health among youth than adults provides a descriptive rationale for testing this assertion.

Part of the complexity of SES effects on health is in the multi-causality and multi-finality of the processes involved in the link between SES and health. The effects of SES are broad, influencing a wide range of domains of functioning, such as a person’s physical environment (e.g., exposure to pathogens, toxic hazards, and carcinogens), social environment (e.g., exposure to violence, stress, and access to social capital), and health behaviors. (e.g., cigarette smoking, alcohol drinking). Theoretical literature linking SES and health proposes a variety of mechanisms from these domains as potential mediators of the link between SES and health. Many of these mechanisms have not been formally tested among adolescents (as is the case where there is evidence for the SES effects on the proposed mediating variable and of mediating variable on the health outcome, but no formal tests of the mediation pathway) or have been tested in some age groups but not others. Nonetheless, these mediating models provide theoretical background to guide future research and offer promise of clarifying mechanisms explaining SES and health associations.