Life-course criminology is a major criminological paradigm that acknowledges stability/continuity of behavior as well as change in behavior at different points in the life course as the result of various life-altering events (Sampson & Laub, 2003). This perspective acknowledges the possibility that the factors that influence the timing of the onset of crime may or may not be the same factors that influence criminal persistence, desistance, or intensity. Consequently, the perspective considers the whole stretch of the human life as potentially relevant to the explanation of criminal behavior, not solely the adolescent or young adult years. This approach to the study of crime is developmental in nature and encompasses a number of theories. Two of the most well-known life-course theories in criminology are Moffittâs developmental taxonomy of offenders (1993) and Sampson and Laubâs age-graded theory of informal social control (1993, 2003). Life-course theorizing has much to offer if thoughtfully integrated with extant health disparities frameworks for better elucidating the intersections between delinquency and health. In this chapter, we discuss the untapped potential of these intersections and reveal ways in which health disparities and related public health reasoning can enrich the criminological life-course paradigm.
Moffittâs Developmental Taxonomy
Moffittâs (1993) developmental taxonomy proposes that the causes of criminality differ depending on the nature and duration of the offending. Specifically, she posits that there are two distinct types of offenders: life-course-persistent (LCP) and adolescence-limited (AL) offenders. Moffitt theorizes that the offending of these two groups is distinct, both in its patterns and etiology. She proposes that LCP offenders consist of a small group of offenders who demonstrate substantial continuity in offending behaviors (i.e., offending begins prior to adolescence and continues into adolescence and adulthood). According to the theory, the origins of LCP offending is an amalgam of childhood neuropsychological deficits, negative/impulsive temperament, and adverse familial environments across development, resulting in a stable propensity for antisocial behavior. The early, multifaceted origins of LCP offending are thought to place individuals on a path of cumulative disadvantage and social dysfunction across the life course. As a result, they are at risk of more severe and/or violent criminal behaviors. AL offenders, on the other hand, have (1) shorter offending trajectories, and (2) consist of the majority of offending individuals. The cause of their offending is rooted in a social group phenomenon that Moffitt called the âmaturity gapâ (Moffitt, 1993). Moffitt described this gap as a disjuncture between biological and social maturity, where youth are biologically âadultsâ, but are denied the autonomy or legal permission to make many adult decisions. As a result, AL offenders are temporarily compelled to engage in rebellious delinquency that can take the form of âadult-likeâ behaviors, such as drinking and smoking, in an effort to attain power and status. However, by the time they reach early adulthood, the motivation behind their offending dissipates and they no longer offend. In sum, AL offending is short-term and is explained by an age-dependent motivational state (i.e., the maturity gap), whereas LCP offending is more severe, more chronic, and is rooted in biological and social risks that are compounded early in life (Moffitt, 1993). Overall, Moffittâs theory has received a substantial degree of empirical support (for a review, see Jennings & Reingle, 2012), despite some evidence that Moffittâs conceptualization of persistent offending may be too narrow (Blokland, Nagin, & Nieuwbeerta, 2005; Gunnison, 2015; Odgers et al., 2008). Some studies also suggest that race/ethnicity and social class may moderate associations between neuropsychological deficits, adverse parenting, and offending behaviors (Jackson & Beaver, 2016; Turner, Hartman, & Bishop, 2007).
Sampson and Laubâs Age-Graded Theory of Informal Social Control
Another seminal life-course theory in criminology is Sampson and Laubâs Age-Graded Theory of Informal Social Control (1993). Sampson and Laubâs theory is similar to Moffittâs in that it emphasizes life trajectories and divergent pathways. Even so, the theories differ in many respects. The age-graded theory of informal social control is rooted in the theoretical developments of Elder (1995,1998) and underscores the importance of two distinct, yet co-occurring phenomena: state dependence and population heterogeneity. Sampson and Laub argue that future behavior is both a reflection of (a) the social consequences of past experiences and behaviors, and (b) individual differences in propensity towards that behavior. To illustrate, Sampson and Laub recognize that delinquency and social bonds (to conventional persons and institutions) have a reciprocal relationship over the life course, such that early childhood and adolescent bonds diminish the likelihood of adolescent offending, but that such offending (as well as a criminal record) can also interfere with future adult bonds, like marriage and employment. Thus, the mutual reinforcement of attenuated social bonds and delinquency over time is a potent explanation of stability. Nevertheless, to explain change, they also make room in their theory for various serendipitous, fortunate life occurrences that can serve as turning points that deflect individuals off of the criminal course and âknife offâ the past from the future. For example, important life transitions like marriage, serving in the military, and access to gainful employment, may all operate as mechanisms of informal social control that place individuals on a law-abiding path. Sampson and Laub also contend that elements of luck/randomness and human agency can play a role in criminal desistance (Sampson & Laub, 2003). Thus, the theory is an age-graded theory of informal social control in that different sources of informal control have the potential to be turning points at different points during the life course. A number of studies support Sampson and Laubâs postulations (Doherty, 2006; Sampson, Laub, & Wimer, 2006; Wright & Cullen, 2004), though many scholars have emphasized that properly accounting for social selection (i.e., environmental selection on the basis of preexisting traits, like self-control) tends to attenuate support for social causation (see Barnes & Beaver, 2012; Barnes et al., 2014; Wright et al. 2001).
The Untapped Relevance of Health Disparities Research for Life-Course Criminological Theorizing
Despite the impact that the life-course perspective has had on the field of criminology over the past two decades (Barnes & Beaver, 2012; Barnes et al., 2014; Blokland, Nagin, & Nieuwbeerta, 2005; Doherty, 2006; Gunnison, 2015; Jennings & Reingle, 2012; Odgers et al., 2008; Sampson, Laub, & Wimer, 2006; Wright et al., 2001; Wright & Cullen, 2004), the most influential theories under this paradigm adhere to a somewhat limited scope of potentially criminogenic variables, such as attenuated social bonds (e.g., marriage, employment), negative childhood temperament, and neuropsychological deficits (Laub & Sampson, 1993; Moffitt, 1993; Sampson & Laub, 2003). The theoretical emphasis on a fairly narrow range of risk factors has prevented life-course criminologists from systematically integrating relevant research and theoretical developments from related fields into this criminological perspective. For instance, scholars from fields such as sociology (e.g., sociology of health and illness, medical sociology), demography, epidemiology, and public health have frequently engaged in cross-disciplinary efforts to examine health disparities, or the existence of heightened health risks (and diminished health status) in the context of social disadvantage (Adler & Newman, 2002; Amone-PâOlak et al., 2009; CerdĂĄ et al., 2014; Skalamera & Hummer, 2016; White & Borrell, 2011). At the turn of the twenty-first century, the reduction of socioeconomic and racial/ethnic disparities in health was identified as a major priority for public health practice and scholarship by the U.S. Public Health Service and the National Institute of Health (House & Williams, 2000; U.S. Department of Health and Human Services, 1999 see also House, 2002). Consequently, this area of research has the potential to significantly enhance the criminological life-course paradigm, and render it increasingly relevant to cross-disciplinary evidence-based prevention and intervention efforts, particularly in light of the well-established associations between the socioeconomic status, race/ethnicity, and involvement in violent crime (Heimer, 1997; Markowitz, 2003; McNulty & Bellair, 2003; Stewart & Simons, 2006), early-onset delinquency (Aguilar et al., 2000; Staff et al., 2015), and LCP offending (Moffitt & Caspi, 2001; Piquero, Moffitt, & Lawton, 2005). In short, while criminologists acknowledge that racial/ethnic minorities and lower class individuals are exposed to early, criminogenic conditions more consistently, they do not systematically examine the criminogenic effects of racial and socioeconomic disparities in high-risk health conditions/behaviors or diminished health resources, particularly during the early life course. Instead, when criminologists study health, they typically examine it as an outcome of criminal justice involvement and/or involvement in chronic offending (Manninen et al., 2015; Moffitt et al., 2002; Odgers et al., 2007; Piquero et al., 2007; Piquero et al., 2014; Shepherd, Farrington, & Potts, 2004; Vaughn et al., 2014). This is an unfortunate gap in the literature that, if addressed, can greatly enhance the theoretical and practical contributions of life-course criminological research.
To date, research has yielded substantial evidence for the existence of health disparities among individuals with varying social identities and/or positions within the social structure. For instance, research has revealed that inequalities in income, education, and employment widen the gap in physical and mental health between the haves and the have-nots (Adler & Newman, 2002; Amone-PâOlak et al., 2009; Schreier & Chen, 2013; Skalamera & Hummer, 2016; Quon & McGrath, 2015). To illustrate, research has provided evidence for socioeconomic disparities in depression (Zimmerman & Katon, 2005), asthma (Schreier & Chen, 2013), obesity (Schreier & Chen, 2013), hypertension (Quon & McGrath, 2015), and LDL cholesterol (Quon & McGrath, 2015). This process can occur in various contexts and through several mediating mechanisms, including adverse housing conditions (Krieger & Higgins, 2002), neighborhood disadvantage or disorder and associated deficits in social capital (Ross & Mirowsky, 2001; Vyncke et al., 2013), school physical activities practices (Carlson et al., 2014), and diminished access to fundamental health resources, including food (Cook & Frank, 2008) and medical care (Alder & Newman, 2002; Larson & Halfon, 2010). In general, explanations of socioeconomic disparities in health are rooted in the understanding of socioeconomic disparities in exposure to sources of chronic stress (Adler & Newman, 2002; Brunner, 1997; Lantz et al., 2005) and the capacity to manage or cope with chronic stress (Gallo & Matthews, 2003). Research has also indicated socioeconomic disparities in behaviors associated with health and wellbeing. Results from a sample of 2,071 Australian children indicated that higher income children spend significantly more time playing sports and music, whereas low-income individuals spend significantly more time watching television and playing video games (Ferrar, Olds & Walters, 2012). The researchers propose that differential engagement in these behaviors may be an important source of health inequalities between socioeconomic groups across development. A study examining a Finnish sample of adolescents yielded similar findings, as youths engaging in more health-protective behaviors (e.g., physical exercise, hygiene, seatbelt use, abstention from smoking, limited TV viewing) were on a more advanced educational track than adolescents who did not engage in health-protective behaviors (Koivusilta, Rimpelä, & Rimpelä, 1999; see also Skalamera & Hummer, 2016). Research also suggests that dietary behaviors among adolescents are stratified by household SES (Quon & McGrath, 2015).
Apart from socioeconomic disparities in health, research has also provided evidence for racial/ethnic disparities in health, particularly in the U.S. (for a review, see Williams & Sternthal, 2010). In general, this body of research suggests that racial disparities in health status and exposure to health risks may be partly explained by four interrelated phenomena: (1) differential access to social capital (Ard et al., 2016), (2) de facto residential segregation into unequal neighborhoods (CerdĂĄ et al., 2014; Kravitz-Wirtz, 2016; Williams & Collins, 2001), (3) an ongoing history of racial discrimination (Keene, Lynch & Baker, 2014; Saegert, Fields, & Libman, 2011; Tobler et al., 2013), and (4) differential engagement in high-risk health behaviors by minority groups, particularly blacks (Block, Scribner & DeSalvo, 2004...
