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Abstract

French

This article focuses on the biosocial perspective in criminology. Its purpose is to highlight public health approaches on biosocial interactions that can be drawn from to develop more theorization on the social environment and to provide new possibilities in studying how socio-environmental macro–micro characteristics interact with neurobiology in developing antisocial, violent, and criminal behaviors. Extant biosocial research in criminology examines and understands the social environment as characteristics proximal to the individual, more so than those that are distal. Examples of proximal level characteristics are family, education, or individual socioeconomic status and examples of distal level ones are income inequality and institutional racial discrimination. Although the field of criminology traces the history of the biosocial perspective to Cesare Lombroso, the concept of “biosocial” and its onto-epistemological approach is also linked to that of public health. In relinking criminological biosocial research to public health, this article highlights how trends within the latter may have shaped the former; and in relinking, the article also provides “ways of seeing” the role of distal level social factors in biosocial interactions from three public health theoretical frameworks and constructs: Nancy Krieger’s embodiment from ecosocial theory; Merrill Singer’s syndemics; and Johan Galtung’s structural violence.

Keywords

biosocial criminology ecosocial theory public health structural violence syndemic

Introduction

The biosocial perspective in criminology underscores the importance of biology, and how it interacts with the social environment to increase the likelihood of antisocial behavior, including violence and offending, which not only enables a better understanding into which social characteristics are important, but also why the same characteristics are detrimental to certain individuals exposed to them and not to others (Walsh, 2024; Wright and Cullen, 2012). According to this perspective, violence and crime themselves are not inherited, but our biology may increase the likelihood that we behave a certain way in a particular social environment. Living in areas that are chronically violent crime hot spots, for example—characterized by high crime and victimization and the fear of them; density of mental health issues; low trust in neighbors—are thought to harm human development through long-term changes in genetic expression and brain growth, possibly explaining the development of physical aggression (Leshem and Weisburd, 2019).

Supporters of this perspective even regard it as a paradigm shift, seeing it as radically changing old ways of thinking and doing science on crime and justice (Heylen et al., 2015; Rudo-Hutt et al., 2014; Wright and Cullen, 2012).¹ Biosocial interactions that have been identified have to do with genes and child maltreatment; changes in cognition and receiving treatment; taking nutritional supplements which reduce malnourishment and increase better parent-child relations; low physiological arousal and treatment effects; and low resting heart rate and parental characteristics/family dynamics (see reviews from Barnes et al., 2016, 2022; Bedoya and Portnoy, 2022; Brennan and Raine, 1997; Brennan et al., 1997; Chen et al., 2016; Raine, 2002; Rudo-Hutt et al., 2011; van Hazebroek et al., 2019); policy implications for prevention and treatment have also been discussed (Raine and Liu, 1998; Rocque et al., 2012, 2014). According to Barnes et al. (2022), however, there is no question about whether there are interactions between biology and the social environment, but “questions are to what extent do these factors interact, what is the meaning of the interaction, and what are the implications?” They noted this because, similar to concerns raised in social epidemiology, there was a need for more theory-guided tests for interactions.

One possibility of addressing these questions may be to enhance the development of the perspective’s social environment, so to better understand the social context in which these interactions operate. The social environment comprises “groups to which we belong, the neighborhoods in which we live, the organization of our workplaces, and the policies we create to order our lives” (Yen and Syme, 1999), but the “social” of the biosocial perspective focuses more on proximal level characteristics such as family, education, or individual socioeconomic status compared with distal level factors at the structural level such as income inequality and institutional racial discrimination.² Because of the perspective’s inadequate attention to the social environment, Rocque and Posick (2017) observed that the consequences were that criminological biosocial research created a false dichotomy between nature and nurture; inflated the significance of biological factors; deemphasized the importance of language; became atheoretical; and was uninformed by history. In a recent review of criminological bio(psychological) and social-environmental interactions, Barnes et al. (2022)³ concluded that the research would benefit from integrating empirical and theoretical insights on socioenvironmental risks, including those from medical sociology focused on inequalities in social conditions. Thus, the purpose of the present article is to highlight public health approaches on biosocial interactions that can be drawn from to enhance theorization about and conceptualization of the social environment. Doing so may encourage more integrated theoretical and empirical advances on interactions between biological and social-environmental characteristics.

The concept of “biosocial” is not exclusive to the study of antisocial behavior (which includes violence and crime), but has been used across diverse fields and research approaches, particularly focused on mental health (see Fletcher and Birk, 2022). This concept shares a history with developments in public health, but is not acknowledged in the specific history of “biosocial criminology.” Consequently, divorced from this larger scholarly context, this could be why biosocial crime scholars observe an underdevelopment of inquiry on the social environment, specifically a focus more on proximal-level factors than on distal-level factors. This article is based on the observation that the literature on biosocial criminology focuses on proximal-level interactions. The gap that the article addresses has to do with the incorporation of distal-level social factors into biosocial theorizing, which is often focused on the proximal level. It contributes to “bridging this gap” by exploring an underacknowledged historical link to public health that may be conducive to thinking about and understanding these biosocial interactions within the larger social environment and the role of distal-level social factors in these interactions. In doing so, this article elaborates on discussions of and calls on developing and enhancing theorization on the social environment and processes in the biosocial perspective by: (1) introducing public health theoretical frameworks and constructs that highlight the importance of distal-level social factors in its relationship to biosocial interactions; (2) proposing these theoretical frameworks and constructs are applied to said interactions so to contextualize these within the broader social context; and (3) emphasizing that basic theorizing in which the role of distal-level social factors is considered may reveal new possibilities and directions in studying these interactions. The article does not construct a theory to test, but provides an approach to theorizing how these interactions may operate when distal-level social factors are considered. An example using the interaction between low resting heart rate and social adversity is provided to illustrate the aforementioned.

In relinking this literature to public health, it introduces and discusses three public health theoretical frameworks and constructs, or “ways of seeing,” that focus on these interactions and their relationship to the larger social environment: Nancy Krieger (1994)’s embodiment from ecosocial theory; Merrill Singer’s (2009) syndemics; and Johan Galtung’s (1969) structural violence. These may help develop more theorization on the social environment and provide new possibilities in studying how socioenvironmental macro–micro characteristics interact with neurobiology in developing criminological outcomes—how it “gets under the skin.” The phrase “gets under the skin” has been used on several occasions in biosocial research across different fields (see Moffitt and The Klaus-Grawe 2012 Think Tank, 2013; Rocque and Posick, 2017; Singer et al., 2017). The phrase has its origins in the contemporary psychosocial and population health literature and is used to describe how social conditions affect individuals internally (Krieger, 2011: 222).

Although there are already a number of criminological theories that focus on the social environment and can be drawn on to address the dearth of social theorizing in the biosocial perspective, this article addresses an issue that is much more basic: it echoes previous works on the biosocial perspective that have called for more consideration about the “social”; what it does differently, however, is elaborate on what possibilities and advancements, including methodological challenges, may be revealed if distal level social factors and processes, as examined and understood in public health, are incorporated in the thinking and doing of criminological biosocial research. Not only that, but to theorize at this basic level is to also clarify the biosocial perspective’s specific outcome of interest: in a review of findings from this perspective, outcomes of antisocial behavior, crime, aggression, and violence are muddled together, giving the impression that outcomes do not matter conceptually and what binds them all is merely that their explanations are biosocial.

For the purposes of this article, which draws from both criminological and public health literatures, violence is the outcome of focus and research on it will be used as illustrative. Preventing violence globally takes on a public health approach, addressing characteristics across individual, relational, community, and societal levels to substantially reduce adverse behavioral, mental health, and physical health outcomes (Violence Prevention Alliance and Education Development Center, 2011); violence is also likely to occur from an interaction between individual characteristics and the social environment (Krug et al., 2002). Violence is understood as “the intentional use of physical force or power, threatened or actual, against oneself, another person, or against a group or community, that either results in or has a high likelihood of resulting in injury, death, psychological harm, maldevelopment or deprivation” (Krug et al., 2002). This definition from the World Health Organization (WHO) is referred to in this article because it is informed by a public health approach with global policy implications for prevention—it takes on a wide lens understanding of violence, and helps to consider and think more about the role of distal-level social factors/processes in criminological biosocial interactions.

The definition used reveals that violence is not merely direct or interpersonal, and requires a public health response (Rutherford et al., 2007). Avoidable consequences may manifest immediately or much later in time and in various ways that stunt growth, whether intentional use of physical force actually happens (see Adlam et al., 2018; Lee, 2019); violence also comprises power, such that one’s relative social influence or authority and, so, ability to dominate and control others, can be wielded against those very others (Parsons, 2007; Wrong, 1993). Violence and its consequences, then, are much broader and insidious than is popularly understood, as visible and immediate.

On history and the perspective’s connection to public health

In criminology, the history of the biosocial perspective can be traced to the biological work of Cesare Lombroso, Charles Goring, and Earnest A. Hooton (Bedoya and Portnoy, 2022). The biosocial perspective is distinct from this early biological work, but its onto-epistemological influences can be traced back to public health: the concept of risk factors and risk-focused prevention had appeared in criminology from public health (Farrington, 2007; Hawkins and Catalano, 1992; Welsh et al., 2014), and had a significant impact on the field’s understanding of offending and on practice (Bui and Deakin, 2021; Loeber and Farrington, 2000; Mahony, 2009). Biology and the social environment were condensed to individual and social characteristics known as risk factors that increased the risk for violence and offending (Barnes et al., 2016; Brennan et al., 1997; Brennan and Raine, 1997; Chen et al., 2016; Rudo-Hutt et al., 2011; van Hazebroek et al., 2019). This approach itself has its own history and reflects larger trends in the natural and social sciences.

Tracing epidemiology’s own history of knowledge production, Krieger (2011) noted that, in the 1950s, an individualist and reductionist approach became influential in the majority of the natural and social sciences, and remained so even in the present day. This approach was characterized by the idea that societal phenomena could be reduced to and explained by individual behaviors and exposures. Unlike “holism,” this “individualism” predictably became dominant in the West, especially as, during that time, the rivalry between communist and capitalist ideologies was tense. The biosocial perspective has strong traces of this legacy, likely deriving from the mid-twentieth-century biomedical approach and the subsequent “multiple causation” idea, which viewed causes of disease to be the consequence of risk factors. Often, these risk factors, like behaviors, exposures, and genes, were depicted as “disembodied” and “decontextualized” aversive characteristics (Krieger, 2005).

The consequence of this “disembodied” and “decontextualized” approach relates to the underdevelopment of the social environment. A couple of times in a recent comprehensive review of biosocial research on violence and offending, Barnes et al. (2022), noted this underdevelopment, calling not only for more theory-guided tests for interactions, but for more attention to social processes that affected biological changes, so as to “sharpen” popular criminological theories (see also Choy et al., 2015).

Without thinking and reflecting more carefully about the social environment, many biosocial findings are not anchored to a larger context in which to make sense of themselves. Consequently, this may affect how results are communicated and understood, giving the inaccurate impression that the context in which biosocial integration⁴ is situated is simplistic, and, therefore, this supposedly complex integration itself is also simplistic. Theorizing about the role of distal-level social phenomena expands the social environment of biosocial interactions and creates a better-informed context for prevention. To do so is to reveal three ways of seeing that: one, clarifies possible causal pathways; two, considers the role of social disparities and the meaning of interaction; and three, emphasizes the long reach of violence that produces various adverse outcomes. Again, public health theoretical frameworks and constructs on biosocial interactions that are focused on violence are used to illustrate these.

Seeing causality through embodiment: Krieger’s ecosocial theory

Extant biosocial research often views the social environment as characteristics immediate to the individual. In past reviews of biosocial integration (see previous sections), these proximal-level social characteristics were to do with familial relationships, statuses, and dynamics; peers and social networks; parenting and parental mental illness; neighborhood; and childhood maltreatment. These empirical findings, in turn, inform prevention strategies. Prevention from a biosocial perspective is informed by a developmental approach, which emphasizes the importance of early life experiences on later human development (Welsh and Farrington, 2012). This form of prevention has been shown to be effective in targeting violent and criminal behavior by enhancing health and nutrition; parenting skills and the quality of the child–parent bond; and intellectual and cognitive abilities (Rocque et al., 2012, 2014). For example, prevention can comprise home visitations from health nurses for new and expecting parents or environmental enrichment programs from nursery school teachers lasting for more than 1 year.

If prevention is already considered effective at the proximal level, why bother theorizing how to link proximal level phenomena to distal ones? Even in other types of prevention, whose principles are similar, Gupta et al. (2008), in reviewing theoretical frameworks on broader social approaches for HIV prevention, note that it is more difficult to establish causality with distal-level social factors than with proximal ones, and that health officials often deem distal factors like gender inequality beyond their area of focus. Distal issues are vital for social justice, according to Freilich et al. (2020) in their article on applying situational crime prevention to preventing public mass violence, but argue that these are not vital for prevention as they are unable to directly impact on the situation in which violence occurs; later, though, they noted that distal factors⁵ can influence situations of interest, but as facilitating conditions that can be targeted.

Incorporating distal-level social factors, then, provides “the context of vulnerability” whereby mapping how each of these factors increase risk and the specific pathways leading to that risk are important in identifying the “most appropriate type and level of response” (Gupta et al., 2008). Although it is more difficult establishing causality than that at the proximal level, a broader social approach does help to clarify possible causal pathways in order to locate which points are best to intervene in order to change the outcome. In addition, prevention that considers the distal is able to affect more lives and for a longer period of time compared with one that only has the proximal social environment in mind (Yen and Syme, 1999).

For example, initiatives for global violence prevention from the World Health Organization (WHO, 2010) focus on seven evidence-based strategies, in which one recommends altering cultural and social norms that support violence, especially when tackling violence against girls and women. In a scoping review, Montesanti and Thurston (2015) mapped out how distal social forces contributed to interpersonal violence toward women, recognizing that most of this research focused on proximal-level factors rather than distal ones known to determine women’s health. Their concept map made clear that structural factors like social and cultural norms such as male dominance, acceptance of violence, and divorce as socially ostracizing contributed to gender-based violence, which, in turn, may directly contribute to interpersonal violence where women were disproportionally the victims, or indirectly so through social determinants of health like control over and access to financial resources. They recommended that structural elements are targeted in interventions to indirectly effect positive change toward interpersonal violence.

Considering distal level social factors in the biosocial perspective (in criminology) clarifies the theorizing and subsequent testing of possible causal pathways, as ecosocial theory emphasizes. Ecosocial theory (Krieger, 1994) emerged at a time when “multiple causation” was the dominant framework from which epidemiology understood population patterns of health and disease—as a web of interlinked risk and protective factors. Consequently, more attention was given to modeling these complex relationships than was to theorizing possible explanations and generating hypotheses to test. Noticing that this metaphorical web was “spiderless” (in other words, atheoretical), the primary concern that ecosocial theory aimed to address had to do with the spider: who and what is responsible for social inequities in health (Krieger, 2011, 2012). It explicitly frames population health and disease over the life course as the consequence of the societal conditions to which we are exposed and with which we engage: we embody our interactions with our social environment that is shaped by our particular society’s economic, political, and social relationships.

The biosocial perspective is considered to be one that applies the premises of ecosocial theory in criminology as observed by Skinner and Farrington (2023) because of its focus on both biology and the social environment and their integration; according to the authors, the theory may be useful in guiding insight into the relationship between offending and health, in that a criminal career may be seen as a social determinant of health and that offenders may embody their social conditions that increase risk for poor health and premature death. The theory’s central notion of “embodiment” enables clarity on possible causal pathways for violence by: first, moving away from the assumption that the cause is inside the individual. Instead of gravitating toward the assumption that biological differences (or any other differences) are innate or natural, “embodiment” moves toward thinking about how changes in societal contexts, like group relations, manifest biologically (Krieger, 2005); second, it better hypothesizes about who and what is responsible for the outcome of interest. “Embodiment” can guide the hypothesizing to identify and elaborate on multilevel processes and how relevant phenomena operate across and within time and space, and in specific historical time periods and contexts (Krieger, 2011). It also sees distal level social factors as more likely to influence proximal level factors rather than the other way around; and third, specifying which metrics of distance like space, time, and level are of interest. Often, the three metric items are conflated with each other, which has implications for causality (Krieger, 2008). For example, if distal and proximal factors are not clarified (also see endnote 2), then it will be assumed that what is proximal will have a stronger effect on the outcome than what is distal; yet it is unclear what exactly about the factor is proximal or distal (in time, space, or level?), and these relationships can actually be non-linear and non-sequential.

Thus, seeing through the prism of ecosocial theory’s tenets, particularly that of “embodiment,” inevitably expands the social environment in the biosocial perspective to consider distal-level social factors. Although both ecosocial theory and the biosocial perspective share similar individualist scientific legacies,⁶ the theory is focused on population health and disease. It provides, however, an informative way of approaching and hypothesizing about violence—by seeing the conditions for it as something one can embody.

Seeing clustering as unnatural: Singer’s syndemics

Variation in characteristics among and between groups is of interest to the biosocial perspective. Accordingly, the criticism lodged against biology proponents is that it seems to assume that “criminality” is inherent to certain people (Larregue and Rollins, 2019). This speaks to a wider issue of mainstream understanding on social phenomena: variation of said phenomena in the human population is expected. If, however, a certain phenomenon is concentrated in a particular group, the oft-too-common and mistaken assumption is that this is a natural occurrence—this is something inherent to those people.

This persistent assumption of individual characteristics as the reason for racial disparities in interpersonal violence was tested by Sampson et al. (2005), for example, and compared to other prevalent explanations. Their results showed that neighborhood context, like concentration of poverty and diminished informal community controls, was the most important explanation for the differences in violence perpetration between Black and White people, whereas the least important explanation was individual characteristics, impulsivity, and intelligence. It should be emphasized, however, that impulsivity and intelligence did indeed predict violence, but not so much specifically for racial disparities in violence. This study and later related work on social disparities (see Sampson, 2019) evidence that, although variation is “natural,” its distribution may be “unnatural.”

Theorizing about whether and why certain biosocial interactions concentrate in certain populations can refine previous knowledge accumulated on the perspective, and this requires thinking about social disparities. The aforementioned work was on a visible form of violence, but subtle and invisible forms may be difficult to articulate, let alone identify, and their manifestations may lie beyond the proximal social environment. Their effects, however, may be patterned, and these materialize as a host of adverse biosocial interactions, in addition to possible interpersonal and self-directed violence.

The syndemic model of health (Singer, 1994; Singer and Snipes, 1992) provides an informative framework to think about violence and biosocial interactions. Whereas “embodiment” can provide seeing social conditions as materializing in the body, syndemics frame the clustering of and exposure to social and health problems, disease, and other vulnerabilities as the result of social and structural inequalities, implying a violence emanating from institutional and systemic levels; these social disparities are considered to be the main cause of syndemics because they enable detrimental coexisting health conditions to persist and thrive (Singer and Rylko-Bauer, 2021). Syndemics are either biosocial interactions or interactions between biological characteristics that arise from a wider harmful social environment that encourages the adverse effects of these co-occurring diseases and health conditions (Singer et al., 2017). The framework gives equivalent importance to social and biological elements in explaining clustering of disease and health problems, so to examine connections between biological and social factors, their causes and consequences for health and well-being, and the most appropriate interventions (Singer et al., 2020).

The earliest identified syndemic is what is known as SAVA—substance abuse, violence, and AIDs (Singer, 1996). Although SAVA seemed to comprise separate American epidemics that occurred during the nineties, through ethnographic and survey research among a Puerto Rican community, Singer (1996) demonstrated the interrelatedness of these phenomena: poverty and social marginalization increased risk for joining a street gang, which in turn increased risk in violent perpetration and victimization; drug use and involvement; and having multiple sexual partners; all of these were also mutually reinforcing. Even though more than two factors are involved in a syndemic, they must demonstrate an interaction to be considered such, not merely be linked with each other. Many studies that claim to study syndemics actually do not, as rigorous empirical analysis of this approach has been lacking (Tsai, 2018). In a review of the literature between 2015 and 2019, Singer et al. (2020) found that only 12% of the 188 selected texts featured syndemics as originally intended; the majority (38%) used syndemics to mean an additive approach whereby the sum of adverse health and social conditions aggravates the outcome of interest instead of their interaction with each other.

A syndemic approach in the context of the biosocial perspective and violence prevention, however, encourages thinking about whether biosocial interactions cluster in certain populations and the possible causal pathways to these that may extend from the distal level social environment, which could provide more pertinent points in intervening, or at least helps to clarify the pathway from distal to proximal level. Seeing these interactions as potentially unnatural disparities frames them as an issue of public health and of social equality—are such social arrangements for health just? In addition to the issue of variation and innate characteristics that the syndemic approach can address in biosocial research, it can also clarify what specific interaction is of interest using this approach.

Tsai (2018), in a critique of the empirical literature on syndemics, underscored the conceptual confusion over “interaction.” How biosocial (or bio-bio) factors “interact” can differ even though they are labeled as syndemic. The three models that informed the different types of interactions were mutually causal, synergistically interacting, and serially causal epidemics. The first one is the type of interaction the SAVA syndemic is meant to describe: substance abuse, violence, and AIDs mutually cause and reinforce each other; the second one is the common understanding, which is the interaction elicits a stronger effect on the outcome of interest (using SAVA as an example, this would presumably be AIDs) than the factors independently (substance abuse and violence); and the third one means that the factors accumulate or “build on” each other to cause the outcome of interest. The reason for clarifying what exactly the interaction is that each model has different ideas about effective prevention and treatment. For example, the serially causal epidemic model implies identifying one causal factor in this interaction of vulnerabilities to target so as to reduce the adverse outcome; in contrast, the mutually causal epidemic model requires targeting all interacting factors.

Although the biosocial perspective provides the impression that biological and social factors are distinct from each other, Raine (2002) had noted that there was much overlap in the character of these factors, so that it was a false dichotomy, but this dichotomy was made mainly for illustrative purposes. The false dichotomy, however, should not mean that the factors are in essence the same, but, instead, is indicative of the extent to which they are intertwined; their interactions with each other may co-occur so closely that, in order to identify causal pathways and their mechanisms, careful attention to these co-occurrences should be heeded.

Seeing biosocial integration as a consequence of violence: Galtung’s structural violence

The previous section noted that disparities are what produce syndemics. The concept, structural violence, is relevant to syndemics because it is considered a cause of the disparities that give rise to biosocial interactions (Singer et al., 2017). Structural violence was first introduced by the sociologist and pioneer of peace and conflict studies, Johan Galtung (1969), who argued that violence should be defined “as the cause of the difference between potential and actual realization, between what could have been and what is.” What Galtung meant by this was that if death or injury was a potential outcome, for example, and happened anyway even though, in actuality, it was avoidable because of prevention and treatment advances, then violence had occurred—what potentially could have happened should not have happened.

He provided the example of tuberculosis and how, today, if someone were to die from it, compared to the eighteenth century, when there was no treatment for it, it would be an apt illustration of violence. The term has also been attributed to Latin American liberation theologians who described social structures that promoted social inequalities as “sinful” (see Farmer, 2004). Structural violence is a social force—like gender inequality, racism, and war—embodied in political and economic institutions and systems that generate and sustain social inequalities; these unnecessarily harm certain individuals or populations of people through invisible and slow processes that prevent them from reaching their full potential (Farmer et al., 2006; Montesanti and Thurston, 2015). This form of violence is an “avoidable impairment of fundamental human needs” (Galtung, 1969) and can only be observed from the disproportional number of negative life outcomes like disability, illness, and premature death in one social group compared to another (Galtung and Höivik, 1971; Shackel, 2018).

Similar to the syndemic approach, what structural violence emphasizes is that the unequal distribution of adverse conditions to certain populations is no coincidence, and the coincidence is unrelated to anything intrinsic. In addition, like the other two concepts of embodiment and syndemics, structural violence views both biology and social phenomena and their interweaving with each other as essential to understanding public health. In making a case for the importance of a biosocial understanding of medical phenomena in public health, Farmer et al. (2006) questioned a “natural history” of chronically infectious diseases by noting a number of successful biosocial interventions that took a structural approach. One was for people living with HIV in the American city of Baltimore: race and poverty were found to be associated with the standard of HIV care, whereby Black people infected with HIV were less likely than their White counterparts to receive the latest therapy, which, in other research, translated to excess mortality among Black people without insurance. The distribution and outcome of infection were intimately linked with social arrangements whereby social forces influenced the effectiveness of diagnosis, staging, and treatment of HIV. To address these disparities in care, interventions targeting comorbid conditions, community stigma, and barriers to access like transportation issues were developed, and, consequently, these social inequalities in care were significantly lessened. The effectiveness of interventions and treatments, according to Farmer et al. (2006), is limited by social forces and will continue to be so if they are ignored. In preventing violence using the biosocial perspective, distal-level social factors may well take the form of structural violence.

The structural violence approach informs theorizing in the biosocial perspective in two ways: first, as the above has explained, to expand the social environment is to consider structural phenomena and its role in creating, sustaining, or exacerbating biosocial interactions that: increase likelihood of individual-level violence that is visible (interpersonal, self-directed, and exposure) and may cluster in certain populations; and emphatically, two, that violence of the invisible kind, like structural violence, will also produce outcomes that appear unrelated and are biopsychosocial like mental illness, disease, and social isolation; even the biosocial interactions themselves.

An example

Figure 1 provides a simple illustration of what elaborating on and expanding the social environment to consider distal-level social factors would look like with the aforementioned frameworks and concepts. To show how the three frameworks and concepts can be used to “expand” the social environment in order to gain theoretical insights into biosocial interactions, we use, as an example, the relationship between low resting heart rate (RHR) and social adversity (SA) on violence. This relationship is used as an example because research on it has engaged with developing the social environment in the biosocial perspective and is informed by a “social neuroscience theoretical framework” (Barnes et al., 2022; Choy et al., 2015; Fagan et al., 2017); this social neurocriminology perspective emphasizes more consideration of the role of the social environment in affecting biological processes. Low RHR is the most well-replicated biological correlate of antisocial behavior (ASB) in children and adolescents (Armstrong et al., 2009; Choy et al., 2017; Farrington, 1997; Ortiz and Raine, 2004; Portnoy and Farrington, 2015; Raine et al., 2014), and compared with other forms of ASB, it most reliably and strongly predicts violence (de Looff et al., 2022; Murray et al., 2016). Low RHR seems indicative of low arousal, so those with this heart rate are thought to engage more in impulsive sensation seeking to increase their level of arousal (Choy et al., 2018; Portnoy et al., 2014). Hence, its robust association with ASB broadly.

Figure 1.

Application of the three public health frameworks and concepts to biosocial interactions in criminology.

A few studies have examined low RHR, as well as other measures of autonomic nervous system activity such as pre-ejection period and heart rate variability, and their relationship to SA in influencing ASB. SA broadly encompasses various socio-environmental risks ranging from exposure to violence, segregation, poverty, and adverse home and parental conditions (Fagan et al., 2017). These studies have evidenced two ways of understanding this relationship between SA, low RHR, and ASB: (1) as the expected biosocial interaction to affect ASB (Barnes et al., 2022; Bertoldi et al., 2022; Raine et al., 2014); and (2) low RHR as a mediator, whereby SA leads to low RHR, which, in turn, gives rise to ASB (Choy et al., 2015; Fagan et al., 2017).

It could be that both forms of these relationships occur, but it would help to understand under what conditions that may happen. In addition, measures of SA in these studies focus on parental, familial, and accommodation characteristics. For example, Choy et al. (2015) measured SA with 18 items about the parents (e.g., parents’ employment status, parental physical or mental illness) and a couple of items on accommodation.⁷ As different aspects of SA are measured in these studies, it would also help to further consider the “composition” of SA and how those aspects relate to low RHR.

The three public health frameworks and concepts are applied to the biosocial relationship of focus to theorize about further directions that can be taken with the broader social environment in mind. Again, the aims of this are to (1) clarify potential causal pathways to investigate; (2) consider the role of any social disparities in their relation to the interaction(s) of interest and their meaning; and (3) apply a broader understanding of violence that may illuminate how relevant but seemingly disparate factors are linked. This is not an exhaustive example and is not a criticism of the studies that have investigated this relationship; the example is intended to suggest possible directions for further investigation.

Embodiment

Embodiment is a core concept in ecosocial theory and emphasizes how people “embody” their social conditions. If the social “gets under the skin,” then understanding what is being embodied in the relationship between low RHR, SA, and violence is needed. As empirical findings show two different relationships for low RHR, SA, and ASB, referred to is ecosocial theory’s tenets to clarify potential causal pathways. If we evoke the larger social environment, we have in mind the question of what or who might be causing the social disparity in health outcomes. The larger social environment is seen as an unknown cause of social inequity or inequality (SI_X), so that there are three possible theorized relationships:

(1) SI_X → SA → Low RHR → Violence

(2) SI_X → SA x Low RHR → Violence

(3) SI_X → Low RHR x SA → Violence

The first relationship incorporates the mediation model, whereas the latter incorporates two variations of the interaction model. These two types of interactions are also included because if SI_X is applied, the moderator might be different. In this case, it is unclear whether the health outcome should be differing levels of RHR (as emphasized in Relationship 3), or if low RHR is seen as a mechanism in the pathway for health-related outcomes of those involved in violence (as implied in Relationships 1 and 2). Including SI_X in the mediation model suggests, and as Relationship 1 depicts, that SI_X gives rise to SA. This makes sense, but as previously mentioned, SA is conceptualized primarily as parenting, familial, and accommodation characteristics; sometimes these are combined to form an overall measure of it. The question then is what is SI_X influencing to be adverse? Would SI_X give rise to parental characteristics such as mental illness and substance use? It might but accommodation and socioeconomic indicators may be underlying proximal measures of SI_X. It would help to understand what would likely lead to differences in aspects of SA if inequality played a role.

SI_X influences the presence of SA in Relationship 2, but SA interacts with low RHR. Questions from Relationship 1 are applicable here too, but if it is an interaction in this exact direction, it suggests that low RHR is innate and its influences are independent from the measured proximal social environment. This may explain why not everyone who is exposed to the same socioenvironmental characteristics will go on to be involved in violence (see Portnoy et al., 2020). It could be that those who have relatively lower RHR and are exposed to SA are specifically the ones who go on to be involved in violence.

Relationship 3 theorizes that SI_X influences differences in RHR. Disparities in autonomic functioning have been attributed to social inequality (Fuller-Rowell et al., 2013; Kim et al., 2020; Pope et al., 1999; Ugarte et al., 2022). Here, it could be that SI_X influences disparities in RHR and that low RHR interacts with a specific form of social adversity—familial and parental factors—to amplify its relationship with violence. In terms of which factors would be distal or proximal, when these terms are used, it is to do with space (again see endnote 2), but like with Relationship 2, though low RHR would be considered innate, it would be influenced by socioenvironmental factors that may be proximal in space but are distal in time. For example, low RHR may have been affected by familial stress experienced as an infant. Familial stress would be considered proximal in space, but its experience was distal in time.

Although SI_X may be unknown at this particular point in this example, applying the ecosocial theory’s tenets encourages thinking about how the existing relationships work and embody social conditions in producing violence, as it is presumed that there are preceding causes that are distal.

Syndemics

A syndemic framework emphasizes that social and health conditions can interact with each other and cluster in certain populations, increasing physical and behavioral vulnerability, which is indicative of social inequality (SI_X). It is the nature of the interaction that is of interest, and the syndemic framework helps to clarify this and theorize broader and interrelated social and health conditions relevant to the interaction between low RHR and SA to produce violence. In a syndemic, however, all of these factors would co-occur and interact with each other to cluster and aggravate conditions:

(4) SI_X → (Low RHR x SA x Violence) → Increased disease transmission, progression, and negative health outcomes

Relationship 4 theorizes that, instead of seeing each phenomenon as independent conditions, it could be that SI_X influences the emergence of all three phenomena that coexist and are closely linked, and are transmitted and progressed by the same underlying characteristics such as exposure to community violence and high allostatic load, which also promotes adverse health outcomes (see Massey, 2004, 2018; Moffitt and The Klaus-Grawe 2012 Think Tank, 2013). Low RHR, in this relationship, could represent psychophysiological under-arousal or blunted reactivity, which could also be linked to neurodevelopmental issues (Glenn and Raine, 2014). As the syndemic framework highlights, those who are likely to be disproportionately affected by a syndemic are from impoverished or marginalized populations (Singer et al., 2017). The measure of SA in its relationship to low RHR and antisocial behavior generally seems to allude to impoverishment and marginalization, especially as the literature draws from sociological findings (Choy et al., 2015; Fagan et al., 2017).

Most studies on the interaction between autonomic functioning and socioenvironmental factors have understood the interaction to be characterized by the diathesis-stress and differential susceptibility models (Barnes et al., 2022; Hazebroek et al., 2019). The former proposes that the outcome is highest for those exposed to both social-environmental and biological risk whereas the latter proposes that biological factors may make an individual more susceptible to the outcome but only in certain social environments. These forms of interactions are relevant because they highlight that the presence of adverse social conditions will make outcomes particularly potent. In either case, they are understood to be synergistically interacting to produce violence, but it could be as Relationship 4 theorizes, that by theoretically expanding the social environment, the relationship between low RHR, SA, and violence may completely change and is mutually causal.

Broadening the social environment under the syndemic framework also highlights pertinent health outcomes. Health outcomes of those who are involved in violence may have an overlap with those found among persistent offenders. Empirical findings show that, compared with those not involved in offending, those who do are likely to experience more illness, injury, and hospitalization over the life course, and that those who persistently offend have overall poor physical and mental health (Reising et al., 2019; Skinner and Farrington, 2023; Skinner et al., 2020; Testa and Semenza, 2020). Specifically for persistent male violence, early health risks such as lead exposure, poor nutrition, and birth complications are understood to influence later neurodevelopmental issues, which in turn can lead to significant problems functioning in social, educational, and work settings (Raine, 2019).

Structural violence

From a structural violence lens, if the syndemic of low RHR, SA, and violence can be prevented and occurs anyway in certain populations and not others, then applying the concept of structural violence may help develop thinking about the causal mechanisms that precede the syndemic to empirically test; this further can help clarify where intervention or preventive measures can be applied to be most effective.

Empirical and theoretical literature on the neurobiological basis for antisocial behavior as well as on social inequality and health have some overlap, particularly that of lead exposure. The former literature conceptualizes lead exposure as a biological characteristic, as it is neurotoxic and exposure “gets under the skin” to negatively affect development particularly in the prefrontal cortex (Raine, 2013, 2019); whereas the latter literature conceptualizes lead exposure as a “toxic inequality” that has long-term effects on child development and adult life outcomes and concentrates in poor neighborhoods of color (Muller et al., 2018; Sampson and Winter, 2016). Lead exposure is considered a pathway in which inequality is embodied because it concentrates in impoverished and marginalized areas. It also has macro-level social causes (concentrated disadvantage, regulatory environment, and community organization) so that “its eradication is a central component of tackling broader racial and other social inequalities in human development” (Sampson, 2022: 2).

Lead exposure has also been shown to predict later violence and other forms of antisocial behavior (Boutwell et al., 2017; Sampson and Winter, 2018; Talayero et al., 2023; Wright et al., 2008), and that concentrated disadvantage—isolation from “beneficial social institutions”—interacted with lead exposure to affect violent crime rates (Martin and Wolfe, 2020). Although lead exposure is relevant to biosocial interactions and violence, most evidence supports its direct relevance for neurodevelopment. Emerging evidence, however, shows that it negatively affects heart rate as well (Halabicky et al., 2022; Park et al., 2008), and is associated specifically with low RHR among community adolescent boys (Liu et al., 2021). Applying the concept of structural violence to what is understood so far about lead exposure (LE) on low RHR, SA, and violence, the theorized relationship looks like the following and points to other avenues to explore:

(5) SI_X → LE → (Low RHR x SA x Violence) → Increased disease transmission, progression, and negative health outcomes

Further investigations could attempt to reproduce the relationship between LE and low RHR within the context of social disparities, or, if showing the proposed syndemic exists, understand how changes in LE by one of the social causes (SI_X) may affect the biosocial interactions. Figure 2 provides a summative illustration of how these frameworks and concepts can be applied to theorize further directions and possibilities on the relationship between low RHR, SA, and violence.

Figure 2.

Summative illustration of “an example.”

Conclusion

The purpose of this article is basic: reviews of criminological biosocial interactions reveal mostly interactions between proximal-level factors, but it is a literature that has links and relevance to the broader literature on biosocial interactions on health that has advanced knowledge on the role and influence of broader social factors and processes. The article focuses on three public health frameworks and concepts using violence as an example that may help guide the direction of scientific inquiry on these interactions. In seeing criminological biosocial interactions situated and related to a broader social context is a way of also developing better insight into the role and influence of the social environment.

Why this basic theorizing also matters is that it influences the way biosocial explanations are presented and understood. Wright and Cullen (2012) characterize critics of the biosocial perspective as anti-science⁸ whose hostility toward the area stems from beliefs that certain ideas should not be examined because they are seen as unquestionably wrong; these are to do with racial and sex differences, blaming the victim, supporting stereotypes, and nativism. Moffitt’s (1993) Developmental Taxonomy, then, although considered by the authors a biosocial theory, is believed to receive mainstream criminological support because it attributes biological risk factors to the social environment and uses more palatable language so that biological pathology was replaced with terms like “neuropsychological deficits.”

Perhaps, though, Moffitt’s theory was accepted more than any other biological theorizing, not because of its subtlety, but because it recognized the complexity of everyday life and attempted to explain how and why, in this case, antisocial behavior manifested in specific social environments. The developmental taxonomy provided a thoughtful account of a biosocial integration that scholars understood as likely occurring in the real world. Language like “biological pathology,” aside from its negative and stigmatizing connotations, does not capture what is likely to happen in reality, especially in light of neurodiversity. Consequently, underdevelopment in understanding the social environment may manifest as explanations with little context and language that is perceived as reductive and crude; it is these that critics are perhaps also reacting to, rather than just the product of their stubborn adherence to uncritical beliefs and values.

There may be other reasons why theory, particularly on the social environment, has been underdeveloped in biosocial criminology: according to Larregue (2024), the social sciences became receptive to advances in behavioral genetics, and genetic data became widely available in the early 2000s. Thus, social sciences research combining environmental and genetic factors proliferated, including that from the biosocial perspective in criminology, whereby testing of proposed interactions could now be done instead of mere theorizing.

The doing of the science in the biosocial perspective could do more with thinking about the science. Wright and Cullen (2012) had stated that the biosocial perspective will push scholars to “abandon their obsessive focus on theory in favor of empirical discoveries that have real policy and treatment ramifications,” and the perspective has certainly done so. It now, however, could benefit from more theorization on distal social factors that are informed by its empirical observations to date—who and what could be responsible for these observations? Why and how are biosocial interactions disproportional to one group and not to another? What is the role of structures and institutions in producing the various violent outcomes, and do these phenomena link, and if so, how? Thinking about and doing the science are not separate activities: thinking about, in fact, is part of the doing of science.

Footnotes

Acknowledgements

Much thanks to Adrian Raine, Daniel Marshall, Caroline Miles, Nicholas Lord, Julia Buxton, and anonymous reviewers for comments/feedback on earlier versions of this work. Any omissions or errors are those of the author.

ORCID iD

Laura Bui

Ethical considerations

Ethical approval not required.

Funding

The author disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This research was supported in part by the Independent Social Research Foundation (ISRF).

Declaration of conflicting interests

The author declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Notes

Author biography

Laura Bui is Senior Lecturer in Criminology at the University of Manchester.

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Gets under the skin: Elaborating on and expanding the “social” in biosocial criminology

Abstract

Keywords

Introduction

On history and the perspective’s connection to public health

Seeing causality through embodiment: Krieger’s ecosocial theory

Seeing clustering as unnatural: Singer’s syndemics

Seeing biosocial integration as a consequence of violence: Galtung’s structural violence

An example

Embodiment

Syndemics

Structural violence

Conclusion

Footnotes

Acknowledgements

ORCID iD

Ethical considerations

Funding

Declaration of conflicting interests

Notes

Author biography

References