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For an amusing look at how scientists think, check out The Pleasure of Finding Things Out: The Best Short Works of Richard Feynman (1999, New York, Harper Collins). Here we focus on the essentials of the scientific method originally inspired by Robert Boyle, and then look at how science is practiced today. Scientific method refers to a standardized protocol for observing, asking questions about, and investigating natural phenomena. Simply put, it says look/listen, infer a cause and test your inference. As captured by the Oxford English Dictionary, the essential inviolable commonality of all scientific practice is that it relies on “systematic observation, measurement, and experiment, and the formulation, testing and modification of hypotheses."
A. The Method
Adherence to the method is not strict, and may sometimes breach adherence to protocol! In the end, scientific method in actual practice recognizes human biases and prejudices and allows deviations from the protocol. Nevertheless, an understanding of scientific method will guides the prudent investigator to balance personal bias against the leaps of intuition that successful science requires. The practice of scientific method by most scientists would indeed be considered a success by almost any measure. Science “as a way of knowing” the world around us constantly tests, confirms, rejects and ultimately reveals new knowledge, integrating that knowledge into our worldview.
Here in the usual order are the key elements of the scientific method:
- Observe natural phenomena (includes reading the science of others).
- Infer and propose an hypothesis (explanation) based on objectivity and reason. Hypotheses are declarative sentences that sound like a fact, but aren’t! Good hypotheses are testable, easily turned into if/then (predictive) yes-or-no questions.
- Design an experiment to test the hypothesis: results must be measurable evidence for or against the hypothesis.
- Perform the experiment and then observe, measure, collect data and test for statistical validity (where applicable). Then, repeat the experiment.
- Consider how your data supports or does not support your hypothesis and then integrate your experimental results with earlier hypotheses and prior knowledge.
But, how do theories and laws fit into the scientific method?
A scientific theory, contrary to what many people think, is not a guess. Rather, a theory is a statement well supported by experimental evidence and widely accepted by the scientific community. One of the most enduring, tested theories is of course the theory of evolution. Among scientists, theories might be thought of as ‘fact’ in common parlance, but we recognize that they are still subject to testing and, modification, and may even be overturned. While some of Darwin’s notions have been modified over time, in this case, those modifications have only strengthened our understanding that species diversity is the result of natural selection. You can check out some of Darwin’s own work (1859, 1860; The Origin of Species] at Origin of Species. For more recent commentary on the evolutionary underpinnings of science, check out Dobzhansky T (1973, Nothing in biology makes sense except in the light of evolution. Am. Biol. Teach. 35:125-129) and Gould, S.J. (2002, The Structure of Evolutionary Theory. Boston, Harvard University Press).
A scientific Law is thought of as universal and even closer to ‘fact’ than a theory! Scientific laws are most common in math and physics. In life sciences, we recognize Mendel’s Law of Segregation and Law of Independent Assortment as much in his honor as for their universal and enduring explanation of genetic inheritance in living things. But Laws are not facts! Laws too, are always subject to experimental test.
Astrophysicists are actively testing universally accepted laws of physics. Strictly speaking, even Mendel’s Law of Independent Assortment should not be called a law. Indeed, it is not true as he stated it! Check the Mendelian Genetics section of an introductory textbook to see how chromosomal crossing over violates this law.
In describing how we do science, the Wikipedia entry states: “the goal of a scientific inquiry is to obtain knowledge in the form of testable explanations (hypotheses) that can predict the results of future experiments. This allows scientists to gain an understanding of reality, and later use that understanding to intervene in its causal mechanisms (such as to cure disease).” The better an hypothesis is at making predictions, the more useful it is, and the more likely it is to be correct. In the last analysis, think of Hypotheses as educated guesses and think of Theories and/or Laws as one or more experimentally supported hypothesis that everyone agrees should serve as guideposts to help us evaluate new observations and hypotheses.
A good hypothesis is a rational guess that explains scientific observations or experimental measurements. Therefore by definition, hypotheses are testable based on predictions based on logic. Additional observation can refine or change the original hypothesis, and/or lead to new hypothesis whose predictive value can also be tested. If you get the impression that scientific discovery is a cyclic process, that’s the point! Exploring scientific questions reveals more questions than answers!
We now recognize that a key component of the scientific method is the requirement that the work of the scientist be disseminated by publication! In this way, shared data and experimental methods can be repeated and evaluated by other scientists.
B. Origins of the Scientific Method
Long before the word scientist began to define someone who investigated natural phenomena beyond simple observation (i.e., by doing experiments), philosophers developed formal rules of deductive and inferential logic to try to understand nature, humanity’s relationship to nature, and the relationship of humans to each other. In fact, Boyle was not alone in doing experimental science. We therefore owe the logical underpinnings of science to philosophers who came up with systems of deductive and inductive logic so integral to the scientific method. The scientific method grew from those beginnings, along with increasing empirical observation and experimentation. We recognize these origins when we award the Ph.D. (Doctor of Philosophy), our highest academic degree! We are about to learn about the life of cells, their structure and function, and their classification, or grouping based on those structures and functions. Everything we know about life comes from applying the principles of scientific method.
Biological theories within the field of criminology attempt to explain behaviors contrary to societal expectations through examination of individual characteristics. These theories are categorized within a paradigm called positivism (also known as determinism), which asserts that behaviors, including law-violating behaviors, are determined by factors largely beyond individual control. Positivist theories contrast with classical theories, which argue that people generally choose their behaviors in rational processes of logical decision making, and with critical theories, which critique lawmaking, social stratification, and the unequal distribution of power and wealth.
Positivist theories are further classified on the basis of the types of external influences they identify as potentially determinative of individual behavior. For example, psychological and psychiatric theories look at an individual’s mental development and functioning sociological theories evaluate the impact of social structure on individuals (e.g., social disorganization, anomie, subcultural theories, opportunity, strain) and the impact of social function and processes on individuals (e.g., differential association, social learning, social bonds, labeling). Biological theories can be classified into three types: (1) those that attempt to differentiate among individuals on the basis of certain innate (i.e., those with which you are born) outward physical traits or characteristics (2) those that attempt to trace the source of differences to genetic or hereditary characteristics and (3) those that attempt to distinguish among individuals on the basis of structural, functional, or chemical differences in the brain or body.
This research paper is organized in rough chronological order and by historical figures associated with an important development. It is difficult to provide an exact chronology, because several important developments and movements happened simultaneously in various parts of the world. For example, although biological theories are considered positivist, the concept of positivism did not evolve until after the evolution of some early biological perspectives. In addition, biological theories of behavior that involve some aspect of evolution, genetics, or heredity are discussed in terms of those scientific developments, although physical trait theories still continued to be popular.
The following sections discuss some of the more important and relevant considerations in scientific developments that impacted biological theories of behavior. A brief history of positivism also is provided, tracing the development and use of the biological theories from early (largely discredited) beliefs, to the most current theories on the relationship of biology to behavior. This section also provides a conclusion that discusses the role of biological theories in the future of criminological thought.
Biological explanations of criminal behavior
There is a growing literature on biological explanations of antisocial and criminal behavior. This paper provides a selective review of three specific biological factors – psychophysiology (with the focus on blunted heart rate and skin conductance), brain mechanisms (with a focus on structural and functional aberrations of the prefrontal cortex, amygdala, and striatum), and genetics (with an emphasis on gene-environment and gene-gene interactions). Overall, understanding the role of biology in antisocial and criminal behavior may help increase the explanatory power of current research and theories, as well as inform policy and treatment options.
A growing body of literature has indicated the importance of considering neurobiological factors in the etiology of antisocial and criminal behavior. Behaviors, including criminality, are the result of complex, reciprocally influential interactions between an individual’s biology, psychology, and the social environment (Focquaert, 2018). As research progresses, the misconception that biology can predetermine criminality is being rectified. Elucidating the biological underpinnings of criminal behavior and broader, related outcomes such as antisocial behavior can provide insights into relevant etiological mechanisms. This selective review discusses three biological factors that have been examined in relation to antisocial and criminal behavior: psychophysiology, brain, and genetics.
Psychophysiology, or the levels of arousal within individuals, has become an important biological explanation for antisocial and criminal behavior. Two common psychophysiological measures are heart rate and skin conductance (i.e. sweat rate). Both capture autonomic nervous system functioning skin conductance reflects sympathetic nervous system functioning while heart rate reflects both sympathetic and parasympathetic nervous system activity. Blunted autonomic functioning has been associated with increased antisocial behavior, including violence (Baker et al., 2009 Choy, Farrington, & Raine, 2015 Gao, Raine, Venables, Dawson, & Mednick, 2010 Portnoy & Farrington, 2015). Longitudinal studies have found low resting heart rate in adolescence to be associated with increased risk for criminality in adulthood (Latvala, Kuja-Halkola, Almqvist, Larsson, & Lichtenstein, 2015 Raine, Venables, & Williams, 1990). However, there is likely a positive feedback loop whereby blunted autonomic functioning may lead to increased antisocial/criminal behavior, which in turn may reinforce disrupted physiological activity. For example, males and females who exhibited high rates of proactive aggression (an instrumental, predatory form of aggression elicited to obtain a goal or reward) in early adolescence were found to have poorer skin conductance fear conditioning in late adolescence (Gao, Tuvblad, Schell, Baker, & Raine, 2015 Vitiello & Stoff, 1997).
Theories have been proposed to explain how blunted autonomic functioning could increase antisociality. The fearlessness hypothesis suggests that antisocial individuals, due to their blunted autonomic functioning, are not deterred from criminal behavior because they do not experience appropriate physiological responses to risky or stressful situations nor potential aversive consequences (Portnoy et al., 2014 Raine, 2002). Alternatively, the sensation-seeking hypothesis suggests that blunted psychophysiology is an uncomfortable state of being, and in order to achieve homeostasis, individuals engage in antisocial behavior to raise their arousal levels (Portnoy et al., 2014 Raine, 2002).
Another mechanism that could connect disrupted autonomic functioning to antisocial behavior is the failure to cognitively associate physiology responses with emotional states. Appropriately linking autonomic conditions to emotional states is important in socialization processes such as fear conditioning, which is thought to contribute to the development of a conscience. The somatic marker hypothesis (Bechara & Damasio, 2005) suggests that ‘somatic markers’ (e.g. sweaty palms) may reflect emotional states (e.g. anxiety) that can inform decision-making processes. Impairments in autonomic functioning could lead to risky or inappropriate behavior if individuals are unable to experience or label somatic changes and connect them to relevant emotional experiences. Indeed, psychopathic individuals exhibit somatic aphasia (i.e. the inaccurate identification and recognition of one’s bodily state Gao, Raine, & Schug, 2012). Moreover, blunted autonomic functioning impairs emotional intelligence, subsequently increasing psychopathic traits (Ling, Raine, Gao, & Schug, 2018a). Impaired autonomic functioning and reduced emotional intelligence may impede the treatment of psychopathy (Polaschek & Skeem, 2018) and disrupt development of moral emotions such as shame, guilt, and empathy (Eisenberg, 2000). Such moral dysfunction, a strong characteristic of psychopaths, may contribute to their disproportionate impact on the criminal justice system (Kiehl & Hoffman, 2011).
While there is evidence that antisocial/criminal individuals typically exhibit abnormal psychophysiological functioning, it is important to acknowledge that there are different antisocial/criminal subtypes, and they may not share the same deficits. Whereas individuals who are high on proactive aggression may be more likely to exhibit blunted autonomic functioning, individuals who are high on reactive aggression (an affective form of aggression that is elicited as a response to perceived provocation) may be more likely to exhibit hyperactive autonomic functioning (Hubbard, McAuliffe, Morrow, & Romano, 2010 Vitiello & Stoff, 1997). This may have implications for different types of offenders, with elevated autonomic functioning presenting in reactively aggressive individuals who engage in impulsive crimes and blunted autonomic functioning presenting in proactively aggressive offenders engaging in more premediated crimes. Similarly, psychopaths who are ‘unsuccessful’ (i.e. convicted criminal psychopaths) exhibit reduced heart rate during stress while those who are ‘successful’ (i.e. non-convicted criminal psychopaths) exhibit autonomic functioning similar to non-psychopathic controls (Ishikawa, Raine, Lencz, Bihrle, & LaCasse, 2001). Despite differences among subgroups, dysfunctional autonomic functioning generally remains a reasonably well-replicated and robust correlate of antisocial and criminal behavior.
There has been increasing interest in the role of the brain in antisocial/criminal behavior. In general, research suggests that antisocial/criminal individuals tend to exhibit reduced brain volumes as well as impaired functioning and connectivity in key areas related to executive functions (Alvarez & Emory, 2006 Meijers, Harte, Meynen, & Cuijpers, 2017 Morgan & Lilienfeld, 2000), emotion regulation (Banks, Eddy, Angstadt, Nathan, & Phan, 2007 Eisenberg, 2000), decision-making (Coutlee & Huettel, 2012 Yechiam et al., 2008), and morality (Raine & Yang, 2006) while also exhibiting increased volumes and functional abnormalities in reward regions of the brain (Glenn & Yang, 2012 Korponay et al., 2017). These prefrontal and subcortical regions that have been implicated in antisocial/criminal behavior are the selective focus of this review.
Conventional criminal behavior has typically been associated with prefrontal cortex (PFC) structural aberrations and functional impairments (Brower & Price, 2001 Yang & Raine, 2009). The PFC is considered the seat of higher-level cognitive processes such as decision-making, attention, emotion regulation, impulse control, and moral reasoning (Sapolsky, 2004). In healthy adults, larger prefrontal structures have been associated with better executive functioning (Yuan & Raz, 2014). However, structural deficits and functional impairments of the PFC have been observed in antisocial and criminal individuals, suggesting that PFC aberrations may underlie some of the observed behaviors.
While many studies on brain differences related to criminal behavior have consisted of correlational analyses, lesion studies have provided some insight into causal neural mechanisms of antisocial/criminal behavior. The most well-known example of the effects of prefrontal lobe lesions is the case of Phineas Gage, who was reported to have a dramatic personality change after an iron rod was shot through his skull and damaged his left and right prefrontal cortices (Damasio, Grabowski, Frank, Galaburda, & Damasio, 1994 Harlow, 1848, 1868). Empirical studies suggest that prefrontal lesions acquired earlier in life disrupt moral and social development (Anderson, Bechara, Damasio, Tranel, & Damasio, 1999 Taber-Thomas et al., 2014). A study of 17 patients who developed criminal behavior following a brain lesion documented that while these lesions were in different locations, they were all connected functionally to regions activated by moral decisionmaking (Darby, Horn, Cushman, & Fox, 2018), suggesting that disruption of a neuromoral network is associated with criminality. Nevertheless, while lesion studies have implicated specific brain regions in various psychological processes such as moral development, generalizability is limited because of the heterogeneity of lesion characteristics, as well as subjects’ characteristics that may moderate the behavioral effects of the lesion.
In recent years, non-invasive neural interventions such as transcranial magnetic stimulation and transcranial electric stimulation have been used to manipulate activity within the brain to provide more direct causal evidence of the functions of specific brain regions with regard to behavior. These techniques involve subthreshold modulation of neuronal resting membrane potential (Nitsche & Paulus, 2000 Woods et al., 2016). Using transcranial electric stimulation, upregulation of the PFC has been found to decrease criminal intentions and increase perceptions of moral wrongfulness of aggressive acts (Choy, Raine, & Hamilton, 2018), providing support for the causal influence of the PFC on criminal behavior.
Importantly, there is evidence of heterogeneity within criminal subgroups. Successful psychopaths and white-collar offenders do not seem to display these prefrontal deficits (Raine et al., 2012 Yang et al., 2005). While unsuccessful psychopaths exhibit reduced PFC gray matter volume compared to successful psychopaths and non-offender controls, there are no prefrontal gray matter volume differences between successful psychopaths and non-offender controls (Yang et al., 2005). Similarly, while prefrontal volume deficits have been found in conventional criminals (i.e. blue-collar offenders), white-collar offenders do not exhibit frontal lobe reductions (Brower & Price, 2001 Ling et al., 2018b Raine et al., 2012) and in fact may exhibit increased executive functioning compared to blue-collar controls (Raine et al., 2012). Lastly, antisocial offenders with psychopathy exhibited reduced gray matter volumes in the prefrontal and temporal poles compared to antisocial offenders without psychopathy and non-offenders (Gregory et al., 2012). It is therefore important to acknowledge that there are various types of antisocial and criminal behavior that may have different neurobiological etiologies.
The amygdala is an important brain region that has been implicated in emotional processes such as recognition of facial and auditory expressions of emotion, especially for negative emotions such as fear (Fine & Blair, 2000 Murphy, Nimmo-Smith, & Lawrence, 2003 Sergerie, Chochol, & Armony, 2008). Normative amygdala functioning has been thought to be key in the development of fear conditioning (Knight, Smith, Cheng, Stein, & Helmstetter, 2004 LaBar, Gatenby, Gore, LeDoux, & Phelps, 1998 Maren, 2001), and appropriate integration of the amygdala and PFC has been argued to underlie the development of morality (Blair, 2007). The amygdala is thought to be involved in stimulus-reinforcement learning that associates actions that harm others with the aversive reinforcement of the victims’ distress and in recognizing threat cues that typically deter individuals from risky behavior. However, amygdala maldevelopment can lead to a diminished ability to recognize distress or threat cues disrupting the stimulus-reinforcement learning that discourages antisocial/criminal behavior (Blair, 2007 Sterzer, 2010). Indeed, while reduced amygdala volume in adulthood has been associated with increased aggressive and psychopathic characteristics from childhood to early adulthood, it is also associated with increased risk for future antisocial and psychopathic behavior (Pardini, Raine, Erickson, & Loeber, 2014).
Although the amygdala has been implicated in criminal behavior, there may be important differences between subtypes of offenders. Whereas psychopathic antisocial individuals may be more likely to exhibit cold, calculating forms of aggression, non-psychopathic antisocial individuals may be more likely to engage in impulsive, emotionally-reactive aggression (Glenn & Raine, 2014). Research suggests the former may exhibit amygdala hypoactivity and the latter, amygdala hyperactivity (Raine, 2018a). Indeed, violent offenders have been found to exhibit increased amygdala reactivity in response to provocations (da Cunha-Bang et al., 2017). Spousal abusers have also been found to exhibit increased amygdala activation when responding to aggressive words compared to nonabusers (Lee, Chan, & Raine, 2008). In a community sample of healthy adults, psychopathy scores were negatively related to amygdala reactivity while antisocial personality disorder scores were positively associated with amygdala reactivity after adjusting for overlapping variance between psychopathy and antisocial personality disorder (Hyde, Byrd, Votruba-Brzal, Hariri, & Manuck, 2014). Nevertheless, more research is needed to determine whether the presence of callous-unemotional traits (e.g. lack of guilt Lozier, Cardinale, VanMeter, & Marsh, 2014 Viding et al., 2012) or severity of antisocial behavioral traits (Dotterer, Hyde, Swartz, Hariri, & Williamson, 2017 Hyde et al., 2016) are most relevant to the observed amygdala hypo-reactivity.
The striatum has recently garnered more attention as a region that could be implicated in the etiology of criminal behavior because of its involvement in reward and emotional processing (Davidson & Irwin, 1999 Glenn & Yang, 2012). Dysfunction in the striatum has been hypothesized to be a neural mechanism that underlies the impulsive/antisocial behavior of criminals. Indeed, individuals with higher impulsive/antisocial personality traits have been found to exhibit increased activity in the striatum (Bjork, Chen, & Hommer, 2012 Buckholtz et al., 2010 Geurts et al., 2016). Psychopathic individuals, compared to non-psychopathic individuals, demonstrate a 9.6% increase in striatal volumes (Glenn, Raine, Yaralian, & Yang, 2010). Moreover, striatal enlargement and abnormal functional connectivity of the striatum has specifically been associated with the impulsive/antisocial dimension of psychopathy (Korponay et al., 2017), suggesting this dimension of psychopathy is related to reward processes (Hare, 2017).
While much of the literature on striatal abnormalities in antisocial individuals has focused on psychopathic individuals, there is some evidence that offenders in general exhibit striatal abnormalities. Increased volume (Schiffer et al., 2011) and increased reactivity to provocations (da Cunha-Bang et al., 2017) have both been found in violent offenders as compared to non-offendersMoreover, weak cortico-striatal connectivity has been associated with increased frequency of criminal convictions (Hosking et al., 2017). In contrast, one study found reduced striatal activity to be associated with antisocial behavior (Murray, Shaw, Forbes, & Hyde, 2017). While more research is needed, current literature suggests that striatal deviations are linked to criminal behavior. One important consideration for future studies is to determine a consistent operationalization for the striatum, as some studies examine the dorsal striatum (i.e. putamen and caudate Yang et al., 2015), others assess the corpus striatum (i.e. putamen, caudate, and globus pallidus Glenn et al., 2010), and still others analyze the role of the ventral striatum (i.e. nucleus accumbens and olfactory tubercle Glenn & Yang, 2012) in relation to antisocial/criminal behavior.
The neuromoral theory of antisocial behavior
Abnormalities in brain regions other than the PFC, amygdala, and striatum are also associated with antisocial behavior. The neuromoral theory of antisocial behavior, first proposed by Raine and Yang (2006), argued that the diverse brain regions impaired in offenders overlap significantly with brain regions involved in moral decision-making. A recent update of this theory (Raine, 2018b) argues that key areas implicated in both moral decision-making and the spectrum of antisocial behaviors include frontopolar, medial, and ventral PFC regions, and the anterior cingulate, amygdala, insula, superior temporal gyrus, and angular gyrus/temporoparietal junction. It was further hypothesized that different manifestations of antisocial behavior exist on a spectrum of neuromoral dysfunction, with primary psychopathy, proactive aggression, and life-course persistent offending being more affected, and secondary psychopathy, reactive aggression, and crimes involving drugs relatively less affected. Whether the striatum is part of the neural circuit involved in moral decision-making is currently unclear, making its inclusion in the neuromoral model debatable. Despite limitations, the neuromoral model provides a way of understanding how impairments to different brain regions can converge on one concept – impaired morality – that is a common core to many different forms of antisocial behaviors.
One implication of the model is that significant impairment to the neuromoral circuit could constitute diminished criminal responsibility. Given the importance of a fully developed emotional moral capacity for lawful behavior, moral responsibility would appear to require intactness of neuromoral circuity. To argue that the brain basis to moral thinking and feeling are compromised in an offender comes dangerously close to challenging moral responsibility, a concept which in itself may be just a short step removed from criminal responsibility.
There is increasing evidence fora genetic basis of antisocial/criminal behavior. Behavioral genetic studies of twins and adoptees have been advantageous because such designs can differentiate the effects of genetics and environment within the context of explaining variance within a population (Glenn & Raine, 2014). Additionally, a variety of psychological and psychiatric constructs associated with antisociality/criminality, such as intelligence, personality, and mental health disorders, have been found to be heritable (Baker, Bezdjian, & Raine, 2006). While individual study estimates vary, meta-analyses have suggested the level of heritability of antisocial behavior is approximately 40% (Raine, 2013). Shared environmental factors have been estimated to explain approximately 11% of the variance in antisocial/criminal behavior and non-shared environmental influences approximately 31% (Ferguson, 2010 Gard, Dotterer, & Hyde, 2019). However, the heritability of antisocial/criminal behaviors vary in part based upon the specific behaviors examined (Burt, 2009 Gard et al., 2019).
Inspired by prominent theories of the neurobiology of aggression, there have been several candidate genes implicated in the serotonergic and catecholaminergic neurobiological systems that have been examined in relation to antisocial/criminal behavior (Tiihonen et al., 2015). However, a meta-analysis of genetic variants related to antisocial/criminal behavior yielded null results at the 5% significance level (Vassos, Collier, & Fazel, 2014). Nevertheless, genes do not operate in isolation, thus it is important to consider the context in which genes are activated.
Gene-environment (G x E) interactions have garnered increasing attention over the years, as these can increase risk for antisocial behavior and/or produce epigenetic changes within individuals. Longitudinal studies and meta-analyses have documented the moderating effect of the monoamine oxidase A (MAOA) gene on the relationship between maltreatment and antisocial behaviors, with the maltreatment-antisocial behavior relationship being stronger for individuals with low MAOA than high MAOA (Byrd & Manuck, 2014 Caspi et al., 2002 Fergusson, Boden, & Horwood, 2011 Kim-Cohen et al.,2006). Similarly, in a large study of African-American females, having the A1 allele of the DRD2 gene or a criminal father did not individually predict antisocial outcomes, but having both factors increased risk for serious delinquency, violent delinquency, and police contacts (Delisi, Beaver, Vaughn, & Wright, 2009). This type of G x E interaction reflects how genotypes can influence individuals’ sensitivity to environmental stressors. However, there may be important subgroup differences to consider when examining genetic risk for criminal behavior. For example, low-MAOA has been associated with higher risk for violent crime in incarcerated Caucasian offenders but not incarcerated non-Caucasian offenders (Stetler et al., 2014). Additionally, high-MAOA may protect abused and neglected Caucasians from increased risk of becoming violent or antisocial, but this buffering effect was not found for abused and neglected non-Caucasians (Widom & Brzustowicz, 2006). Thus, while the MAOA gene has been associated with antisocial/criminal behavior, there are still nuances of this relationship that should be considered (Goldman & Rosser, 2014).
Another way in which G x E interactions manifest themselves is when environmental stressors result in epigenetic changes, thus becoming embedded in biology that result in long-term symptomatic consequences. For example, females exposed to childhood sex abuse have exhibited alterations in the methylation of the 5HTT promoter region, which in turn has been linked to subsequent antisocial personality disorder symptoms (Beach, Brody, Todorov, Gunter, & Philibert, 2011). There has been a growing body of work on such epigenetic mechanisms involved in the biological embedding of early life stressors and transgenerational trauma (Kellermann, 2013 Provencal & Binder, 2015). Thus, just as biological mechanisms can influence environmental responses, environmental stressors can affect biological expressions.
While genes may interact with the environment to produce antisocial/criminal outcomes, they can also interact with other genes. There is evidence that dopamine genes DRD2 and DRD4 may interact to increase criminogenic risk (Beaver et al., 2007 Boutwell et al., 2014). The effect of the 7-repeat allele DRD4 is strengthened in the presence of the A1 allele of DRD2, and has been associated with increased odds of committing major theft, burglary, gang fighting, and conduct disorder (Beaver et al., 2007 Boutwell et al., 2014). However, there is some evidence that DRD2 and DRD4 do not significantly affect delinquency abstention for females (Boutwell & Beaver, 2008). Thus there may be demographic differences that moderate the effect of genetic interactions on various antisocial outcomes (Dick, Adkins, & Kuo, 2016 Ficks & Waldman, 2014 Rhee & Waldman, 2002 Salvatore & Dick, 2018), and such differences warrant further research.
Interactions between biological factors
Importantly, biological correlates of antisocial and criminal behavior are inextricably linked in dynamical systems, in which certain processes influence others through feedback loops. While a detailed summary is beyond the scope of this review, some interactions between biological mechanisms are briefly illustrated here. Within the brain, the PFC and amygdala have reciprocal connections, with the PFC often conceptualized as monitoring and regulating amygdala activity (Gillespie, Brzozowski, & Mitchell, 2018). Disruption of PFC-amygdala connectivity has been linked to increased antisocial/criminal behavior, typically thought to be due to the impaired top-down regulation of amygdala functioning by the PFC. Similarly, the brain and autonomic functioning are linked (Critchley, 2005 Wager et al., 2009) output from the brain can generate changes in autonomic functioning by affecting the hypothalamic-pituitary-adrenal axis, but autonomic functions also provide input to the brain that is essential for influencing behavioral judgments and maintaining coordinated regulation of bodily functions (Critchley, 2005). While not comprehensive, these examples illustrate that biological systems work together to produce behavior.
While biological processes can contribute to antisocial/criminal behavior, these do not guarantee negative outcomes. Considering that many of the aforementioned biological risk factors are significantly influenced by social environment, interventions in multiple spheres may help mitigate biological risks for antisocial behavior.
With regard to psychophysiological correlates of antisocial behavior, research suggests differential profiles of arousal impairment depending on the type of antisocial behavior (Hubbard et al., 2010 Vitiello & Stoff, 1997). Treatments designed to address the issues associated with psychophysiological differences are typically behavioral in nature, targeted at associated symptoms. Studies of mindfulness have suggested its utility in improving autonomic functioning (Delgado-Pastor, Perakakis, Subramanya, Telles, & Vila, 2013) and emotion regulation (Umbach, Raine, & Leonard, 2018), which may better help individuals with reactive aggression and hyperarousal. Hypo-arousal has been associated with impaired emotional intelligence (Ling et al., 2018a), but emotional intelligence training programs have shown some promise in reducing aggression and increasing empathy among adolescents and increasing emotional intelligence among adults (Castillo, Salguero, Fernandez-Berrocal, & Balluerka, 2013 Hodzic, Scharfen, Ropoll, Holling, & Zenasni, 2018), and in reducing recidivism (Megreya, 2015 Sharma, Prakash, Sengar, Chaudhury, & Singh, 2015).
Regarding healthy neurodevelopment, research has supported a number of areas to target. Poor nutrition, both in utero and in early childhood, have been associated with negative and criminal outcomes (Neugebauer, Hoek, & Susser, 1999). Deficits of omega-3 fatty acids have been linked with impaired neurocognition and externalizing behavior (Liu & Raine, 2006 McNamara & Carlson, 2006). The opposite relationship is also supported increased intake of omega-3 fatty acids has been associated with a variety of positive physical and mental health outcomes (Ruxton, Reed, Simpson, & Millington, 2004), increased brain volume in regions related to memory and emotion regulation (Conklin et al.,2007), and reduction in behavioral problems in children (Raine, Portnoy, Liu, Mahoomed, & Hibbeln, 2015). Studies examining the effect of nutritional supplements have suggested that reducing the amount of sugar consumed by offenders can significantly reduce offending during incarceration (Gesch, Hammond, Hampson, Eves, & Crowder, 2002 Schoenthaler, 1983). Thus, nutritional programs show some promise in reducing antisocial and criminal behavior.
A healthy social environment is also crucial for normative brain development and function. Early adversity and childhood maltreatment have been identified as significant risk factors for both neurobiological and behavioral problems (Mehta et al., 2009 Teicher et al., 2003 Tottenham et al., 2011). A review of maltreatment prevention programs supports the efficacy of nurse-family partnerships and programs that integrate early preschool with parent resources in reducing childhood maltreatment (Reynolds, Mathieson, & Topitzes, 2009). Promoting healthy brain development in utero and in crucial neurodevelopmental periods is likely to reduce externalizing behaviors, as well as other psychopathology.
Knowing that the social context could help to buffer biological risks is promising because it suggests that changing an individual’s environment could mitigate biological criminogenic risk. Rather than providing a reductionist and deterministic perspective of the etiology of criminal behavior, incorporating biological factors in explanations of antisocial/criminal behaviors can highlight the plasticity of the human genome (Walsh & Yun, 2014). They can also provide a more holistic understanding of the etiologies of such behavior. For example, sex differences in heart rate have been found to partially explain the gender gap in crime (Choy, Raine, Venables, & Farrington, 2017). Social interventions that aim to provide an enriched environment can be beneficial for all, but may be particularly important for individuals at higher biological risk for antisocial behavior. While biological explanations of antisocial and criminal behavior are growing, they are best thought of as complementary to current research and theories, and a potential new avenue to target with treatment options.
For example, when a person achieves tremendous academic success, did they do so because they are genetically predisposed to be successful or is it a result of an enriched environment? If a man abuses his wife and kids, is it because he was born with violent tendencies or is it something he learned by observing his own parent's behavior?
A few examples of biologically determined characteristics (nature) include certain genetic diseases, eye color, hair color, and skin color. Other things like life expectancy and height have a strong biological component, but they are also influenced by environmental factors and lifestyle.
An example of a nativist theory within psychology is Chomsky's concept of a language acquisition device (or LAD). According to this theory, all children are born with an instinctive mental capacity that allows them to both learn and produce language.
Some characteristics are tied to environmental influences. How a person behaves can be linked to influences such as parenting styles and learned experiences. For example, a child might learn through observation and reinforcement to say 'please' and 'thank you.' Another child might learn to behave aggressively by observing older children engage in violent behavior on the playground.
One example of an empiricist theory within psychology is Albert Bandura's social learning theory. According to the theory, people learn by observing the behavior of others. In his famous Bobo doll experiment, Bandura demonstrated that children could learn aggressive behaviors simply by observing another person acting aggressively.
Even today, research in psychology often tends to emphasize one influence over the other. In biopsychology, for example, researchers conduct studies exploring how neurotransmitters influence behavior, which emphasizes the nature side of the debate. In social psychology, researchers might conduct studies looking at how things such as peer pressure and social media influence behaviors, stressing the importance of nurture.
Methods of Studying the Brain
Methods of Studying the Brain
It is important to appreciate that the human brain is an extremely complicated piece of biological machinery. Scientists have only just “scratched the surface” of understanding the many functions of the workings of the human brain. The brain can influence many types of behavior.
In addition to studying brain damaged patients, we can find out about the working of the brain in three other ways.
Children begin to plan activities, make up games, and initiate activities with others. If given this opportunity, children develop a sense of initiative and feel secure in their ability to lead others and make decisions.
1. Neuro Surgery
1. Neuro Surgery
We know so little about the brain and its functions are so closely integrated that brain surgery is usually only attempted as a last resort. H.M. suffered such devastating epileptic fits that in the end a surgical technique that had never been used before was tried out.
This technique cured his epilepsy, but in the process the hippocampus had to be removed (this is part of the limbic system in the middle of the brain.) Afterwards, H.M. was left with severe anterograde amnesia. I.e., He could remember what happened to him in his life up to when he had the operation, but he couldn’t remember anything new. So now we know the hippocampus is involved in memory.
2. Electroencrphalograms (EEGs)
2. Electroencrphalograms (EEGs)
This is a way of recording the electrical activity of the brain (it doesn’t hurt, and it isn’t dangerous). Electrodes are attached to the scalp and brain waves can be traced.
EEGs have been used to study sleep, and it has been found that during a typical night’s sleep, we go through a series of stages marked by different patterns of brain wave.
One of these stages is known as REM sleep (Rapid Eye Movement sleep). During this, our brain waves begin to resemble those of our waking state (though we are still fast asleep) and it seems that this is when we dream (whether we remember it or not).
3. Brain Scans
3. Brain Scans
More recently methods of studying the brain have been developed using various types of scanning equipment hooked up to powerful computers.
The CAT scan (Computerised Axial Tomography) is a moving X-ray beam which takes “pictures” from different angles around the head and can be used to build up a 3-dimensional image of which areas of the brain are damaged.
Even more sophisticated is the PET scan (Positron Emission Tomography) which uses a radioactive marker as a way of studying the brain at work.
The procedure is based on the principle that the brain requires energy to function and that the regions more involved in the performance of a task will use up more energy. What the scan, therefore, enables researchers to do is to provide ongoing pictures of the brain as it engages in mental activity.
These (and other) methods for producing images of brain structure and functioning have been extensively used to study language and PET scans, in particular, are producing evidence that suggests that the Wernicke-Gerschwind model may not after all be the answer to the question of how language is possible.