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Contemporary Biological and Integrated Perspectives


by Diana Fishbein  

Q1: Why is it important that criminological inquiry include the perspectives, findings, and methods of the behavioral sciences (e.g., behavioral genetics, psychophysiology, neuroscience, biochemistry, psychology, and developmental biology)?  
Q2: In studying genetic and biological factors in the field of criminology, why should there be a concentration on various dimensions of “antisocial” behavior as opposed to “criminal” behavior?  
Q3: Why are chronic patterns of antisocial behavior more strongly influenced by genetics and biology than single acts?  
Q4: What is the Diathesis-Stress Model of behavior, and how does it apply to the study of antisocial behavior?  
Q5: What are some examples of the interaction between biology and the environment in human behavior?
Q6: What is “Developmental Criminology” and how does it help us to understand how antisocial behaviors develop over time, are influenced by both biology and environment, and change in response to changing conditions?  
Q7: How do antisocial behavior and drug abuse relate to one another and what are the common antecedents?
Q8: What are the measurable features (or phenotypes) that place an individual at risk for antisocial behavior and/or drug abuse?
Q9: What designs are used to estimate the influence of genetic factors relative to environmental factors in the study of antisocial behaviors? In general, what do these studies show?  
Q10: What biological mechanisms are believed to be involved in the risk for antisocial and violent behavior (brain anatomy and function)?  
Q11: What biological mechanisms (brain anatomy and function) are believed to be involved in the risk for drug abuse?  
Q12: What is the role of stress in antisocial behavior?
Q13: What is psychopathy, how does it increase risk for antisocial behavior and drug abuse, and what biological and environmental mechanisms have been associated with it?  
Q14: How do genetic and biological factors (i.e., nature) interact with environmental conditions (i.e., nurture) to increase or decrease risk for antisocial behavior?  
Q15: What are the implications of this research for the criminal justice system and the offender?  
Q16: What are the controversies surrounding this research?  

Additional Readings and References

 

There are many competing and “integrated” theories within the field of criminology. It is important to distinguish the literature and findings discussed in this lecture, however, from the theories of any particular discipline. While these findings are an extension of certain models and perspectives proposed in the behavioral sciences, they should not be considered theories that are competitive with others in criminology. Instead, research that is described has been generated from a broad range of scientific inquiries and methodologies into the generators of human behavior that are highly relevant to the inquiries of criminologists. Findings from the behavioral sciences should, therefore, be viewed as having the potential to fill existing gaps in our knowledge pertaining to the development of antisocial behavior, and to eventually be understood in the context of social forces that we have identified as significant players in this dynamic equation.  

 

Q1: Why is it important that criminological inquiry include the perspectives, findings, and methods of the behavioral sciences (e.g., behavioral genetics, psychophysiology, neuroscience, biochemistry, psychology, and developmental biology)?

 

A1: There are many subdisciplines within the behavioral sciences that have been intensively studying various dimensions of antisocial behavior that are relevant to the field of criminology. They include molecular and behavioral genetics, neurobiology, physiology, psychology, cognitive neuroscience, endocrinology, and forensic psychiatry, among many others. To date, their findings have provided substantial evidence to suggest that individuals are different in the extent to which they are vulnerable to both antisocial behavior and drug abuse. Researchers in these fields are studying the tendency to engage in criminal behavior by attempting to identify genetic and biological mechanisms that underlie or contribute to these problem behaviors. The antecedents or conditions that underlie some types of criminal behavior are psychological traits and behaviors that highly correlate with the development of antisocial behavior and occur early in a child’s life; thus, they are believed to be important in a developmental sense. For example, hyperactivity, attention and other cognitive deficits, conduct disorder (CD), aggressiveness, and negative affect all tend to co-occur with and predict criminal behavior. Each of these so-called antecedents, among others, has been associated with various disturbances or irregularities in brain function, physiological and neuropsychological processes, and biochemical balance. In interaction with certain conditions in the physical and social environment, these disturbances are thought to increase the likelihood for an antisocial outcome.

 

The vast array of reported studies on vulnerability to Antisocial Personality Disorder  (ASPD), violence, and drug abuse may seem unintelligible at first, but several consistencies across studies reveal a pattern that may characterize vulnerable individuals. Findings indicate that vulnerability to antisocial behavior is partially a function of genetic and biological make-up that manifests during childhood as particular behavioral, cognitive, and psychological traits (e.g., impulsivity, attention deficits, conduct disorder (CD) and are measurable in physiological and biochemical responses (such as heart rate, hormone levels, or EEG recordings) to environmental inputs. Instead of viewing evidence from these various disciplines as independent indicators of biological and social dysfunction, these sources of evidence should be seen as a continuous, developmental sequence of interacting factors; i.e., basic genetic or acquired biological traits contribute to measurable biochemical and physiological conditions that predispose individuals to a constellation of particular behavioral and temperamental outcomes.

 

The resulting integration of research findings from various disciplines has direct relevance to criminological inquiry, informing ideology with science, which should appeal to social scientists who hold widely divergent views and beliefs but are in search of reliable scientific answers. This research is persuasive in that it compels the reader to acknowledge several decades of serious scientific criminological research in psychology, psychiatry, and the bio-behavioral sciences. Findings account for both intra-psychic (from within) and extra-psychic (from external sources) variables in their emphasis on the recent explosion of genetic and biological evidence that neurobiological conditions often underlie violent and impulsive behaviors by sensitizing the actor to adverse social stimuli. Behavioral sciences research should, therefore, be viewed as having the potential to fill existing gaps in our knowledge pertaining to the development of antisocial behavior, and to eventually be understood in the context of social forces that we have identified as significant players in this dynamic equation.

 

See Fishbein (1990); Reiss and Roth (1993).

 

Q2: In studying genetic and biological factors in the field of criminology, why should there be a concentration on various dimensions of “antisocial” behavior as opposed to “criminal” behavior?

 

A2: The development of a framework for incorporating biological perspectives into criminological theory requires that we first identify behaviors of interest. This exercise is essential given that not all “illegal” behaviors are dysfunctional or antisocial and not all “legitimate” behaviors are moral, acceptable, or adaptive. The term “criminality” includes behaviors that do not necessarily offend all members of society, such as certain “victimless” acts, and also behaviors that may be considered adaptive or rational given the social conditions and circumstances. Also, the concept of criminality excludes behaviors that may be antisocial or illegal but that are not detected by the criminal justice system. Antisocial behaviors, on the other hand, are costly to citizens and society overall. Such behaviors do not necessarily violate legal norms or come to official attention, however. Antisocial individuals have a high probability of being labeled as delinquent or criminal, but being so labeled is not a sufficient criterion to be identified as antisocial. For example, schizophrenics’ behavior is poorly regulated, detrimental to their own well‑being, and considered “deviant,” but they rarely engage in crime. Individuals identified as psychopathic, conversely, are at high risk for crime by virtue of their behavior. Yet, there are psychopathic individuals who find legal, albeit not always ethical, avenues for channeling their behavioral tendencies (e.g., a subgroup of those involved in competitive sports, high‑risk activities, corporate life, and politics). The focus of this lecture is on antisocial behaviors, including both criminal and undetected behaviors, that are detrimental to the individuals affected and/or their milieu; in other words, behaviors that increase risk for criminal stigmatization, for example, violence or drug abuse.

 

In addition, studies generated from this perspective in criminology should focus on the dimensions of antisocial behavior that can be reliably and precisely measured. This way, investigators are able to replicate studies to identify consistencies in findings and eventually base conclusions on rigorous and reliable methods of measuring behavior. Thus, it is important that researchers isolate the behavioral phenotypes of interest that correlate or co-occur with criminal behavior. A phenotype is the measurable outcome of genetic factors that interact dynamically with the environment. For example, even something as simple as eye color is a result of both genetic influence and the gestational environment. Behavioral phenotypes are much more complex than appearance, but are still amenable to observation, measurement, and manipulation. Thus, they are imminently better candidates for investigation than criminality, which is a socially constructed concept. Phenotypes of interest to the criminologist, which correlate or co-occur with criminal behavior, include aggressiveness, impulsivity, attention and other cognitive deficits, hyperactivity, and negative affect. Each of these behavioral phenotypes is influenced by both genetic and environmental conditions.

 

Q3: Why are chronic patterns of antisocial behavior more strongly influenced by genetics and biology than single acts?

 

A3: Phenomenologically, “antisocial behavior” is a complex concept defined variably in different disciplines and arising from widely diverging origins. No single mental disorder is uniquely associated with antisocial behavior, nor are particular behavioral patterns, childhood experiences, or social circumstances. From the various ways of characterizing individuals, however, emerges a subgroup who persistently engage in impulsive (not instrumental) antisocial behavior, potentially violent (resulting in physical injury), typified not simply by the behavioral outcome, but by relatively stable personality and temperamental traits, including impulsivity, negative affect, and cognitive deficits. Displays of impulsive antisocial behavior are, thus, an outgrowth of these traits in interaction with crime-prone situations in the social environment. Conversely, individuals who exhibit only isolated displays of antisocial behavior may be more influenced by social and situational factors and probably do not possess the requisite conditions to produce a true “vulnerability” to a destructive behavioral pattern. This depiction corresponds with the pattern described by Moffitt (1993), who characterizes a subgroup of chronic offenders by “life-course persistent antisocial behavior culminating in a pathologic personality.”   Individuals possessing these features also appear to be unusually susceptible to the abuse of alcohol or drugs.

 

Due to the nature of the phenomenon of antisocial behavior, studies of the underpinnings of criminal behavior should focus on the measurable dimensions of antisocial behavior that may increase the risk for criminal activity rather than crime, per se, which is an abstract legal and social construct, not a measurable behavioral construct. Criminal acts that occur only once or rarely in an individual may be more a result of a situation than an ongoing predisposition. But a longstanding or recurrent pattern of antisocial behavior is more likely due to the cumulative, developmental influence of interacting biological and environmental factors.

 

Q4: What is the Diathesis-Stress Model of behavior, and how does it apply to the study of antisocial behavior?

 

A4: The theoretical framework for biological perspectives in criminology is consistent with the diathesis‑stress model constructed to explain many forms of antisocial behavior. According to this model, individuals vary considerably with respect to their biological strengths and weaknesses. Biological weaknesses, referred to as a "vulnerability," influence the degree to which the individual is at risk for antisocial behavior. Rather than acting alone, however, these biological features operate by setting the stage for how adaptively an individual will respond to personal stressors. In other words, a stressful environment is more likely to contribute to some form of psychopathology when it is received by a biological system that is somehow compromised. Learning disability, brain damage or functional irregularity, drug exposure, genetic predisposition to temperamental disturbances, and other biological disadvantages lay the groundwork for a pathological response to stress. Prior learning experiences contribute further by either increasing or decreasing the risk.

 

 Although the probability of a pathological response is a function of the number of these risk factors present, the probability is even greater in the presence of an adverse environment with severe stressors (e.g., poverty, unemployment, crime and drug infestation, poor parenting, lack of education, abuse/neglect, social immobility). For example, hyperactive children may function well given appropriate intervention. In the presence of family instability, alcoholism, absence of educational programs, and a delinquent peer group, however, the child may be more prone to antisocial behavior, possibly resulting in criminal acts. Thus, environmental factors play a facilitating role in determining an antisocial outcome in vulnerable persons. Environmental factors may be even more potent determinants of antisocial outcomes than strictly biological vulnerabilities when the environment is unusually harsh or conducive to such behavior, as we may readily observe in our inner cities. Once again, however, not all inner-city residents engage in antisocial behavior; that outcome remains somewhat dependent on individual vulnerability. The reverse may be also apply—even in the presence of a protective environment, a biological disadvantage may be so severe as to overwhelm the positive environmental influence. An example of that particular outcome may be seen in fetal alcohol syndrome, when the biological odds frequently outweigh prosocial influences.

 

Q5: What are some examples of the interaction between biology and the environment in human behavior?

 

A5:  The neurotransmitter serotonin is of particular interest for its role in impulsivity and aggressiveness. An individual’s range for synthesis and metabolism of serotonin is largely determined by his genes, although its activity is exquisitely sensitive to changes in the environment. Animal studies show that, when the social hierarchy is altered, the loss in status by dominant monkeys results in decreases in serotonin activity and vice versa, and they become more impulsive and subordinate. Human studies consistently report lower levels of serotonin in individuals exposed to high and chronic amounts of stress (e.g., Post-Traumatic Stress Disorder [PTSD]) than individuals not exposed to high levels of stress. There are indications that poor parenting is also associated with low-serotonin levels in the child and good parenting techniques can raise serotonin activity levels, subsequently minimizing the impact of other risk factors for negative behavioral outcomes.

 

 

Temperament, the second example, is known to be largely heritable (i.e., a significant amount of variation in the trait is genetic) and stable across the life span. Nevertheless, the behavioral expression of any given temperament is strongly contingent upon environmental circumstances, such as stressors, situational factors, opportunities, and learning experiences. Shyness is one form of temperament with biological and genetic origins that can be environmentally altered to influence its behavioral manifestations. Overactivity of the autonomic nervous system (ANS) (peripheral to the central nervous system  [CNS]) is, in part, responsible for behavioral withdrawal in social situations in susceptible individuals. Strategies to combat shyness in a child may result in more extroverted behavior and less nervousness in social situations by lowering levels of reactivity of the  ANS.

 


 

Third, alcoholism, known to be significantly heritable and associated with several genetic markers contributing to its expression, is also susceptible to environmental influence. While alcoholism is considered to be in large part a genetic disease state, its expression is significantly dependent upon family stability factors. The same may also be true for other forms of drug abuse and addiction in which genetics plays a role, but the environment and learning experiences help to determine their actual expression.

 

A significant population of children chronically exposed to cocaine prenatally have been characterized as difficult to manage, temperamental, hyper-responsive to environmental stimuli (e.g., lights and noises), developmentally delayed, learning disabled, impulsive, and sometimes aggressive. Cocaine can dramatically alter the developing nervous system to increase the likelihood of these behaviors in predictable ways. Because the brain continues to develop for twelve months after birth, however, the provision of supportive therapies and interventions can substantially alter these negative outcomes. Children raised by the “crack mothers” who gave birth to them exhibit significantly worse behavioral and cognitive outcomes than cocaine-exposed children raised in more supportive and nurturing environments, suggesting that, although prenatal cocaine exposure is a highly preventable cause of behavioral and cognitive disorders, environmental enrichment during the formative years can substantially improve the outcome.

 



Illustration by Susan Gilbert

 

One final example is that of cognitive differences between males and females. Similar to other parts of the anatomy, the structure of the developing fetal brain is influenced after the seventh week of pregnancy by the introduction of testosterone, a male hormone, in the presence of a Y chromosome. Subsequent changes in neuroanatomy differentiate the male from the female brain, in addition to promoting the development of external genitalia, a larger musculature and, eventually, facial hair in the male. One result of these differences is distinctive cognitive styles, with males and females performing somewhat differently in various cognitive tasks. Interestingly, however, the gender gap in these cognitive differences has been narrowing in recent decades. Can the environment produce such significant changes in a trait known to be largely genetic? Researchers believe that differences in the way parents treat their children may contribute to cognitive styles and actually alter brain development in the early years. A few decades ago, psychological studies found that parents were more likely to encourage exploration of the environment and active play in baby boys, while little girls were coddled, comforted and “kept safe” from their environment. In contrast, parents in more recent years tend to treat male and female babies more equally, a practice that can, theoretically, lead to a smaller magnitude of gender differences in cognitive abilities by increasing activity levels in baby girls.

 
 
The male and female brain differ in some important ways in their structure
and function.  For the most part, differences are due to the introduction of
relatively large amounts of testosterone to the male fetus during pregnancy.
They help to explain some statistical gender-group differences in brain
function, from verbal and motor skills to the incidence of certain dis
orders
and learning disabilities.

 

Q6: What is “Developmental Criminology” and how does it help us to understand how antisocial behaviors develop over time, are influenced by both biology and environment, and change in response to changing conditions?



 

A6: Research into the multiple determinants of the liability to antisocial behavior requires a developmental perspective to place in context the fluid interaction between environmental and biological factors described in this lecture. The age of onset for antisocial behaviors is not equally distributed throughout the life span among the population of individuals who exhibit these behaviors. This variability is a direct function of changes over time in biological and behavioral processes that result from ongoing interactions with many different environments. For example, family situations, peer interactions, school settings, and work environments are typically not static in an individual’s lifetime, and produce measurable changes in biological systems and behavioral outcomes as the individual ages. Epidemiological data provides support for the notion that some external conditions are more important influences at certain points in the life span than others; for example, maternal influences during childhood, peer influences during adolescence, and perhaps the use of drugs with analgesic (pain relieving) or euphorigenic (pleasurable or euphoric) properties later in life when stress or pain becomes more prevalent. Thus, there is an essential feedback loop between extant traits, phenotypic behaviors, and environmental influences that fluctuate throughout the life span and contribute to varying degrees of “risk” or liability for antisocial behavior at any given stage of life.

 

Tarter has employed a developmental approach for understanding the etiology of substance abuse disorder. His developmental model can readily be applied to an understanding of antisocial behaviors in general:

 

This perspective emphasizes the influence of cumulative prior experience as the major determinant of the emergence of each successive phenotype. This epigenetic process allows understanding of the etiology of drug abuse in the context of an orderly process in which the outcome is the culmination of an ongoing developmental trajectory concomitant to person-environment interactions. It is important to note, however, that other outcomes (e.g., AIDS, criminality, dementia) can likewise be investigated through continued monitoring of the trajectory across the life span. Thus, drug abuse is not necessarily the only or final outcome of interest but instead is commonly intermediary to other negative outcomes. The epigenetic approach enables, therefore, the integration and sequencing of adverse outcomes associated with drug abuse as well as quantitative analysis of the patterning of other outcomes.

 

Although Tarter’s model addresses the development of drug abuse specifically, the implications are relevant to all complex human behavior. Healthy, normal development is characterized by the mastery of particular developmental tasks, such as cognitive and verbal skills, honesty, understanding rights of possession, respect for authority, independence, and basic trust. Maturing or developing successfully is defined by the mastery of these tasks, and is conducive to prosocial behavior and incompatible with antisocial behavior, generally resulting in a well-adjusted social behavioral repertoire. And while there are bases in evidence for the tendency of resultant behavioral patterns to wax and wane over time (contingent upon both physical and experiential stages of development), most assume a predictable trajectory (or life course), absent intervention or drastic socio-environmental change.

 

Antisocial behavior tends to have an early onset and often persists into adolescence and adulthood, suggesting that it is (1) a developmental trait, and (2) somewhat a function of the inability to assimilate the above developmental tasks. Early manifestations may include difficult temperament, impulsivity, social adjustment problems, poor academic achievement, distractibility and, oftentimes, depressed or negative affect. Attention deficit hyperactivity disorder (ADHD) is especially prevalent in early onsetters who progress to more serious criminal offending. These early signs commonly originate in genetic, congenital, and prenatal processes that subsequently interact with contextual factors to further condition the relationship between biology and behavior. A few of the contextual variables that exacerbate this developmental process, constituting a negative feedback loop, include parental rejection, ineffective parenting practices or severe disciplinary responses, child abuse, negative peer influences, poverty, and negative feedback from teachers. In short, the child’s responses to environmental input stimulate predictable reactions from the social environment, reinforcing or counteracting the child’s reactions, contributing to further changes in reactions from both the social environment and the child. Each step in this action-reaction sequence puts the antisocial child more at risk for long-term social maladjustment and criminal behavior. Rather than replacing one behavior with another in response to changing socio-environmental conditions, however, behaviors diversify and either strengthen, weaken, or reverse the developmental path over time.

 

See Loeber and Le Blanc (1990).

 

Q7: How do antisocial behavior and drug abuse relate to one another and what are the common antecedents?

 

A7: Susceptibility to chronic, excessive use of an abusable drug, increasing risk for dependency and related behavioral and lifestyle complications, is both biologically and socially constructed. Research reveals that a subgroup of the population is especially vulnerable to drug abuse and addiction, that its population exhibits early onset of drug use, finds drugs unusually rewarding, and more quickly develops a pattern of dependency and behavioral dysfunction than less vulnerable populations. This subgroup also exhibits a greater incidence of chronic maladaptive behaviors and demonstrates a tendency to be antisocial and at times violent irrespective of social conditions. Several investigators have proposed that drug abuse and antisociality may share common antecedents in susceptible individuals. These unusually vulnerable drug users are likely responsible for a major portion of drug-related offenses, particularly serious, chronic, violent crimes.

 


Certain parts of the brain govern specific functions. Areas including the sensory (orange), motor (blue) and visual cortex (yellow) highlight their specific functions. The cerebellum (pink) is involved in coordination and the hippocampus (green) regulates memory. Nerve cells or neurons connect one area to another via pathways to send and integrate information. The distances that neurons extend can be short or long. For example; the reward pathway (orange). This pathway is activated when a person receives positive reinforcement for certain behaviors ("reward"). This occurs when a person takes an addictive drug. As another example, the thalamus (magenta) receives information about pain coming from the body (magenta line within the spinal cord), and passes the information up to the cortex.

 

Given the commonalities in personality and temperament among populations considered vulnerable to drug abuse and antisocial behavior, it is plausible that underlying mechanisms in addictive behaviors may be interrelated with the specific proclivity to become antisocial under certain social and biological (e.g., drug- or stress-related) conditions. Antisocial behavior is self-stimulating, provides an outlet for frustration, is empowering, and is frequently a result of poor coping skills—properties that resemble those of drug abuse. Simply that these two behavioral outcomes are reinforced by their stimulating effects, however, does not sufficiently explain why only a subgroup of drug users respond with antisocial behavior while the overwhelming majority of users does not. We do not yet fully understand why only some individuals are attracted to and rewarded by these properties.

 

Individual differences, or unique characteristics, significantly determine both vulnerability to abuse drugs and various antisocial behaviors when sober or under the influence. The presence of conditions conducive to drug taking does not, however, necessitate that result; if drugs are unavailable or if other protective forces are strongly in place (e.g., family stability, strong religious affiliations, or high I.Q.), then drug misuse may not occur. Nevertheless, those “at risk” but who do not partake, may suffer from other chronic problems, for example, violence, depression, compulsive gambling, overeating, overmedicating, or unusual religiosity. Drug abuse may, therefore, be only one form of compulsive or excessive behavior resulting from existing psychopathology. Antisocial behavior may be another outcome. Findings that both antisocial behavior and drug abuse often coexist with other forms of psychopathology are consistent with the idea that both behavioral patterns are symptoms rather than syndromes in and of themselves.  For example, the abuse of psychoactive drugs would, therefore, likely lead to an intensification of underlying traits or psychopathology that predated and perhaps contributed to the onset of drug use, such as violence or another antisocial outcome. And similarly, the presence of antisocial tendencies may increase the likelihood that drug abuse would be one manifestation.

 

See Web site: www.nida.nih.gov

 

The co-occurrence of certain forms of psychopathology and cocaine use exemplifies the relationship between propensity to drug abuse and childhood behavioral disorders that antedate antisocial behavior, e.g., ADHD and CD. Alterations in the neurotransmitters serotonin and dopamine appear to be involved in both. There is evidence that individuals with ADHD are particularly vulnerable to cocaine dependence; they progress more quickly from casual use to dependence and experience a greater “crash” upon withdrawal. ADHD is often treated with medications that affect dopamine systems, as does cocaine. Cocaine addicts have also demonstrated a genetic susceptibility to dependence, found as a defect in the metabolism of the neurotransmitter dopamine. Subjects have a high incidence of early deviant behaviors, including CD. Although violence among cocaine users occurs more often in those with a history of violence, chronic use increases the likelihood irrespective of a predisposition as a result of neurotransmitter disruptions. In either event, characterizing users according to an underlying symptomatology may increase the effectiveness of treatment efforts; drug abusers with co-occurring psychiatric disorders, for example, drug abuse and depression, respond more favorably to treatment efforts that incorporate therapies—both pharmacologic and behavioral—appropriate for the underlying disorder.

 

The relationship between ASPD and alcoholism is also illustrative of neurobiological mechanisms that may underlie propensity to drug abuse and aggressiveness by virtue of common psychosocial traits. Alcoholics diagnosed as having ASPD tend to begin drinking at an earlier age, progress to alcohol dependence more rapidly, evidence greater impairment in social and occupational functioning, and have an increased number of arrests associated with their drinking. The genetic, biological, and psychological conditions discussed herein characterize those at risk for both ASPD and alcoholism: 1) higher levels of ANS activity during alcohol intake, suggesting unusual reward value of alcohol; 2) sensation-seeking which increases displays of impulsivity or aggression when sober and under alcohol's influence; 3) aberrations in serotonin and dopamine activity levels; 4) relatives with alcoholism and ASPD; and 5) a history of childhood hyperactivity among adults with alcoholism,  ASPD, and aggressive behavior. Co-occurring behavioral disorders are purportedly due to impaired impulse control functions that characterize each of them.

 

TRAITS OF TYPE I AND TYPE II ALCOHOLICS
CHARACTERISTICS
ALCOHOLIC TYPE
 
TYPE 1
TYPE 2
Problems Related to Alcohol
Common age of onset After 25 Before 25
Gender most afflicted Male and Female Mostly Male
Severity of alcohol dependence Relatively mild Unable to abstain
Fighting and arrests when drinking Not common Very common to be violent with or without alcohol
Psychological dependence (loss of control over drinking) High Not common
Guilt and fear about drinking problem Common Not common
Inheritance Questionable Most likely through father
Other Drug Use Less common More common
Personality Traits
Reward dependence
-------Eager to please
-------Sensitive
-------Dependent
High Low
Harm avoidance
-------Cautious
-------Inhibited and shy
High Low

Novelty seeking
-------Impulsive
-------Excitable
-------Distractible

Low High
Family History
Criminal History Less Common Common (especially father)
Treatment
Effectiveness More successful Resistant to treatment

Two types of alcoholism have been proposed by Cloninger.  Type I occurs
later in life, is less insidious, is not as often associated with
criminality, and is not believed to be strongly genetically influenced.
Type II alcoholism, on the other hand, occurs earlier in life, is more
destructive, is more often associated with criminality, and is believed to
be largely inherited.

See Fishbein and Pease (1996).  

 

                     

Q8: What are the measurable features (or phenotypes) that place an individual at risk for antisocial behavior and/or drug abuse?

 

A8: Neither antisocial behavior nor drug abuse is a direct manifestation of any classifiable (Diagnostic and Statistical Manual of the American Psychiatric Association [DSM-IV]) syndrome or psychological disorder. An increased risk for a spectrum of disorders that includes antisocial behavior and drug abuse is more likely a function of deviations in neurobiological systems that basically destabilize, or disturb, functions of the CNS. Given that several psychopathological states are associated with destabilization of the CNS, prediction of particular behavioral outcomes becomes impossible. Instead, as mentioned above, specific personality and behavioral traits may be a more direct reflection of neurobiological functions that underlie antisocial behavior and drug abuse than a larger syndrome or diagnosable disorder. The constellation of co-occurring personality and behavioral traits that may arise from such deviations includes:

 

Þ    impulsivity

Þ    negative affect or hostility

Þ    risk-taking

Þ    sensation- and novelty-seeking

Þ    oppositional defiance disorder

Þ    paucity of avoidance responses

Þ    aggressiveness unrelated to instrumental gain

Þ    longstanding behavioral patterns of  CD

Þ    learning disabilities

Þ    attention and other cognitive deficits

Þ    unusual sensitivity to rewarding properties of abusable drugs

 

Accordingly, psychological traits that increase vulnerability to the co-occurrence of drug abuse and antisocial behavior form the functional bridge between biological status and the behavioral outcome.

 

See Pallone and Hennessy (1996).

   

 

 

Individuals exhibiting the cluster of high-risk neurobiological and psychological traits described above often have a childhood history of the above-mentioned constellation of traits that present themselves as early warning signs. Irregularities in brain function that characterize those with antisocial behavior and substance abuse, particularly those suggestive of neurotransmitter imbalance, are more pervasive among affected children than those without.

 

See Raine (1993: 97).

 

Affected children often demonstrate CNS instability that prevents proper regulation over processes such as cognitive flexibility, attention, verbal fluency, and problem solving. These and other skills normally enable an individual to cope, assess consequences, control impulses, make decisions, and mature at a reasonable rate.  ADHD, in particular, has been cited as a precursor for both drug abuse and delinquency. The brains of ADHD children often show low levels of activity in areas responsible for arousal and alertness that may contribute to their stimulation-seeking behaviors. Such a childhood history may predict antisocial behavior while sober and under the influence of a psychoactive drug; as adults these children may possess both the susceptibility and the trigger.

 

See Farrington (1995); Fishbein (1990).

 

Q9: What designs are used to estimate the influence of genetic factors relative to environmental factors in the study of antisocial behaviors? In general, what do these studies show?

 

A9: “Heritability” studies estimate that the minimum extent to which different individuals vary in a trait within a particular human population is genetically determined. For example, I.Q. is considered to be highly heritable based on the extent to which monozygotic (identical) twins are more similar in I.Q. than dizygotic (fraternal) twins. Because identical twins are 100% genetically similar and fraternal twins only 50% similar, a higher rate of concordance, or similarity, in a behavioral trait between identical twins than fraternal twins is reflective of a genetic influence. Thus, the levels and ratios of concordance rates in identical and fraternal twins are used to estimate heritability. In adoption studies, concordance rates are compared for children and their biological parents relative to children and their adoptive parents. Given that children and their biological parents are 50% genetically identical by descent, while adopted children are unrelated to their adoptive parents, higher concordance rates between biological parents and their adopted-away children indicates a genetic influence on the trait.

   

 

Heritability studies of various dimensions of criminal behavior have most often focused on impulsivity, aggressiveness, and antisocial personality. Such phenotypes are more likely to be genetically influenced than the more complex, socially bound concepts of criminality and violence. However, high heritability for a trait in a population does not preclude the identification of environmental influences nor effective prevention or treatment. There may be an inclination towards a particular behavioral pattern, but not predestination. So even traits with genetic roots are not immutable and can be altered via environmental manipulations. Nevertheless, inborn differences are a starting point for understanding the web of interactions that leads to complex traits, including impulsive-aggression and other antisocial behaviors. In terms of public policy, treatment, prevention, or research aimed at identifying specific genes in aggression, what is important is not the level of heritability; rather, the focus should be on an understanding of the underlying processes and of the particular vulnerabilities and needs of individuals.

 

Individuals are vulnerable to different degrees to antisocial behavior, and interactions between genetic and environmental sources of variation underlie these individual differences. The extent of genetic influence is surprisingly high for behavioral traits, particularly alcoholism, impulsivity, and various other dimensions of antisocial behavior. One might think that traits such as these would not be measurably influenced by genetic factors because they are, in reality, crudely estimated and strongly influenced by cross-cultural and other environmental factors. However, data from large, methodologically sound twin and adoption studies, too numerous to delineate here, suggest that traits related to repetitive aggressive behavior (e.g., impulsivity, negative affect, drug abuse, alcoholism, and cognitive deficits) are significantly heritable. Furthermore, similar findings have been reported for the heritability of personality factors, like extroversion, introversion, cognitive deficits, CD, or anxiety, which are strongly predictive of substance abuse and aggression. Identification of genetic contributions does not reduce behavior to a gene level, but can help explain the origins of behavioral variation in a population. Specifically, the role of genetics in modulating behaviors that centrally involve impulse control and negative affect is thought to be substantial. According to this view, genetic factors help to explain individual vulnerability to certain behavioral patterns or orientations. Nevertheless, other factors such as choice and volition are more important in explaining behavior on a population-wide scale.

 

While we know that traits associated with impulsivity, aggressiveness, and alcoholism have significant heritability, twin and adoption studies do not identify the underlying biological mechanisms that may directly contribute to these traits. New techniques in molecular genetics have resulted in important discoveries that implicate certain biological systems in these disorders, and it is on this level that both environmental and clinical interventions may be effective. Irregularities or variations in genes, which lead to functionally significant differences in the way genes are expressed, have been discovered in humans and can be reliably measured. The genetic markers (associated with gene action) and variants (variations in gene structure) that most often relate to behavioral disorders involve the neurotransmitters dopamine and serotonin, and include the way they are synthesized, metabolized, and interact with receptors. The breakdown of dopamine and serotonin into their metabolic end products is orchestrated by two forms of the enzyme monoamine oxidase (MOA): MAOA and MAOB. Levels of these enzymes have also been associated with the behavioral phenotypes impulsivity and aggressiveness, as discussed in the following section.

 

A variety of genetically influenced psychiatric disorders are accompanied by increased liabilities for impulsive and aggressive behaviors, including   ASPD, CD, and Borderline Personality Disorder. Alcoholism, a largely genetic disorder, also mediates liability to impulsive and aggressive behaviors. Aggressive behavior is frequently triggered by intake of relatively small amounts of alcohol, and more than half of violent crimes occur under the influence of alcohol (see Reiss and Roth [1993]). The early-onset subtype of alcoholism, Type II, is itself associated with antisocial behavior and impulsiveness.

 

See the table depicting Type I and Type II alcoholics above.

 

Other associations between aggression and genetically influenced psychiatric diagnoses include suicide in depression, schizophrenia, alcoholism, self-directed violence in borderline personality disorder, self-destructive behaviors in Lesch-Nyhan syndrome, and other mental retardation syndromes. Therefore, identification of genetic factors contributing to these disorders would contribute to an understanding of the antecedents of aggressiveness.

 

Identification of variants (or irregularities) in genetic markers for neurotransmitter (e.g., dopamine and serotonin), enzyme (e.g., MAOA), and hormone (e.g., thyroid hormone receptors) function in impulsive aggression and related disorders encourages the conclusion that scanning of additional candidate genes will detect alleles (one of a set of genetic variants at a given gene) significant for antisocial behaviors. It is important to recognize that these genes will be scanned and the variants detected independent of any research program specifically directed towards criminality or   ASPD. Direct gene analyses have revealed functionally significant genetic variants, many common, at most of the dopamine and serotonin-related genes previously implicated in impulsive and aggressive behavior.

 

Questions addressed in the following sections describe the neurochemical, physiological, and neuropsychological mechanisms through which genetic markers for behavioral vulnerabilities are often expressed. Before entering this discussion, two critical points that condition the relationship between genetic traits and behavioral outcomes should be noted. First, there is a genetically determined range of potential responses to environmental inputs by chemical and physiological systems in the brain. Within this range, many environmental influences play a role in determining which sector of the spectrum of responses will be elicited. Thus, many behavioral outcomes are possible at any given time; each situation is unique, although consistency in experiences (e.g., adverse or positive) will be cumulative to produce predictable and consistent patterns of behavior. Second, and following from the first, biological functions are substantially influenced by environmental factors and cannot always be directly attributed to genetic traits. The social and physical environment have the potential to significantly alter brain function irrespective of genotypic features; e.g., prenatal drug exposure and traumatic experience disrupt neurotransmitter function, hormonal release, and neuropsychological development. Importantly, as will be discussed in a later section, genetically influenced temperament can also alter environmental responses to the individual, thereby either exacerbating or subduing the behavioral outcome (e.g., irritability or negative emotionality in an infant can elicit more severe parenting responses, thereby compounding the child’s difficulties).

 

See Moffitt (1993).

 

Q10: What biological mechanisms are believed to be involved in the risk for antisocial and violent behavior (brain anatomy and function)?

 

A10: Studies conducted so far implicate deviations in a) activity levels for neurotransmitters and hormones in vulnerability to antisocial behaviors, b) physiological processes, and
c) neuropsychological function. Each area is summarized below.

 

         Neurotransmitters

 

Current studies of biochemical mechanisms underlying various forms of antisocial behavior focus on the role of central neurotransmitter systems in modulating impulse control and levels of arousal. The neurotransmitters dopamine and serotonin help to regulate and modulate aggressive behaviors, even in the absence of pathology. The dopamine system appears to facilitate responses to cues in the environment that were previously paired or associated with a reward or an object that satisfies some basic or social need. When something potentially useful is nearby, like food or a mate, dopamine activity sets in motion a physiological process to elicit an emotional response that activates behavior to explore the possibilities. Excitement, anxiety, curiosity, or pleasure provide an impetus for flight or fight, exploration of something novel, or avoidance of something aversive or painful. So when the dopamine system is activated, novelty seeking and self-stimulation behaviors increase. When this system goes awry, however, behavior may be activated in the absence of a threat or other appropriate stimulus. This approach system can produce dangerous asocial and disruptive behavior.

 
 "Pathway for sensation of pain and reaction to pain".  This is a long pathway, in which neurons make connections in both the brain and the spinal cord. When a person one slams a door on one's finger, here's what happens. First, nerve endings in the finger sense the injury to thefinger (sensory neurons) and they send impulses along axons to the spinal cord (magenta pathway).  The incoming axons form a synapse with neurons that project up to the brain. The neurons that travel up the spinal cord then form synapses with neurons in the thalamus, which is a part of the midbrain (magenta circle). The thalamus organizes this information and sends it to the sensory cortex (blue), which interprets the information as pain and directs the nearby motor cortex (orange) to send information back to the thalamus (green pathway). Again, the thalamus organizes this incoming information and sends signals down the spinal cord, which direct motor neurons to the finger and other parts of the body to react to the pain (e.g., shaking the finger or screaming "ouch!").

 

The dopamine system has been implicated in displays of aggressive or violent behavior. Dopamine metabolism increases when laboratory animals are provoked to behave aggressively. Amongst humans, the over-production of dopamine has been associated with psychosis and has been linked to antisocial behavior and violence. Antipsychotic drugs that decrease dopamine levels tend to decrease fighting behaviors. Nevertheless, meta-analyses of neurotransmitter levels in antisocial populations show inconsistencies across studies that have been conducted and no main effects have been identified for individual neurotransmitter systems. Variations in populations studied and definitions of antisociality employed may explain these discrepancies. Moreover, main effects were examined to the neglect of interactions between neurotransmitter systems, an omission that precludes identification of significant players in a total neurobiological environment.

 

See Raine (1993).

 

 An abnormally low level of serotonin activity is regarded as another collaborator in the production of both antisocial behavior and depression. In rats, lesions in (or damage to) particular brain regions dense with serotonin connections produce rage and attack. Genetic strains of mice that show lower serotonin activity than other strains are more aggressive, and intraspecies aggression is suppressed when serotonin metabolism is blocked, resulting in increased activation of serotonin. Several indicators of lowered serotonin activity in humans characterized as violent or impulsive, in contrast to those who are not, have also been reported. Post-mortem studies of the brain show serotonin deficits in those who committed a violent suicide (e.g., using a gun or knife) as compared with those who committed a “nonviolent” suicide (e.g., using pills or gas). Thus, it seems that a deficit in serotonin activity produces disinhibition, resulting in an increased likelihood of impulsive-aggressiveness or other excessive and inappropriate behavior.

 

Studies reveal that serotonin has a modulating influence in excessive drinking behavior and alcoholism, a finding that is particularly noteworthy in light of reports that impulsive and violent individuals have also shown low-serotonin activity levels and are prone to antisocial behavior while drinking. A decline in serotonin activity may be partially responsible for alcohol-induced behavioral and neurological disinhibition, leading to the expression of underlying violent tendencies. Alcoholics believed to be at genetic risk for comorbid alcoholism and aggressiveness/criminality may be the product of a preexisting deficit in serotonin function. When drinking, such individuals are more likely to experience dysphoria and display impulsive-aggressive behavior as alcohol brings serotonin-activity levels below “the floor.”   As serotonin activity declines during alcohol consumption, compromising impulse control, dopamine activity simultaneously rises, leading to the expression of underlying violent tendencies.  The use of drugs or environmental manipulations that stimulate serotonin activity in such cases may be a helpful therapy for co-occurring alcoholism and violence by reducing 1) co-occurring depression and/or anxiety; 2) alcohol craving; 3) some of the reinforcing properties of alcohol; and 4) aggressiveness.

 

Norepinephrine (NE) is a transmitter substance produced from dopamine; dopamine is converted to NE through the action of the enzyme, dopamine beta-hydroxylase. Excess NE is destroyed by MOA (see below), and 3-methoxy-4-hydroxyphenylglycol (MHPG) is one of NE’s principal metabolites. NE has been of particular interest due to its involvement in stress responses, emotions, attention and arousal. It plays a primary role in the initiation of the so-called “fight and flight” response by eliciting the release of adrenal stress hormones and exciting the CNSs and ANSs. Brain structures from the frontal cortex, to the limbic system, to the brainstem are responsible for NE’s stimulatory effects on these functions.  



The synapse and synaptic neurotransmission.
This figure describes the synapse and the process of chemical
neurotransmission. As an electrical impulse arrives at the terminal, it
triggers vesicles containing a neurotransmitter, such as dopamine (in blue),
to move toward the terminal membrane . The vesicles fuse with the terminal
membrane to release their contents (in this case, dopamine). Once inside the
synaptic cleft (the space between the 2 neurons) the dopamine can bind to
specific proteins called dopamine receptors (in pink) on the membrane of a
neighboring neuron. 

 

Significant changes in NE have been documented during preparation for, execution of, and recovery from activities that involve high-arousal states, including violent behavior, although the direction of these changes is variable from situation to situation, and from brain site to brain site. While NE activity is related to states of arousal, affect, and behavioral activation, NE activity is not predictive of particular behavioral outcomes; rather, it may characterize a patterned orientation to environmental stimuli. For example, NE activation as a result of amphetamine use is strongly associated with agitation and aggression, but the actual behavioral outcome is contingent on circumstance, setting, and individual predisposition.

 

Several studies have established a link between changes in NE and violence, although discrepancies exist. Subjects with convictions exclusively for violent crimes had higher levels of NE than those convicted of mixed violence and property crimes. MHPG levels in cerebrospinal fluid (CSF) have been positively related to aggression in military personnel, and stress-related urinary NE values were reportedly higher in violent incarcerated males.  Also, drugs that increase NE activity are known to exacerbate violence in patients who are already agitated. On the other hand, Virkkunen and his colleagues reported that CSF MHPG was positively correlated with the number of property crimes, not violent crimes, in a subgroup of arsonists. Both arsonists and violent offenders had lower levels of MHPG than controls. Various psychiatric populations with antisocial behavior have shown significantly lower NE levels than controls.

 

Directionality is obviously an unresolved issue when relating NE levels to violence. The majority of studies indicate that higher levels of NE are associated with aggression and violence; however, because NE values are highly variable, the most promising approach for the use of NE levels as a marker for violence is under conditions of stress or provocation, rather than of a resting state. Although it is unknown at the present time what the precise role of NE is in contributing to violence—because NE activity levels are suppressed by beta-blockers and reserpine—these medications have been used in the treatment of violence. Thus, there are clear indications that NE’s role in violence is significant but highly dependent on its interaction with other central neurotransmitters and environmental conditions.

           

MAO, an enzyme responsible for the breakdown of several neurotransmitters (e.g., dopamine, serotonin, and NE), is involved in several aspects of brain function via regulation of neurotransmitter concentrations and activity levels. MAO helps to flush used neurotransmitter molecules from the nervous system. While there is a broad range of optimal-MAO levels, unusually high or low levels are believed to adversely affect social behaviors. Low-MAO activity is thought to result in excessive neurotransmitter accumulation in brain cells, leading to excessive levels of dopamine and NE, in particular, which may contribute to aggression, loss of self-control, and inappropriate motivations to behave (see above). Because MAO concentrations within the brain are particularly high in areas of the brain involved in executive cognitive functions (ECFs), affect and mood state, impulse control, and aggressiveness (the brainstem, hypothalamus, and prefrontal cortex), the relationship between deviations in its activity and effects on social and emotional behaviors is understandable.  

 

Since the early 1980s, deviations in MAO levels have been linked with certain forms of criminality, particularly those involving psychopathy, aggression and violent behavior. Several studies have related variations in MAO activity to tendencies toward alcoholism, sensation-seeking behavior, impulsivity, psychopathy, and excessive alcohol use, all of which are often associated with antisocial behavior.  Low-platelet MAO levels were also found in male student volunteers with histories of psychosocial problems, including convictions for various offenses and among relatives of low-MAO subjects. One recent study of a large Dutch kindred spanning four generations found 14 males to be affected by a complex behavioral syndrome that includes borderline mental retardation and severely impulsive aggressive behavior. A genetic defect was discovered in affected males and found to be associated with abnormalities in MAO metabolism. Because this defect is rare, it is impossible to extrapolate these findings to other families in which impulsive aggression appears prevalent. Nevertheless, investigators are considering the possibility that subtler forms of MAO deficiency may exist in a subgroup of the population that exhibits these behaviors, although the causal relationship between a MAO metabolic abnormality and behavioral disturbance is not a simple one.

 

Hormones

 

A large body of literature reflecting both animal and human studies conducted over the past decade reports an association between aggressiveness and various “sex” and “stress” hormones. Animal studies are briefly mentioned because they provide the models for human investigation; however, the focus is on human studies since the literature is rife with discrepancies between human and animal findings, indicating that extrapolation between species is unjustifiable.  The most informative studies of the role of hormones in human behavior include either a pharmacological challenge (e.g., administering of an agent that either antagonizes or agonizes the release of a particular hormone or set of hormones) or a behavioral challenge (e.g., provoking anger under laboratory conditions or inducing a stressful state) to identify group differences in hormonal responses. Nevertheless, reports also suggest that basal levels of hormones also often differ between test subjects and controls.

 

Probably the most studied hormone in relation to aggression is testosterone, a male androgen (females also produce this hormone, but in lower amounts and with somewhat differing effects). Animal studies suggest that testosterone facilitates aggression, although findings of an association from human studies have not been as consistent. Studies of subjects with congenital adrenal hyperplasia (CAH), a disorder characterized by exposure to high levels of androgens in the prenatal and early postnatal periods, provide evidence for testosterone’s role in human aggression across the life span. Testosterone concentrations in plasma have been reported to correlate positively with self-rated measures of aggression in some studies of non-psychiatric subjects and have recently been reported to be higher in alcoholics with a history of repeated episodes of domestic violence.  Dabbs and Hargrove have reported several studies of violent offenders showing that testosterone is related to criminal violence and aggressive dominance in both male and female inmates. In a laboratory investigation of normal male controls, the administration of testosterone resulted in a significantly higher level of aggressive responding relative to responding resulting from the administration of a placebo.

 

Higher CSF testosterone concentrations in antisocial impulsive violent offenders have been reported, but not in non-antisocial impulsive or non-impulsive violent offenders, compared with healthy volunteers. Another study concluded that adrenal androgen functioning plays an important role in aggression in young boys, although these findings were significant for two male hormones other than testosterone. Interestingly, high levels of testosterone were found to augment rates and intensity of aggression in subjects with indicators of low-serotonin activity; the interactive effects of these two conditions on aggression were significant. Overall, data from both animals and humans suggest that the biological and behavioral responses to androgens such as testosterone are substantially context-dependent and that testosterone not only affects dominance behavior (involving either competition or aggression), but also responds to it.

 

Biological or integrated studies of aggressive or antisocial females are scarce—too few to draw conclusions about underlying mechanisms. There is some evidence, however, for the role of deviations in sex hormonal secretions in female antisocial behavior. Exposure of a female fetus to heightened levels of androgens, or a genetic hypersensitivity in the brain’s receptor sites to these hormones, during prenatal development can masculinize the fetus by altering both the neuroanatomy and the physical constitution.  Strong evidence exists for the influence of male hormones on a masculine physique, a masculine self-identity, and increased aggressiveness in adult females.

 

Prenatal drug exposures, genetic defects, neurotransmitter imbalances, certain medical conditions, and even social factors can all affect sexual and social development by altering sex hormone influences.  Dabbs and his colleagues, for example, have reported high levels of testosterone among violent female inmates and delinquents relative to those considered nonviolent. Also, females exposed to high levels of androgen in the prenatal and early postnatal periods (due to a congenital disorder) had significantly higher aggression scores than controls. Unusually high testosterone levels in females may contribute to the increased incidence of mesomorphy among female offenders and may function to reinforce aggressive tendencies under certain environmental conditions.

 

Hormone release initiated by the hypothalamus and secreted by the pituitary and adrenal glands are known to be exquisitely sensitive to environmental stressors, including novel situations; thus, they are referred to as stress hormones (e.g., ACTH [sp