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Contemporary Biological and Integrated Perspectives
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.” 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.
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.
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.
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.
Two types of alcoholism have
been proposed by Cloninger. Type I occurs 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
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.
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.” 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.
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
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 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||