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 [spell out], cortisol, and prolactin). In general, studies report increased cortisol reactivity in individuals with unusually heightened reactions to challenging situations, and an increased incidence in conduct disordered behavior and depression. On the other hand, low cortisol increases may reflect a low ANS arousal characteristic of those considered to be at risk for psychopathy. Consistent with that possibility is previous research showing low concentrations of cortisol in aggressive youth and violent adult offenders who lack anxiety. Alcohol consumption may further strengthen the link between stress hormones and antisocial behavior, but in the opposite direction; [word is missing here] found increased levels of cortisol in violent alcoholics, suggesting a relationship between impulsive violence and heightened stress responses.

See Raine (1993); Raine et al. (1997).

Psychophysiological Correlates

Both genetic and acquired deviations in physiological activity of the nervous system attributable to neurotransmitter dysfunction have been consistently associated with behavioral and psychological risk factors for both violence and drug abuse. Although discrepancies exist due to differences in methodologies, measures, and subjects, numerous studies suggest that stimulation-seeking, impulsivity, aggressiveness, hyperactivity, ADHD, lack of avoidance responses, and inability to empathize are possible behavioral outcomes of serotonin and dopamine system abnormalities with measurable psychophysiological consequences. The overwhelming majority of the evidence is supportive of the notion that individuals prone to violent, psychopathy, and/or drug abuse have unusually low levels of ANS and CNS activity and subsequent sensation seeking.

See Fishbein (1990); Raine (1993); Pallone and Hennessy (1996).

Physiological markers indicative of CNS instability have been repeatedly found in subjects with antisocial behavior, including drug abuse and violence, as reflected in electroencephalogram (EEG) differences, and electrodermal, cardiovascular and other nervous system measures. Individuals with histories of both drug abuse and impulsive aggression, for example, tend to show relatively more slow wave activity in their spontaneous EEG and delayed brainstem evoked potentials (evoked potentials are electrical brain waves that occur in response to a stimulus, such as a visual or auditory stimulus; thus delayed evoked potentials indicate slow CNS information processing) as compared to controls, findings which may be related to differences in cognitive abilities. Relatively high levels of EEG slowing and EP delays in these subjects are thought to reflect a lag in the maturity level of brain development and function, although such findings lack specificity. These processes are often a function of neurotransmitter defects that alter CNS arousal levels and, thus, may contribute to excessive stimulation needs.

Skin conductance (SC), a measure of peripheral nervous system functioning, is a measure of the level of arousal and, therefore, emotional state. Most studies of SC and its relationship to aggressiveness or antisocial behavior have focused on a subgroup of criminal offenders classified as “psychopathic.” Nearly consistently, investigators have reported findings of low SC arousal in this population. Deficits in measures of SC arousal are believed to be indicative of both structural and functional abnormalities in the ANS and the area behind the forehead, the frontal cortex, responsible for higher intellectual cognitive functions. In psychopathic subjects, such deficits are outwardly expressed as reduced levels of responding to socially meaningful stimuli. Both serotonin and dopamine play a mediating role in the production of skin conductance, leading to speculation that SC deficits result from a central neurotransmitter imbalance.

Low resting heart rate has been reliably found in antisocial and aggressive youngsters. A meta-analysis reported an average effect size of 0.53, indicating that low resting heart rates are predictive of CDs in various childhood samples. Furthermore, it has been reported that resting heart rate at age 18-19 years in a sample of non-institutionalized males predicted violent offending by age 25. Resting heart rate, like SC, is a reflection of ANS tone; thus, a low heart rate is indicative of low ANS arousability, consistent with the widely tested hypothesis that subjects with antisocial, psychopathic, and repeatedly violent behavior are more likely to be physiologically underaroused and, consequently, sensation-seeking.

Many of these psychophysiological markers are nonspecific for psychiatric, psychological or behavioral disorders; the particular behavioral outcome may be more a function of socio-environmental experiences. Nevertheless, taken together they show deviations in arousal level that are consistent with findings of neurotransmitter irregularities. 

Neuropsychological and Imaging Studies

Reviews of a large body of research unanimously conclude that impairments ECFs are implicated in the regulation of impulsive and aggressive behaviors. The evidence specifically suggests that various types of antisocial behavior may be characterized by impairments in ability to assess consequences and act on that assessment, as reflected in the personality trait of impulsivity. Underlying such impairments are putative brain function abnormalities that alter cognitive capacities, particularly those involving ECFs such as attention, concentration, verbal ability, abstract reasoning, problem solving, and programming and planning goal-oriented behaviors. Giancola has hypothesized that ECF impairment compromises the ability to interpret social cues during interpersonal interactions, which may lead to misperceptions of threat or hostility in conflict situations. ECF impairment may further undermine the ability to generate alternative socially-adaptive behavioral responses and to execute a sequence of responses necessary to avoid aggressive or stressful interactions. Finally, compromised cognitive control over behavior may permit hostility and negative affective states, and other maladaptive responses (e.g., violence or drug abuse) to dominate.

The prefrontal cortex and some of its subcortical connections (e.g., regions of the limbic system and basal ganglia) represent the neural structures most involved in subserving ECF, suggesting their involvement in concomitant aggressive behavior. Damage to areas of the prefrontal cortex reduces inhibitions and self-concern, causing an indifference to the consequences of one’s behavior. Thus, areas of the prefrontal cortex are thought to modulate social skills. Features of impaired judgment, inability to assess consequences, attention deficits, and inadequately motivated behavior typify individuals with histories of both violence and drug abuse. Several lines of evidence implicate dysfunction of the prefrontal cortex specifically in violent behavior. For example, head injury affecting the prefrontal cortex has been associated with posttraumatic violent behavior. Patients and offender populations with prefrontal lobe damage show increased extraversion, impulsivity, irritability, aggressiveness, and various antisocial behaviors. Patients with prefrontal lobe head injuries often exhibit impairments in ability to make rational decisions in personal and social matters, in addition to difficulties in the processing of emotion. In brain-injured individuals, a functional disconnect between frontal cortical regions and the limbic system may result in impaired impulse control, reasoning, and decision-making.

Based on the experiences of Phineas Gage and their effects on his personality, temperament and intellect, neuroscientists began to understand that the damaged area was responsible for social skills, impulse control, forethought, and assessment of consequences in all human beings. This area is the orbitofrontal cortex, within the prefrontal cortex, which has remained the focus of numerous investigations into disregulated and disinhibited behavioral problems, including those involving drug abuse, alcoholism, CDs, and antisocial behaviors.

See Volavka (1995).

While neuropsychological tests provide some guidance in the search for neural mechanisms in antisocial behavior, they lack the regional specificity of other more recently developed techniques. Thus, the logical next step in future research is to directly measure neural responses in particular brain regions to various cognitive challenges in individuals with and without violent behavior and substance abuse. The most promising method at present is the use of neuroimaging techniques to identify structural differences and elucidate functional brain responses to cognitive stimuli that challenge regions thought to be involved in ECF (e.g., via positron emission tomography [PET] or functional magnetic resonance imaging).

            In one of the few brain imaging studies examining individuals with persistent aggressive behavior, altered metabolism of glucose in a region of the prefrontal cortex was reported. PET studies of individuals with disruptive behavioral disorders that often antedate impulsive-aggression in adulthood have focused primarily on ADHD.  Zametkin and his colleagues reported lower levels of global and regional glucose metabolism in areas of the prefrontal cortex and limbic system in ADHD adults than in controls without ADHD. Adrian Raine’s study of murderers used PET and demonstrated lower glucose metabolism in prefrontal areas of the brain compared to a control group. In an expanded study, Raine and his colleagues examined 41 murderers and 41 age-matched controls using PET and the Continuous Performance Task (CPT) that produced increases in relative regional glucose metabolism in the frontal lobes in control subjects, in addition to increases in right temporal and parietal lobes. Primary findings were that murderers exhibited reduced glucose metabolism during activation in both sides of the prefrontal cortex, in addition to several other brain regions. Raine concluded that these findings support earlier indications of deficits in the prefrontal cortex. Imaging studies of impulsive and aggressive behavior suffer from one or more shortcomings, including small sample size, technological shortcomings, ambiguity in group assignments, and absence of a condition to activate the brain so that functional responses can be attributed to a particular brain region. Nonetheless, these studies offer provocative information on brain function in impulsive-aggressive individuals and provide the basis for more definitive investigations.

Q11: What biological mechanisms (brain anatomy and function) are believed to be involved in the risk for drug abuse?

A11: Abuse of psychoactive substances in general is a function of the “pharmacological” properties of the drug; the drugs effects on specific neurotransmitter systems in specific anatomic regions of the brain. Most substances are considered to be "abusable" as a function of their ability to produce euphoria, craving and, potentially, dependence, and they exert both excitatory (increasing activity) and inhibitory (decreasing activity) effects. Excitation of reward pathways in the region near the center of the brain (mesolimbic) by psychoactive substances creates the sensation of pleasure and is believed to be the most powerful inducement to abuse and addiction. Many drugs also suppress or inhibit neural systems responsible for the perception of pain, thereby further reinforcing repeated drug‑taking behaviors. Ways in which these drugs alter the balance between excitatory and inhibitory activity in various structures are responsible for influencing so-called motivational systems in the brain. This means that motivations to behave in certain ways are altered by affecting goal-driven behavior, impulse control, and forethought. Because drugs of abuse actually stimulate systems in the brain that motivate us to satisfy our basic drives (like eating, drinking, sex, reproductive activities, child rearing, and need for survival), an addiction to drugs can actually supercede these basic drives and cause the addict to crave the drug more than satisfy these basic human drives.

The Brain's Reward System

Central to the rewarding excitatory effects of psychoactive drug use and the possible eventuality of drug addiction is the role of the brain's dopaminergic neurotransmitter system. Neurons in this system are critical in the mediation of reinforcement; i.e. behaviors that stimulate brain-reward regions rich with dopaminergic neurons are likely to be repeated due to the intrinsic reward value they possess. Stimulation to these systems elicits a range of motivational emotions and responses that encourage adaptive behavior; eating, exercise, sexual behaviors, and personal accomplishments stimulate reward centers and provide motivation for a repeat performance. When systems within reward centers go awry due to injury, stress, genetics, or drug use, however, behavior may become dysfunctional, leading to affective, eating or sexual disorders and other compulsive and excessive behaviors.

Psychoactive drugs produce more intense dopaminergic effects than natural stimulators, so the reward value of drugs may supercede motivations to perform acts that enhance, rather than detract from, adaptations to our environment. Animals will work for opiates, like heroin, directly injected into dopamine-rich structures within these systems (e.g., the nucleus accumbens), and when these neurons are destroyed, the behavioral response is extinguished. Other pleasure-producing psychoactive substances elicit similar responses by their action in the same structures. For example, psychomotor stimulants (e.g., cocaine or amphetamines) activate dopaminergic systems leading to self-stimulation and heightened sensitivity to environmental cues, which may be further reinforced by stress. Use of stimulant drugs sensitizes the dopamine system to other drugs, increasing their reward value. This reverse tolerance partially explains why many drug abusers are polydrug abusers.

 

"Dopamine neurotransmission and modulation by endogenous opiates"
Using the close-up of a synapse, dopamine is shown here as an example of
synaptic function. Dopamine is synthesized in the nerve terminal and
packaged in vesicles. For neurotransmission, the vesicle fuses with the
membrane and releases dopamine. The dopamine molecules can then bind to a
dopamine receptor (in pink). After the dopamine binds, it comes off the
receptor and is removed from the synaptic cleft by uptake pumps (also
proteins) that reside on the terminal (arrows show the direction of
movement). This process is important because it ensures that not too much
dopamine remains in the synaptic cleft at any one time. Also there are
neighboring neurons that release another compound called a neuromodulator.
Neuromodulators help to enhance or inhibit neurotransmission that is
controlled by neurotransmitters such as dopamine. In this case, the
neuromodulator is an "endorphin" (in red). Endorphins bind to opiate
receptors (in yellow) which can reside on the post-synaptic cell (shown
here) or, in some cases, on the terminals of other neurons. The endorphins
are destroyed by enzymes rather than removed by uptake pumps.

"The reward pathway"
This is a view of the brain cut down the middle. An important part of the
reward pathway is shown and the major structures are highlighted: the
ventral tegmental area (VTA), the nucleus accumbens and the prefrontal
cortex. The VTA is connected to both the nucleus accumbens and the
prefrontal cortex via this pathway and it sends information to these
structures via its neurons. The neurons of the VTA contain the
neurotransmitter dopamine which is released in the nucleus accumbens and in
the prefrontal cortex. This pathway is activated by a rewarding stimulus.
[Note: the pathway shown here is not the only pathway activated by rewards,
other structures are involved too, but only this part of the pathway is
shown for simplicity.

The Impulse Control System

Parallel research suggests another neurotransmitter, serotonin, is also involved in drug abuse. Serotonergic systems are largely responsible for the regulation of impulse control, mood, sleep cycles, arousal levels, satiety (satisfaction of certain drives), and aggression. Serotonin mechanisms globally inhibit behavioral responses to emotional stimuli. Abnormalities in serotonin-activity levels have been linked to psychosis, anxiety, obsessive-compulsive disorder, violence, impulsivity, eating disorders, and depression, all of which share mood disturbance, alterations in functions involving basic drives (eating or sex), sleep disruption, and excessive aggression. Studies reveal that serotonin also has a modulating influence in excessive drinking behavior. Alcoholism has been associated with low levels of serotonergic activity; and drugs that increase the concentration of serotonin in active brain sites decrease alcohol intake in animals and humans.

Behaviors related to drug abuse have been attributed partially to an impairment in serotonin's ability to mediate feelings of having a basic drive satisfied, to inhibit behavior, and to regulate sensitivity to stressful stimuli. The net consequence of these effects of serotonin deficiency is that the behavioral response lasts longer, occurs more frequently, and occurs with more intensity: more sexual behavior, more food and water intake, more aggression, higher startle response, increased sensitivity to painful stimulation, and more novelty-induced exploration (activity levels being heightened by exposure to new experiences). Affected individuals will thus appear more depressed and aggressive (more affected by punishment), more appetite-driven (more motivated by food, water, sex, and drugs of abuse, which share psychomotor-stimulant properties), and more impulsive (less able to control behavior in the face of threat). As a result, when individuals consume psychoactive drugs with pre-existing anomalies in the routes and mechanisms for neurotransmitter metabolism, the net effect can be radically unpredictable. Drug activation of relevant limbic and cortical structures compromise both neurological and behavioral inhibitions and can produce dysphoric, or uncomfortable, feelings in susceptible persons, increasing risk for the outward expression of a negative emotional state.

See Pallone and Hennessy (1996).

See Web site: www.nida.nih.gov  

Q12: What is the role of stress in antisocial behavior?

A12: Understanding the dynamics and consequences of stress is key to unraveling etiological mechanisms in antisocial outcomes. Stressors, the cause or precipitants of stress, can be acute or chronic and if severe, can cause damage to internal organs. Stress is the physical and psychological response to an excess of stimulation compared with an individual’s resources for coping.  The source of stimulation may be either environmental (e.g., child abuse, family dysfunction, or sensory deprivation), biological (e.g., lead poisoning, prenatal drug exposure, or head trauma) or an interaction of the two. Resources for coping may also be grounded in conditions that are either biological (e.g., I.Q. and executive cognitive skills), social (e.g., parenting techniques), psychological (e.g., self-esteem) or, most likely, a combination.

Stressful experiences can temporarily or permanently alter brain function and chemistry. An acute stressor occurs in the short term and generally produces only a temporary effect; biological and physiological adjustments in the brain’s response to the stressor take place after the stressor terminates. The presence of a chronic or recurring stressor, in contrast, more often results in a cumulative effect on biological and physiological responses that can impair coping abilities, and constitutes a formidable risk factor. As a direct consequence of these effects, chronic stress primes the brain for maladaptive responses to the environment, thereby increasing the likelihood of psychopathological or antisocial behavior. Inherent susceptibilities or vulnerabilities help to determine particular behavioral outcomes of that stress, e.g., from schizophrenia to depression to violence, while positive attributes of either the individual or the environment can provide some protection from these outcomes.

A stressful experience produces a flurry of physiological and biochemical reactions that differ somewhat in intensity and effectiveness depending upon the individual’s constitution. Bodily reactions to stress are, in essence, an activation of the “flight or fight mechanism” and are designed to help the individual determine which response to the stressor is warranted. The immediate impact of stress is felt by the hypothalamus within the limbic system, which is a primitive part of the brain responsible for survival, mood, emotion, and a variety of other behaviors and states. The hypothalamus, in turn, communicates with the endocrine system (a system of glands that secrete hormones throughout the body) and the ANS to directly affect the function of relevant organs.

Imagine that you are working through a dark alley and you realize that someone is quickly approaching. The first step in the flight and fight mechanism is the perception by the cortex (the gray matter in charge of higher intellectual functions) of the event. This is cognition. The cortex “talks” to various structures, including memory centers of the limbic system, so that the individual can quickly remember the dangerous nature of such a situation. Subsequently, the brain will begin to reason or determine the best plan of action and the motor system becomes active to initiate the necessary moves for coping. As a result of this biochemical and physiological process, the limbic system is thus activated to induce feelings of fear or urgency. Such feelings are necessary to mobilize action within the body for successful survival. Without fear or a sense of urgency, we are likely to be sluggish in our response. The limbic system, in turn, activates the ANS to produce several physiological responses, such as heightened skin conductance, slowed digestion, rapid heart rate and blood pressure, increased oxygen and glucose to the muscles and brain, bronchial tube dilation, pupil dilation, and a host of other responses all designed to mobilize the energy and motivation to cope quickly. Several of these indicators, by the way, are measured by the polygraph that attempts to measure physiological reactions to lying, which produces stress in most people. Simultaneous to ANS activation, the hypothalamus continues to organize a chain reaction of defenses by releasing several stress hormones. The pituitary gland (the master gland at the base of the brain) is signaled to produce ACTH, a stress hormone. Stress hormones subsequently notify the brainstem (responsible for motor movement, among other functions) to alter organ activity. These biochemical reactions further reinforce the physiological processes that lead to increases in heart rate, blood pressure, and so forth. As a result, you are able to decide the best course of action and act on it by either fighting back or fleeing that dark alley.

The hypothalamus coordinates our response to stress by unleashing a flurry of hormonal secretions from the pituitary, thyroid, and adrenal glands. These hormones, in turn, trigger physiological and behavioral reactions that enable us to copy with the stressor. If this biological process is disturbed, our behavior will be disturbed accordingly.

Under these conditions of severe stress, humans have been known to perform unusual feats of strength and endurance. For example, a mother was known to lift a car off her trapped child due to the dramatic increases in energy and strength caused by this flight and fight system. Even under less severe conditions of stress, however, awareness and attention are heightened and physical strength increases.

It is this very system that allows humans and other primates to be conditioned by our environment. For example, when you reach for a cookie as a child and your mother slaps your hand, this stress system is activated to some extent and you are deterred from repeating that behavior. The mere threat of punishment becomes uncomfortable enough that you probably won’t try again without permission. As adults, most of us have been conditioned effectively enough to know not to steal or harm others simply due to the threat of punishment or negative consequence. This entire criminal justice system is premised on the ability to condition our behavior.

What happens when this “stress” system is hyperactive, i.e., when it is too quick to respond or it responds without adequate provocation from the environment? Researchers believe that individuals prone to panic attacks may suffer from a hyperactive ANS that is much too sensitive and causes experiences of panic and fear when the context does not warrant such a reaction. For these individuals, medications that suppress this stress system (also often used in cardiac patients) generally work well to stabilize the ANS. On the other hand, what happens when this system is underactive? What happens when an individual does not experience a sufficient flurry of hormones or physiological activation to produce discomfort? The result can be an underactive CNS and ANS, and the inability to effectively deter that individual merely with threats of punishment. As you will see below, the psychopath is characterized by this paucity of biochemical and physiological responses.

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?

A13: Psychopathy is a syndrome or pattern of behaviors and psychological traits that were characterized by Cleckley as having the following features:

Þ    Charming

Þ    Intelligent

Þ    Lack of nervousness

Þ    Untruthful

Þ    Insincere

Þ    Lack of remorse or shame

Þ    Inadequately motivated antisocial behavior

Þ    Poor judgment

Þ    Failure to learn from experience

Þ    Pathological egocentricity

Þ    Incapacity for love

Þ    Emotionally flat

Þ    Lack of insight

Þ    Unresponsiveness to relationships

There has been great confusion regarding the concept of psychopathy as opposed to sociopathy and   ASPD. Sociopathy is not a psychiatric classification; it is a social construct used often to describe individuals who have no regard for the law or social norms. Sociopaths are simply individuals who break the law, and there are no particular underlying mechanisms to explain their behavior. Often their behavior is described as being a result of a lack of socialization, but the concept of sociopathy has been historically poorly measured or characterized.   ASPD, on the other hand, is an Axis II diagnosis found in the DSM-IV. This diagnosis describes individuals who disobey authority and eventually the law with an early onset of defiant and deviant behavior. While psychopaths also generally fall into the category of ASPD, they are a particular subgroup, believed to differ from others in this category by virtue of deviations in physiological and brain functional measures.

Individuals thought to be psychopathic are not out-of-control, drooling, homicidal maniacs. Quite the contrary, they have been referred to as “reptile-men”, “automatons” or “mechanical men” because they appear to lack emotion and empathy for others. They are cool, calm, and collected. They obtain pleasure from risky behaviors, dangerous situations, and thrill seeking. The epitome of a psychopath is a serial murderer (although some serial murderers instead suffer from paranoid schizophrenia) who kills without remorse and achieves a thrill from the process itself.  They are also more likely to abuse drugs and alcohol; studies have reported that individuals with psychopathy and ASP are more sensitive to the rewarding properties of drugs and less sensitive to their adverse effects.

Psychopaths have been found to differ from nonpsychopathic controls in several physiological parameters. These indices include (a) EEG differences, (b) cognitive and neuropsychological impairment, and (c) electrodermal, cardiovascular, and other nervous system measures. In particular, psychopathic individuals have been found to show relatively slower wave activity in their EEG compared with controls, which may be related to differences in cognitive abilities. Relatively high levels of EEG slowing found in psychopathic subjects may reflect a maturational lag in brain function. Thus, EEG slowing among individuals who also demonstrate immature behavior and an inability to learn from experience reflects a developmental delay. EEG slowing among some psychopaths is consistent with findings of hypoaroused autonomic function and other differences in psychophysiologic parameters. Their need for external stimulation may be higher and more difficult to satisfy than in other populations due to a lower level of internal stimulation.  

When a sound is repeatedly introduced to subjects, the brain processes it
in predictable ways from the auditory nerve, through the brainstem and up
into higher cortical centers.  Electrophysiological recordings of this
process are called "evoked potentials" (EPs).  Research such as this study
have shown that subjects with a significant history of childhood aggression
and/or psychopathy process these stimuli less efficiently than those without
such a history, showing delays in the brain's response.  Along with findings
of an increased amount of slow wave activity in the EEG in aggressive
subjects, these neurophysiological findings suggest the presence of a
developmental lag in this group.

See Raine (1993).

The implications of many decades of research on psychopathy are that affected individuals do not condition the way most of us do. As explained in the previous question, most individuals’ behavioral patterns are conditioned by rewards and punishments. When a behavior results in a painful consequence, we are less likely to repeat that behavior. When a behavior results in a pleasurable consequence, that behavior is reinforced and likely repeated. In order to invoke this process, the physiological responses to environmental input that are necessary to produce the experience of stress must be intact. For example, as children, we are taught that when we engaged in behaviors that are forbidden, we would be punished for that behavior. This is the process of behavioral conditioning. The mere threat of a punishment produces the experience of anxiety, which is uncomfortable and avoidable. Having learned in childhood that certain behaviors are considered “wrong,” we are not likely to engage in them in adulthood for the same reasons. We are, thus, avoiding a negative consequence – the anxiety produced when doing something we know is wrong. Threats of punishment, and even lying, causes a chain of physiological responses, unleashed by the ANS, that make us feel uncomfortable and anxious, which is why we don’t often engage in “wrong” behaviors. Our criminal justice system’s notion of deterrence is based on these principles of behavioral conditioning. The problem with psychopaths, however, is that they do not condition through threats of punishment and are, therefore, not easily deterred using negative sanctions. Research, some of which is mentioned above, suggests that their ANSs are underactive and, consequently, not able to produce the appropriate anxiety responses to environmental input or stressors. Additional research suggests that their ANSs may be underaroused as a result of a disconnect within the CNS between the cortex (the part of the brain responsible for higher intellectual functions) and the limbic system (the region responsible for emotion, mood, memory, and other functions necessary for survival). As a result of their relatively low levels of physiological responsiveness and lack of anxiety, they are notoriously difficult to treat for their antisocial behavior and also for any co-occurring drug abuse disorders they develop.

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?

A14: Although both biological and environmental conditions are powerful predictors of antisocial behavior and drug abuse, neither are “causal” in a deterministic sense – they are probabilistic. The intensity and frequency of exposure to negative environmental conditions, and the number and severity of internal risk factors present, determine the extent to which an individual is liable or vulnerable to behavioral disorders in general. Inherently vulnerable individuals (by virtue of their genetic make-up or biological constitution) who are subsequently exposed to an adverse environment are at imminently greater risk, particularly when adverse external influences are cumulative over time. The cumulative presence of many of these factors can result in antisocial or drug-taking behaviors (or other psychopathology) by altering brain function, disengaging coping mechanisms and compromising ability to formulate and act on rational choices.

Research in neurobiology and behavioral genetics have demonstrated that individuals vary considerably with respect to their biological strengths (protective factors) and weaknesses (risks). Biological weaknesses or vulnerabilities are influential in an individual's risk for antisocial behavior. Rather than acting alone, however, this body of research suggests that these biological features operate by setting the stage for how adaptively an individual will respond to personal stressors. 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. Thus, although the probability of a pathological response is a function of the number of these individual risk factors present, the probability is even greater in the presence of an adverse environment with severe stressors.

So far, neurobiological research shows that stress, both internally and externally induced, affects neurological processes and behavioral outcomes during particular phases of development for better or for worse. The environment can contribute to changes in behavior by altering the following:

*        Neurotransmitter responses

*        CNS and behavioral activity levels

*        Blood flow and glucose metabolic rates in the brain

*        Development of neuronal connections over time

*        Psychoneuroimmunological responses

*        Density of autoreceptors affecting regulatory capabilities

*        Hormonal responses

*        Physiological responses and tone

Deviations in these biological processes often underlie many forms of psychopathology.

Social, economic, and physical deprivation, poverty, traumatic stress, family dysfunction, prenatal drug exposures, and other deleterious childhood experiences and environmental conditions all have a profound impact on brain function. Conversely, brain dysfunction has an impact on environmental or social responses to the individual, compounding the risk for an adverse outcome. Manifestations of these impacts are measurable in cognitive processes (e.g., attention deficits), behavioral patterns (e.g., CD), temperamental traits (e.g., impulsivity or sensation-seeking), psychophysiological indices (e.g., EEG or skin conductance) and/or neurochemical aberrations (e.g., serotonin or cortisol). Of relevance here is that these indicators of brain function are now known to be at least partially alterable by our environment in ways that may decrease liability for antisocial behavior and drug abuse. Brain functional substrates for these disorders are both genetically determined and environmentally influenced; thus, their presence can cumulatively alter an individual’s developmental trajectory to influence subsequent development and behavioral outcomes. Scientific examinations are needed to isolate the neurological effects of these factors, providing greater insight into specific brain-environment interactions. A few selected examples of this interaction are highlighted below.

Environmental Triggers

Þ    Pregnancy and birth complications

Þ    Child abuse and neglect

Þ    Lack of social and physical stimulation

Þ    PTSD and trauma

Þ    Learned helplessness and stress

Integrity of the internal environment of the developing fetus is strongly predictive of future outcomes in terms of organ function, anatomical features, cognitive ability, intelligence level, psychiatric status, and behavioral patterns. The mother’s experiences and mental state influence this internal environment and, consequently, play an active role in determining the range of abilities the child will have in interaction with his or her genetic make-up. Her nutritional intake, use of substances, and even stress levels directly affect fetal development. Hundreds of studies document the relationship between suboptimal prenatal conditions and later behavioral and psychological disorders. One of the most profound and preventable precipitants of psychopathology that occur during pregnancy is prenatal drug exposure. Animal and human studies indicate that repeated prenatal exposures to abusable drugs leads to disruptions in normal neurotransmitter function and may enhance development of tolerance and/or sensitization to later drug use in the offspring. Research suggests that prenatal exposure to alcohol, cocaine, and nicotine may either alone or additively contribute to executive cognitive deficits, neurological dysfunction, low academic achievement, impaired impulse control, and other syndromes which place individuals at increased risk for socially inappropriate and, in some cases, antisocial behaviors. Conditions that often prevail in the homes of children exposed prenatally to illicit drugs or excessive alcohol intake may further impair intellectual capacity and social ethical behavior, such as a chaotic environment, lack of appropriate stimulation, lack of parenting skills, mother with impaired mental functioning by virtue of her addiction, inappropriate developmental modeling, and abuse and neglect.

The social environment of a mother during pregnancy can also alter the prenatal biological environment, subsequently affecting outcomes for the offspring. Exposure to high levels of stress during pregnancy can compromise integrity of physiological, hormonal, and neurotransmitter systems developing in the fetus, subsequently increasing the risk for psychopathology in the child. Recent studies suggest that environmental stress during this period can activate genes linked to various mental problems. Increased activity of these genes is believed to create abnormal neural connections, causing neurons to fire in the absence of a trigger that may elicit feelings or behaviors that are out-of-context given environmental conditions. Children who experience high levels of stress, either in utero or in early life, may become sensitized to future stressful experiences and exhibit inappropriate emotions associated with mental disorders.

Several studies have identified multiple minor physical anomalies (MPAs)[1] in behavioral and developmental disorders associated with antisocial outcomes that are reflective of genetic defects or prenatal insults. High MPA counts were strongly predictive of short attention span, high-activity level and aggressive-impulsive behavior, in addition to hyperactivity in normal and clinical populations of boys. Kandel and her colleagues measured the number of MPAs at 11 to 13 years of age, and police records of criminal behavior were ascertained at 20 to 22 years of age. Recidivistic violent offenders evidenced an elevated level of MPAs compared to subjects with one violent offense and subjects with no violent offenses. Mednick and his colleagues further reported that MPAs appear to be strongly related to hyperactivity and later criminal involvement, but only in the presence of an unstable, nonintact family. They concluded that indices of perinatal problems relate to later violent crime, rather than to property crime, and may have as their basis some form of trauma occurring very early in life.

Perinatal conditions, which occur between the seventh month of pregnancy to 28 days after birth, include prematurity and delivery complications. These conditions may increase risk for negative outcomes, including impulsive and aggressive behavior, as a result of the increased incidence of fetal brain damage. Piquero and Tibbetts provided a thorough overview of research on the relationship between perinatal factors and criminal or antisocial behavior. The predominance of literature they review, in addition to their own research, shows support for the relationship, although there are some discrepancies. More importantly, however, are the studies they cite that suggest a strong interactive relationship between the effects of perinatal complications and the social environment on antisocial outcomes. They conclude from their review that “poor or deficient familial and socioeconomic environments may magnify the effects of pre/perinatal complications.” Piquero and Tibbetts surmise that perinatal complications may contribute to neuropsychological deficits that impede the socialization process. In the dual presence of neuropsychological impairment and a poor familial environment, the socialization process is further compromised, exponentially increasing risk for an antisocial outcome.

Social and physical stimulation, from mother-child bonds to visual and tactile explorations of the environment, is essential to develop and maintain proper brain function. Deprived of adequate sensory experiences, the brain atrophies and neural connections are lost; an impoverished environment where sensory stimulation is inadequate can decrease neural connections by 25% or more. When stimulation from the environment is inadequate, due either to sensory deprived conditions or physiological deficiencies within the brain, the tendency to seek stimulation elsewhere increases. Stimulation needs in children are primarily manifested in increased physical activity, often resulting in distractibility, constant motion, inability to sit still, and excessive physical contact with others, as seen in hyperactivity. As the child matures, however, high-stimulation needs may be met in more sophisticated ways by risk-taking activities, thrill- or novelty-seeking, drug use, criminal activity, and other excessive behaviors.  Thus, environmental stimulus deprivation can simulate a condition such as hyperactivity or sensation seeking by creating a deficiency state and increasing needs for external stimulation. There is evidence that brain function changes incurred through environmental enrichment, where complex and intensive stimulation is provided, may endure through adulthood.

Child abuse and other traumatic experiences play a distinct and significant role in the risk for behavioral disorders. What is less well known, however, is the impact of child abuse on the developing brain, which may actually mediate the behavioral response. Child abuse has been associated with alterations in neurotransmitter activity (e.g., serotonin) and stress hormone levels. Also, poor parenting has been related to low-serotonin levels in the child, which could be both environmentally and genetically transmitted. Furthermore, fewer neural connections, EEG abnormalities, and aberrant cortical development have been reported in individuals with a history of child abuse. The increase in hormone release associated with chronic stress can compound deficits in learning and memory by the damage “stress” hormones cause in the hippocampus, a brain structure responsible for memory and learning.  Later in life, the stress associated with traumatic events has been associated with social rank, self-esteem and competency in animals and humans. These findings help to explain the higher incidence of developmental delays and behavioral disorders in this population. Fortunately, there is speculation that high-quality parenting can minimize problems associated with abnormal levels of neurotransmitter and hormonal activity, regardless of whether the deficit was a function of genetics, environment, or a combination thereof.

The interaction between prenatal conditions and parenting is critical to behavioral outcomes. Babies exposed to prenatal or perinatal disturbances, or those simply predisposed to a difficult temperament, are often more troublesome to care for. While some prenatally or genetically disadvantaged babies sleep excessively, others are more volatile, temperamental and colicky, cry more frequently, do not develop normal sleep or eating patterns, and are difficult to soothe. Furthermore, delays in brain development and greater physical needs are often coupled with a lack of appropriate stimulation from their caretakers, particularly in cases where the mother is a drug abuser, a teenager, or unusually stressed or anxious; all conditions associated with improper prenatal care, drug exposure and pre/perinatal complications. As a result, these more “difficult” children commonly elicit harsher responses from their primary caretaker, who may not have the psychological or physical resources to cope with their baby’s special problems and needs. For example, adopted children who were at genetic risk by virtue of their biological mother’s antisocial behavior were found to be more likely to receive negative parenting. Thus, in a developmental sense, these children enter the world disadvantaged and, subsequently, experience harsh, inconsistent or inadequate parenting. Upon entering school, their difficulties are compounded and risk for antisocial outcomes heightened when they exhibit learning disabilities, failure in school, social isolation, and further parental rejection.

See Moffitt (1993).

Severe and/or chronic traumatic experiences throughout the life span can alter brain function by disrupting neurotransmitter and hormonal activity and metabolism. Separation from the mother and social isolation have been shown to increase vulnerability to drug abuse in the affected individual (or animal), with abnormalities in DNA synthesis, hormone responses, and neurotransmitter systems as the mediator of this effect.  PTSD has been specifically associated with low levels of serotonin activity and other neurotransmitters; PTSD is not only associated with conditions of battle, but with conditions in many inner cities. There is further evidence that severe stress during adolescence can damage coping responses by disrupting neurotransmitter responses. Parental divorce, for example, can have serious psychological and behavioral consequences, including problems in peer relationships and a high incidence of aggressive behavior and alcohol consumption. Studies cited above suggest that impairments may be due to changes in the secretion patterns of neurohormones induced by the stress of the parental divorce, thereby reducing adaptation to stress in the adolescent. Fortunately, several factors offer some protection from these deleterious conditions, including quality of the home life, relationships with others, and intimate bonds.

Evidently, exposure to highly stressful and/or novel situations can alter sensitivity of the brain’s dopamine reward system; the same system which mediates the rewarding effects of drugs of abuse. Recent studies shed light on individual differences in drug-seeking behavior by demonstrating that heightened sensitivity of this system, due to environmental stress or novelty, may increase susceptibility to abuse and addiction. Stress can switch genes on or off at the “wrong” times, leading to the development of abnormal networks of brain cell connections, which can result in, for example, excessive secretion of stress hormones. When levels of stress hormones are excessive, their presence increases sensitivity of dopamine neurons to drugs, further exacerbating the risk for drug abuse. Damage to key brain structures has also been associated with stress, producing irregularities in brain function that are similar to those associated with propensity to both drug abuse and impulsive-aggressive behavior. Consequences may include learning deficits, mood disturbances, drug abuse, tension, depression, and an inability to cope with external stressors, each of which is associated with antisocial outcomes.

Q15: What are the implications of this research for the criminal justice system and the offender?

A15: In order to determine the relevance and significance of biological perspectives for criminology, researchers must estimate the incidence of biological disorders among antisocial populations, identify etiologic mechanisms, assess the dynamic interaction among biological and socio-environmental factors, and determine whether improvements in behavior follow large‑scale therapeutic manipulations.

We are beginning to identify markers of antisocial behavior using biological tests (e.g., EEG slowing, body lead burden, neurotransmitter imbalance). While some of these correlations may prove to be spurious, several of these factors appear to influence an individual's risk status in substantial ways. Demands in the criminal justice system for evaluation of causal relationships are made in decisions regarding the granting of bail, release on personal recognizance, competency, guilty pleas, sentencing options, probation and parole, and proclivity to recidivate. Conclusions and prognoses regarding the role of biological factors, however, are not definitive at this time, regardless of the informational source.

To further establish the relevance of biology to criminology, we must demonstrate the ability to reliably predict antisocial behavior using a combination of biological and social variables. The central question thus becomes: Can we explain more of the variance in the incidence of antisocial behavior with an integrated approach than with an unidisciplinary perspective? Many clinicians and researchers have concluded that predicting antisocial behavior with social or legal variables is inherently unreliable. Prediction studies incorporating biological measures into sociological databases promises to significantly increase the predictive and explanatory power of conditions associated with antisocial behavior and enhance explanatory power.

A comprehensive study of the effects of numerous environmental and biological variables on criminal behavior, juvenile delinquency, and disciplinary problems was conducted by Denno. Denno concluded that “biological and environmental variables exert strong and independent influences on juvenile crime” and that “crime appears to be directly related to familial instability and, most important, a lack of behavioral control associated with neurological and central nervous system disorders.” She cautioned, however, that behavior should be predicted in terms of a series of probabilities of expected behavior, not in terms of cause and effect.  Future research into practical problems in criminology may find considerable solutions in an approach that neither neglects nor places undue emphasis on socio-environmental or biological features of behavior.

At the very least, the inclusion of biological measures holds promise in explaining individual variation within a social context. Why is it, for example, that not all children exposed to child abuse become violent as adults? Research suggests that whether child abuse contributes to violent behavior partially depends on the presence of a biological vulnerability, e.g., brain damage. Perhaps abused children without concomitant or resultant brain damage would be less aggressive and more in control of their impulses. Research yet to be conducted may also show that individuals with biological “disadvantages” respond with more violent or criminal behavior in a criminogenic environment than those equipped with biological “insulators,” for example, high intelligence or adequate serotonergic activity.

Treatment efforts that focus on the underlying mechanisms in antisocial behaviors will more likely succeed in reversing or redirecting these behavioral outcomes. Successful regimens attempt to comprehensively identify the unique underlying precursors of an individual's antisocial behavior and may employ a combination of pharmaceutical, behavioral, cognitive, and family therapies. Nevertheless, while a clinical approach to treatment and prevention may be achieved with knowledge of individual risks and vulnerabilities, global prevention and intervention programs can be implemented now to increase resiliency to prevailing risk factors in a population. Building safety nets, providing recourse for those without options, increasing availability of alternative modes of behavior, revitalizing neighborhoods, assembling multidisciplinary teams to intervene, and enhancing community involvement could have an immediate impact on the problem by providing insulation to those who are particularly “vulnerable.”  For example, recognition that a deprived environment can induce below normal levels of nervous system arousal, or that stress lowers serotonergic activity, may enhance our understanding of why some individuals under these circumstances develop an unusual need for stimulation, often expressed as risk-taking behaviors in the absence of more constructive alternatives. Manipulations of the social environment, therefore, may profoundly alter an individual’s biological stamina, possibly improving impulse control and coping mechanisms.

We are also closer to enacting prevention programs aimed at populations who are at risk for exposure to biological and socio-environmental hazards that are known to increase the incidence of behavioral problems. Factors that may prove to be important contributors to relevant behavioral disorders could subsequently be manipulated on a wide scale to prevent the onset of behavioral disorders in the general population. Early detection programs could be implemented by school systems, and parents could be educated to recognize signs of an impairment. Screening clinics, regulating environmental toxins, school programs, prenatal care facilities, and public educational programs are only a few of the preventative measures possible. The number of “risk” factors could, in essence, be reduced or minimized.

An excellent example of this strategy was suggested by Moffitt and her colleagues in their review of MPAs, that is, observable minor malformations that result from a disturbance in fetal development. MPAs are reflective of other hidden anomalies, such as CNS impairment, that may result from some perinatal trauma (e.g., illness, poor diet, drug use, or stress). A relatively large number of MPAs have been observed among hyperactive and violent populations. There is no acceptable mode of individual remediation in such cases, particularly because of the remote association of MPAs with behavior. These consistent observations, however, emphasize the need for a global effort to provide proper prenatal care. Such programs may reduce the incidence of developmental deficits related to behavioral disorders.

Criminal justice policies must be based on well-founded theories and findings that survive scientific scrutiny. The application of scientific findings to criminal justice programs that are well recognized and accepted by the discipline have more value than trial and error approaches in preventing or minimizing antisocial behavior. Although biological techniques in the assessment of human behavior are still under the microscope and definitive answers have yet to surface, the foregoing description of biological foundations for behavior provides evidence of their applicability and value. By undertaking a collaborative strategy, we can develop more effective prevention and therapeutic programs, and develop a legal system that reflects public consensus, meets human needs, and maintains an ethical and organized social structure.

Q16: What are the controversies surrounding this research?

A16: Critics of this research worry that, in looking for criminal predispositions, researchers rely on oversimplified views of genetic and biological influences and of criminal behavior. Critics also worry that even if this research is focused entirely on individuals and is apolitical on its face, it will be publicly perceived as supporting racial stereotypes and justifying repressive social policies. At the same time, some of the opposition to the research arises from a concern that such research may be used in efforts to establish racial differences in genetic predisposition or to justify conservative programs of social control.

The issues that arise in discussions of biological mechanisms in criminal behavior fall into two categories. One concerns the scientific, philosophical, and moral problems involved in claiming any sort of causal relationship between biology and crime. These problems raise questions about the ways in which the brain interacts with the physical and social environment, about the prospects for explaining voluntary actions in terms of neurobiological processes, and about the possibility of finding biological predispositions to behaviors that are, in essence, socially defined.

The other set of issues concerns the social and ethical implications of research on biology and crime. Critics and proponents of this research set it against the backdrop of two very different legacies. On the one hand, humanity has a long, dark history of “discovering” sources of inferiority in certain individuals or groups, then using the “discovery” to justify gross inequalities and coercive social programs. On the other hand, it has been a hallmark of enlightenment to recognize that undesirable traits and behaviors often arise from biological or psychiatric problems, rather than moral defects, and to offer humane treatments rather than to impose harsh punishments.

Advocates of this research hope that its findings will be used to prevent crime and violence by recognizing the warning signs and intervening before its onset, with benefits to both potential perpetrators and potential victims. Critics fear that the research will lead to large-scale neglect and abuse. Its actual or reported findings may convince legislators that social and economic reforms are doomed to failure because they attempt to apply social solutions to a biological problem. Critics also believe that viewing crime as a medical problem to be treated, rather than as a response to oppressive social and economic conditions or as a matter of individual choice, may result in policies that are patronizing, disrespectful, and highly coercive. On the other hand, advocates argue that if we continue to examine only 50% of the equation (the social causes), then we will continue to mistreat the problem and support programs with low success rates.

Finally, critics insist that biological research must be seen in the context of our racial history and racist attitudes. In our society, any research that links criminal behavior to biological features may be mistakenly seen as implicating the black community and contribute to its stigmatization. Many Americans see violent crime as a minority problem, in part because of the disproportionate number of African Americans in prison, and in part because of deep prejudices that make violent crime seem more characteristic of blacks than whites. Defenders of the research, however, deny that it must be captive to our racial history, and argue that it will ultimately do far more to alleviate than exacerbate racial tensions. Because this research focuses on both biological deviations and adverse social circumstances that trigger the expression of existing vulnerabilities, it may highlight the profound impact that adverse environmental factors can have. Thus, we may eventually be able to concentrate on and alleviate those social problems that are differentially and disproportionately distributed throughout our society and  which trigger underlying vulnerabilities and lead to an increased prevalence of various behavioral disorders.

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Diana H. Fishbein, Ph.D has a Ph.D. in Criminology with a concentration in Psychobiology from Florida State University. She currently directs the Transdisciplinary Behavioral Science Program for the Research Triangle   Institute (dfishbein@rti.org). Previously, she was Prevention Coordinator

Diana Fishbein, Ph.D. 
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