SWAP/DIRE Personality Disorder Test
The document "Identifying Personality Disorders that are Security Risks: Field Test Results" states:
"Certain clinical personality disorders, namely psychopathy, malignant narcissism, and borderline personality organization, can increase the likelihood of unreliable behavior, poor judgment, and compromised motivation to protect classified information and/or sensitive materials."
The Defense Personnel Security Research Center (PERSEREC) performed research to review and rescind Department of Defense Security Clearances. They used: a personality disorder screening tool (the Shedler-Westen Assessment Procedure [SWAP]) and a metric of security risk developed from Phase I (Dispositional Indicators of Risk Exposure [DIRE]).
According to swapassessment.org, "We have partnered with agencies of the United States Federal Government to develop a special edition of SWAP for security risk assessment. The National Security Edition is used to assess personnel for sensitive positions such as those requiring access to classified information."
"Certain clinical personality disorders, namely psychopathy, malignant narcissism, and borderline personality organization, can increase the likelihood of unreliable behavior, poor judgment, and compromised motivation to protect classified information and/or sensitive materials."
The Defense Personnel Security Research Center (PERSEREC) performed research to review and rescind Department of Defense Security Clearances. They used: a personality disorder screening tool (the Shedler-Westen Assessment Procedure [SWAP]) and a metric of security risk developed from Phase I (Dispositional Indicators of Risk Exposure [DIRE]).
According to swapassessment.org, "We have partnered with agencies of the United States Federal Government to develop a special edition of SWAP for security risk assessment. The National Security Edition is used to assess personnel for sensitive positions such as those requiring access to classified information."
Psychopath Brain Research
The following data is excerpted from Quora.com. Please see full original source for reference links.
What is the latest research on brain structure, chemistry, physiology and genetics as well as emerging theories regarding psychopathy?
By Athena Walker
Updated Aug 19, 2017
Part 1 of 2: What is the latest research on brain structure, chemistry, physiology and genetics as well as emerging theories regarding psychopathy?
This answer is a collaboration between Athena Walker and Dr. Natalie Engelbrecht, BA MSc ND RP. As such, it is divided between two posts. The first half is presented in Athena Walker’s post with a link to Natalie Engelbrecht’s, and the second half is presented in Natalie Engelbrecht’s post with a link to Athena Walker’s. Please start with Athena Walker’s post. Both posts were a collaboration, with neither being written solely by either individual.
Care was taken to use the most up-to-date research (<5 years)—older if nothing recent was available (<15 years)—and in places with appropriate seminal work. It is important to recognize that in the DSM-V, psychopathy is referred to as antisocial personality disorder (ASPD). However, researchers such as Blair have indicated that the two are not synonymous. That said, all attempts have been made to utilize studies that are indicative of psychopathy, not ASPD or sociopathy; however, researchers still utilize a variety of terms when referring to psychopathy, making it challenging at times to identify the population they used in their study.
Psychopathy as a Neurobiological Variant
Psychopathy is a born condition. It is marked by a unique formation of the brain that results in a different experience of emotions. Most emotions in a psychopath are very blunted, and some are missing entirely. Psychopathy is not predicated on abuse, neglect, or trauma, though these things can have an effect on the manifestation of traits within the person that has a psychopathic brain.
ASPD is a personality disorder that is characterized by antisocial behaviors. This makes it a sweeping condition that is difficult to nail down as to causation and reasoning, short of saying that environment is involved, as well as factors such as abuse, and neglect.
Personality characteristics have been demonstrated to be due to epigenetic influences on genes. As such, it is necessary to consider psychopathy as researchers such as Dutton (a research psychologist) and Fallon (a neuroscientist), and Blair (a researcher responsible for one of the two major theories on psychopathy) have done. This has been via separating it away from mental conditions to a variation in neurological formation. As such psychopathy is not in the DSM-V because it is not a mental illness, but that the antisocial aspects that may accompany it are.
Imagining Genetics – fuses Genotype with Phenotype
You need both the genes and changes in brain pattern to result in psychopathy. By themselves neither will result in psychopathy.
PET scan: Measures the amount of sugar that is taken up. A PET gives the most amount of information, but is the most expensive to do—and is also no longer done, but was used in previous studies.
fMRI: Measures the amount of blood flow in each area. An fMRI is moderately expensive and gives more information than a SPECT scan, but less than a PET scan.
SPECT scan: measures blood flow in the brains and gives the least amount of information, but is the cheapest scan to do.
Brain Structure (Phenotype)
Introduction
The use of brain scan technology to study mental health and disease began in the 1990s. Research has made correlations between areas of the brain and symptoms like increased anxiety or decreased empathy, and have begun to map out phenology of different personalities and disorders. The field of psychopathy has seen rapid growth in the use of neuroimaging to understand the condition. In some cases scientists are beginning to be able to predict pathology and personalities based on brain scans; however due to brain plasticity, controversy exists as to whether the personality alters the brain or the brain changes themselves create the personality.
James Fallon, a leading neuroscientist at the forefront of psychopathy has been exploring the map of the psychopathic mind for the better part of two decades. Fallon describes a great loop that starts in the front of the brain including the parahippocampal gyrus and the amygdala and other regions tied to emotion and impulse control and empathy. Under certain circumstances these regions light up dramatically on a neurotypical person’s MRI scan, but are darker on a psychopath’s.
Brain function structural models of psychopathy
Two researchers, Blair and Kiehl have proposed two distinctive but prominent models on the neurological origins of psychopathy. Both researchers suggest that there are changes in the function and structure in specific emotional processing areas of the brain. Both models suggest dysfunction of the amygdala and orbitofrontal cortex, however, Khiel’s model also includes additional paralympic region alterations, such as the anterior superior temporal gyrus and the anterior and posterior cingulate cortex.
The key points of the Blair model are that the amygdala and ventromedial prefrontal cortex alterations are indicative of psychopathy. These brain regions allow for communication between the thinking and feeling centers of the brain. Blair further states that although psychopaths can sync normally, they do not integrate feelings appropriately. A metaphor to describe Blair’s model is that psychopaths know the words but not the music, and this is supported by behavioral and imaging data. Blair’s model indicates that while both psychopaths and neurotypicals recognize that running into a burning building is dangerous, only the neurotypical feels negative emotions associated with the act.
Paralympic hypothesis of psychopathy: Kiehl Model
Kiehl’s model of psychopathy developed via research of the behavior changes associated with acquired brain injuries that resulted in psychopathic behavior. This led the researchers to develop the term pseudopsychopathy and acquired sociopathic personality (or secondary psychopathy). His model states that it is a result of structural and functional abnormalities in the paralimbic structures of the brain, and that psychopathy has a developmental course. While this model is not related to primary psychopathy, it does however demonstrate the behavioral changes associated with alterations in brain structure, and function in the paralimbic structures.
Changes in Brain Region Connectivity in Psychopathy
It is important to understand that research shows not only structural changes, but also diminished activity in areas of the brain, including diminished connectivity between areas of the brain. It is a combination of these factors that result in the personality that is unique to psychopaths. In 2011 Kiehl, Joseph Newman (a heavyweight in psychopathy) and colleagues demonstrated via imaging that psychopathy is associated with reduced structural integrity in the right uncinate fasciculus, the primary white matter connection between the vmPFC and anterior temporal lobe. The team further demonstrated that psychopathy is associated with reduced functional connectivity between the vmPFC and the amygdala as well as between the vmPFC and the medial parietal cortex. These findings indicate that diminished vmPFC connectivity is a characteristic neurobiological feature of psychopathy. The study’s most important finding centered on impairments in the link between the ventromedial prefrontal cortex (a control node for regulating emotion, threats, decision-making and social behavior) and the amygdala—a locus of emotional processing.
What is the latest research on brain structure, chemistry, physiology and genetics as well as emerging theories regarding psychopathy?
By Athena Walker
Updated Aug 19, 2017
Part 1 of 2: What is the latest research on brain structure, chemistry, physiology and genetics as well as emerging theories regarding psychopathy?
This answer is a collaboration between Athena Walker and Dr. Natalie Engelbrecht, BA MSc ND RP. As such, it is divided between two posts. The first half is presented in Athena Walker’s post with a link to Natalie Engelbrecht’s, and the second half is presented in Natalie Engelbrecht’s post with a link to Athena Walker’s. Please start with Athena Walker’s post. Both posts were a collaboration, with neither being written solely by either individual.
Care was taken to use the most up-to-date research (<5 years)—older if nothing recent was available (<15 years)—and in places with appropriate seminal work. It is important to recognize that in the DSM-V, psychopathy is referred to as antisocial personality disorder (ASPD). However, researchers such as Blair have indicated that the two are not synonymous. That said, all attempts have been made to utilize studies that are indicative of psychopathy, not ASPD or sociopathy; however, researchers still utilize a variety of terms when referring to psychopathy, making it challenging at times to identify the population they used in their study.
Psychopathy as a Neurobiological Variant
Psychopathy is a born condition. It is marked by a unique formation of the brain that results in a different experience of emotions. Most emotions in a psychopath are very blunted, and some are missing entirely. Psychopathy is not predicated on abuse, neglect, or trauma, though these things can have an effect on the manifestation of traits within the person that has a psychopathic brain.
ASPD is a personality disorder that is characterized by antisocial behaviors. This makes it a sweeping condition that is difficult to nail down as to causation and reasoning, short of saying that environment is involved, as well as factors such as abuse, and neglect.
Personality characteristics have been demonstrated to be due to epigenetic influences on genes. As such, it is necessary to consider psychopathy as researchers such as Dutton (a research psychologist) and Fallon (a neuroscientist), and Blair (a researcher responsible for one of the two major theories on psychopathy) have done. This has been via separating it away from mental conditions to a variation in neurological formation. As such psychopathy is not in the DSM-V because it is not a mental illness, but that the antisocial aspects that may accompany it are.
Imagining Genetics – fuses Genotype with Phenotype
You need both the genes and changes in brain pattern to result in psychopathy. By themselves neither will result in psychopathy.
PET scan: Measures the amount of sugar that is taken up. A PET gives the most amount of information, but is the most expensive to do—and is also no longer done, but was used in previous studies.
fMRI: Measures the amount of blood flow in each area. An fMRI is moderately expensive and gives more information than a SPECT scan, but less than a PET scan.
SPECT scan: measures blood flow in the brains and gives the least amount of information, but is the cheapest scan to do.
Brain Structure (Phenotype)
Introduction
The use of brain scan technology to study mental health and disease began in the 1990s. Research has made correlations between areas of the brain and symptoms like increased anxiety or decreased empathy, and have begun to map out phenology of different personalities and disorders. The field of psychopathy has seen rapid growth in the use of neuroimaging to understand the condition. In some cases scientists are beginning to be able to predict pathology and personalities based on brain scans; however due to brain plasticity, controversy exists as to whether the personality alters the brain or the brain changes themselves create the personality.
James Fallon, a leading neuroscientist at the forefront of psychopathy has been exploring the map of the psychopathic mind for the better part of two decades. Fallon describes a great loop that starts in the front of the brain including the parahippocampal gyrus and the amygdala and other regions tied to emotion and impulse control and empathy. Under certain circumstances these regions light up dramatically on a neurotypical person’s MRI scan, but are darker on a psychopath’s.
Brain function structural models of psychopathy
Two researchers, Blair and Kiehl have proposed two distinctive but prominent models on the neurological origins of psychopathy. Both researchers suggest that there are changes in the function and structure in specific emotional processing areas of the brain. Both models suggest dysfunction of the amygdala and orbitofrontal cortex, however, Khiel’s model also includes additional paralympic region alterations, such as the anterior superior temporal gyrus and the anterior and posterior cingulate cortex.
The key points of the Blair model are that the amygdala and ventromedial prefrontal cortex alterations are indicative of psychopathy. These brain regions allow for communication between the thinking and feeling centers of the brain. Blair further states that although psychopaths can sync normally, they do not integrate feelings appropriately. A metaphor to describe Blair’s model is that psychopaths know the words but not the music, and this is supported by behavioral and imaging data. Blair’s model indicates that while both psychopaths and neurotypicals recognize that running into a burning building is dangerous, only the neurotypical feels negative emotions associated with the act.
Paralympic hypothesis of psychopathy: Kiehl Model
Kiehl’s model of psychopathy developed via research of the behavior changes associated with acquired brain injuries that resulted in psychopathic behavior. This led the researchers to develop the term pseudopsychopathy and acquired sociopathic personality (or secondary psychopathy). His model states that it is a result of structural and functional abnormalities in the paralimbic structures of the brain, and that psychopathy has a developmental course. While this model is not related to primary psychopathy, it does however demonstrate the behavioral changes associated with alterations in brain structure, and function in the paralimbic structures.
Changes in Brain Region Connectivity in Psychopathy
It is important to understand that research shows not only structural changes, but also diminished activity in areas of the brain, including diminished connectivity between areas of the brain. It is a combination of these factors that result in the personality that is unique to psychopaths. In 2011 Kiehl, Joseph Newman (a heavyweight in psychopathy) and colleagues demonstrated via imaging that psychopathy is associated with reduced structural integrity in the right uncinate fasciculus, the primary white matter connection between the vmPFC and anterior temporal lobe. The team further demonstrated that psychopathy is associated with reduced functional connectivity between the vmPFC and the amygdala as well as between the vmPFC and the medial parietal cortex. These findings indicate that diminished vmPFC connectivity is a characteristic neurobiological feature of psychopathy. The study’s most important finding centered on impairments in the link between the ventromedial prefrontal cortex (a control node for regulating emotion, threats, decision-making and social behavior) and the amygdala—a locus of emotional processing.
By Natalie Engelbrecht, Psychotherapist
Updated Mar 10, 2017
Part 2 of 2
Changes to Specific Areas of the Brain that Relate to Psychopathy
Amygdala
Location: Studies have revealed that the amygdala is not a homogeneous structure and can be differentiated into approximately 13 nuclei. Although the functional specificity of the nuclei in the human amygdala remains unclear, considerable evidence from animal studies suggests that several nuclei of the amygdala are involved in the processing of emotion. For example seminal research demonstrated that monkeys with damaged amygdalas have been shown to lack fear cue processing, and attempt to pick up live cobras.
Function: Significant correlations were found between reduced amygdala volumes and increased total and facet psychopathy scores, with correlations strongest for the affective and interpersonal facets of psychopathy.
Psychopath Phenology: Individuals with psychopathy showed significant bilateral volume reductions in the amygdala compared with controls (left, 17.1%; right, 18.9%). Surface deformations were localized in regions in the approximate vicinity of the basolateral, lateral, cortical, and central nuclei of the amygdala.
This article introduces a novel hypothesis regarding amygdala function in psychopathy. The first part of this article introduces the concept of psychopathy and describes the main cognitive and affective impairments demonstrated by this population; that is, a deficit in fear-recognition, lower conditioned fear responses and poor performance in passive avoidance, and response-reversal learning tasks. Evidence for amygdala dysfunction in psychopathy is considered with regard to these deficits; however, the idea of unified amygdala function is untenable. A model of differential amygdala activation in which the basolateral amygdala (BLA) is underactive while the activity of the central amygdala (CeA) is of average to above average levels is proposed to provide a more accurate and up-to-date account for the specific cognitive and emotional deficits found in psychopathy. In addition, the model provides a mechanism by which attentional-based models and emotion-based models of psychopathy can coexist. Data to support the differential amygdala activation model are provided from studies from both human and animal research. Supporting evidence concerning some of the neurochemicals implicated in psychopathy is then reviewed. Implications of the model and areas of future research are discussed. (PsycINFO Database Record (c) 2012 APA, all rights reserved).
A model of differential amygdala activation in psychopathy.
Insula
Location: Located deep in the cerebral cortex.
Function: Processing of disgust cues is not believed to rely upon amygdala; rather the relevant circuitry is thought to be the anterior insular cortex. The insula exhibits higher activity when neurotypicals make decisions and difficult personal moral dilemmas that they consider as repugnant acts.
Psychopath Phenology: Hypofunctioning in psychopathy.
Nucleus Accumbens
Location: In the basal forebrain rostral to the preoptic area of the hypothalamus.
Function: Plays a central role in the reward circuit. Its operation is based chiefly on two essential neurotransmitters: dopamine (promotes desire), and serotonin (satiety and inhibition).
Psychopath Phenology: The volume of the nucleus accumbens was 13% smaller in psychopathy. The atypical morphology consisted of predominant anterior hypotrophy bilaterally.
Orbitofrontal Cortex
Location: The part of the prefrontal cortex that is positioned directly over the orbits or eye sockets. It is located at the base of the frontal lobe.
Function: Social interactions, inhibition of impulsive behavior, ethics, morality, reward and punishment, regret, and projection of future outcomes based on implied expectations of planned near term actions. Involved in the regulation of many social functions, which include ethics and morality.
Psychopath Phenology: Lower activity in psychopathy.
Note: The terms Orbitofrontal Cortex and Prefrontal Cortex in research are sometimes used interchangeably, and at other times, ‘ventromedial prefrontal cortex’ is used to describe a broad area in the lower (ventral) central (medial) region of the prefrontal cortex, of which the medial orbitofrontal cortex constitutes the lowermost part.
Ventromedial Prefrontal Cortex (Lower)
Location: The frontal lobe, located at the front of the brain, is one of the four major lobes of the cerebral cortex.
Function: The frontal lobe contains most of the dopamine-sensitive neurons in the cerebral cortex. The dopamine system is associated with reward, short term memory, planning and motivation. The function of the frontal lobe involves the ability to project future consequences resulting from current actions, the choice between good and bad actions (or better and best) (also known as conscience), the override and suppression of socially unacceptable responses, and the determination of similarities and differences between things or events. The vmPFC is critical in regulating emotion, threats, decision-making and social behavior. Furthermore, the vmPFC also plays an important part in integrating longer non-task-based memories stored across the brain. These are often memories associated with emotions derived from input from the brain’s limbic system. The frontal lobe modifies those emotions to generally fit socially acceptable norms. It is known as the ethics and morality section of the brain.
Psychopath Phenology: Notice that the normal scan shows much more activity (yellow and red) in the lower frontal lobe than Fallon’s (mostly blue).
Conclusion
Brain structural and functional changes in psychopathy suggest that psychopathic individuals have a different way of seeing the world. Further research suggests they may use alternative strategies—such as cognitive empathy and rationality—more than neurotypicals use to make moral judgments. Much of the current research presents psychopathy brain alterations as pathological. Words like “healthy people” (meaning neurotypicals), “brain damage” and “brain dysfunction” serve to bias readers and researchers to view psychopathy as a dysfunction. As psychopathy is inherited and not caused by environmental triggers such as abuse, the word variant may be a better alternative, and lead to less bias.
Brain Chemistry Difference of Psychopathy.
High resolution PET and fMRI scans suggest that alterations in the function of the brain’s reward system may contribute to psychopathy.
Research indicates that dopamine genes leading to alterations in an increased amount of dopamine released in comparison with neurotypicals brains is associated with psychopathy. In fact research indicated that psychopaths release four times more dopamine in the nucleus accumbens than neurotypicals.
Dopamine plays important roles in executive functions, motor control, motivation, arousal, reinforcement, and reward. Studies found that increases in dopamine resulted in a trait aggression and impulsive-antisocial psychopathic traits. Further, an increase in dopamine reduces a hyper-altruistic tendency, altering it to prefer harming others over harming oneself.
Research of the gene 5-HIAA also indicates lower levels of serotonin occur in psychopathy. Studies demonstrated that a decrease in serotonin resulted in a decrease in harm aversion for both self and others.
Psychopathy also demonstrates higher methylation of oxytocin resulting in lower oxytocin levels. Lower circulating oxytocin results in decreased in interpersonal empathy. Although known for increasing bonding and trust, recent studies found that people who were given oxytocin had more envy and gloating during a game of chance. It appears that oxytocin increases both negative and positive emotions. Thus researchers are unclear as of yet whether the effect on increasing oxytocin will be to make a psychopath more social, as well as enhancing anger and aggression.
Genes:
Introduction
Fourteen years ago (2003) the human genome was fully sequenced (in the year 2000 a rough draft was first identified). With this momentous discovery, the genetic basis of some of the most common disorders have begun to be revealed. One area of such research has been the genetics associated with psychopathy. Twin studies do support that psychopathy is strongly heritable. However no single SNP has shown a large or even moderate effect size for psychopathy. The idea of nature/ nurture is outdated. Instead it seems the effect of genes for psychopathy appears to be both polymorphic (tendencies are conferred by multiple genes of small effect size that probabilistically increase the risk for poor behavioural outcome), as well as epistatic (where one gene interacts with another gene at a different location) and epigenetic (environmental buffers that can be used to moderate the effects of risk genes).
There are no good genes or bad genes, but there are alleles that are associated with violence and also a lack of empathy. For example antisocial behaviour (AB) is strongly heritable for callous-unemotional traits in children. AB+/ CU+ children show low emotional reactivity to punishment and distress, as well as poor ability to empathize with others. On the other hand non-callous AB (AB+/CU–) children show mainly environmental influences for their antisocial behaviour. They are emotionally reactive to threat, and are created via environmental risk influences (such as harsh parenting) epigenetically driving the expression of antisocial behaviour for this group. However, certain genes create a significant risk for violence when activated via appropriate epigenetic factors. Studies demonstrate that it is unlikely that genes directly code for violence; rather, allelic variations are responsible for individual differences in neurocognitive functioning that, in turn, may determine differential predisposition to violent behavior. Of the genes associated with psychopathy, MAOA-L is the most well-known and was among the first evidence that the variant MAOA-L interacts with childhood maltreatment to modulate antisocial tendencies (Caspi et al, 2002). “Specifically, severely maltreated participants carrying the low-activity allele of the MAOA gene displayed the highest scores in disposition toward violence and antisocial personality disorder scores, and demonstrated the greatest proportions of adolescent conduct disorder and convictions due to violent behavior.” (Buades-Rotger & Gallardo-Pujol, 2014). Recent research suggests that genetic vulnerability to violence conferred by the low-activity allele of MAOA-L variant may only become evident in the presence of environmental triggers of maltreatment. In favorable conditions, genetic predisposition alone may be of little consequence for behavior.
Gene & Their Associated SNPs (alphabetical order)
5-HTTLPR (serotonin transporter gene)
SNP: rs25531 (G;G) The long allele of the serotonin transporter gene is a potential risk factor for psychopathy. It is associated with less pain sensitivity.
ARL6IP6 (ADP-ribosylation-like factor 6 interacting protein 6 )
Associated with autistic psychopathy (form of autism spectrum disorder that is less severe than other forms, characterized by difficulty with social interaction and communication and by repetitive behavior or restricted interests) in childhood.
SNP rs11682518
DRD2 and DRD4
Positively correlated with a continuously coded psychopathic personality traits scale.
HTR1B (Serotonin 1B Receptor Gene)Serotonin 1B Receptor Gene (HTR1B)
Methylation as a Risk Factor for Callous-Unemotional Traits in Antisocial Boys. One neurochemical system that has been implicated both theoretically and empirically in CU traits and psychopathy is the serotonin system. For example, recent research identified an association between SNPs in the genes encoding serotonin receptor 2A (HTR2A) and serotonin receptor 1B (HTR1B) as well as CU traits in children with antisocial behaviour problems.
HTR1B is of particular interest because it has been found to be linked with behaviors and characteristics commonly associated with CU traits. Most notable are the animal studies which have demonstrated that mice without the serotonin 1B receptor gene show significantly elevated levels of aggression and lower levels of anxiety; both of which are typically associated with psychopathy. Studies in humans have also found an association between HTR1B and impulsive aggression, suggesting that serotonin 1B receptors may be involved in the control of aggression and impulsivity in humans.
SNP rs11568817 (T;T)
Associated with traits linked with ‘psychopathy’ including alcohol dependence, self-reported anger and hostility in young men, and autism spectrum disorder which is characterized by deficits in empathy that overlap those found in people with high CU traits. However, as psychopaths have been shown to be immune to dependence on addictive substances, it is unclear whether this gene is present in psychopathy, or if it may be a genetic marker for ASPD, which does have significant issues with substance dependence.
HTR2A (serotonin receptor 2A)
Provoked aggression associated with primary psychopathy traits. Hostility, Anger and Physical Aggression—but not verbal aggression—were associated with this gene, but only for provoked incidents.
SNP rs7322347 (T;T)
MAOA-L (Monoamine oxidase A)
“MAO-A has been named the ‘warrior gene’, and also more unfavourably the ‘psycho gene’. The gene is a variation of a gene on the X chromosome and therefore inherited from your mother. Females have two X chromosomes and males have an X and a Y chromosome. Mothers always pass an X chromosome on to their children. While if a father passes on his X chromosome (leading to a pair of X chromosomes and a female offspring) or his Y chromosome (leading to one X and one Y chromosomes and a male offspring).
This variation occurs in the X chromosome gene that produces monoamine oxidase A (MAOA), an enzyme in the brain that breaks down the neurotransmitters such as noradrenaline, adrenaline, serotonin, and dopamine.
People with the low-activity MAO-A gene (2R, 3R) are overall more prone to violence, impulsiveness and aggression. Specifically, when people with the MAOA-L feel very provoked or socially isolated their aggression will come out. Again, from an evolutionary perspective, this makes sense; a warrior needs to respond to threat, rather than act in a chaotic manner. Research demonstrates that low-activity MAO-A people are more likely to take revenge for someone who does something to leave them in a bad situation; however they do not act on small misdeeds.
Those with MAOA-L also showed hyperresponsiveness of the amygdala during tasks such as copying facial expressions. This accounts for an increased ability in this group to recognize emotions and also mimic them (the psychopathic mask).”
Natalie Engelbrecht's answer to What are the effects of having MAOA?
What are the effects of having MAO-A? Scientists believe it leads to impulsive behavior (such as as hypersexuality), sleep disorders, mood swings, and violent tendencies.
SNP: rs909525: Warrior; M: C= 3 allele; F: CC= 3 allele
SNP: rs12551906(G;G)
SNP: rs10865864 (G;G)
SNP: rs151997 (T;T)
OXTR (oxytocin receptor gene)
Polymorphisms in the oxytocin receptor gene are associated with the development of psychopathy. Evidence suggests that epigenetic changes in the OXT receptor gene (OXTR) are associated with lower circulating OXT and social–cognitive difficulties. Oxytocin promotes emotional and cognitive aspects of empathy; however increasing oxytocin can have the effect of increasing aggression.
SNP: rs53576 (A;A) Associated with lack of empathy.
SNP: rs2254298 (A;A) Smaller amygdala volume, both right and left sides.
SNP: rs1042778(T;T) Polymorphisms in the oxytocin receptor gene are associated with the development of psychopathy.
SNP: rs237887 (A;A) Lower emotional empathy.
SNP: rs4686302 (T;T) Lower emotional empathy.
Other Top Potential SNPs: rs124111132; rs7531603; rs2514788; rs4383690; rs6846114; rs2376016; rs2311846; rs11088618; rs41516949; rs7640807; rs1490666; rs293844; rs4241597; 6446569; rs1441990; rs1893815; rs11637779; rs10859716; rs1785633; rs4479686; rs10050093; rs12647756; rs1345959; rs13064369; rs8059321; rs6560704
In conclusion
Emerging research in psychopathy has begun to focus on psychopathy as a normal variant of neurotypical personality and brain function. Genetic brain scans and brain chemistry are all lending to this turn in the tides form psychopathy as a mental illness to psychopathy as a unique personality.
Summary
Updated Mar 10, 2017
Part 2 of 2
Changes to Specific Areas of the Brain that Relate to Psychopathy
Amygdala
Location: Studies have revealed that the amygdala is not a homogeneous structure and can be differentiated into approximately 13 nuclei. Although the functional specificity of the nuclei in the human amygdala remains unclear, considerable evidence from animal studies suggests that several nuclei of the amygdala are involved in the processing of emotion. For example seminal research demonstrated that monkeys with damaged amygdalas have been shown to lack fear cue processing, and attempt to pick up live cobras.
Function: Significant correlations were found between reduced amygdala volumes and increased total and facet psychopathy scores, with correlations strongest for the affective and interpersonal facets of psychopathy.
Psychopath Phenology: Individuals with psychopathy showed significant bilateral volume reductions in the amygdala compared with controls (left, 17.1%; right, 18.9%). Surface deformations were localized in regions in the approximate vicinity of the basolateral, lateral, cortical, and central nuclei of the amygdala.
This article introduces a novel hypothesis regarding amygdala function in psychopathy. The first part of this article introduces the concept of psychopathy and describes the main cognitive and affective impairments demonstrated by this population; that is, a deficit in fear-recognition, lower conditioned fear responses and poor performance in passive avoidance, and response-reversal learning tasks. Evidence for amygdala dysfunction in psychopathy is considered with regard to these deficits; however, the idea of unified amygdala function is untenable. A model of differential amygdala activation in which the basolateral amygdala (BLA) is underactive while the activity of the central amygdala (CeA) is of average to above average levels is proposed to provide a more accurate and up-to-date account for the specific cognitive and emotional deficits found in psychopathy. In addition, the model provides a mechanism by which attentional-based models and emotion-based models of psychopathy can coexist. Data to support the differential amygdala activation model are provided from studies from both human and animal research. Supporting evidence concerning some of the neurochemicals implicated in psychopathy is then reviewed. Implications of the model and areas of future research are discussed. (PsycINFO Database Record (c) 2012 APA, all rights reserved).
A model of differential amygdala activation in psychopathy.
Insula
Location: Located deep in the cerebral cortex.
Function: Processing of disgust cues is not believed to rely upon amygdala; rather the relevant circuitry is thought to be the anterior insular cortex. The insula exhibits higher activity when neurotypicals make decisions and difficult personal moral dilemmas that they consider as repugnant acts.
Psychopath Phenology: Hypofunctioning in psychopathy.
Nucleus Accumbens
Location: In the basal forebrain rostral to the preoptic area of the hypothalamus.
Function: Plays a central role in the reward circuit. Its operation is based chiefly on two essential neurotransmitters: dopamine (promotes desire), and serotonin (satiety and inhibition).
Psychopath Phenology: The volume of the nucleus accumbens was 13% smaller in psychopathy. The atypical morphology consisted of predominant anterior hypotrophy bilaterally.
Orbitofrontal Cortex
Location: The part of the prefrontal cortex that is positioned directly over the orbits or eye sockets. It is located at the base of the frontal lobe.
Function: Social interactions, inhibition of impulsive behavior, ethics, morality, reward and punishment, regret, and projection of future outcomes based on implied expectations of planned near term actions. Involved in the regulation of many social functions, which include ethics and morality.
Psychopath Phenology: Lower activity in psychopathy.
Note: The terms Orbitofrontal Cortex and Prefrontal Cortex in research are sometimes used interchangeably, and at other times, ‘ventromedial prefrontal cortex’ is used to describe a broad area in the lower (ventral) central (medial) region of the prefrontal cortex, of which the medial orbitofrontal cortex constitutes the lowermost part.
Ventromedial Prefrontal Cortex (Lower)
Location: The frontal lobe, located at the front of the brain, is one of the four major lobes of the cerebral cortex.
Function: The frontal lobe contains most of the dopamine-sensitive neurons in the cerebral cortex. The dopamine system is associated with reward, short term memory, planning and motivation. The function of the frontal lobe involves the ability to project future consequences resulting from current actions, the choice between good and bad actions (or better and best) (also known as conscience), the override and suppression of socially unacceptable responses, and the determination of similarities and differences between things or events. The vmPFC is critical in regulating emotion, threats, decision-making and social behavior. Furthermore, the vmPFC also plays an important part in integrating longer non-task-based memories stored across the brain. These are often memories associated with emotions derived from input from the brain’s limbic system. The frontal lobe modifies those emotions to generally fit socially acceptable norms. It is known as the ethics and morality section of the brain.
Psychopath Phenology: Notice that the normal scan shows much more activity (yellow and red) in the lower frontal lobe than Fallon’s (mostly blue).
Conclusion
Brain structural and functional changes in psychopathy suggest that psychopathic individuals have a different way of seeing the world. Further research suggests they may use alternative strategies—such as cognitive empathy and rationality—more than neurotypicals use to make moral judgments. Much of the current research presents psychopathy brain alterations as pathological. Words like “healthy people” (meaning neurotypicals), “brain damage” and “brain dysfunction” serve to bias readers and researchers to view psychopathy as a dysfunction. As psychopathy is inherited and not caused by environmental triggers such as abuse, the word variant may be a better alternative, and lead to less bias.
Brain Chemistry Difference of Psychopathy.
High resolution PET and fMRI scans suggest that alterations in the function of the brain’s reward system may contribute to psychopathy.
Research indicates that dopamine genes leading to alterations in an increased amount of dopamine released in comparison with neurotypicals brains is associated with psychopathy. In fact research indicated that psychopaths release four times more dopamine in the nucleus accumbens than neurotypicals.
Dopamine plays important roles in executive functions, motor control, motivation, arousal, reinforcement, and reward. Studies found that increases in dopamine resulted in a trait aggression and impulsive-antisocial psychopathic traits. Further, an increase in dopamine reduces a hyper-altruistic tendency, altering it to prefer harming others over harming oneself.
Research of the gene 5-HIAA also indicates lower levels of serotonin occur in psychopathy. Studies demonstrated that a decrease in serotonin resulted in a decrease in harm aversion for both self and others.
Psychopathy also demonstrates higher methylation of oxytocin resulting in lower oxytocin levels. Lower circulating oxytocin results in decreased in interpersonal empathy. Although known for increasing bonding and trust, recent studies found that people who were given oxytocin had more envy and gloating during a game of chance. It appears that oxytocin increases both negative and positive emotions. Thus researchers are unclear as of yet whether the effect on increasing oxytocin will be to make a psychopath more social, as well as enhancing anger and aggression.
Genes:
Introduction
Fourteen years ago (2003) the human genome was fully sequenced (in the year 2000 a rough draft was first identified). With this momentous discovery, the genetic basis of some of the most common disorders have begun to be revealed. One area of such research has been the genetics associated with psychopathy. Twin studies do support that psychopathy is strongly heritable. However no single SNP has shown a large or even moderate effect size for psychopathy. The idea of nature/ nurture is outdated. Instead it seems the effect of genes for psychopathy appears to be both polymorphic (tendencies are conferred by multiple genes of small effect size that probabilistically increase the risk for poor behavioural outcome), as well as epistatic (where one gene interacts with another gene at a different location) and epigenetic (environmental buffers that can be used to moderate the effects of risk genes).
There are no good genes or bad genes, but there are alleles that are associated with violence and also a lack of empathy. For example antisocial behaviour (AB) is strongly heritable for callous-unemotional traits in children. AB+/ CU+ children show low emotional reactivity to punishment and distress, as well as poor ability to empathize with others. On the other hand non-callous AB (AB+/CU–) children show mainly environmental influences for their antisocial behaviour. They are emotionally reactive to threat, and are created via environmental risk influences (such as harsh parenting) epigenetically driving the expression of antisocial behaviour for this group. However, certain genes create a significant risk for violence when activated via appropriate epigenetic factors. Studies demonstrate that it is unlikely that genes directly code for violence; rather, allelic variations are responsible for individual differences in neurocognitive functioning that, in turn, may determine differential predisposition to violent behavior. Of the genes associated with psychopathy, MAOA-L is the most well-known and was among the first evidence that the variant MAOA-L interacts with childhood maltreatment to modulate antisocial tendencies (Caspi et al, 2002). “Specifically, severely maltreated participants carrying the low-activity allele of the MAOA gene displayed the highest scores in disposition toward violence and antisocial personality disorder scores, and demonstrated the greatest proportions of adolescent conduct disorder and convictions due to violent behavior.” (Buades-Rotger & Gallardo-Pujol, 2014). Recent research suggests that genetic vulnerability to violence conferred by the low-activity allele of MAOA-L variant may only become evident in the presence of environmental triggers of maltreatment. In favorable conditions, genetic predisposition alone may be of little consequence for behavior.
Gene & Their Associated SNPs (alphabetical order)
5-HTTLPR (serotonin transporter gene)
SNP: rs25531 (G;G) The long allele of the serotonin transporter gene is a potential risk factor for psychopathy. It is associated with less pain sensitivity.
ARL6IP6 (ADP-ribosylation-like factor 6 interacting protein 6 )
Associated with autistic psychopathy (form of autism spectrum disorder that is less severe than other forms, characterized by difficulty with social interaction and communication and by repetitive behavior or restricted interests) in childhood.
SNP rs11682518
DRD2 and DRD4
Positively correlated with a continuously coded psychopathic personality traits scale.
HTR1B (Serotonin 1B Receptor Gene)Serotonin 1B Receptor Gene (HTR1B)
Methylation as a Risk Factor for Callous-Unemotional Traits in Antisocial Boys. One neurochemical system that has been implicated both theoretically and empirically in CU traits and psychopathy is the serotonin system. For example, recent research identified an association between SNPs in the genes encoding serotonin receptor 2A (HTR2A) and serotonin receptor 1B (HTR1B) as well as CU traits in children with antisocial behaviour problems.
HTR1B is of particular interest because it has been found to be linked with behaviors and characteristics commonly associated with CU traits. Most notable are the animal studies which have demonstrated that mice without the serotonin 1B receptor gene show significantly elevated levels of aggression and lower levels of anxiety; both of which are typically associated with psychopathy. Studies in humans have also found an association between HTR1B and impulsive aggression, suggesting that serotonin 1B receptors may be involved in the control of aggression and impulsivity in humans.
SNP rs11568817 (T;T)
Associated with traits linked with ‘psychopathy’ including alcohol dependence, self-reported anger and hostility in young men, and autism spectrum disorder which is characterized by deficits in empathy that overlap those found in people with high CU traits. However, as psychopaths have been shown to be immune to dependence on addictive substances, it is unclear whether this gene is present in psychopathy, or if it may be a genetic marker for ASPD, which does have significant issues with substance dependence.
HTR2A (serotonin receptor 2A)
Provoked aggression associated with primary psychopathy traits. Hostility, Anger and Physical Aggression—but not verbal aggression—were associated with this gene, but only for provoked incidents.
SNP rs7322347 (T;T)
MAOA-L (Monoamine oxidase A)
“MAO-A has been named the ‘warrior gene’, and also more unfavourably the ‘psycho gene’. The gene is a variation of a gene on the X chromosome and therefore inherited from your mother. Females have two X chromosomes and males have an X and a Y chromosome. Mothers always pass an X chromosome on to their children. While if a father passes on his X chromosome (leading to a pair of X chromosomes and a female offspring) or his Y chromosome (leading to one X and one Y chromosomes and a male offspring).
This variation occurs in the X chromosome gene that produces monoamine oxidase A (MAOA), an enzyme in the brain that breaks down the neurotransmitters such as noradrenaline, adrenaline, serotonin, and dopamine.
People with the low-activity MAO-A gene (2R, 3R) are overall more prone to violence, impulsiveness and aggression. Specifically, when people with the MAOA-L feel very provoked or socially isolated their aggression will come out. Again, from an evolutionary perspective, this makes sense; a warrior needs to respond to threat, rather than act in a chaotic manner. Research demonstrates that low-activity MAO-A people are more likely to take revenge for someone who does something to leave them in a bad situation; however they do not act on small misdeeds.
Those with MAOA-L also showed hyperresponsiveness of the amygdala during tasks such as copying facial expressions. This accounts for an increased ability in this group to recognize emotions and also mimic them (the psychopathic mask).”
Natalie Engelbrecht's answer to What are the effects of having MAOA?
What are the effects of having MAO-A? Scientists believe it leads to impulsive behavior (such as as hypersexuality), sleep disorders, mood swings, and violent tendencies.
SNP: rs909525: Warrior; M: C= 3 allele; F: CC= 3 allele
SNP: rs12551906(G;G)
SNP: rs10865864 (G;G)
SNP: rs151997 (T;T)
OXTR (oxytocin receptor gene)
Polymorphisms in the oxytocin receptor gene are associated with the development of psychopathy. Evidence suggests that epigenetic changes in the OXT receptor gene (OXTR) are associated with lower circulating OXT and social–cognitive difficulties. Oxytocin promotes emotional and cognitive aspects of empathy; however increasing oxytocin can have the effect of increasing aggression.
SNP: rs53576 (A;A) Associated with lack of empathy.
SNP: rs2254298 (A;A) Smaller amygdala volume, both right and left sides.
SNP: rs1042778(T;T) Polymorphisms in the oxytocin receptor gene are associated with the development of psychopathy.
SNP: rs237887 (A;A) Lower emotional empathy.
SNP: rs4686302 (T;T) Lower emotional empathy.
Other Top Potential SNPs: rs124111132; rs7531603; rs2514788; rs4383690; rs6846114; rs2376016; rs2311846; rs11088618; rs41516949; rs7640807; rs1490666; rs293844; rs4241597; 6446569; rs1441990; rs1893815; rs11637779; rs10859716; rs1785633; rs4479686; rs10050093; rs12647756; rs1345959; rs13064369; rs8059321; rs6560704
In conclusion
Emerging research in psychopathy has begun to focus on psychopathy as a normal variant of neurotypical personality and brain function. Genetic brain scans and brain chemistry are all lending to this turn in the tides form psychopathy as a mental illness to psychopathy as a unique personality.
Summary
- Psychopathy is a distinct personality variation. In psychology, psychopathy is referred to as a personality disorder, often associated with criminal behaviour, however researchers are now arguing that psychopathy is a neurological variation.
- Researchers in the area of psychopathy have stated that psychopathy does not equal ASPD, but that ASPD is a behavior that may co-occur in some with psychopathy.
- The preferred method of assessment is no longer the PCL-R, but instead is now the PPI-R. It is intended to measure the psychopathic personality traits on a spectrum, without assuming particular links to antisocial or criminal behaviors. The test has been standardized to a non-prison population.
- Emerging research in genetics shows that MAOA-L has a significant role in psychopathy, however psychopathy is polygenetic, and it is the interplay of the genes and the effects of the environment that creates the person.
- Brain scan images demonstrate a smaller amygdala, a lower activity PFC, and a down-regulated pathway between the two in psychopathy, along with other brain changes.
- Areas such as the insula and nucleus accumbens are also different in psychopathy. An increased amount of dopamine is released in psychopathy in comparison with neurotypicals. Serotonin levels and oxytocin levels are lower in psychopathy.
