Antisocial personality disorder
Antisocial personality disorder (ASPD), also known as dissocial personality disorder (DPD) and sociopathy, is apersonality disorder, characterized by a pervasive pattern of disregard for, or violation of, the rights of others.
An international team of Finnish, American, British, and Swedish researchers examined data from the Finnish CRIME sample — a database of psychological tests and genetic material from 794 Finnish prisoners taken between 2010-2011.
The findings of this study cannot be implemented for any prediction purposes, or brought into courthouses to be given any legal weight.
Of the 794 prisoners, a full 568 screened positive for ASPD. By comparing that group’s genetic material to a large control sample from the general population, the researchers identified a number of genes that may play a role in at least some ASPD cases.
Hormones and neurotransmitters
Traumatic events can lead to a disruption of the standard development of the central nervous system, which can generate a release of hormones that can change normal patterns of development. Aggressiveness and impulsivity are among the possible symptoms of ASPD. Testosterone is a hormone that plays an important role in aggressiveness in the brain. For instance, criminals who have committed violent crimes tend to have higher levels of testosterone than the average person. The effect of testosterone is counteracted by cortisol which facilitates the cognitive control on impulsive tendencies.
One of the neurotransmitters that have been discussed in individuals with ASPD is serotonin, also known as 5HT. A meta-analysis of 20 studies found significantly lower 5-HIAA levels (indicating lower serotonin levels), especially in those who are younger than 30 years of age.
J.F.W. Deakin of University of Manchester‘s Neuroscience and Psychiatry Unit has discussed additional evidence of a connection between 5HT (serotonin) and ASPD. Deakin suggests that low cerebrospinal fluid concentrations of 5-HIAA, and hormone responses to 5HT, have displayed that the two main ascending 5HT pathways mediate adaptive responses to post and current conditions. He states that impairments in the posterior 5HT cells can lead to low mood functioning, as seen in patients with ASPD. It is important to note that the dysregulated serotonergic function may not be the sole feature that leads to ASPD but it is an aspect of a multifaceted relationship between biological and psychosocial factors.
While it has been shown that lower levels of serotonin may be associated with ASPD, there has also been evidence that decreased serotonin function is highly correlated with impulsiveness and aggression across a number of different experimental paradigms. Impulsivity is not only linked with irregularities in 5HT metabolism but may be the most essential psychopathological aspect linked with such dysfunction. Correspondingly, the DSM classifies “impulsivity or failure to plan ahead” and “irritability and aggressiveness” as two of seven sub-criteria in category A of the diagnostic criteria of ASPD.
Researchers have linked physical head injuries with antisocial behavior. Since the 1980s, scientists have associated traumatic brain injury, including damage to the prefrontal cortex, with an inability to make morally and socially acceptable decisions. Children with early damage in the prefrontal cortex may never fully develop social or moral reasoning and become “psychopathic individuals … characterized by high levels of aggression and antisocial behavior performed without guilt or empathy for their victims.” Additionally, damage to the amygdala may impair the ability of the prefrontal cortex to interpret feedback from the limbic system, which could result in uninhibited signals that manifest in violent and aggressive behavior.
Some studies suggest that the social and home environment has contributed to the development of antisocial behavior. The parents of these children have been shown to display antisocial behavior, which could be adopted by their children.
Cortisol, serotonin and depression: all stressed out?
The fact that patients with major depression exhibit decreased brain serotonin (5-hydroxytryptamine, 5-HT) function and elevated cortisol secretion has reached the status of textbook truism. More recent formulations have suggested that elevated cortisol levels, probably caused by stressful life events, may themselves lower brain 5-HT function and this in turn leads to the manifestation of the depressive state (see Dinan, 1994). This elegant proposal neatly ties abnormalities of cortisol secretion and 5-HT function into a causal chain in which cortisol is the key biological mediator through which life stress lowers brain 5-HT function, thereby causing depression in vulnerable individuals.
The importance, and occasional discomfort, of testing cherished beliefs is shown in a ground-breaking study from the Manchester University Department of Psychiatry published in this issue of the journal (Strickland et al, 2002). In a large group of women the authors found no evidence of increased salivary cortisol levels in those with depression or in the majority of those vulnerable to depression through adverse social or personal circumstances. Moreover, in women with depression, brain 5-HT function (as judged by the prolactin response to the 5-HT releasing agent, d-fenfluramine) was increased rather than diminished. These findings pose serious problems for hypotheses linking hypercortisolaemia with lowered brain 5-HT function and depression.
Massage therapy on cortisol and serotonin
In this article the positive effects of massage therapy on biochemistry are reviewed including decreased levels of cortisol and increased levels of serotonin and dopamine. The research reviewed includes studies on depression (including sex abuse and eating disorder studies), pain syndrome studies, research on auto-immune conditions (including asthma and chronic fatigue), immune studies (including HIV and breast cancer), and studies on the reduction of stress on the job, the stress of aging, and pregnancy stress. In studies in which cortisol was assayed either in saliva or in urine, significant decreases were noted in cortisol levels (averaging decreases 31%). In studies in which the activating neurotransmitters (serotonin and dopamine) were assayed in urine, an average increase of 28% was noted for serotonin and an average increase of 31% was noted for dopamine. These studies combined suggest the stress-alleviating effects (decreased cortisol) and the activating effects (increased serotonin and dopamine) of massage therapy on a variety of medical conditions and stressful experiences.
Correlation between cortisol level and serotonin uptake in patients with chronic stress and depression
In a recent study (Tafet, Toister-Achituv, & Shinitzky, 2001), we demonstrated that cortisol induces an increase in the expression of the gene coding for the serotonin transporter, associated with a subsequent elevation in the uptake of serotonin. This stimulatory effect, produced upon incubation with cortisol in vitro, was observed in peripheral blood lymphocytes from normal subjects. In the present work we investigated the cortisol-induced increase in serotonin uptake in lymphocytes from hypercortisolemic patients, including subjects with major depressive disorder (n = 8), and subjects with generalized anxiety disorder (n = 12), in comparison with a control group of normal healthy subjects (n = 8). A significant increase in serotonin uptake (+37% + 14, M + SD) was observed in the control group, whereas neither the generalized anxiety disorder nor the major depression group exhibited changes in serotonin uptake upon incubation with cortisol. It is likely that under chronic stress or depression, the capacity for increase in serotonin transporter has reached its limit due to the chronically elevated blood cortisol level.
Connie’s comments: A stressed baby can lead to personality disorder in adulthood. Nurture prevents many personality disorders.