Antisocial Personality Disorder (ASPD) is a pervasive pattern of disregard for and violation of the rights of others, with the average age of onset being 15 years; the diagnosis is based on three or more of the following indicators: failure to conform to social norms concerning lawful behaviors, deceitfulness, impulsivity, irritability, and aggressiveness, reckless disregard for the safety of self or others, consistent irresponsibility, and lack of remorse (1). To meet the diagnosis criteria, an individual must be at least 18 years old and have evidence of a Conduct Disorder (CD) with onset before the age of 15 years (2). The requirement of this childhood criterion serves to portray ASPD as a persistent personality disorder with roots early in development (3). Individuals with ASPD are more prone to be violent; they tend to violate the rights of others, be manipulative, commit crimes, and the disease produces extraordinary societal costs and aggregate social burden (2, 4). The maladaptive behaviors may include suicidal behavior, self-harm, aggression, criminal behavior, and substance misuse (2, 4).

Goldstein et al. (5) also found that individuals with ASPD are more likely to have comorbid substance misuse and other psychiatric disorders. The ASPD is associated with greater odds of any substance use disorder (SUD), specifically alcohol, nicotine, and any drug use disorder (6). Similarly, data from cohorts of prisoners has shown that alcohol dependence syndrome (ADS) shows high comorbidity with ASPD, suggesting that there may be common biological risk mechanisms (7). Furthermore, individuals with ASPD, SUD, and their co-occurrence (ASPD/SUD) have similar personality traits (8). Low agreeableness, low conscientiousness, high impulsivity, high excitement-seeking, low deliberation, and low self-discipline were characteristic of these disorders (8). The ASPD exhibited lower neuroticism than SUD and ASPD/SUD, which is consistent with the high levels of mood and anxiety disturbance often reported in individuals with SUD (8).

Alcohol dependence syndrome is characterized by alcohol use that causes serious impairment. It is characterized by preoccupation with alcohol, impaired control over drinking, usage of alcohol despite adverse consequences, and distortions in thinking. Alcoholism is characterized by craving, loss of control, withdrawal symptoms, and tolerance (9). Alcohol use disorder (AUD) is defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) as “a problematic pattern of alcohol use leading to clinically significant impairment or distress.” An alcohol dependence syndrome aligns symptomatically with the current diagnoses of moderate or severe AUD as per DSM-5. To diagnose a patient with AUD, the patient needs to meet at least two criteria: alcohol usage in larger amounts or for longer periods than intended, unsuccessful efforts to cut down or control alcohol use, spending a long time in obtaining alcohol, using alcohol, or recovering from its effects, failure to fulfil major role obligations due to alcohol, reduction in activities due to alcohol, continued alcohol use despite having persistent or recurrent problems due to alcohol, recurrent alcohol use in situations in which it is physically hazardous, craving, tolerance, and withdrawal. Alcohol Dependence Syndrome is a chronic, relapsing brain disease that presents a significant public health issue (1). There are links between developmental changes in personality and alcohol use (10). Across adolescence and early adulthood, individuals with steeper declines in impulsivity and neuroticism demonstrated steeper declines in problematic alcohol use (10). Individuals with a less substantial decline (or even an increase) in impulsivity and neuroticism had either increases or smaller decreases in problematic alcohol use (10). Similarly, increases in risk-taking behavior across development are associated with increased alcohol use among adolescents (11).

The ADS remains to be the actual topic in the field of psychiatry. Although its exact etiology remains unknown, susceptibility to the disorder is likely multifactorial. The cultural aspects are likely to play a very important role in the prevention and treatment of ADS. In Slovakia, 75% of adults consume alcohol occasionally or regularly. Alcohol is socially more accepted than other substances, and in Slovakia, its consumption is socially promoted (12). Alcoholism is the most commonly seen psychiatric diagnosis amongst Slovakians, and 26.5% of all psychiatric hospitalizations are due to alcohol (13). To our knowledge, the present study is a first study analyzing the prevalence of ASPD amongst the Slovak population. In the present study, we compared the characteristics of subjects with ADS and ADS comorbid with ASPD and compared their cognitive abilities. Knowledge of any cognitive deficits associated with ASPD would be valuable in working toward understanding the neurobiology of this disorder and its relationship with other conditions and developing more targeted treatment interventions.

The primary finding of the present study is that 35% of study participants met the criteria for ASPD and featured distinct demographical, clinical, and psychological characteristics. Our findings are in line with previous reports suggesting that antisocial behavior is associated with an increased risk of alcohol use and predicts later problems with alcohol use (25). These findings also provide additional evidence for the high prevalence of ADS in individuals with ASPD (3). Data from a large epidemiological study of psychopathology highlights the intertwined nature of ADS and personality disorders (26). In the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), 42% of individuals who met the diagnostic criteria for any personality disorder also fulfilled the criteria for DSM-IV alcohol dependence (26). Those with ASPD showed a notably higher likelihood, being 7 to 8 times more prone to meeting the criteria for alcohol dependence (26).

An existing personality disorder elicits environmental responses, such as interpersonal or occupational problems, that provoke the onset of ADS (10). The comorbidity may result from overlapping genetic and environmental underpinnings (10). Shared environmental risk factors such as childhood trauma, coercive parenting, and antisocial peer affiliation are associated with the ADS comorbid with ASPD (10). On the other hand, ASPD incapacitates one’s ability to ignore the immediate reward offered by alcohol (10). This jeopardizes the ability to inhibit habitual use of alcohol regardless of the significant psychological and physical distress it causes, leading to the genesis of ADS (10). Conversely, excessive alcohol consumption may lead to a neuroadaptation that results in increased impulsivity or negative emotionality, as seen in ASPD (10).

On the other hand, earlier substance abuse causes aggression and/or antisocial behavior and may transform into ASPD later in life, further increasing aggression (27). Although the literature is limited in this aspect, it may be reasonable to suggest that the search for stimulus may be the initial reason that adolescents succumb to drug use, leading to antisocial/violent behavior and finally forming a vicious cycle embodied by ASPD (27). Findings indicate that proneness to act out aggressively may be linked to a reduced differentiation (at a neural and behavioral level) between threatening and non-threatening interpersonal cues, in line with the hypothesis of a hostile filter that biases the perception of the entire social environment, thus increasing the likelihood for aggressive encounters (28). Alterations of fronto-temporal-limbic regions and neuromodulatory systems, such as the serotonergic or endocannabinoid signaling systems, may also connect impulsive behavior to aggressive responding (28). Weaker cortico-striatal connectivity could relate to greater risk-taking and greater proclivity for violence (28).

Furthermore, we found that participants with ASPD had lower MoCA scores and had more problems with vigilance, attention, and linguistic skills ( Figure 1 ). This is in line with previous literature findings that antisocial symptoms have been significantly associated with cognitive control defects, attentional problems, abnormalities in decision-making, deficits in flexible responding, such as reversal learning, planning impairments, neural regions governing inhibitory control, and verbal deficits/delayed language development (29, 30). The young offenders scored approximately half a standard deviation lower on verbal domains of intelligence than on performance-related domains of general intelligence (31). Moreover, in subjects with ASPD, spatial convergence in brain regions belonging to ventral and dorsal attention networks (the anterior midcingulate cortex/the pre-supplementary motor area (aMCC/pre-SMA), superior parietal lobule (SPL), and premotor (frontal eye field, and the cuneus) were found (32). Indeed, the aMCC/pre-SMA mainly corresponded to the ventral network, whereas the SPL and premotor cortex were associated with the dorsal network (32). These regions are frequently co-activated in tasks requiring attentional processes such as shifting: sustained, oddball, and working memory (32). Ventral network regions (e.g., aMCC/pre-SMA) may correspond to a stimulus-driven attentional system. In contrast, regions subserving the dorsal attentional network (e.g., SPL, premotor cortex) may play a crucial role in top-down or goal-driven attentional control (32). Subjects with ASPD have significant connectivity deficits in the amygdala, middle cingulate cortex, ventral posterior cingulate cortex-precuneus, ventromedial and dorsomedial prefrontal cortex, premotor cortex, and superior parietal lobule and increased connectivity in the ventral posterior cingulate cortex and decreased connectivity in the parietal operculum, calcarine cortex, and cuneus (32). There is a negative relationship between the severity of antisocial behaviors and connectivity with the ventromedial prefrontal cortex (32). These findings overlapped with socio-affective and attentional processes (32). The ASPD is associated with variability in neural functioning during reward and loss processing (33). In particular, impulsive-antisocial traits appeared to be specifically associated with hypersensitivity in the ventral striatum (VS) and prefrontal cortex (PFC) (VS reactivity or VS-PFC functional connectivity) during the anticipation, but not the receipt of rewards (33). Beyond VS reactivity, ASPD was related to the greater orbitofrontal cortex (OFC), medial PFC reactivity, and VS-dorsomedial PFC connectivity during reward processing (33). The ASPD was linked to greater reactivity in several regions, including the posterior cingulate, precuneus, and insula, during error-related loss receipt and decreased VS reactivity during loss anticipation (33).

Our finding of younger age among ADS participants with comorbid ASPD corresponds with the literature (34). In our sample, individuals diagnosed with ASPD tend to start drinking alcohol at younger ages, which is in line with literature findings (35), and were more likely to seek treatment at a younger age, which was previously described (10). Studies also reported that prevalence rates of ASPD steadily decline with age (36). Over the years, researchers have proposed multiple factors that may contribute to the decline in the prevalence of ASPD with age, including increased rates of mortality and incarceration and a change in personality traits over the lifespan (37).

We found that individuals with ASPD had more frequent hospitalizations and more problems with alcohol consumption, as shown in the AUDIT test, which aligns with literature findings - more than half of subjects dependent on alcohol relapse within a year (38). Relapse can be attributed to several psychosocial and biological factors. Among others, marital status, traumatic experiences, psychological distress, and the presence of co-existing psychopathology, including anxiety and depression, and alteration in the brain’s dopamine system may influence relapse (10). If individuals with ASPD seek treatment, their chances of adhering to the treatment are low because they tend to violate rules (10). The comorbidity leads to poorer treatment outcomes, thereby increasing the chance of relapse or drop-out (10).

We reported that subjects with comorbid ASPD had lower education levels, tended to be unemployed more often, and tended to be married less often. The results align with the literature finding, which revealed significantly higher odds of a diagnosis among individuals with less than a high school education, lower income, and those not married (37). Using the NESARC-III data, Goldstein et al. (5) found similar results with adults of any age. In their study, individuals with ASPD were more likely to be 18-29 years old, widowed/separated/divorced, had less than a college degree and a lower family income (5). Also, more knowledge on the effect of education level on this relation is required since research suggests that school failure is overrepresented in offenders and related to aggressive antisocial behaviors (39). It is hypothesized that behavioral disorders and impulsivity in individuals with ASPD negatively affect their academic and professional achievements, which results in lower income levels and employment compared to healthy individuals (40).

We reported that participants with ADS+ASPD more often have family members who suffer from ADS, are incarcerated, or are otherwise mentally ill. Similarly, a state hospital study (41) of 740 individuals admitted for alcoholism treatment concluded that ADS+ASPD subjects had a higher prevalence of familial alcoholism when compared with alcohol abusers without ASPD. This points us toward the etiopathogenesis of the disease, which combines genetic and environmental influences (42–44). Notably, Rhee and Waldman’s (45) meta-analysis reported additive and non-additive genetic contributions to antisocial behavior (32% and 9%, respectively), 16% of the variance explained by shared environment, and 43% explained by individual-specific environmental influences. A genetic basis for ASPD is supported by the finding that a first-degree biological relative with ASPD constitutes a risk factor for the disorder (43). The ASPD, like most mental disorders, is thought to have a complex, multifactorial etiology characterized by polygenic inheritance and genetic heterogeneity across individuals. The genetic contribution is not stable over time, suggesting that partly different genes contribute to ASPD at different stages of the lifespan (44). Recently, GWAS meta-analysis identified a novel genome-wide significant signal with rs9806493 chromosome 15q26.1 close to SLCO3A1, possibly contributing to the genetic risk factor for ADS and ASPD (42). Many environmental risk factors were described in the literature. Of the prenatal risk factors, maternal smoking, alcohol use, drug use, and stress during pregnancy are among the best documented (44). Perinatal risk factors include obstetric complications, parental psychopathology, malnutrition, and exposure to heavy metals (44). Postnatal risk factors include more strained family relationships, child maltreatment, parental substance abuse, lower income, childhood residential mobility, and bullying (43).

Subjects with ASPD reported experiencing traumatic events more often ( Figure 2 ), which is in agreement with previous literature findings (10). Adverse childhood experiences, which encompass various forms of abuse, neglect, and impoverishment during childhood, are prime examples of negative socialization experiences that engender antisocial traits and behaviors (2). Clinical evidence suggests that trauma may contribute to ASPD features such that the experience of trauma provides a template for which people who develop ASPD learn to interact with others (46). People with ASPD traits may use the betrayal trauma they experienced earlier in life as a template for perpetrating trauma on others later in life (2). One way of understanding the relationship between antisocial behaviors preceded by traumatic experiences is to suggest that individuals who have experienced severe trauma develop insensitivity to stressful situations. In addition to numbing reactions of sadness and fear, these individuals would tend to behave aggressively. Traumatic experiences compromise the functioning of neurotransmitters, the neuroendocrine, and the immune system, generating a dysfunction of the hypothalamic-pituitary-adrenal system affecting control and stress response (4). The average correlation between trauma and ASPD traits were both high. Exposure to traumas at all levels of betrayal predicts ASPD traits for women, but only exposure to high betrayal trauma predicts ASPD traits for men (2). Fergusson et al. (47) examined the association between childhood sexual abuse, childhood physical abuse, and ASPD and found that the prevalence of ASPD at ages 18–21 and 21–25 was two to four times greater among those who had been sexually abused compared to those who had not. Similarly, those who experienced regular physical abuse or severe physical abuse had ASPD at a prevalence that was two to seven times higher than those who were not physically abused. In multivariate models, sexual abuse predicted ASPD; however, physical abuse did not occur in the fully adjusted model (2).

Our next finding was that depression, anxiety, and stress were all statistically significantly correlated with ASPD) ( Figure 3 ), which is in line with the literature findings (40). However, we failed to replicate this finding in a linear regression model, possibly due to the small sample size. Symptoms reflecting impulsivity and emotional dysregulation are found in ASPD, psychopathy, anxiety, and mood disorders. Interestingly, the relationship between psychopathy and ASPD with mood and anxiety disorders has been a controversial topic, as many experts associate ASPD and psychopathy with very low levels of anxiety and depression (3). In contrast, in the DSM-5, it is noted that those with an ASPD diagnosis may also experience anxiety disorders and/or depressed mood (1). Evidence from epidemiological samples indicates that individuals with ASPD are four times more likely to experience a mood disorder, and up to half of the individuals with ASPD may also experience an anxiety disorder in their lifetime, particularly posttraumatic stress disorder and social anxiety disorder. These individuals with comorbid ASPD and anxiety disorders were found to be at increased risk for major depression and substance dependence (48, 49). Drinking is sometimes used as a coping strategy and/or method of self-medication among individuals with substance abuse disorder before, during, and after anxiety-provoking events (3).

Our last finding was that individuals with ADS-ASPD reported worse sleep, which showed a statistical trend. Previous sleep problems were reported in individuals with ASPD and ADS (50). A similar relationship between sleep and ASPD was described in a study conducted by Van Veen in 112 patients with antisocial personality disorder and borderline personality disorder. The study found a relationship between behavioral disinhibition and/or emotional dysregulation and poor sleep. Poor sleep quality was reported in 53.6% of the patients, especially with problems falling asleep, and 22.3% suffered from severe chronic insomnia, which was particularly characterized by major problems with sleep initiation, resulting in much shorter total sleep times. Problems with sleep were significantly associated with greater impulsivity. Subjects with greater insomnia or lower sleep quality reported more difficulties with focusing and controlling their thoughts (51). However, to our knowledge, this is the first study comparing sleep problems in individuals with ADS with and without ASPD.

A recent meta-analysis on 24,801 subjects did not find enough evidence to determine whether or not medication is a helpful treatment for people with ASPD (52). There is also minimal evidence available on psychological interventions for adults with ASPD (53). A recent meta-analysis of 605 adults found that three interventions (schema therapy, contingency management, and dialectic behavior therapy) may be more effective than other approaches (53). However, the certainty of the evidence was low or very low to recommend or reject any psychological treatment for people with a diagnosis of ASPD (53).

Our findings may not apply to all participants with alcohol dependence syndrome as the sample we studied was small. Nevertheless, the group was homogenous; all subjects were from the same region, and the same team of psychiatrists evaluated them. The results might differ in a sample of outpatients with the same problems and a sample of people recovering from ADS. Many of the participants in the present study were using benzodiazepines at the time of the examination, which can worsen some cognitive parameters.

Since this study extensively uses questionnaire methods, it was not possible to objectively evaluate variables such as sleep parameters or the incidence of traumatization. Specifically, in cases of memory decline, they may be unable to recall all the events. In addition, a limited insight into one’s problems is very common in this population. The present results are preliminary, and the study is still ongoing. Further studies are warranted to evaluate the impact of various comorbidities and their treatment on cognitive skills.

The strength of the current study is that it provides a comprehensive analysis of comorbid ASPD among adults with ADS based on the in-depth analysis of the selected demographic and psychological variables controlling for key covariates in analyses. Another strength is that it explored familial psychopathology among subjects, providing deeper insights into their conditions. Overall, the study advances understanding of the complexities of comorbid ASPD in individuals with ADS, providing valuable insights for research and clinical practice.

The study demonstrated that more than one-third of the individuals with ADS met the criteria for ASPD. The prevalence of depression, anxiety, stress, traumatization, and sleep problems was high among all subjects. All these difficulties were closely related to ASPD. Participants with ADS+ASPD had lower MoCA scores and had more problems with attention and linguistic skills. The findings implicate that screening for ASPD might be helpful in the complex management of ADS.