Socioeconomic status has also been looked at as a potential cause for personality disorders. There is a strong association with low parental/neighborhood socioeconomic status and personality disorder symptoms. In a recent study comparing parental socioeconomic status and a child's personality, it was seen that children who were from higher socioeconomic backgrounds were more altuistic, less risk seeking, and had overall higher IQs. These traits correlate with a low risk of developing personality disorders later on in life. In a study looking at female children who were detained for disciplinary actions found that psychological problems were most negatively associated with socioeconomic problems. Furthermore, social disorganization was found to be inversely correlated with personality disorder symptoms.

Child abuse and neglect consistently show up as risk factors to the development of personality disorders in adulthood. A study looked at retrospective reports of abuse of participants that had demonstrated psychopathology throughout their life and were later found to have past experience with abuse. In a study of 793 mothers and children, researchers asked mothers if they had screamed at their children, and told them that they did not love them or threatened to send them away. Children who had experienced such verbal abuse were three times as likely as other children (who did not experience such verbal abuse) to have borderline, narcissistic, obsessive-compulsive or paranoid personality disorders in adulthood. The sexually abused group demonstrated the most consistently elevated patterns of psychopathology. Officially verified physical abuse showed an extremely strong correlation with the development of antisocial and impulsive behavior. On the other hand, cases of abuse of the neglectful type that created childhood pathology were found to be subject to partial remission in adulthood.

Individual differences in women's estrogen cycles may be related to the expression of BPD symptoms in female patients. A 2003 study found that women's BPD symptoms were predicted by changes in estrogen levels throughout their menstrual cycles, an effect that remained significant when the results were controlled for a general increase in negative affect.

There is a strong correlation between child abuse, especially child sexual abuse, and development of BPD. Many individuals with BPD report a history of abuse and neglect as young children, but causation is still debated. Patients with BPD have been found to be significantly more likely to report having been verbally, emotionally, physically, or sexually abused by caregivers of either gender. They also report a high incidence of incest and loss of caregivers in early childhood. Individuals with BPD were also likely to report having caregivers of both sexes deny the validity of their thoughts and feelings. Caregivers were also reported to have failed to provide needed protection and to have neglected their child's physical care. Parents of both sexes were typically reported to have withdrawn from the child emotionally and to have treated the child inconsistently. Additionally, women with BPD who reported a previous history of neglect by a female caregiver and abuse by a male caregiver were significantly more likely to experience sexual abuse by a non-caregiver.

It has been suggested that children who experience chronic early maltreatment and attachment difficulties may go on to develop borderline personality disorder. Writing in the psychoanalytic tradition, Otto Kernberg argues that a child's failure to achieve the developmental task of and failure to overcome splitting might increase the risk of developing a borderline personality. A child's inability to tolerate delayed gratification at age four does not predict later development of BPD.

Another theory suggests a possible relationship between histrionic personality disorder and antisocial personality disorder. Research has found 2/3 of patients diagnosed with histrionic personality disorder also meet criteria similar to those of the antisocial personality disorder, which suggests both disorders based towards sex-type expressions may have the same underlying cause. Women are hypersexualized in the media consistently, ingraining thoughts that the only way women are to get attention is by exploiting themselves, and when seductiveness isn't enough, theatricals are the next step in achieving attention. Men can just as well be flirtatious towards multiple women yet feel no empathy or sense of compassion towards them. They may also become the center of attention by exhibiting the "Don Juan" macho figure as a role-play.

Some family history studies have found that histrionic personality disorder, as well as borderline and antisocial personality disorders, tend to run in families, but it is unclear if this is due to genetic or environmental factors. Both examples suggest that predisposition could be a factor as to why certain people are diagnosed with histrionic personality disorder, however little is known about whether or not the disorder is influenced by any biological compound or is genetically inheritable. Little research has been conducted to determine the biological sources, if any, of this disorder.

There is evidence that narcissistic personality disorder is heritable, and individuals are much more likely to develop NPD if they have a family history of the disorder. Studies on the occurrence of personality disorders in twins determined that there is a moderate to high heritability for narcissistic personality disorder.

However the specific genes and gene interactions that contribute to its cause, and how they may influence the developmental and physiological processes underlying this condition, have yet to be determined.

The causes of narcissistic personality disorder are unknown. Experts tend to apply a biopsychosocial model of causation, meaning that a combination of environmental, social, genetic and neurobiological factors are likely to play a role in formulating a narcissistic personality.

Genetic

Schizotypal personality disorder is widely understood to be a "schizophrenia spectrum" disorder. Rates of schizotypal personality disorder are much higher in relatives of individuals with schizophrenia than in the relatives of people with other mental illnesses or in people without mentally ill relatives. Technically speaking, schizotypal personality disorder may also be considered an "extended phenotype" that helps geneticists track the familial or genetic transmission of the genes that are implicated in schizophrenia. But there is also a genetic connection of STPD to mood disorders and depression in particular.

Social and environmental

There is now evidence to suggest that parenting styles, early separation, trauma/maltreatment history (especially early childhood neglect) can lead to the development of schizotypal traits. Neglect or abuse, trauma, or family dysfunction during childhood may increase the risk of developing schizotypal personality disorder. Over time, children learn to interpret social cues and respond appropriately but for unknown reasons this process does not work well for people with this disorder.

Schizotypal personality disorders are characterized by a common attentional impairment in various degrees that could serve as a marker of biological susceptibility to STPD. The reason is that an individual who has difficulties taking in information may find it difficult in complicated social situations where interpersonal cues and attentive communications are essential for quality interaction. This might eventually cause the individual to withdraw from most social interactions, thus leading to asociality.

Reported prevalence of STPD in community studies ranges from 0.6% in a Norwegian sample, to 4.6% in an American sample. A large American study found a lifetime prevalence of 3.9%, with somewhat higher rates among men (4.2%) than women (3.7%). It may be uncommon in clinical populations, with reported rates of 0% to 1.9%.

Together with other Cluster A personality disorders, it is also very common among homeless people.

A University of Colorado Colorado Springs study comparing personality disorders and Myers-Briggs Type Indicator types found that the disorder had a significant correlation with the Introverted (I), Intuitive (N), Thinking (T), and Perceiving (P) preferences.

DID is rarely diagnosed in children, despite the average age of appearance of the first alter being three years. This fact is cited as a reason to doubt the validity of DID, and proponents of both etiologies believe that the discovery of DID in a child that had never undergone treatment would critically undermine the SCM. Conversely, if children are found to only develop DID after undergoing treatment it would challenge the traumagenic model. , approximately 250 cases of DID in children have been identified, though the data does not offer unequivocal support for either theory. While children have been diagnosed with DID before therapy, several were presented to clinicians by parents who were themselves diagnosed with DID; others were influenced by the appearance of DID in popular culture or due to a diagnosis of psychosis due to hearing voices—a symptom also found in DID. No studies have looked for children with DID in the general population, and the single study that attempted to look for children with DID not already in therapy did so by examining siblings of those already in therapy for DID. An analysis of diagnosis of children reported in scientific publications, 44 case studies of single patients were found to be evenly distributed (i.e., each case study was reported by a different author) but in articles regarding groups of patients, four researchers were responsible for the majority of the reports.

The initial theoretical description of DID was that dissociative symptoms were a means of coping with extreme stress (particularly childhood sexual and physical abuse), but this belief has been challenged by the data of multiple research studies. Proponents of the traumagenic hypothesis claim the high correlation of child sexual and physical abuse reported by adults with DID corroborates the link between trauma and DID. However, the DID-maltreatment link has been questioned for several reasons. The studies reporting the links often rely on self-report rather than independent corroborations, and these results may be worsened by selection and referral bias. Most studies of trauma and dissociation are cross-sectional rather than longitudinal, which means researchers can not attribute causation, and studies avoiding recall bias have failed to corroborate such a causal link. In addition, studies rarely control for the many disorders comorbid with DID, or family maladjustment (which is itself highly correlated with DID). The popular association of DID with childhood abuse is relatively recent, occurring only after the publication of "Sybil" in 1973. Most previous examples of "multiples" such as Chris Costner Sizemore, whose life was depicted in the book and film "The Three Faces of Eve", disclosed no history of child abuse.

Little is known about prognosis of untreated DID. It rarely, if ever, goes away without treatment, but symptoms may resolve from time to time or wax and wane spontaneously. Patients with mainly dissociative and posttraumatic symptoms face a better prognosis than those with comorbid disorders or those still in contact with abusers, and the latter groups often face lengthier and more difficult treatment. Suicidal ideation, failed suicide attempts, and self-harm also occur. Duration of treatment can vary depending on patient goals, which can extend from elimination of all alters to merely reducing inter-alter amnesia, but generally takes years.

Data from the 2001–02 National Epidemiologic Survey on Alcohol and Related Conditions indicates a prevalence rate of 2.36% in the American general population. It appears to occur with equal frequency in males and females. In one study, it was seen in 14.7% of psychiatric outpatients.

According to Professor Emily Simonoff of the Institute of Psychiatry, Psychology and Neuroscience, "childhood hyperactivity and conduct disorder showed equally strong prediction of antisocial personality disorder (ASPD) and criminality in early and mid-adult life. Lower IQ and reading problems were most prominent in their relationships with childhood and adolescent antisocial behaviour."

Causes of avoidant personality disorder are not clearly defined, but appear to be influenced by a combination of social, genetic, and psychological factors. The disorder may be related to temperamental factors that are inherited. Specifically, various anxiety disorders in childhood and adolescence have been associated with a temperament characterized by behavioral inhibition, including features of being shy, fearful, and withdrawn in new situations. These inherited characteristics may give an individual a genetic predisposition towards avoidant personality disorder. Childhood emotional neglect and peer group rejection are both associated with an increased risk for the development of avoidant personality disorder. Some researchers believe that a combination of high sensory processing sensitivity coupled with adverse childhood experiences may heighten the risk of an individual developing AvPD.

Approximately 1–3% of the general population may be diagnosed with HPD. Major character traits may be inherited, while other traits may be due to a combination of genetics and environment, including childhood experiences. This personality is seen more often in women than in men. It has typically been found that at least two thirds of persons with HPD are female, however there have been a few exceptions. Whether or not the rate will be significantly higher than the rate of women within a particular clinical setting depends upon many factors that are mostly independent of the differential sex prevalence for HPD. Those with HPD are more likely to look for multiple people for attention which leads to marital problems due to jealousy and lack of trust from the other party. This makes them more likely to become divorced or separated once married.

SPD can be first apparent in childhood and adolescence with solitariness, poor peer relationships, and underachievement in school. This may mark these children as different and make them subject to teasing.

Being a personality disorder, which are usually chronic and long-lasting mental conditions, schizoid personality disorder is not expected to improve with time without treatment; however, much remains unknown because it is rarely encountered in clinical settings.

Dependent personality disorder occurs in about 0.6% of the general population. The disorder is diagnosed more often in females than males; however, research suggests that this is largely due to behavioural differences in interviews and self-reporting rather than a difference in prevalence between the sexes. A 2004 twin study suggests a heritability of 0.81 for developing dependent personality disorder. Because of this, there is significant evidence that this disorder runs in families. Children and adolescents with a history of anxiety disorders and physical illnesses are more susceptible to acquiring this disorder.

Genetically informed studies of the personality characteristics typical of individuals with psychopathy have found moderate genetic (as well as non-genetic) influences. On the PPI, fearless dominance and impulsive antisociality were similarly influenced by genetic factors and uncorrelated with each other. Genetic factors may generally influence the development of psychopathy while environmental factors affect the specific expression of the traits that predominate. A study on a large group of children found more than 60% heritability for "callous-unemotional traits" and that conduct problems among children with these traits had a higher heritability than among children without these traits.

A study by Farrington of a sample of London males followed between age 8 and 48 included studying which factors scored 10 or more on the PCL:SV at age 48. The strongest factors included having a convicted parent, being physically neglected, low involvement of the father with the boy, low family income, and coming from a disrupted family. Other significant factors included poor supervision, harsh discipline, large family size, delinquent sibling, young mother, depressed mother, low social class, and poor housing. There has also been association between psychopathy and detrimental treatment by peers. However, it is difficult to determine the extent of an environmental influence on the development of psychopathy because of evidence of its strong heritability.

It is unclear what causes alexithymia, though several theories have been proposed.

Early studies showed evidence that there may be an interhemispheric transfer deficit among people with alexithymia; that is, the emotional information from the right hemisphere of the brain is not being properly transferred to the language regions in the left hemisphere, as can be caused by a decreased corpus callosum, often present in psychiatric patients who have suffered severe childhood abuse. A neuropsychological study in 1997 indicated that alexithymia may be due to a disturbance to the right hemisphere of the brain, which is largely responsible for processing emotions. In addition, another neuropsychological model suggests that alexithymia may be related to a dysfunction of the anterior cingulate cortex. These studies have some shortcomings, however, and the empirical evidence about the neural mechanisms behind alexithymia remains inconclusive.

French psychoanalyst Joyce McDougall objected to the strong focus by clinicians on neurophysiological at the expense of psychological explanations for the genesis and operation of alexithymia, and introduced the alternative term "disaffectation" to stand for psychogenic alexithymia. For McDougall, the disaffected individual had at some point "experienced overwhelming emotion that threatened to attack their sense of integrity and identity", to which they applied psychological defenses to pulverize and eject all emotional representations from consciousness. A similar line of interpretation has been taken up using the methods of phenomenology. McDougall has also noted that all infants are born unable to identify, organize, and speak about their emotional experiences (the word "infans" is from the Latin "not speaking"), and are "by reason of their immaturity inevitably alexithymic". Based on this fact McDougall proposed in 1985 that the alexithymic part of an adult personality could be "an extremely arrested and infantile psychic structure". The first language of an infant is nonverbal facial expressions. The parent's emotional state is important for determining how any child might develop. Neglect or indifference to varying changes in a child's facial expressions without proper feedback can promote an invalidation of the facial expressions manifested by the child. The parent's ability to reflect self-awareness to the child is another important factor. If the adult is incapable of recognizing and distinguishing emotional expressions in the child, it can influence the child's capacity to understand emotional expressions.

Molecular genetic research into alexithymia remains minimal, but promising candidates have been identified from studies examining connections between certain genes and alexithymia among those with psychiatric conditions as well as the general population. A study recruiting a test population of Japanese males found higher scores on the Toronto Alexithymia Scale among those with the 5-HTTLPR homozygous long (L) allele. The 5-HTTLPR region on the serotonin transporter gene influences the transcription of the seretonin transporter that removes serotonin from the synaptic cleft, and is well studied for its association with numerous psychiatric disorders. Another study examining the 5-HT1A receptor, a receptor that binds serotonin, found higher levels of alexithymia among those with the G allele of the Rs6295 polymorphism within the HTR1A gene. Also, a study examining alexithymia in subjects with obsessive-compulsive disorder found higher alexithymia levels associated with the Val/Val allele of the Rs4680 polymorphism in the gene that encodes Catechol-O-methyltransferase (COMT), an enzyme which degrades catecholamine neurotransmitters such as dopamine. These links are tentative, and further research will be needed to clarify how these genes relate to the neurological anomalies found in the brains of people with alexithymia.

Although there is evidence for the role of environmental and neurological factors, the role and influence of genetic factors for developing alexithymia is still unclear. A single large scale Danish study suggested that genetic factors contributed noticeably to the development of alexithymia. However, such twin studies are controversial, as they suffer from the "equal environments assumption" and the "heritability" estimates in no way correspond to actual DNA structures.

Traumatic brain injury is also implicated in the development alexithymia, and those with traumatic brain injury are six times more likely to exhibit alexithymia.

Some evidence suggests the Cluster A personality disorders have shared genetic and environmental risk factors and there is an increased prevalence of schizoid personality disorder in relatives of people with schizophrenia and schizotypal personality disorder. Twin studies with schizoid personality disorder traits (e.g. low sociability and low warmth) suggest these are inherited. Besides this indirect evidence, the direct heritability estimates of SPD range from 50-59%. To Sula Wolff, who did extensive research and clinical work with children and teenagers with schizoid symptoms, "schizoid personality has a constitutional, probably genetic, basis." The link between SPD and being underweight may also point to the involvement of biological factors.

In general, prenatal caloric malnutrition, premature birth and a low birth weight are risk factors for being afflicted by mental disorders and may contribute to the development of schizoid personality disorder as well. Those who have experienced traumatic brain injury may be also at risk of developing features reflective of schizoid personality disorder.

Other researchers had hypothesized excessively perfectionist, unloving or neglectful parenting could play a role.

Research into genetic associations in antisocial personality disorder is suggestive that ASPD has some or even a strong genetic basis. Prevalence of ASPD is higher in people related to someone afflicted by the disorder. Twin studies, which are designed to discern between genetic and environmental effects have reported significant genetic influences on antisocial behavior and conduct disorder.

In the specific genes that may be involved, one gene that has seen particular interest in its correlation with antisocial behavior is the gene that encodes for Monoamine oxidase A (MAO-A), an enzyme that breaks down monomamine neurotransmitters such as serotonin and norephinephrine. Various studies examining the gene's relationship to behavior have suggested that variants of the gene that results in less MAO-A being produced, such as the 2R and 3R alleles of the promoter region have associations with aggressive behavior in men. The association is also found influenced by negative experience in early life, with children possessing a low-activity variant (MAOA-L) with who experienced such maltreatment being more likely to develop antisocial behavior than those with the high-activity variants (MAOA-H). Even when environmental interactions (e.g. emotional abuse) are controlled for, a small association between MAOA-L and aggressive and antisocial behavior remains.

The gene that encodes for the serotonin transporter (SCL6A4), a gene that is heavily researched for its associations with other mental disorders, is another gene of interest in antisocial behavior and personality traits. Genetic associations studies have suggested that the short "S" allele is associated with impulsive antisocial behavior and ASPD in the inmate population. However, research into psychopathy find that the long "L" allele is associated with the Factor 1 traits of psychopathy, which describes its core affective (e.g. lack of empathy, fearlessness) and interpersonal (e.g. grandiosity, manipulativeness) personality disturbances. This is suggestive of two different forms, one associated more with impulsive behavior and emotional dysregulation, and the other with predatory aggression and affective disturbance, of the disorder.

Various other gene candidates for ASPD have been identified by a genome-wide association study published in 2016. Several of these gene candidates are shared with attention-deficit hyperactivity disorder, with which ASPD is comorbid.

Impulsive behavior, and especially impulsive violence predisposition has been correlated to a low brain serotonin turnover rate, indicated by a low concentration of 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF). This substrate appears to act on the suprachiasmatic nucleus in the hypothalamus, which is the target for serotonergic output from the dorsal and median raphe nuclei playing a role in maintaining the circadian rhythm and regulation of blood sugar. A tendency towards low 5-HIAA may be hereditary. A putative hereditary component to low CSF 5-HIAA and concordantly possibly to impulsive violence has been proposed. Other traits that correlate with IED are low vagal tone and increased insulin secretion. A suggested explanation for IED is a polymorphism of the gene for tryptophan hydroxylase, which produces a serotonin precursor; this genotype is found more commonly in individuals with impulsive behavior.

IED may also be associated with lesions in the prefrontal cortex, with damage to these areas, including the amygdala, increasing the incidence of impulsive and aggressive behavior and the inability to predict the outcomes of an individual's own actions. Lesions in these areas are also associated with improper blood sugar control, leading to decreased brain function in these areas, which are associated with planning and decision making. A national sample in the United States estimated that 16 million Americans may fit the criteria for IED.

The cause of OCPD is unknown. However, it is believed to involve a combination of genetic and environmental factors. Under the genetic theory, people with a form of the DRD3 gene will probably develop OCPD and depression, particularly if they are male. But genetic concomitants may lie dormant until triggered by events in the lives of those who are predisposed to OCPD. These events could include trauma faced during childhood, such as physical, emotional, or sexual abuse, or other psychological trauma. Under the environmental theory, OCPD is a learned behavior.

Externalizing disorders are frequently comorbid or co-occurring with other disorders. Individuals who have the co-occurrence of more than one externalizing disorder have homotypic comorbidity, whereas individuals who have co-occurring externalizing and Internalizing disorders have heterotypic comorbidity. It is not uncommon for children with early externalizing problems to develop both internalizing and further externalizing problems across the lifespan.