Risk factors for mental illness include genetic inheritance, such as parents having depression, or a propensity for high neuroticism or "emotional instability".

In depression, parenting risk factors include parental unequal treatment, and there is association with high cannabis use.

In schizophrenia and psychosis, risk factors include migration and discrimination, childhood trauma, bereavement or separation in families, and abuse of drugs, including cannabis, and urbanicity.

In anxiety, risk factors may include family history (e.g. of anxiety), temperament and attitudes (e.g. pessimism), and parenting factors including parental rejection, lack of parental warmth, high hostility, harsh discipline, high maternal negative affect, anxious childrearing, modelling of dysfunctional and drug-abusing behaviour, and child abuse (emotional, physical and sexual).

Environmental events surrounding pregnancy and birth have also been implicated. Traumatic brain injury may increase the risk of developing certain mental disorders. There have been some tentative inconsistent links found to certain viral infections, to substance misuse, and to general physical health.

Social influences have been found to be important, including abuse, neglect, bullying, social stress, traumatic events and other negative or overwhelming life experiences. For bipolar disorder, stress (such as childhood adversity) is not a specific cause, but does place genetically and biologically vulnerable individuals at risk for a more severe course of illness. The specific risks and pathways to particular disorders are less clear, however. Aspects of the wider community have also been implicated, including employment problems, socioeconomic inequality, lack of social cohesion, problems linked to migration, and features of particular societies and cultures.

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.

Correlations of mental disorders with drug use include cannabis, alcohol and caffeine, use of which appears to promote anxiety. For psychosis and schizophrenia, usage of a number of drugs has been associated with development of the disorder, including cannabis, cocaine, and amphetamines. There has been debate regarding the relationship between usage of cannabis and bipolar disorder.

Epidemiological data are limited, but reactive attachment disorder appears to be very uncommon. The prevalence of RAD is unclear but it is probably quite rare, other than in populations of children being reared in the most extreme, deprived settings such as some orphanages. There is little systematically gathered epidemiologic information on RAD. A cohort study of 211 Copenhagen children to the age of 18 months found a prevalence of 0.9%.

Attachment disorders tend to occur in a definable set of contexts such as within some types of institutions, in the presence of repeated changes of primary caregiver or of extremely neglectful identifiable primary caregivers who show persistent disregard for the child's basic attachment needs, but not all children raised in these conditions develop an attachment disorder. Studies undertaken on children from Eastern European orphanages from the mid-1990s showed significantly higher levels of both forms of RAD and of insecure patterns of attachment in the institutionalized children, regardless of how long they had been there. It would appear that children in institutions like these are unable to form selective attachments to their caregivers. The difference between the institutionalized children and the control group had lessened in the follow-up study three years later, although the institutionalized children continued to show significantly higher levels of indiscriminate friendliness. However, even among children raised in the most deprived institutional conditions the majority did not show symptoms of this disorder.

A 2002 study of children in residential nurseries in Bucharest, in which the DAI was used, challenged the current DSM and ICD conceptualizations of disordered attachment and showed that inhibited and disinhibited disorders could coexist in the same child.

There are two studies on the incidence of RAD relating to high risk and maltreated children in the U.S. Both used ICD, DSM and the DAI. The first, in 2004, reported that children from the maltreatment sample were significantly more likely to meet criteria for one or more attachment disorders than children from the other groups, however this was mainly the proposed new classification of disrupted attachment disorder rather than the DSM or ICD classified RAD or DAD. The second study, also in 2004, attempted to ascertain the prevalence of RAD and whether it could be reliably identified in "maltreated" rather than "neglected" toddlers. Of the 94 maltreated toddlers in foster care, 35% were identified as having ICD RAD and 22% as having ICD DAD, and 38% fulfilled the DSM criteria for RAD. This study found that RAD could be reliably identified and also that the inhibited and disinhibited forms were not independent. However, there are some methodological concerns with this study. A number of the children identified as fulfilling the criteria for RAD did in fact have a preferred attachment figure.

It has been suggested by some within the field of attachment therapy that RAD may be quite prevalent because severe child maltreatment, which is known to increase risk for RAD, is prevalent and because children who are severely abused may exhibit behaviors similar to RAD behaviors. The APSAC Taskforce consider this inference to be flawed and questionable. Severely abused children may exhibit similar behaviors to RAD behaviors but there are several far more common and demonstrably treatable diagnoses which may better account for these difficulties. Further, many children experience severe maltreatment and do not develop clinical disorders. Resilience is a common and normal human characteristic. RAD does not underlie all or even most of the behavioral and emotional problems seen in foster children, adoptive children, or children who are maltreated and rates of child abuse and/or neglect or problem behaviors are not a benchmark for estimates of RAD.

There are few data on comorbid conditions, but there are some conditions that arise in the same circumstances in which RAD arises, such as institutionalization or maltreatment. These are principally developmental delays and language disorders associated with neglect. Conduct disorders, oppositional defiant disorder, anxiety disorders, post-traumatic stress disorder and social phobia share many symptoms and are often comorbid with or confused with RAD. Attachment disorder behaviors amongst institutionalized children are correlated with attentional and conduct problems and cognitive levels but nonetheless appear to index a distinct set of symptoms and behaviors.

Currently, genetic research for the understanding of the development of personality disorders is severely lacking. However, there are a few possible risk factors currently in discovery. Researchers are currently looking into genetic mechanisms for traits such as aggression, fear and anxiety, which are associated with diagnosed individuals. More research is being conducted into disorder specific mechanisms.

The AACAP guidelines state that children with reactive attachment disorder are presumed to have grossly disturbed internal models for relating to others. However, the course of RAD is not well studied and there have been few efforts to examine symptom patterns over time. The few existing longitudinal studies (dealing with developmental change with age over a period of time) involve only children from poorly run Eastern European institutions.

Findings from the studies of children from Eastern European orphanages indicate that persistence of the inhibited pattern of RAD is rare in children adopted out of institutions into normative care-giving environments. However, there is a close association between duration of deprivation and severity of attachment disorder behaviors. The quality of attachments that these children form with subsequent care-givers may be compromised, but they probably no longer meet criteria for inhibited RAD. The same group of studies suggests that a minority of adopted, institutionalized children exhibit persistent indiscriminate sociability even after more normative caregiving environments are provided. Indiscriminate sociability may persist for years, even among children who subsequently exhibit preferred attachment to their new caregivers. Some exhibit hyperactivity and attention problems as well as difficulties in peer relationships. In the only longitudinal study that has followed children with indiscriminate behavior into adolescence, these children were significantly more likely to exhibit poor peer relationships.

Studies of children who were reared in institutions have suggested that they are inattentive and overactive, no matter what quality of care they received. In one investigation, some institution-reared boys were reported to be inattentive, overactive, and markedly unselective in their social relationships, while girls, foster-reared children, and some institution-reared children were not. It is not yet clear whether these behaviors should be considered as part of disordered attachment.

There is one case study on maltreated twins published in 1999 with a follow-up in 2006. This study assessed the twins between the ages of 19 and 36 months, during which time they suffered multiple moves and placements. The paper explores the similarities, differences and comorbidity of RAD, disorganized attachment and post traumatic stress disorder. The girl showed signs of the inhibited form of RAD while the boy showed signs of the indiscriminate form. It was noted that the diagnosis of RAD ameliorated with better care but symptoms of post traumatic stress disorder and signs of disorganized attachment came and went as the infants progressed through multiple placement changes. At age three, some lasting relationship disturbance was evident.

In the follow-up case study when the twins were aged three and eight years, the lack of longitudinal research on maltreated as opposed to institutionalized children was again highlighted. The girl's symptoms of disorganized attachment had developed into controlling behaviors—a well-documented outcome. The boy still exhibited self-endangering behaviors, not within RAD criteria but possibly within "secure base distortion", (where the child has a preferred familiar caregiver, but the relationship is such that the child cannot use the adult for safety while gradually exploring the environment). At age eight the children were assessed with a variety of measures including those designed to access representational systems, or the child's "internal working models". The twins' symptoms were indicative of different trajectories. The girl showed externalizing symptoms (particularly deceit), contradictory reports of current functioning, chaotic personal narratives, struggles with friendships, and emotional disengagement with her caregiver, resulting in a clinical picture described as "quite concerning". The boy still evidenced self-endangering behaviors as well as avoidance in relationships and emotional expression, separation anxiety and impulsivity and attention difficulties. It was apparent that life stressors had impacted each child differently. The narrative measures used were considered helpful in tracking how early attachment disruption is associated with later expectations about relationships.

One paper using questionnaires found that children aged three to six, diagnosed with RAD, scored lower on empathy but higher on self-monitoring (regulating your behavior to "look good"). These differences were especially pronounced based on ratings by parents, and suggested that children with RAD may systematically report their personality traits in overly positive ways. Their scores also indicated considerably more behavioral problems than scores of the control children.

Elements of the family and social environment may also play a role in the development and maintenance of conduct disorder. For instance, antisocial behavior suggestive of conduct disorder is associated with single parent status, parental divorce, large family size, and young age of mothers. However, these factors are difficult to tease apart from other demographic variables that are known to be linked with conduct disorder, including poverty and low socioeconomic status. Family functioning and parent-child interactions also play a substantial role in childhood aggression and conduct disorder, with low levels of parental involvement, inadequate supervision, and unpredictable discipline practices reinforcing youth's defiant behaviors.

Peer influences have also been related to the development of antisocial behavior in youth, particularly peer rejection in childhood and association with deviant peers. Peer rejection is not only a marker of a number of externalizing disorders, but also a contributing factor for the continuity of the disorders over time. Hinshaw and Lee (2003) also explain that association with deviant peers has been thought to influence the development of conduct disorder in two ways: 1) a “selection” process whereby youth with aggressive characteristics choose deviant friends, and 2) a “facilitation” process whereby deviant peer networks bolster patterns of antisocial behavior. In a separate study by Bonin and colleagues, parenting programs were shown to positively affect child behavior and reduce costs to the public sector.

The development of conduct disorder is not immutable or predetermined. A number of interactive risk and protective factors exist that can influence and change outcomes, and in most cases conduct disorder develops due to an interaction and gradual accumulation of risk factors. In addition to the risk factors identified under cause, several other variables place youth at increased risk for developing the disorder, including child physical abuse and prenatal alcohol abuse and maternal smoking during pregnancy. Protective factors have also been identified, and most notably include high IQ, being female, positive social orientations, good coping skills, and supportive family and community relationships.

However, a mere correlation between a particular risk factor and a later developmental outcome (such as conduct disorder) cannot be taken as definitive evidence for a causal link. Co-variation between two variables can arise, for instance, if they represent age-specific expressions of similar underlying genetic factors. For example, the tendency to smoke during pregnancy (SDP) is subject to substantial genetic influence (D'Onofrio et al., 2007), as is conduct disorder. Thus, the genes that dispose the mother to SDP may also dispose the child to CD following mitotic transmission. Indeed, Rice et al. (2009) found that in mother-fetus pairs that were not genetically related (by virtue of in-vitro fertilisation), no link between SDP and later conduct problems arose. Thus, the distinction between causality and correlation is an important consideration.

According to Michael First of the DSM-5 working committee the focus of a relational disorder, in contrast to other DSM-IV disorders, "is on the relationship rather than on any one individual in the relationship".

Relational disorders involve two or more individuals and a disordered "juncture", whereas typical Axis I psychopathology describes a disorder at the individual level. An additional criterion for a relational disorder is that the disorder cannot be due solely to a problem in one member of the relationship, but requires pathological interaction from each of the individuals involved in the relationship.

For example, if a parent is withdrawn from one child but not another, the could be attributed to a relational disorder. In contrast, if a parent is withdrawn from both children, the dysfunction may be more appropriately attributable to a disorder at the individual level.

First states that "relational disorders share many elements in common with other disorders: there are distinctive features for classification; they can cause clinically significant impairment; there are recognizable clinical courses and patterns of comorbidity; they respond to specific treatments; and they can be prevented with early interventions. Specific tasks in a proposed research agenda: develop assessment modules; determine the clinical utility of relational disorders; determine the role of relational disorders in the etiology and maintenance of individual disorders; and consider aspects of relational disorders that might be modulated by individual disorders."

The proposed new diagnosis defines a relational disorder as "persistent and painful patterns of feelings, behaviors, and perceptions" among two or more people in an important personal relationship, such a husband and wife, or a parent and children.

According to psychiatrist Darrel Regier, MD, some psychiatrists and other therapists involved in couples and marital counseling have recommended that the new diagnosis be considered for possible incorporation into the Diagnostic and Statistical Manual of Mental Disorders (DSM IV).

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.

Traumatic grief or complicated mourning are conditions where both trauma and grief coincide. There are conceptual links between trauma and bereavement since loss of a loved one is inherently traumatic. If a traumatic event was life-threatening, but did not result in death, then it is more likely that the survivor will experience post-traumatic stress symptoms. If a person dies, and the survivor was close to the person who died, then it is more likely that symptoms of grief will also develop. When the death is of a loved one, and was sudden or violent, then both symptoms often coincide. This is likely in children exposed to community violence.

For C-PTSD to manifest, the violence would occur under conditions of captivity, loss of control and disempowerment, coinciding with the death of a friend or loved one in life-threatening circumstances. This again is most likely for children and stepchildren who experience prolonged domestic or chronic community violence that ultimately results in the death of friends and loved ones. The phenomenon of the increased risk of violence and death of stepchildren is referred to as the Cinderella effect.

Similar to adult personality disorders there are multiple causes and causal interactions for personality development disorders. In clinical practice it is important to view the disorder multi-perspectively and from an individual perspective. Biological and neurological causes need to be observed just as much as psychosocial factors. Looking at the disorder from only one perspective (e.g. (s)he had a bad childhood) often results in ignorance of important other factors or causal interactions. This might be one of the main reasons why traditional treatment methods often fail with these disorders. Only a multi-perspective view can provide for a multi-dimensional treatment approach which seems to be the key for these disorders.

The diagnosis personality development disorder should only be given carefully and after a longer period of evaluation. Also a thorough diagnostic evaluation is necessary. Parents should be questioned separately and together with the child or adolescent to evaluate the severity and duration of the problems. In addition standardized personality tests might be helpful. It is also useful to ask the family what treatment approaches they have already tried so far without success.

Medical conditions associated with an increased risk of PTSD include cancer, heart attack, and stroke. Intensive-care unit (ICU) hospitalization is also a risk factor for PTSD. Some women experience PTSD from their experiences related to breast cancer and mastectomy.

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.

MIltiary service is a risk factor for developing PTSD. Around 78% of people exposed to combat do not develop PTSD; in about 25% of military personnel who develop PTSD, its appearance is delayed.

Refugees are also at an increased risk for PTSD due to their exposure to war, hardships, and traumatic events. The rates for PTSD within refugee populations range from 4% to 86%. While the stresses of war impact everyone involved, displaced persons have been shown to be more affected than nondisplaced persons.

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 Adam und Breithaupt-Peters personality development disorders are defined as complex disorders

- which show similarity to a certain type of personality disorder in adulthood

- which persist over a long period of time (more than a year) and show a tendency towards being chronic

- which have a severe negative impact on more than one important area of functioning or social life

- which show resistance to traditional educational and therapeutic treatment methods

- which result in a reduced insight into or ignorance of the own problem behavior. The family usually suffers more than the child or adolescent and has a hard time dealing with the diminished introspection.

- which make positive interactions between the children/adolescents and other people merely impossible. Instead social collisions are part of everyday life.

- which threaten the social integration of the young person into a social life and might result in an emotional disability.

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.

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.

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.

Complex post-traumatic stress disorder (C-PTSD; also known as complex trauma disorder) is a psychological disorder thought to occur as a result of repetitive, prolonged trauma involving harm or abandonment by a caregiver or other interpersonal relationships with an uneven power dynamic. C-PTSD is associated with sexual, emotional or physical abuse or neglect in childhood, intimate partner violence, victims of kidnapping and hostage situations, indentured servants, victims of slavery, sweatshop workers, prisoners of war, victims of bullying, concentration camp survivors, and defectors of cults or cult-like organizations. Situations involving captivity/entrapment (a situation lacking a viable escape route for the victim or a perception of such) can lead to C-PTSD-like symptoms, which include prolonged feelings of terror, worthlessness, helplessness, and deformation of one's identity and sense of self.

Some researchers argue that C-PTSD is distinct from, but similar to PTSD, somatization disorder, dissociative identity disorder, and borderline personality disorder, with the main distinction being that it distorts a person's core identity, especially when prolonged trauma occurs during childhood development . It was first described in 1992 by Judith Herman in her book "Trauma & Recovery" and an accompanying article. Though peer-reviewed journals have published papers on C-PTSD, the category is not yet adopted by either the American Psychiatric Association's (APA) "Diagnostic and Statistical Manual of Mental Disorders", 5th Edition (DSM-5), or in the World Health Organization's (WHO) "International Statistical Classification of Diseases and Related Health Problems", 10th Edition (ICD-10). However, it is proposed for the ICD-11, to be finalized in 2018.

Alexithymia is considered to be a personality trait that places affected individuals at risk for other medical and psychiatric disorders while reducing the likelihood that these individuals will respond to conventional treatments for the other conditions. Alexithymia is not classified as a mental disorder in the fourth edition of the "Diagnostic and Statistical Manual of Mental Disorders". It is a dimensional personality trait that varies in severity from person to person. A person's alexithymia score can be measured with questionnaires such as the Toronto Alexithymia Scale (TAS-20), the Bermond-Vorst Alexithymia Questionnaire (BVAQ), the Online Alexithymia Questionnaire (OAQ-G2) or the Observer Alexithymia Scale (OAS). It is distinct from the psychiatric personality disorders, such as antisocial personality disorder or borderline personality disorder, with which it shares some characteristics, and is likewise distinct from the abnormal conditions of sociopathy or psychopathy.

Alexithymia is defined by:

1. difficulty identifying feelings and distinguishing between feelings and the bodily sensations of emotional arousal

2. difficulty describing feelings to other people

3. constricted imaginal processes, as evidenced by a scarcity of fantasies

4. a stimulus-bound, externally oriented cognitive style.

In studies of the general population the degree of alexithymia was found to be influenced by age, but not by gender; the rates of alexithymia in healthy controls have been found at: 8.3%; 4.7%; 8.9%; and 7%. Thus, several studies have reported that the prevalence rate of alexithymia is less than 10%. A less common finding suggests that there may be a higher prevalence of alexithymia amongst males than females, which may be accounted for by difficulties some males have with "describing feelings", but not by difficulties in "identifying feelings" in which males and females show similar abilities.

Psychologist R. Michael Bagby and psychiatrist Graeme J. Taylor have argued that the alexithymia construct is strongly related (negatively) to the concepts of psychological mindedness and emotional intelligence and there is "strong empirical support for alexithymia being a stable personality trait rather than just a consequence of psychological distress". Other opinions differ and can show evidence that it may be state-dependent.

Bagby and Taylor also suggest that there may be two kinds of alexithymia, "primary alexithymia" which is an enduring psychological trait that does not alter over time, and "secondary alexithymia" which is state-dependent and disappears after the evoking stressful situation has changed. These two manifestations of alexithymia are otherwise called "trait" or "state" alexithymia.

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.

Intellectual disability in children can be caused by genetic or environmental factors. The individual could have a natural brain malformation or pre or postnatal damage done to the brain caused by drowning or a traumatic brain injury, for example. Nearly 30 to 50% of individuals with intellectual disability will never know the cause of their diagnosis even after thorough investigation.

Prenatal causes of intellectual disability include:

- Congenital infections such as cytomegalovirus, toxoplasmosis, herpes, syphilis, rubella and human immunodeficiency virus

- Prolonged maternal fever in the first trimester

- Exposure to anticonvulsants or alcohol

- Untreated maternal phenylketonuria (PKU)

- Complications of prematurity, especially in extremely low-birth-weight infants

- Postnatal exposure to lead

Single-gene disorders that result in intellectual disability include:

- Fragile X syndrome

- Neurofibromatosis

- Tuberous sclerosis

- Noonan's syndrome

- Cornelia de Lange's syndrome

These single-gene disorders are usually associated with atypical physical characteristics.

About 1/4 of individuals with intellectual disability have a detectable chromosomal abnormality. Others may have small amounts of deletion or duplication of chromosomes, which may go unnoticed and therefore, undetermined.

There are many possible causes for this disorder. One such possibility is an underlying personality disorder. Individuals with FD may be trying to repeat a satisfying childhood relationship with a doctor. Perhaps also an individual has a desire to deceive or test authority figures. The underlying desire to resume the role of a patient and be cared for can also be considered an underlying personality disorder. Abuse, neglect, or abandonment during childhood are also probable causes.

These individuals may be trying to reenact unresolved issues with their parents. A history of frequent illnesses may also contribute to the development of this disorder. In some cases, individuals afflicted with FD are accustomed to actually being sick, and thus return to their previous state to recapture what they once considered the 'norm.' Another cause is a history of close contact with someone (a friend or family member) who had a severe or chronic condition. The patients found themselves subconsciously envious of the attention said relation received, and felt that they themselves faded into the background. Thus medical attention makes them feel glamorous and special.