The Marchessault, 1996). Guzder et al conducted

 The American Psychiatric Association defines psychological disorders as a pattern of behaviour that is disturbing and harmful to a person which can lead to dysfunction in important areas of one’s life and is accompanied by an increased risk of additional suffering or even death. Further to that a personality disorder involves a person’s personality traits becoming rigid and inflexible and behaviour that deviates from the social norm which causes severe impairment or distress to the individual. This essay will discuss the view that the causes of personality disorders are multifactorial and will focus on the six specific personality disorders outlined in the DSM-V; in particular, the focus will be on Borderline, Schizotypal and Obsessive Compulsive Personality Disorder. Borderline Personality Disorder (BPD) is characterised by a life of instability, this includes their relationships, their emotions and their self-image. They are often intense, volatile and have a strong fear of abandonment. One argument is that this is a result of loss of or abuse by the parents in early childhood leading the child to have unstable attachments with their primary caregivers which translates on into adulthood in the form of unstable behaviour (Guzder, Paris, Zelkowitz & Marchessault, 1996). Guzder et al conducted a study of 98 children 41 of which were identified as having Borderline Personality Disorder using the Child Diagnostic Interview for Borderliners. They assessed their parental dysfunction and abuse and scored them individually comparing them to the non-borderline children. They found similar levels of dysfunction but significantly higher levels of sexual abuse, physical abuse, severe neglect, and parental substance abuse or criminality in the Borderline group suggesting these are the risk factors that make an individual susceptible to BPD. This is further supported by an abundance of research on childhood abuse, outlining it as a significant antecedent to BPD (Herman, Perry & van der Kolk, 1989; Fossati, Madeddu & Maffei, 1999. However, the study fails to account for the fact that not all children who suffer abuse go on to have BPD as well as, although the number is significant, not all adults with BPD have suffered abuse as children. This would suggest that while childhood abuse could be part of the cause of BPD it does not account for all cases therefore there must be other components in its cause for example it is possible that trauma is a trigger for children with a biological vulnerabilityFurthermore, no definitive conclusions can be drawn about the aetiology of borderline personality disorder from correlational studies despite the importance of it as a factor being well supported by numerous studies (Guzder et al; Herman et al; Fossati et al).Although it would appear that biological factors play a minimal role in borderline personality order there is evidence showing a genetic link between borderline personality disorder and the Five Factor Model personality traits in a study of 11,000 monozygotic and dizygotic twins, and siblings (Distel et al, 2009). The broad-sense heritability for borderline personality was found to be 45%. Phenotypic correlations between FFM traits and BPD ranged from .06 for openness to .68 for neuroticism and they found a combination of low agreeableness and high neuroticism best predicts BPD(Widgier and Costa 2002). Despite these figures suggesting a significant influence from genetics it is not large enough to be solely biological and would suggest an interaction of factors. However, the phenotype of a person is an interaction of their genetic makeup and environmental influences therefore, in itself it is not a wholly biological explanation and acknowledges the influence of an individual’s environment.  Schizotypal Personality Disorder (SPD) is characterised by acute discomfort in social relationships and a feeling of not fitting in, they are often eccentric and odd and violate social norms, such as eye contact and colour schemes. Schizotypal personality disorder is much more commonly investigated and explained in terms of biological factors due to individuals diagnosed as schizotypal also being referred to as high risk for schizophrenia due to genetic similarities between the two (Nigg and Goldsmith, 1994). Furthermore, the first degree relatives of an individual with schizophrenia are much more likely to show traits of schizotypal personality disorder than a member of the general population (Kendler & Diehl, 1993). Siever (1985) studied schizotypal as a schizophrenic disorderand found decreased activities of plasma amine oxidase and platelet monoamine oxidase have been associated with SPD in biological high risk studies (Baron, Levitt, and Perlman 1980) and in the families of schizophrenics, Baron and Levitt (1980, as cited in Siever, 1985). However, these findings contradict previous research which found no associations between schizophrenic disorders and low platelet MAO activity highlighting the frailty of this argument (Coursey, Buchsbaum, and Murphy 1979; Haier, Buchsbaum and Murphy, 1980). Other studies using psychophysiological methods have been applied to subjects with psychological traits similar to SPD and found biological abnormalities similar to those reported in schizophrenia. These studies are in line with the possibility that some individuals with SPD may share common biological abnormalities with schizophrenic individuals and may further our understanding of SPD and its relationship to schizophrenia (Siever, 1985). However, the majority of research into SPD tends to focus more on schizophrenia’s causes under the assumption that SPD has a lot of genetic similarities but since no single gene or combination of genes has been identified as the cause of schizophrenia any genetic similarities between it and SPD could merely be circumstantial or due to something else and cannot be proved as causes (Siever, 1985). Furthermore, again a single major gene or combination of genes has yet to be identified in the cause of SPD and therefore this could suggest that while genetics play a large role it is again a combination of factors such as genetics and environment where perhaps genetic make an individual susceptible and environment acts as a trigger for the disorder (Kendler & Diehl, 1993).  Obsessive Compulsive personality disorder (OCPD) is characterised by a need to be perfect in a person with very high standards who is often preoccupied with order and considered a workaholic. They often appear inflexible in their ethics and morals and are highly conscientious, they also appear to have little time for leisure or friendships choosing to focus on demanding hobbies. As with SPD and schizophrenia research of OCPD has focused much on similarities and differences between OCPD and OCD and evidence of increased OCD in families of PD patients would suggest an association between the two (Nigg and Goldsmith, 1994). However, this means while there is an abundance of research on OCD there are a lot of references to OCPD possibly having the same causes but no concrete evidence. The biological explanation of OCPD focuses on genetics and heritability of traits for example Clifford et al (1984) assessed 419 pairs of twins reared together in England (175 MZ female, 75 MZ male, 99 DZ female, 44 DZ male, and 55 opposite-sex DZ), administering a brief form of the Leyton Obsessional Inventory (Cooper & Kelleher, 1973) and the Eysenck EPQ. The Leyton conception of obsessiveness included incompleteness, cleanliness, tidiness, gloomy thoughts, and checking. The Leyton inventory correlations were .50 for MZ males, .22 for DZ males, .44 for MZ females, and. 13 for DZ females. The correlation for the opposite-sex DZ pairs was .11. These figures showed estimated heritability of obsession at .46 for males and .62 for females, with non-shared environment effects sufficient to account for the remaining variance. They then analysed the relation of Leyton obsessiveness to EPQ neuroticism and found that the obsession scale could be subdivided into two factors, the first strongly correlated with neuroticism. That correlation was mostly explained by shared genetic variance. However, a similar Norwegian study conducted by Torgersen and Psychol(1980) found that the heritability of obsessiveness as a personality trait was modest or non-existent in their sample. The highly contradictory findings of these two studies would suggest a certain uncertainty in the area. Although the two studies used somewhat different measures of obsessiveness which could account for the difference in findings especially since the measure of obsessiveness is very objective and is influenced by a number of personal and cultural factors making these studies very had to compare. In addition, you cannot separate the effects of genes and environment especially in sibling reared together.  In this area of research true experiments are impossible due to the nature of the topic therefore most of the research in this area is correlational and can only show a relationship between two factors not a cause and effect. Furthermore, we cannot say which factor comes first for example is inherited obsessiveness a factor that could lead to OCPD or is it a result of already having OCPD. Personality disorders are shown as having no singular factor that could cause them each personality disorder is different and has to be considered individually as some are more biologically based while others are more psychological and environmentally based. Typically, personality disorders are a result of the interaction between an individual’s genetic predisposition and environment which accounts for the individual differences in personality disorders better as a collaboration than individually.