After weighing all perspectives and sources of evidence, it is clear that there are problems on multiple levels. Our conceptualizations are fuzzy, our samples are biased, our measures are biased, and our clinicians fall prey to their own biases. The question of what to do is even more difficult to address. At the theoretical level, we have great room for improvement. A logical place to start is at the DSM level. However, tales of how DSM committees work are horrifying (see Caplan, 1991, for details on how the self-defeating personality diagnosis was retained in the DSM). What we put faith in as an unbiased and scientific system for diagnosing mental disorders is often a very political and even random set of criteria. To add further fuel to the fire, the vast majority of DSM authors and committee members on personality disorder workgroups have been male. Eighty-nine percent of DSM-III personality disorder workgroup members (8 of 9) were male, 84% for DSM-III-R (32 of 38), and 78% for the DSM-IV (7 of 9; Widiger, 1998). Future revisions of the DSM need to draw on the resources of a far wider clinical base than the 1,000 individuals involved in the production of the DSM-IV Additionally, if our clinical samples are biased, as a community, we need to make the investment in solid epidemiological research to determine real prevalence rates, even if we are using our flawed diagnostic criteria. It is difficult to obtain a clear picture of where to fix a problem if we do not know how pervasive the problem is.

The fairly convincing evidence that clinicians do not adhere to the existing criteria when making diagnoses is also troubling. How to tackle these failures is a complex issue. Perhaps raising awareness of biases is a first step. If clinicians have taken the time to introspect a little on why they assume histrionics are female and narcissists are male, they may pause to consider alternative diagnoses. The DSM-IV contains only one sentence about this issue buried within the general discussion of personality disorders:

Although these differences in prevalence probably reflect real gender differences in the presence of such patterns, clinicians must be cautious not to overdiagnose or underdiagnose certain Personality Disorders in females or in males because of social stereotypes about typical gender roles and behaviors. (APA, 1994, p. 632)

Focus on Gender (Continued)

Perhaps another solution would be to include reminders throughout the DSM, for example, in the histrionic section: "If a female client is presenting with X, Y, and Z symptoms, make sure to consider a diagnosis of antisocial personality disorder as well." While these suggestions are merely stopgap measures to address the larger issues of how our diagnostic criteria and, on a grander scale, our entire mental health system are biased against women, they are a step toward ameliorating the negative effects such biases can have on our mental health.

the defective gene is weakened by the operation of beneficial modifying genes or favorable environmental experiences (Meehl, 1990b). An alternate explanation might be formulated in terms of polygenic action; polygenes have minute, quantitatively similar, and cumulative effects. Thus, a continuum of increasing pathological severity can be accounted for by the cumulative effects of a large number of minor genes acting on the same trait (Millon, 1969).

The idea that psychopathological syndromes comprise well-circumscribed disease entities is an attractive assumption for those who seek a Mendelian or single-gene model of inheritance. Recent thinking forces us to question the validity of this approach to nosology and to the relevance of Mendelian genetic action. Defects in the infinitely complex central nervous system can arise from innumerable genetic anomalies (Plomin, 1990). Moreover, even convinced geneticists make reference to the notion of phenocopies, a concept signifying that characteristics usually traceable to genetic action can be simulated by environmental factors; thus, overtly identical forms of pathology may arise from either genetic or environmental sources. As a consequence, the clinical picture of a disorder may give no clue to its origins since similar appearances do not necessarily signify similar etiologies. To complicate matters further, different genes vary in their responsiveness to environmental influences; some produce uniform effects under all environmental conditions, whereas others can be entirely suppressed in certain environments (Plomin, DeFries, & McClearn, 1990). Moreover, it appears that genes have their effects at particular times of maturation and their interaction with environmental conditions is minimal both before and after these periods.

Despite these ambiguities and complications, there can be little question that genetic factors do play some dispositional role in shaping the morphological and biochemical substrate of certain traits. However, these factors are by no means necessary to the development of personality pathology, nor are they likely to be sufficient in themselves to elicit pathological behaviors. They may serve, however, as a physiological base that makes the person susceptible to dysfunction under stress or inclined to learn behaviors that prove socially troublesome.

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