A Review and Critique of Obsessive-Compulsive Personality Disorder Etiologies: Reckoning With Heritability Estimates

Steven Charles Hertler

doi:10.5964/ejop.v10i1.679

Abstract

The present review and critique of extant etiological theories centers on a single finding: Obsessive-compulsive personality is highly heritable (0.78) and not significantly influenced by “common, shared-in-families environmental factors” (Torgersen et al., 2000, p. 424). This finding, though twelve years old, has remained dissociated from existing etiological accounts. Psychoanalytic theories anachronistically maintain that obsessive personality is familially forged. Biological theories, few, unelaborated and weakened by postulating proximate instead of ultimate explanations, fail to seriously reckon with Torgersen’s findings. Truly integrating heritability estimates into a functional etiological account of obsessive character, it is argued in the discussion section, will come from an evolutionary model that understands obsessive personality to be an evolved strategy rather than a dysfunctional disorder.

Highlights

Both the fourth and fifth editions of the Diagnostic and Statistical Manual of Mental Disorders describe ten personality disorders
Characterized by the American Psychiatric Association (2000, p. 296; 2013) as a pervasive pattern of “preoccupation with orderliness, perfectionism, and mental and interpersonal control, at the expense of flexibility, openness, and efficiency,” Obsessive Compulsive Personality Disorder (OCPD) is comprised of the following symptoms: (1) Preoccupation with details, rules, lists, order, organization, or schedules; (2) shows perfectionism that interferes with task completion; (3) is excessively devoted to work and productivity; (4) is over-conscientious, scrupulous, and inflexible about matters of morality, ethics, or values; (5) is unable to discard worn-out or worthless objects; (6) is reluctant to delegate tasks; (7) adopts a miserly spending style towards both self and others; (8) shows rigidity and stubbornness
Using Baron-Cohen’s scheme, Hummelen et al assert that in the obsessive, the empathizing mechanism is blunted and the systemizing mechanism is sharpened. Obsessives incongruously apply their systemizing mechanism across situations, attempting to subject the vagaries of social life to the order of physical life. This inborn imbalance represents the temperamental seeds of obsessive character, which must be cultivated by parental mismanagement, as described by Hummelen et al (2008, p. 453) in the following passage: We suggest that OCPD develops out of an intersubjective matrix where children with a moderate to high inborn tendency of systemizing mechanism and displaying more rigidity, stubbornness, and perfectionism than average, are met by rigid and inflexible countermeasures by parents who may share the same genetic disposition

Summary

Introduction

Both the fourth and fifth editions of the Diagnostic and Statistical Manual of Mental Disorders describe ten personality disorders. The discussion section will comment on these weaknesses and examine their implications Stated here, these implications are 1) that we need to take seriously and assimilate the behavioral genetics estimates that demonstrate the high heritability of obsessive character; 2) we need abandon psychoanalytic models outright, not as possible adjunctive modifiers of obsessive character, but as primary determinants of it; 3) we need to ask more of biological models, demanding not just localization, but true explanation; 4) we need to either reject or revise those biological etiologies that simultaneously find obsessive character to be both heritable and harmful; 5) we need to consider that the only way to craft a truly convincing model of obsessive origins might be to altogether stop thinking of obsessive character as disorder; 6) instead, we would do better to search for the adaptive logic behind obsessive behavior and posit an evolutionary model on these grounds (Hertler, 2013). Europe's Journal of Psychology 2014, Vol 10(1), 168–184 doi:10.5964/ejop.v10i1.679

A History of Psychoanalytic Etiological Models

Discussion and Conclusions