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5. Judith Rapoport, The Boy Who Couldn’t Stop Washing (New York: Plume, 1990), 90–91. The evidence for heritability that follows comes from M. Lenane, S. Swedo, H. Leonard, et al., “Psychiatric Disorders in First Degree Relatives of Children and Adolescents with Obsessive Compulsive Disorder,” Journal of the American Academy of Child and Adolescent Psychiatry 29 (1990): 407–12.

6. S. Turner, D. Beidel, and R. Nathan, “Biological Factors in Obsessive-Compulsive Disorders,” Psychological Bulletin 97 (1985): 430–50; L. Baxter, M. Phelps, J. Mazziotta, et al., “Local Cerebral Glucose Metabolic Rates in Obsessive-Compulsive Disorder: A Comparison with Rates in Unipolar Depression and Normal Controls,” Archives of General Psychiatry 44 (1987): 211–18; R. Rubin, J. Villanueva-Meyer, J. Ananth, et al., “Regional Xenon 133 Cerebral Blood Flow and Cerebral Technetium 99m HMPAO Uptake in Unmedicated Patients with Obsessive-Compulsive Disorder and Matched Normal Control Subjects,” Archives of General Psychiatry 49 (1992): 695–702.

The latest studies show normalization of brain function with Anafranil (clomipramine) treatment, fluoxetine treatment, and behavior therapy. See C. Benkelfat, T. Nordahl, W. Semple, et al., “Local Cerebral Glucose Metabolic Rates in Obsessive-Compulsive Disorder,” Archives of General Psychiatry 47 (1990): 840–48; L. Baxter, J. Schwartz, K. Bergman, et al., “Caudate Glucose Metabolic Rate Changes with Both Drug and Behavior Therapy for Obsessive-Compulsive Disorder,” Archives of General Psychiatry 49 (1992): 681–89; S. Swedo, P. Pietrini, H. Leonard, et al., “Cerebral Glucose Metabolism in Childhood-Onset Obsessive-Compulsive Disorder,” Archives of General Psychiatry 49 (1992): 690–94.

7. Both Judith Rapoport, in The Boy Who Couldn’t Stop Washing, and Isaac Marks and Adolf Tobena, in “Learning and Unlearning Fear: A Clinical and Evolutionary Perspective,” Neuroscience and Biobehavioral Reviews 14 (1990): 365–84, have argued for an evolutionarily prepared substratum of OCD.

8. For recent studies of Anafranil (clomipramine), see M. Jenike, L. Baer, P. Summergrad, et al., “Obsessive-Compulsive Disorder: A Double-Blind, Placebo-Controlled Trial of Clomipramine in 27 Patients,” American Journal of Psychiatry 146 (1989): 1328–30; R. Katz, J. DeVeaugh-Geiss, P. Landau, “Clomipramine in Obsessive-Compulsive Disorder,” Biological Psychiatry 28 (1990): 401–14; M. Pato, T. Piggott, J. Hill, et al., “Controlled Comparison of Buspirone and Clomipramine in Obsessive-Compulsive Disorder,” American Journal of Psychiatry 148 (1991): 127–29; and M. Mavissakalian, B. Jones, S. Olson, J. Perel, “Clomipramine in Obsessive-Compulsive Disorder: Clinical Response and Plasma Levels,” Journal of Clinical Psychopharmacology 10 (1990): 261–68. See M. Trimble, “Worldwide Use of Clomipramine,” Journal of Clinical Psychiatry 51 (1990): 51–54, for a review of eleven double-blind studies. Overall, slightly fewer than 50 percent of the patients are improved to subclinical levels, and perhaps 25 percent are almost symptom free.

For side effects and the high relapse rate after drug discontinuation, see M. Pato, R. Zohar-Kadouch, J. Zohar, D. Murphy, “Return of Symptoms After Discontinuation of Clomipramine in Patients with Obsessive-Compulsive Disorder,” American Journal of Psychiatry 145 (1988): 1521–25, which shows an 80 percent relapse rate; T. Piggott, M. Pato, S. Bernstein, et al., “Controlled Comparisons of Clomipramine and Fluoxetine in the Treatment of Obsessive-Compulsive Disorder,” Archives of General Psychiatry 47 (1990): 926–32, which shows a comparable effect for fluoxetine to clomipramine and comparable high relapse after drug discontinuation; and J. Greist, “Treating the Anxiety: Therapeutic Options in Obsessive-Compulsive Disorder,” Journal of Clinical Psychiatry 51 (1990): 29–34.

For an articulate critique of the biological viewpoint, see P. DeSilva and S. J. Rachman, Obsessive-Compulsive Disorder: The Facts (Oxford: Oxford