Faculty Bibliography

In support of his Oedipal theory of Little Hans's horse phobia, Freud argues that Hans's assertion that his younger sister Hanna has a penis is a defense against castration anxiety, revealing a key Oedipal component. Freud's argument presupposes that by Hans's term "widdler" (Wiwimacher in German), Hans means "penis," a structural/functional concept. Challenging Freud's interpretation on Wittgensteinian grounds, Jonathan Lear argues that Hans lacks rationally structured concepts and instead applies category terms associatively according to perceived family resemblance similarities. Recent discoveries in child cognitive-developmental psychology, especially regarding young children's essentialist and teleological conceptual understanding, suggest that Hans was conceptually more sophisticated than either Freud or Lear allow. Both developmental research and a close examination of the case evidence suggest that Hans used "widdler" to express a functional/essentialist concept referring not to penises but to "organs for urinating," irrespective of perceived structural form. Knowing that Hanna urinates, Hans's attribution of a widdler to Hanna is logical and does not require hypothesizing castration anxiety. In his reaction to his sister's genitals, rather than a "little Oedipus" or little Wittgensteinian, Hans is best understood as a little essentialist theoretician. Freud's misinterpretation of Hans's assertions about Hanna's widdler holds lessons for all analysts about the need to take into account the full complexity of child and adult conceptualization before attributing dynamic or fantasy derivatives in interpretations.

In this two-part analysis, I analyze Marc Lewis's arguments against the brain-disease view of substance addiction and for a developmental-learning approach that demedicalizes addiction. I focus especially on the question of whether addiction is a medical disorder. In Part 1, I argued that, even if one accepts Lewis's critique of the brain evidence presented for the brain-disease view, his arguments fail to establish that addiction is not a disorder. Relying on my harmful dysfunction analysis of disorder, I defended the view that addiction is a medical disorder and a brain disorder. In Part 2, I consider some broader philosophical issues raised by Lewis's arguments: (1) I consider a larger puzzle, at the heart of the neo-Kraepelinian program in contemporary psychiatry, that is raised by Lewis's argument that addiction is not a disorder because the brain displays no damage but only normal learning: must all mental disorders be brain disorders, or can mental disorders occur in normal brains? I argue that mental disorders can occur in normal brains. (2) I critique Lewis's response to the evolutionary "novel environment" approach to explaining why addiction is a disorder. (3) Lewis agrees with brain-disease proponents that interpreting addiction as brain disorder relieves addicts of moral censure, but I argue that moral defect and brain disease are not exclusive. (4) Finally, I consider Lewis's "developmental-learning" account of addiction that encourages positive and empowering narrativizing of addiction, but I argue that the developmental-learning view is vacuous due to use of an overly broad notion of "development.".

In this two-part analysis, I analyze Marc Lewis's arguments against the brain-disease view of substance addiction and for a developmental-learning approach that demedicalizes addiction. I focus especially on the question of whether addiction is a medical disorder. Addiction is currently classified as a medical disorder in DSM-5 and ICD-10. It is further labeled a brain disease by NIDA, based on observed brain changes in addicts that are interpreted as brain damage. Lewis argues that the changes result instead from normal neuroplasticity and learning in response to the intense rewards provided by addictive substances, thus that addiction is not a brain disease and by implication not a medical disorder at all. I argue that even if one accepts Lewis's reinterpretation of the brain evidence, his conclusions do not follow. Relying on my harmful-dysfunction analysis of medical disorder, I defend the view that substance addiction is in fact a medical disorder and a brain disorder. In Part 1, I identify five arguments Lewis puts forward against the brain-disease view and evaluate them as arguments that addiction is not a disorder: (1) Addiction is not a chronic, relapsing condition; (2) There is no clear boundary between addiction and other strong desires; (3) Negative consequences are not unique to disorders; (4) The brain disease model does not account for behavioral addictions; and, (5) Addiction is like love. I argue that Lewis's arguments are invalid because they fail to take account of the context of addiction and its relation to biological design.

BACKGROUND: "Complicated" subthreshold depression (CsD) includes at least one of six pathosuggestive "complicated" symptoms: >6 months duration, marked role impairment, sense of worthlessness, suicidal ideation, psychotic ideation, and psychomotor retardation. "Uncomplicated" subthreshold depression (UsD) has no complicated features. Whereas studies show that complicated (CMDD) versus uncomplicated (UMDD) major depression differ substantially in severity and prognosis, UsD and CsD severity has not been previously compared. This study evaluates UsD and CsD pathology validator levels and examines whether the complicated/uncomplicated distinction offers incremental concurrent validity over the standard number-of-symptoms dimension as a depression severity measure. METHODS: Using nationally representative community data from the National Comorbidity Survey, seven depression lifetime history subgroups were identified: one MDD screener symptom (n=1432); UsD (n=430); CsD (n=611); UMDD (n=182); and CMDD with 5-6 symptoms (n=518), 7 symptoms (n=217), and 8-9 symptoms (n=291). Severity was evaluated using five concurrent pathology validators: suicide attempt, interference with life, help seeking, hospitalization, and generalized anxiety disorder. RESULTS: CsD validator levels are substantially higher than both UsD and UMDD levels, and similar to mild CMDD, disconfirming the "monotonicity thesis" that severity increase with symptom number. Complicated/uncomplicated status predicts severity, and when complicatedness is controlled, number of symptoms no longer predicts validator levels. LIMITATIONS: Diagnoses were based on respondents' fallible retrospective symptom reports during a lay-administered structured interview, which may not yield diagnoses comparable to clinicians' assessments. CONCLUSION: CsD is more severe than UsD and comparable to mild MDD. Complicated status more validly indicates depression severity than the standard number-of-symptoms measure.

BACKGROUND: Uncomplicated major depressive disorder (UMDD) is defined as MDD that does not include any of six pathosuggestive features: more than six months duration, marked functional impairment, sense of worthlessness, suicidal ideation, psychotic ideation, and psychomotor retardation. Complicated MDD (CMDD) includes all episodes containing one or more of these features. UMDD has been shown to be lower than CMDD and indistinguishable from no-MDD-history on predictive pathology validators. This study's purpose is to establish where on the number-of-symptoms depressive continuum UMDD is located, using the criterion of predictive validity. METHODS: Using two-wave longitudinal community data, seven baseline depression history subgroups were identified: no MDD symptoms (n=23,214), one MDD screener symptom (n=609), subthreshold or "minor" depression (mD; 2-4 MDD symptoms; n=2,623), UMDD (n=505), and complicated MDD with 5-6 symptoms (n=1,106), 7 symptoms (n=1,200), and 8-9 symptoms (n=2,408). Predictive validity was evaluated by four follow-up variables: major depressive episode; generalized anxiety disorder; suicide attempt; and manic/hypomanic episode. RESULTS: UMDD predictive pathology validator rates are not significantly different from rates for subthreshold mD but significantly different from those for all other depression categories; UMDD is higher in symptoms but lower in validator levels than 5-6 symptom CMDD. LIMITATIONS: Baseline and follow-up diagnoses were based on respondents' fallible retrospective symptom reports in response to a lay-administered structured questionnaire, which may not yield diagnoses comparable to clinicians' assessments. CONCLUSION: Uncomplicated MDD's follow-up outcomes resemble subthreshold depression, not CMDD, even when CMDD has less symptoms. Clinical decisions should reflect the relatively benign prognosis of uncomplicated MDD.