DSM-5 includes a number of statements concerning the biology and genetics of mental disorders, and these represent a significant landmark in the history of psychiatry. According to DSM-5, there are no laboratory tests, x-rays, or other biological markers for any mental disorder; there is no physiological specificity to any mental disorder; there is no genetic specificity to any mental disorder; and there is no symptom specificity to DSM-5 disorders. DSM-5 disorders, according to the manual, have porous boundaries with each other, have high rates of comorbidity, and fluctuate a great deal over time. The risk genes for mental disorders number in the hundreds, each contributes perhaps 1%–2% to the overall risk, and the same genes confer risk for multiple DSM-5 categories of disorder. The idea that DSM disorders are separate diseases with distinct pathophysiologies has been disconfirmed by the DSM-5, and therefore by the American Psychiatric Association, as it has by the National Institutes of Mental Health.
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A review of the effectiveness of antipsychotic medications was conducted with a focus on quetiapine, olanzapine, and clozapine. The different antipsychotics are equally effective if given in equivalent doses; therefore, what is true of one is true of all. In large, randomized, placebo-controlled studies, less than 15% of participants respond to antipsychotics, and in many trials less than 10%, if a response is defined as an 80% or greater reduction in symptom scores. Dropout rates are very high in long-term studies such as the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) study (74%). A common definition of a “responder” in antipsychotic studies is a score reduction of 40% or greater, but in most studies, a participant can have a score reduction of 40% and still be psychotic enough to be reenrolled in the trial. Given the high percentage of nonresponders to antipsychotic medications, greater research and clinical emphasis should be placed on psychosocial interventions.
Self-harm is frequently a trauma-driven coping strategy that can be understood from the perspective of the adaptive information processing (AIP) model and treated with eye movement desensitization and reprocessing (EMDR) therapy (Shapiro, 1995, 2001). Self-harm is often connected with memories of adverse and traumatic life experiences. Identifying and processing these memories with EMDR therapy can put an end to the self-injurious behavior. In addition, self-harm is often based on a lack of regulation skills, and these skill deficits can be addressed in EMDR therapy as well. In this article, the authors describe strategies for treating self-harm throughout the 8 phases of EMDR. Although there is no single approach that applies to all cases, the therapist needs to take a careful history of self-harm, its historical origins, and its triggers and functions in the present to formulate a treatment plan. Often, in the authors’ experience, self-harm functions as a self-soothing strategy that redissociates traumatic affect from childhood. Treatment strategies for Phases 3–8 of EMDR therapy are illustrated through case vignettes.
- Go to article: How the Incorrect Belief That Eating Disorders Are Predominantly Genetic Is Maintained
The incorrect belief that anorexia nervosa is predominantly genetic is maintained in the psychiatric literature by a series of misquotations and misrepresentations of research data. An example of this type of scholarship is as an editorial in The American Journal of Psychiatry. Data from family and twin studies referenced in the editorial provide compelling evidence that the genetic contribution to the etiology of anorexia nervosa is small. The incorrect belief that anorexia nervosa is predominantly genetic is maintained, in addition, by statistical procedures such as heritability estimates. The incorrect belief that anorexia nervosa is predominantly genetic should not be endorsed by the American Psychiatric Association, in either its journals, in its published books, or in DSM–V.
The purpose of this article is to analyze and critique repeated claims in the literature that there is a substantial genetic contribution to eating disorders. Data from the existing twin and family studies of eating disorders were tabulated and compared to heritability estimates resulting from complex statistical analyses of the same data. Overall, concordance in monozygotic twins is 26% for bulimia and 35% for anorexia nervosa. Among the relatives of probands with bulimia, 95.1% do not have bulimia, whereas among the relatives of probands with anorexia nervosa, 97.1% do not have the disorder. The raw data refute claims that the genetic heritability of eating disorders is as high as 80%. The erroneous conclusion that there is a substantial genetic contribution to eating disorders needs to be corrected by focusing on the raw data for twin concordance and prevalence in first-degree relatives.
Un trouble dissociatif de l'identité (TDI) jusque-là non diagnostiqué peut exister chez des individus qui sont évalués en vue de l'EMDR (désensibilisation et retraitement par les mouvements oculaires). Un TDI jusque-là non diagnostiqué était présent chez 3,9 % des 1 529 patients adultes hospitalisés en psychiatrie générale dans 10 études menées dans 6 pays différents. Cet article présente un cas de TDI probable qui n'a pas été détecté dans un rapport de cas publié et apporte des lignes directrices pour déterminer quand suspecter et comment diagnostiquer le TDI. De telles lignes directrices manquent à la formation de nombreux professionnels en santé mentale.
The philosophical foundations of reductionist biological psychiatry are internally self-contradictory. Mind is simultaneously disallowed and “explained” by the reductionist approach; this internal self-contradiction invalidates reductionist biological psychiatry at the level of its philosophical foundation. Three theories that dominate science today are based on a reductionist approach: the Big Bang theory, the origins of life 3.7 billion years ago, and the emergent property model of the relationship between mind and brain. The problem with these theories is not with the science, rather it is the way the three theories are used to validate a logically untenable philosophical position, which in biological psychiatry insists on a model of mind as an emergent property of brain function. The universe, evolution, and the human mind, within this reductionist philosophy, are all based on the workings of automatic machinery. The purpose of the present article is to analyze the fundamental logical errors underlying biological psychiatry, which is based on a mechanistic model of the universe.
Las autolesiones suelen ser una estrategia de afrontamiento derivada del trauma, que pueden entenderse desde la perspectiva del modelo de procesamiento adaptativo de la información (PAI) y tratarse con terapia de desensibilización y reprocesamiento mediante movimientos oculares (EMDR) (Shapiro, 1995, 2001). Las autolesiones a menudo están conectadas con recuerdos de experiencias adversas y traumáticas en la vida. Identificar y procesar estos recuerdos con terapia EMDR puede poner fin al comportamiento autodestructivo. Además, las autolesiones suelen tener su base en la falta de habilidades de regulación, y estos déficits de habilidades también se pueden abordar en la terapia EMDR. En este artículo, los autores describen estrategias para tratar las autolesiones a lo largo de las 8 fases de EMDR. Aunque no existe un enfoque único que se aplique en todos los casos, el terapeuta debe hacer una historia meticulosa de las autolesiones, sus orígenes históricos, y sus desencadenantes y funciones en el presente para formular un plan de tratamiento. A menudo, según la experiencia de los autores, las autolesiones funcionan como una estrategia de autorregulación que vuelve a disociar las emociones traumáticas de la infancia. Las estrategias de tratamiento para las Fases 3-8 de la terapia EMDR se ilustran a través de ejemplos de casos.
The author reviewed the placebo-controlled literature on electroconvulsive therapy (ECT) for depression. No study demonstrated a significant difference between real and placebo (sham) ECT at 1 month posttreatment. Many studies failed to find a difference between real and sham ECT even during the period of treatment. Claims in textbooks and review articles that ECT is effective are not consistent with the published data. A large, properly designed study of real versus sham ECT should be undertaken. In the absence of such a study, consent forms for ECT should include statements that there is no controlled evidence demonstrating any benefit from ECT at 1 month posttreatment. Consent forms should also state that real ECT is only marginally more effective than placebo.