Handbook of Clinical Gender Medicine. Группа авторов
Чтение книги онлайн.
Читать онлайн книгу Handbook of Clinical Gender Medicine - Группа авторов страница 38
23 Carney RM, Wolpert CM, Ravan SA, Shahbazian M, Ashley-Koch A, Cuccaro ML, Vance JM, Pericak-Vance MA: Identification of MeCP2 mutations in a series of females with autistic disorder. Pediatr Neurol 2003;28:205–211.
24 Filges I, Rothlisberger B, Blattner A, Boesch N, Demougin P, Wenzel F, Huber AR, Heinimann K, Weber P, Miny P: Deletion in Xp22.11: PTCHD1 is a candidate gene for X-linked intellectual disability with or without autism. Clin Genet 2011;79:79–85.
25 Gong XH, Bacchelli E, Blasi F, Toma C, Betancur C, Chaste P, Delorme R, Durand CM, Fauchereau F, Botros HG, Leboyer M, Mouren-Simeoni MC, Nygren G, Anckarsater H, Rastam M, Gillberg IC, Gillberg C, Moreno-De-Luca D, Carone S, Nummela I, Rossi M, Battaglia A, Jarvela I, Maestrini E, Bourgeron T, IMGSAC: Analysis of X chromosome inactivation in autism spectrum disorders. Am J Med Genet B Neuropsychiatr Genet 2008;147B:830–835.
26 Johnston CM, Lovell FL, Leongamornlert DA, Stranger BE, Dermitzakis ET, Ross MT: Large-scale population study of human cell lines indicates that dosage compensation is virtually complete. PLoS Genet 2008;4:e9.
27 Creswell CS, Skuse DH: Autism in association with Turner syndrome: genetic implications for male vulnerability to pervasive developmental disorders. Neurocase 1999;5:511–518.
28 Bruining H, van Rijn S, Swaab H, Giltay J, Kates W, Kas MJH, van Engeland H, de Sonneville L: The parent-of-origin of the extra X chromosome may differentially affect psychopathology in Klinefelter syndrome. Biological Psychiatry 2010;12:1156–1162.
29 Botbol M, Roubertoux PL, Carlier M, Trabado S, Brailly-Tabard S, Perez-Diaz F, Bonnot O, Bronsard G, Tordjman S: Modulation of brain beta-endorphin concentration by the specific part of the Y chromosome in mice. PLoS One 2011;6:e16704.
30 Ridley M: The Red Queen. London, Penguin, 1993.
31 Mouridsen SE, Rich B, Isager T: Sibling sex ratio of individuals diagnosed with autism spectrum disorder as children. Dev Med Child Neurol 2010;52:289–292.
32 Gualtieri T, Hicks RE: An immunoreactive theory of selective male affliction. Behav Brain Sci 1985;8:427–441.
33 Warren RP, Cole P, Odell JD, Pingree CB, Warren WL, White E, Yonk J, Singh VK: Detection of maternal antibodies in infantile autism. J Am Acad Child Adolesc Psychiatry 1990;29:873–877.
34 Wang PY, Koishi K, McGeachie AB, Kimber M, MacLaughlin DT, Donahoe PK, McLennan IS: Mullerian inhibiting substance acts as a motor neuron survival factor in vitro. Proc Natl Acad Sci USA 2005;102:16421–16425.
35 Lai MC, Lombardo MV, Pasco G, Ruigrok AN, Wheelwright SJ, Sadek SA, Chakrabarti B, Baron-Cohen S, MRC AIMS Consortium: A behavioral comparison of male and female adults with high functioning autism spectrum conditions. PLoS One 2011;6:e20835.
Rebecca Knickmeyer, PhD
Department of Psychiatry, Medical Wing C, Room 343
School of Medicine, University of North Carolina at Chapel Hill
336 Emergency Drive
Chapel Hill, NC 27599 (USA)
Tel. +1 919 966 2216, E-Mail [email protected]
Central Nervous System and Clinical Applications
Schenck-Gustafsson K, DeCola PR, Pfaff DW, Pisetsky DS (eds): Handbook of Clinical Gender Medicine.
Basel, Karger, 2012, pp 92–98
______________________
David R. Rubinow · Claire D. Craft
Department of Psychiatry, Neurosciences Hospital, University of North Carolina at Chapel Hill, Chapel Hill, N.C., USA
______________________
Abstract
The translation of observed sex differences in depression and its treatment into clinical practice is in an immature stage of development. Indeed, the literature to date provides no compelling clear-cut guidelines for the selection or avoidance of any psychotropic medication on the basis of sex alone. The current lack of translation, however, is counterbalanced by a voluminous body of literature suggesting that sex, as one of several critical contextual factors, impacts the regulation and dysregulation of affect.
Copyright © 2012 S. Karger AG, Basel
Sex differences that may impact the presentation and treatment of depression will often remain undisclosed unless clinicians remain vigilant to their possible influence. For instance, victims of sexual abuse, who are most often women, frequently exhibit dysregulation of the hypothalamic-pituitary-adrenal axis and experience depressions that typically are responsive to psychotherapy. However, without specific inquiries, this contextual information will often go undisclosed. Similarly, drug abuse, which is more prevalent in men, can greatly complicate the presentation and treatment of depression. Finally, there are culture-bound sex differences in presentation that often reflect the relative reluctance in men to endorse symptoms of sadness. Consequently, the likelihood of overlooking clinically relevant depressive episodes in men will be substantial unless the physician makes a concerted effort to elicit evidence of either a past or a present depressive disorder. Failure to detect comorbid depression is particularly problematic, as it results in increased treatment costs for the primary illness, greater pathological progression of illness, and an increased likelihood of death.
The goal of individualized medicine is the prediction of therapeutic interventions that will have the greatest efficacy and the least adverse effects. This goal will be met only when our clinical databases are sufficiently populated and integrated to permit identification of relevant contextual predictors (be they genomic, historical, psychological, or physiological). Currently available genetic, psychobiological, brain imaging, and pharmacological evidence for the existence of meaningful sex differences makes unimaginable a future in which sex will not be viewed as one of the most powerful predictors of vulnerability to and expression of depression and other affective disorders.
Epidemiology