Aggression and Medication

Cosgrove, K. P., Mazure, C. M., & Staley, J. K. (2007). Evolving knowledge of sex differences in brain structure, function, and chemistry.  Biological Psychiatry,  62:  847-855.

Hermans, E. J., Ramsey, N. F., van Honk, J. (2008). Exogenous testosterone enhances responsiveness to social threat in the neural circuitry of social aggression in humans.  Biological Psychiatry,  63:  263-270.

An uneasy, and to my mind unearned, peace has settled over battlefield on which the warring camps of psycho-pharmacology and “pure” psychoanalysis wrangled during the late 1980s and most of the 1990s. Back then it was not at all uncommon for the first-time analysand, complaining of frequent social anxiety, to be told in Brenner-influenced fashion that by no means should he/she take an anxiety-dampening medication. To stop all anxiety is to stop signal anxiety; to stop signal anxiety is to smooth over conflict; to leave conflict unresolved is to perpetuate neurotic suffering (or worse); which is to say, to remain unanalyzed. Many analysts held the line against medication because, they sensed, these molecules had the potential not merely to allay suffering but to ablate meaning. In the major American centers of psychoanalysis, psychopharmacology is now rather casually practiced, with an unproblematic flair. It is now generally accepted that if a medication can help alleviate suffering— well, great! This procedural integration of medication into practice—the patient says depression, the shrink prescribes Prozac, and then it's back to the talk—obscures the utterly riveting philosophical war that Brenner was on to back in the 1980s: to cure by molecule and to cure by meaning are by no means one and the same. Or put differently, they likely do not share a common final pathway. I recently stumbled across the meaning-destroying capacity of medication in my own practice: a physically healthy woman in very late middle age presented complaining of depression. She had built an addition to her main house