Wednesday, June 29, 2005

The Autonomy Enhancer (in part)--DHS claim #1

Here is what I accomplished today in outline the first point of the Psychopharmacological Hedonist Strategy (this follows my "The Psychopharmacological Hedonist's Orthdoxy: Part 1).

The Autonomy Enhancer

Among bioethicists, the principle of autonomy is one of the most important moral goods. Physicians should not, according to the principle of autonomy, coerce a patient to undergo treatments or therapies; the physician must respect that patient’s innate capacity to make good decisions for him or herself given impartial, comprehensive information. The emphasis on protecting patient autonomy creates the impression that the physician-patient relationship is a free market exchange between equal contractors (see Donchin 2001, 368). Healthcare, on this model, looks dangerously close to a commodity (see Tong 1998, 150). In the case of psychiatry, potential patients are presented with an array of choices: psychotherapy, homeopathy, psychopharmacology, psychoanalysis, or philosophical counseling. Kramer, in part, sees his book as offering good reasons why a consumer of psychiatric care out to consider psychopharmacology over the other options. This is the first sense in which Kramer is appealing to the principle of autonomy in Listening to Prozac. He is presenting a book that offers consumers good information about why Prozac and the pharmaceutical therapy in general is a good practice for dealing with subclinical mental illnesses.

The second, and more important sense, in which Kramer appeals to autonomy, is to argue that Prozac is actually a chemical promoter of it. This might seem like the worst kind of science-fiction nightmare: medical science in the service of making better consumers. Moreover, its not clear that after 15 years of Prozac (and its cousins), we can conclude that it actually does deliver on Kramer’s promise for better living through chemistry. However, let’s put aside, for the moment, the question of whether Prozac actually does make us more autonomous, and consider the abstract moral question: is there anything ethically problematic about a drug that makes humans better able to make choices and thereby fully participate in a liberal, democratic society? Afterall, Kramer disclaims many times in Listening to Prozac that his speculations about the positive impact of Prozac for rewriting our cultural narrative on what makes us who we are—biology or biography?—are simply that, speculations: “[t]he biological study of the self is so primitive as to be laughable” (1993, 283). When we attend to his abstract, speculative, and gender-neutral claims—Prozac is good for autonomy—some very interesting problems emerge.

First, how is it that Prozac is a chemical autonomy enhancer? Remember, Kramer has encouraged his readers to give up old psychiatric paradigms—long, drawn out analytic sessions directed toward spurring anxious analysands to choose their authentic paths—and replace that paradigm with a neuroscientific view of mood, i.e. biography becomes biology and hence responds best to biological interventions. If we accept this paradigm, then what follows is the metaphor of psychopharmacology “mending” or “restoring” us to a better biological state of existence. A psychopharmacological intervention into our badly bruised biology may be a far more effective way of “leveling the playing field,” one could argue, than striving toward building more just and equitable institutions. Consider what ethicist Mike Martin has to say about weighing the choice of treating a subclinical, yet unhappy patient suffering from an unjust world or dedicating energies toward making the world more just:

Depression can be ‘normal,’ in the sense of an understandable and expected response to harmful social structures and yet have pathological aspects that disrupt our ability to carry on with our lives. We cannot wait until the vaster problems of community are resolved before dealing with the suffering generated by those problems (1999, 284, my emphasis).

Unjust social institutions, Martin concedes, do injure people. Sexism, for example, may impact a woman’s sense of self, leading her to mistrust herself and thereby ability to make good decisions. Such women, Kramer’s reasons, might make themselves too dependent on men, and more dangerously abusive men (1993, 68). Ostensibly, though he doesn’t spell this out, women might become dependent on men, precisely because they project a competent, autonomous self. The old-style feminist approach was to challenge—through protest, educational and legal reforms, and “consciousness raising”—cultural cultural assumptions that women are simply incapable of self-determination. Second-wavers—“modern” feminism—want to create a world that taught their daughters to see themselves as powerful and capable as men are, while the new style—“postmodern” feminism—is too impatient for this work, and opts for personal enhancement drugs that more effectively transform the female self into a powerful and autonomous self (see Zita 1998; Metzl 2003).

Kramer helps sell this “postmodern” feminism—this elixir for a “masculine” self-determination in his chapter on “Sensitivity.” I want to point out two moves that Kramer makes in this chapter: (1) he offers up a new mental health diagnosis facilitated by Prozac interactions on “needy” women and then, (2) names this diagnosis “rejection-sensitivity,” which, I will argue, deemphasizes gender. We learn about rejection-sensitivity in connection with “Lucy,” who has low self-esteem and a pronounced need for male attention. Lucy is not clinically depressed, but she does suffer from a perception that her boyfriend does not love her enough, which she builds from the slightest insensitivity on his part. Kramer finds that Lucy responds well to Prozac and then launches into an exploration of a new mental illness category—rejection-sensitivity—that is reified by Prozac. Psychopharmacology, therefore, does more than merely treat patients, but it also acts like a diagnostic tool, enabling the psychiatrist to discover pathology where he didn’t see it before. If you give Prozac to a “normal,” albeit overly sensitive person, and she becomes less sensitive, and therefore efficacious in the world, then what you thought was a normal state may in fact be an abnormal state, or at least potentially abnormal state. Jennifer Radden (2003) refers to this type of diagnostic methodology as “drug cartography,” a practice whose problems which I will outline in the next chapter.

Kramer credits the discovery of rejection-sensitivity to Donald Klein, who was a pioneer in biological psychiatry. However, Klein’s nomenclature for the illness was “hysteroid dysphorics” who he described as:

. . . usually females whose general psychopathological state is an extremely brittle and shallow mood ranging from giddy elation to desperate unhappiness. Their mood level is markedly responsive to external sources of admiration and approval. Such a patient may feel hopelessly bereft when a love affair terminates, then meet a new attentive man and feel perfectly fine and even slightly elated within a few days. Their emotionality markedly affects their judgment. . . .They are fickle, emotionally labile, irresponsible, shallow, love-intoxicated, giddy and short-sighted. They tend to be egocentric, narcissistic, exhibitionistic, vain and clothes-crazy. They are seductive, manipulative, exploitative, sexually provocative, and think emotionally and illogically (cited in Kramer 1993, 74-75).

Kramer acknowledges that this syndromal description reads more like a “misogynist’s picture of womankind,” however he nonetheless champions Klein’s work from moving us away from the even worse misogyny inherent to Freudianism. What Klein discovered the “psychobiological defect” of “hysteroid dysphorics,” who were so traumatized by any perceived or actual rejection, that to compensate maladapted the above personality style (75, 77). When Klein intervened with MAOI inhibitors—an older generation antidepressant—these women no longer degenerated into self-destructive behavior as a result of rejection.