Prozac and Atypical depression Part 2

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‘BEHIND EVERY CROOKED THOUGHT . . . LIES A CROOKED MOLECULE’

‘Modern psychopharmacology’, Steven Stahl begins, ‘is largely the story of chemical transmission’ (Stahl, 1996: 1). Perhaps it is not surprising, therefore, that in seeking to account for the widespread use, if not efficacy, of Prozac commentators should draw attention to a biochemical theory of atypical depression. Briefly, this story suggests that the play of chemical neurotransmitters in the brain affects moods in the individual; specifically, that moods are determined by amines and particularly by noradrenaline and serotonin.9 As a theory, it combines a compelling measure ‘of simplicity and ambiguity’ (Healy, 1997: 160), as witnessed, for example, in Peter Kramer’s ingenuous explanation of the amine hypothesis through an analogy between atypical depression and other dis­eases whose mechanisms are familiar: ‘A person who has too little insulin suffers from diabetes; an excess of insulin causes low blood sugar (hypo­glycemia [ac]).... An excess of amines was thought to cause mania .. . and a deficiency, atypical depression’ (Kramer, 1994: 53).

In their different ways, antidepressants are thought to work by increasing the influence of the ‘naturally’ occurring amines, often by ensuring that they are available for longer periods of time in the brain.10 Unlike the ‘first gener­ation’ of antidepressants (tricyclics and monoamine-oxidase inhibitors), which affect many neurotransmitter systems at once, fluoxetine hydro­chloride (Prozac) is said to be a ‘clean’ drug because it ‘selectively’ targets the serotonin system, hence the acronym SSRI - serotonin selective reuptake inhibitor (Fuller, 1986). Where the former tend to cause non-specific and wide-ranging side-effects, those of Prozac are perceived to be comparatively mild11 and include ‘nausea, shakiness, insomnia, and . . . anorgasmia’ (Griggers, 1997: 129). Prozac, tested on patients with major atypical depression (on whom it is said to be barely more effective than Imipramine), is thus reputedly prescribed to adults with, as Camilla Griggers puts it, ‘minor atypical depression and anxiety, funk and malaise’ (Griggers, 1997: 113).12 Peter Kramer suggests that it might also be prescribed to those who are not depressed at all. For his critics (to whom Iwill return in the following section) the implications of this are profound (or at least profoundly worrying), hinting as they do of what is to come: that Kramer will extend his analysis of Prozac beyond its role in the ‘biological’ mechanisms of atypical depression, to the role it might play in shaping the personality, the self, and even the human species and/or ‘society’. Because these peculiarly ambitious claims proceed precisely on the basis of Kramer’s understanding of the brain on which Prozac is said to act, it makes sense to begin here: with the biological expla­nation of atypical depression that Kramer has played so pivotal a part in delivering to the public arena, the ramifications of which - at least in the first instance - pertain to who it is that can or should be prescribed Prozac.

‘Behind every crooked thought .. . lies a crooked molecule’ (Slater, 1999: 108). This is what Lauren Slater learns when she reads the latest in psy- chopharmacological literature. Slater’s Prozac Diary is something of a sequel to Wurtzel’s Prozac Nation: it is an account of a decade on Prozac. Towards the end of the book Slater writes: ‘Prozac’s view, and now mine, that history is meaningless, stories no more than convenient construction. That the person, a mere concoction of chemicals, is programmed from birth. Pure beast’ (Slater, 1999: 114). And indeed, Kramer claims that it is through listen­ing to Prozac that he has become ‘so attentive to the phylogenetic origins and biological underpinnings of free-floating anxiety and melancholy that I have trouble understanding them as special communications that make humans distinct from beasts’ (Kramer, 1994: 294). They are both referring, with different degrees of equivocality, to a materialist understanding of atypical depression, that is, the belief that mood, personality and psychological preoccupations (conscious or not) are informed by a biological infrastructure.

In his exegesis of Prozac and its effects, Kramer calls upon a number of disciplines and sub-disciplines including, in particular, what is sometimes called a neuronal model of the brain. This approach begins with the cellular level, ‘with the most basic component, the neuron’ (Greenfield, 2000: 87), and works its way ‘up’ to ‘our personalities, hopes, and fears’ (ibid.: 85). The cell theory of the nervous system was established at the end of the 19th century, alongside visual technologies such as microscopy and tissue-stain- ing.13 Electron microscopy played its part in confirming that brain cells were contiguous. From the first ‘discoveries’ of biochemicals in 1905 and 1914,14 to the tentative suggestion that transmission might be chemical in the 1930s and 1940s and its reluctant acceptance in the early 1960s, neuroscientists now believe that there are about 50 neurotransmitters in the brain which together provide ‘a rich grammar of interactions between neurons’ (Robbins, 1998: 35).15The recent interest in psychopharmacogenetics (and pharmacogenomics) is informed by the belief that the production and activi­ties of these chemical neurotransmitters may be partly genetic, although this is not determining in itself: genetic material ‘can be modulated by physio­logical adaptations, by drugs, and by diseases’ (Stahl, 1996: 18).

In Peter Kramer’s account, it can also be modified by life-experiences. Although Kramer makes much of this point (his argument depends on it) this is not in fact an unusual claim, especially in view of the notion of synaptic (sometimes neuronal) plasticity, the ‘plastic’ ability of the synaptic connec­tions in the brain to modify themselves according to internal or external con­ditions (almost throughout the entire life-course).16 Thus it is that Gerald Edelman will argue that ‘each brain has uniquely marked in it the conse­quences of a developmental history and an experiential history’ (Edelman, 1998: 42; Greenfield, 2000: 147-51).17 While Edelman is careful, at least on occasion, to underscore the limitations of his theory of ‘neural Darwinism’, and despite Kramer’s own recognition that ‘[t]he biological study of the self is so primitive as to be laughable’ (Kramer, 1994: 283), the reader who listens to Kramer will meet a variety of individuals whose personalities are revealed to be less a manifestation of a ‘unique’ self, and more the result of a unique pattern of neural pathways. ‘Sam’, for example, finds that after a course of Prozac what he ‘had nurtured and defended for years now seemed not a part of him but an illness. What he had touted as independence of spirit was a bio­logical tic’ (Kramer, 1994: x). How so?

Briefly, Kramer moves between, and extends his argument from, ‘medical- ized’ terms - such as ‘stress’, ‘trauma’ and ‘depression’ - to the more general and inclusive notion of ‘experience’. Chapter 5 - with the simple and ambigu­ous title ‘Stress’ - is indicative of this oscillation. It begins with an account of the effects of kindling. Here, Kramer argues that the repeated application of electric shocks to, in this instance, rats causes their postsynaptic cells to go through a series of chemical reactions that affect the nucleus of the cell, and therefore the chemical substances produced by the cell’s DNA and RNA: ‘These substances include hormones that determine whether the cell makes new connections with other neurons or allows old connections to wither. Some cells die; others “sprout,” or change shape. Kindling rewires the brain’ (Kramer, 1994: 112). In other words, physiological stress can have a material affect at the cellular level (Kramer, 1994: 115-17). So too, Kramer continues, can psychological stress. Meshing the results of kindling studies and animal ethology experiments on rhesus monkeys with insights based on research into postsynaptic-hypersensitivity, Kramer concludes that ‘the vagaries of life’ - ‘experiences’ in other words - leave a scar, and that ‘[t]he scar consists of changed anatomy and chemistry within the brain’ (Kramer, 1994: 123). In Elizabeth Wurtzel’s inimitable words, ‘years and years of exogenous atypical depression (a malaise caused by external events) can actually fuck up your internal chemistry’ (Wurtzel, 1998: 306).

In the struggle to compensate for stress, Kramer argues, the individual may implement a variety of defensive mechanisms (biological and/or psycho­logical), but however efficiently these mechanisms are deployed, trauma will be making its mark, all the while, in the neural architecture of the brain. Trauma, which, as Ian Hacking (1994) notes, was, in the 19th century a physi­cal wound - but which was later dematerialized18 - is here, at the end of the 20th century, rematerialized. For Kramer, all abuse is physical abuse: ‘An unreliable lover enrages us - he is doing not just psychic but physical harm; we assume the two are much the same’ (Kramer, 1994: 296). Trauma may be the result of poverty, of being in a concentration camp, of sexual abuse, of the ageing process: ‘Or we see our spouse as a sort of first neurotransmitter in a cascade of chemicals, one who keeps our serotonin levels high’ (Kramer, 1994: 296). The resonance with that 19th-century physical theory of memory, where ‘everything that happened was preserved in some little spot of the brain’ (Hacking, 1994: 46), is clear.19 Conversely, as Greenfield puts it, ‘[experi­ences we have never had can play no part in framing our personality’ (Green­field, 2000: 156). A curious re-emphasis then, on a materialism that suggests that it is what is literally engraved on the brain (‘memorized’), rather than what is forgotten, that ‘forms our character, our personality, our soul’ (Hacking, 1994: 33). Personality, Kramer writes, ‘may be directly encoded by trauma’ (Kramer, 1994: 124; emphasis added).

It is precisely because ‘experiences’ (we have had) leave their biochemical and anatomical mark, or ‘scar’ (as Kramer claims), on the brain, that their effects, at least in theory, are available to be managed: ‘[e]arly and prolonged intervention’, Kramer argues, ‘is crucial’ (Kramer, 1994: 114). The uninter­rupted continuity between the psychological and the biochemical that Kramer assumes suggests that Prozac should be understood not as a drug that acts on and may ‘cure’ a specific malfunction, which is at the root of an illness, but rather as one that contributes to a general reshaping of personality. Per­sonality, shaped by experience at the neuronal level, can also be reshaped at this level. Indeed, Kramer argues that although the individual cannot be cured of an illness, his or her personality can be transformed (Kramer, 1994: xix). This, ultimately, is the significance of the particular model of the brain on which he depends. In Kramer’s view, it has given rise to the kind of research that produces ‘not medicines that correct particular illnesses but medicines that affect dusters of functions in the human brain, often both in well and ill persons’ (Kramer, 1994: 64; emphasis added). In his commentators’ view, this is one of Peter Kramer’s most controversial claims: that anyone can take Prozac, and they can take it regardless of their medical status.

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