In recent years, a growing (and pleasingly interdisciplinary) literature has developed around the intersecting themes of neurogenetic ‘explanatory’ narratives, largely pharmaceutically-driven processes of medicalization, stigma and socioclinical identity in the context of psychiatric disorder. In this post I aim to briefly review two of the most immediate and provocative of these publications, and then launch a more free-ranging reflection on a few key implications.
Daniel Buchman and his colleagues (2012)–all members of the new Neuroethics Core at the University of British Columbia–present analyses of a qualitative study designed to explore the implications of potential future advances in neuroimaging (e.g. imaging-based biomarkers) from the perspective of individuals with diagnoses of depression or bipolar disorder. Participants’ narratives reveal relatively strong convictions that such advances might both increase the socio-medical “legitimacy” of their disorders, and deflect stigmatizing conclusions regarding personal responsibility and culpability. In other words, neuroimaging promises to reframe psychiatric illnesses as unmediated physical insults which, like breast cancer or neurological disease, are understood as external to the self and which the ‘sufferer’ is made to endure but for which she bears no responsibility. As Buchman and his colleagues point out, however, though such blame-deflecting narratives have been advanced by a variety of private and clinical interests, the evidence from both population-based and experimental studies suggests that “biomedical” or “biogenetic” explanatory models in general have not only failed to ameliorate, but in some cases actually worsened, public stigma (e.g. Pescosolido et al., 2010; Rüsch et al., 2010; Schomerus et al., 2012). Participants’ perspectives on neuroimaging may thus reflect the internalization of select politically-motivated perspectives on stigma change (e.g. pharmaceutically-driven linkages between destigmatization and predominantly “neurochemical” explanations of depression) rather than the real-world impacts of biogenetic attributions on stigma change.
Even here, however, existing research suggests a complex picture. In Chicago, Nicholas Rüsch and colleagues, for example, have explored the impact of genetic and neurobiological causal attributions on both explicit and implicit attitudes using a mental illness-specific adaptation of the implicit attitudes test (IAT). Pace the effects fantasied by Buchman’s interviewees, Rüsch (2010) found that service users who strongly endorsed both neurobiological and genetic causes generally affirmed a desire for greater social distance from other individuals with psychiatric diagnoses, and scored significantly higher on implicit measures designed to tap “guilt-prone [mental illness-related] self-concepts” (though, importantly, they did not explicitly endorse higher levels of self-responsibility). Although the authors attribute these findings partly to “genetic essentialism” (i.e. the belief that biogenetic changes implicate the individual’s “self” in an even more intrinsic and permanent way than psychosocial causes), it seems equally possible that those individuals most internally troubled by their own agentic implication are in turn more likely to attempt—ultimately unsuccessfully—to deflect this guilt and shame through the explicit and self-consciously public endorsement of more strongly biogenetic ontologies. Intriguingly, the researchers identified a very different pattern of correlations in members of the general public: endorsement of genetic (but not neurobiological) causes strongly correlated with greater desired social distance form individuals with schizophrenia but lower levels of both implicit and explicit blame. For patients, in other words, explicit endorsement of a biogenetic model was found to correlate with self-blame and guilt, while those non-patients who most strongly endorsed genetic factors were less likely to blame individuals with psychiatric diagnoses but more likely to report discomfort and a desire to avoid social interactions.
A further provocative, if not unexpected, theme of Buchman and colleagues’ paper is the unmistakably visual materialism iterated in participants’ comments. Above all, that is, these service users emphasized the visual immediacy of the neuroimage (rather than the human science behind it) in prospectively persuading the public of the (material and physical) veridicality of psychiatric disorder. Although neuroimages, as the authors underscore, are in fact among the most mediated of contemporary anatomical artifacts, popular assumption remains that such technologies precisely bypass suspect forms of ‘mental’ interpretation, allowing the brain to directly “speak” or show itself. And here—a theme I will return to–we arguably find less evidence of a paradigm shift occasioned by neuro-narratives, than a contemporary reiteration of the historically entrenched binding of visual (re)presentation and medico-anatomical truth. Laqueur (1990), for example, identifies the origin of the conviction that “Truth and progress lay not in texts, but in the opened and properly displayed body” as far back as the 16th century, exemplified by Vesalius’ monumental 1543 frontspiece to De humani corporis fabrica (p. 70).
Where Buchman’s work helps unpack the projected or fantasied consequences of ‘advances’ in neuroimaging, Felicity Callard and colleagues’ (2012) recent paper explores specific deployments of “gene talk” in interviews with (non-user) family members of individuals diagnosed with schizophrenia. Painstakingly attentive to the discursive and nonverbal-affective tensions embedded within participants’ narratives, Callard and colleagues’ analysis highlights family members’ sometimes vigorous invocation of causal genetic mechanisms in an effort to mitigate personal responsibility, but also the ultimate (at least partial) failure of these efforts. Some sense of self-blame or responsibility appears difficult or impossible to shake, in spite of the public legitimacy of explicitly bio-expiatory frameworks.
In the course of interrogating these positions, the authors also help illuminate the ‘real world’ messiness of genetic discourse. In addition to the ways in which participants’ narratives are complicated by concepts stemming from epigenetics and the gene environment interactions literature, these narratives also turn our attention to and even reinforce the irreducibly social nature of the “new” kinship ties between affected (trans-generational) family members. In the same stroke, strange or eccentric relatives are newly pathologized (relative to normal kin) but also “normalized” through the (re)establishment of common behavioral bonds: so-and-so’s schizophrenic daughter is now retrospectively linked, for instance, to a “mad” great aunt, a second cousin who was a recluse, an alcoholic grandfather who died under mysterious circumstances. These complications, in turn, raise further questions regarding agency: is a mother responsible for not recognizing “early warning signs” in her son, consistent with a relative’s behavior, or even overlooking a family history of mental illness altogether? Do “bad genes” implicate a larger trans-generational family unit in a way irreducible to any given individual, and yet for which all members nevertheless retain some unspoken (perhaps only implicit) culpability? Does gene talk ultimately decrease responsibility or simply displace it to other spheres of reproductive and parental decision-making?
Without any claim to having comprehensively reviewed Buchman and Callard’s papers, let me now turn to a few select implications.
(1) The myth of the biopsychosocial model. Although psychiatric textbooks, by and large, almost ubiquitously reference “biopsychosocial” models of psychiatric disorder, such models mostly function, as critics have pointed out, as disciplinary “shibboleths” or empty “catchphrases” rather than substantive attempts to deconstruct relationships within and across domains (Markova & Berrios, 2012; McLaren, 2002). Or, as philosophers are more likely to put it, we might say that we simply haven’t solved the “brain-mind problem”. Given these academic difficulties—effects, at least in part, of the resilience of physical-mental dualism(s) in Euro-American culture—it should come as no surprise that members of the “general public,” forced to negotiate the complexities of causality in the context of increasingly complex iterations of neuroscience, genetics and critical social research, are also unable to do so in any clear or straightforward way. Buchman’s and especially Callard’s work, however, arguably underscores an even greater difficulty: not the difficulty of integrating or relating diverse factors that, in isolation, are clear and distinct, but rather the dilemma of parsing distinctions between “categories” that cross and re-cross to the point of semantic indeterminacy. What “sense” is there in attempting to relegate the neuroimage to the domain of either the social or the biological, for example, or the lineages constructed on the basis of retrospectively identified pathological ties? Or as my colleague Summer Schrader likes to point out, the dietary changes or alternative (“physical”) therapies recommended by critics of “biomedical” approaches to mental distress? What would the purpose be of attempting to determine whether the epigenetic changes occasioned by childhood abuse categorically differ in terms of their social or biological nature from the neurobiological trauma occasioned by a car accident?
Arguably then, following my interpretation of Callard’s lead, we might instead emphasize the often tacit sociopolitical motivations that prompt us to deploy this or that explanatory category (e.g. the social, psychological, genetic, or neural) or cultural script in particular circumstances and not others not because of the veridicality of the category employed but because of its social, cultural and moral effects.
(2) Agency. Although the challenge facing us all is undeniably multidimensional, I want to suggest that possibly more important—more fundamental, more impactful–than the question of where we can or can’t locate the ‘cause’ of a given condition or experience, is the question of human agency. Ultimately, that is, the distinction between the biological, the psychological and the social is perhaps less important than the extent to which we or they (service user, family member, member of society), can or should be held responsible, and are or are not, in terms of our/their personality and self, “synonymous” with (or separable from) ‘our’ or ‘their’ disorder. Undeniably, certain concepts have been culturally vested with specific agentic or expiatory qualities (e.g. the biological qua external insult), but this does not mean, in practice, that these qualities are in any sense stable or guaranteed. This is clear in the construct of “genetic essentialism”: even a disorder that we did not ‘cause’ may so thoroughly consume us that our immediate agency is implicated, even though our “prior” or originary agency is not. Agency is thus arguably one of the most important, and yet most under-researched, trans-disciplinary issues in the domain of psychiatric disorder.
(3) Politics. Finally, in interrogating the politics of these themes, the work of Buchman, Rüsch, Callard and their colleagues reminds us that we should not forget the frequent divergences between fantasy and ‘reality,’ projection and experience, internal doubt and public articulation, the implicit and the explicit. For instance, we might note the disconnect between the similarities Callard (2012) identifies between ‘everyday’ users and family members’ explanatory narratives, and the often intense public disagreements between political advocacy groups historically dominated by “family members” (e.g NAMI in the States) versus user/survivors regarding the origins and nature of psychiatric experiences. Perhaps regardless of any of our (conscious or unconscious) private sentiments, that is, political pressures and motivations often force us to adopt more dogmatic positions, positions that, I tentatively maintain, may again have more to do with the group-specific implications of different (typically significantly simplified) ‘causal attributions’ with respect to agency and responsibility than to ideology or perceived ‘truth.’ (E.g. “schizophrenia is a brain disease that in no way implicates mothers” or “schizophrenia is not a brain disease and therefore cannot be used to justify the infringements on individual freedom, rights, or autonomy so often based in putatively ‘neurological’ anosognosia.”)
In moving forward, then, my brief recommendations are that we (1) recognize the complexities and importance of agency, whether in the context of internal ‘symptom management’, interpersonal ‘explanation’ or public discourse; (2) attend to the popular, political and psychodynamic motivations behind and effects of the deployment of given cultural scripts as separate from their philosophical or scientific ‘semantics’; and (3) grapple with not only the experiences participants report in qualitative investigations, but also, ala Callard, their unspoken and/or affective ‘communications,’ as well as the broader sociopolitical pressures that push public discourse, often regardless of the nuance of the individual experiences that research participants might report, in particular, often vexed, directions.
Buchman, D, Borgelt, E., Whiteley, L. & Illes, J. (in press). Neurobiological narratives: experiences of mood disorder through the lens of neuroimaging. Sociology of Health and Illness. doi: 10.1111/j.1467-9566.2012.01478.x.
Callard, F. (2012). Schizophrenia: Does Talk of Genes and Brains Really Stop a Mother’s Blame? Huffington Post UK, September 9, 2012.
Callard, F., Rose, D., Hanif, E-L., Quigley, J., Greenwood, K. & Wykes, T. (in press). Holding blame at bay? ‘Gene talk’ in family members’ accounts of schizophrenia aetiology. BioSocieties.
Laqueur, T. (1990). Making sex: Body and Gender from the Greeks to Freud. Cambridge: Harvard University Press.
Marková, I. S., & Berrios, G. E. (2012). Epistemology of Psychiatry. Psychopathology, 45(4), 220-227.
McLaren, N. N. (2006). The myth of the biopsychosocial model. Australian And New Zealand Journal Of Psychiatry, 40(3), 277-278.
Pescosolido, B. A., Martin, J. K., Long, J., Medina, T. R., Phelan, J. C., & Link, B. G. (2010). “A disease like any other”? A decade of change in public reactions to schizophrenia, depression, and alcohol dependence. The American Journal Of Psychiatry, 167(11), 1321-1330.
Rüsch, N., Todd, A. R., Bodenhausen, G. V., & Corrigan, P. W. (2010). Biogenetic models of psychopathology, implicit guilt, and mental illness stigma. Psychiatry Research, 179(3), 328 332.
Schomerus, G. G., Schwahn, C. C., Holzinger, A. A., Corrigan, P. W., Grabe, H. J., Carta, M. G., & Angermeyer, M. C. (2012). Evolution of public attitudes about mental illness: a systematic review and meta-analysis. Acta Psychiatrica Scandinavica, 125(6), 440-452.
Nev Jones is currently a psychology doctoral student at DePaul University in Chicago with an extensive background in continental philosophy and enduring interests in the intersections of psychiatry, psychological anthropology, critical neuroscience and cultural theory. See her research website here.
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