Stop the stigma... or whatever

So what exactly causes stigma and what can be done about it? According to the social-psychological concept of attribution theory, if people judge the causes of a mentally ill person’s behaviour to be under the person’s control, then they should be more prejudiced, blaming and unsympathetic. Conversely, if the mentally ill person’s behaviour is attributed to uncontrollable causes, people should be more sympathetic and pitying. So, it would appear to follow that bio-genetic explanations, which attribute mental illness to uncontrollable causes, should encourage less stigmatisation of the mentally ill.

The social policy implications of this reasoning are obvious. However, the evidence linking the promulgation of bio-genetic explanations to a decrease in stigma is mixed and, often enough, bio-genetic explanations seem to be related to greater stigma. Go figure! Let's consider some of the studies done on the subject.

1. STIGMA AND ATTRIBUTION THEORY

In their paper examining whether espousing particular causal models affects the way in which people view and treat those with a mental illness, Mehta and Farina (1997) quote a person with schizophrenia as saying, “Believe me, there is nothing more devastating, discrediting and disabling to an individual recovering from mental illness than stigma.” Dangerous, unpredictable, worthless, dirty, cold, insincere, delicate, slow, tense, foolish, incompetent and unreliable have emerged through many studies as being commonly held beliefs about people suffering from a mental illness (Read and Harré, 2001), prompting the US Surgeon General to note that “people with mental illness suffer not only from their disorders but also from the stigma and discrimination that accompany them” (Phelan, 2002). A National Institute of Mental Health (NIMH) report stated that non-responsibility, unpredictability and dangerousness are the three major attributions underpinning the stigmatisation of the mentally ill (Read and Harré, 2001).

Link and Phelan (2001) have conceptualised stigma as a three-part process in which “a label sets the labelled person apart from others, links them to undesirable characteristics and leads to rejection and discrimination”. The phenomenon of stigma is fertile ground for the application of attribution theory, as developed and elaborated by theorists such as Harald Kelly and Bernard Weiner, and which explores how people explain (‘attribute’) and hence evaluate the behaviour of others. For example, if a person’s disruptive behaviour is judged to be under the person’s control, others are likely to react reproachfully and unsympathetically. In contrast, if the behaviour is assumed to be beyond the person’s control, the expected reaction is sympathy and pity. It has been well established that people with a mental illness are often viewed as being responsible for their conditions, and are to blame for the problems that result. Thus, the phenomenon of stigma appears to accord with the predictions of attribution theory, and it immediately follows that it may be possible to reduce stigma by educating the public that people with a mental illness are not responsible for the conditions, cannot necessarily control their behaviour, and that “mental illness is a brain disease” (Corrigan & Watson, 2004). Indeed, Corrigan and his colleagues have carried out research that supports the attribution theory prediction. After being educated about how mental illness is a biological disorder and not a personal choice, experimental subjects were less likely to sanction blame, anger and social avoidance towards those with a mental illness. However, further research has shown that attributing mental illness to uncontrollable genetic or biological factors has had a complex effect on its stigmatisation, reducing blame and anger on the one hand but exacerbating different kinds of negative attitudes on the other. These mixed results have called into question the adequacy of attribution theory to explain stigma in this context, and inspired the development of alternative models and concepts to help fully explain its genesis and suggest alternatives for its amelioration.

2. WHAT MOST PEOPLE THINK ANYWAY

Before even considering the efficacy of destigmatisation campaigns based on presenting mental illness as a bodily dysfunction, it should be noted that studies have shown that the public, apart from the relatives of people suffering from schizophrenia, does tend to prefer environmental stress as an explanation for mental illness. Even as far back as 1961, the US Joint Commission on Mental Illness lamented that “Psychiatry has tried diligently to make society see the mentally ill [as physically sick] and has railed at the public’s antipathy or indifference”. Psychiatric patients themselves tend to reject ‘medical model’ explanations of their experiences, claiming that they increase stigma, paint a pessimistic picture of the likelihood of recovery, and ignore the multifaceted nature of their situation and experience (Read & Harré, 2001). Ironically, in an era of conceptualising patients as ‘service users’ and ‘consumers’, it does seem that the customer is always right, at least on the first two points, as further studies into the impact of the promulgation of biogenetic explanations for mental illness on stigma have shown.

3. STUDIES LINKING BIOGENETIC CAUSAL MODELS TO INCREASED STIGMA

Research by Read and Harré (2001) found that biogenetic causal beliefs were related to negative attitudes and beliefs, such as people with mental illness are dangerous, anti-social, unpredictable, and undesirable as friends or partners. This accords with the NIMH analysis of stigma cited above. Corrigan and Watson (2004) noted that while biogenetic explanations of mental illness reduce blame and anger, they might also increase other kinds of stigma. They note that Weiner’s theory of attribution accounts only for people’s beliefs about the onset (cause) rather than the offset (consequences) of mental illness, the latter of which may also contribute to stigmatisation. Presenting mental illness as biologically or genetically determined also raises doubts about the likelihood of remission and/or recovery, which in turn encourages patronising and disempowering attitudes. Read and Harré (2001) noted that mental health professionals who prefer biological explanations tend not to allow patient input into the treatment process compared to professionals who take a more psychosocial perspective. Mehta and Farina (1997) examined the assumption that biogenetic explanations for mental illness reduce stigma in a Milgram-esque study that tested both the attitude and behaviour of subjects towards people (actors) with a purported mental illness, where the mental illness was conceptualised in either biogenetic or psychosocial terms. While they were able to replicate some of Corrigan’s results, i.e. that biogenetic explanations reduce blame, they also found that they induced harsher treatment by subjects of the actors, measured via presumed electric shocks. On the other hand, actors whose psychiatric history was described in psychosocial terms did not suffer harsher treatment than actors whose histories were presumed to be normal. Mehta and Farina (1997) speculated that biogenetic explanations lead us to adopt patronising, controlling attitudes to the mentally ill, to perceive them as physically distinct or “another species”, thus invoking callousness, and to fear for our sanity, leading to an increased sense of vulnerability. With respect to this last point, psychosocial explanations enable us to place a person’s mental illness in the context of negative life experiences, which we may not share, while biogenetic explanations imply that anyone may be struck down at any time.

4. THE FASHIONABILITY OF GENETIC ESSENTIALISM

Recent research by Phelan (2002, 2005), Haslam (2005) and Haslam and Levi (2005) has introduced new frameworks through which the stigmatisation of mental illness can be understood, complementing attribution theory and compensating for its inadequacies. Phelan (2002) has argued that the new emphasis on genetics as exemplified by the Human Genome Project has brought about changes in the way in which we view ourselves and our behaviour, modulating concepts such as personal responsibility, the effect of the environment on behaviour, and individuality, to the extent that genetics may become the dominant explanatory mode with respect to these issues and concepts. In contrast to attribution theory, Phelan (2005) describes what earlier researchers have called rise of the genetic essentialist view, in which “genes form the basis of our human and individual identities… and are strongly deterministic of behaviour.” When applied to mental illness, Phelan predicted that genetic essentialism should increase stigma by promoting the beliefs that (i) the mentally ill person is intrinsically different to others (cf. Mehta and Farina, 2005), (ii) mental illness is persistent and serious, and (iii) is likely to affect other members of the mentally ill person’s family. Taken together, all of these beliefs would tend to exacerbate social distance between the mentally ill person and others, and limit their perceived reproductive ‘fitness’, as well as that of other members of his/her family. It is clear that each of these beliefs correspond to the tripartite model of stigma outlined by Link and Phelan (2001) cited above. Setting apart is achieved by viewing biological differences as being more deep-seated and immutable than differences resulting from environmental effects (Phelan, 2001; Mehta & Farina, 2005); linking to undesirable characteristics is exaggerated by the sense that, when genes are involved, mud sticks – “if the problem is in your genes… full and permanent recovery seems less likely” (Phelan, 2001); and rejection and discrimination is exacerbated specifically in the realm of reproductive rights. Phelan tested her predictions using a case study in a nationwide (USA) survey. Like the above researchers, she found little support for attribution theory predictions that biological/genetic explanations for mental illness reduce stigma, except where punishment was concerned. However, she found that, in accordance with genetic essentialist theory, biological/genetic explanations for mental illness increased beliefs about its seriousness, persistence, and the likelihood of it affecting the siblings of a mentally ill person. Interestingly, biological/genetic explanations did not increase social distance from and perceptions of reproductive unfitness of the mentally ill person themselves, but only with respect to their siblings (Phelan, 2005).

It is appropriate at this point to consider whether the public’s genetic essentialist thinking is consistent with the current scientific understanding of how genes influence behaviour. Phelan (2005), following Alper and Beckwith (1993), asserted that “there is no necessary association between the degree of genetic influence on a behaviour and its malleability or persistence.” She also cites studies of people undergoing genetic testing that show that individuals tend to exaggerate the actual risk of developing a disease based on genetic profiles and family histories, and concludes that “public beliefs about the transmissibility of genetic characteristics are likely exaggerated by genetic essentialist thinking”. Her overall conclusion was that “the processes described by attribution theory and genetic essentialism are not mutually exclusive and that [her] findings support the idea that the effects of geneticisation on stigma are complex, ameliorating stigma along some dimensions while exacerbating it along others”. She then noted that conceiving of mental illness as a biogenetic disorder may benefit parents by absolving them of any (environmentally based) causal responsibility, but harm younger relatives of the mentally ill person, such as siblings or children.

5. FRAMEWORKS FOR UNDERSTANDING THE LINK BETWEEN BIOGENETIC CAUSAL MODELS AND STIGMA

Rejecting the notion that laypeople’s ideas about mental illness are merely reflections of professional concepts and allowing for laypeople’s ability to construct their own understanding, Haslam (2005) has developed a model of folk psychiatry, that comprises four dimensions along which the general public seek to understand mental illness. The first of these four dimensions is pathologising, the business of judging a person or his/her behaviour as deviant and abnormal, based on perceptions of infrequency, incomprehensibility, internal attribution, and entitativity, i.e. that those engaged in deviant behaviour form a coherent and ontologically meaningful group. The three other dimensions represent ways of explaining the pathologised behaviour. Moralising involves judging deviant behaviour to be under the actor’s control, and attributing it variously to perversity, sinfulness or criminality. Moralising derives from (the somewhat inaccurate) folk psychology way of explaining human behaviour, in which acts are understood to derive from intentions, which in turn derive from reasons, which are consciously considered beliefs and desires. Moralising assumes that intentionality underlies the deviant behaviour. In contrast, medicalising involves attributing deviance to some kind of physical aberration, a non-intentional causal essence, rendering it “the outward expression of a fixed identity-determining pathological essence” and thus an example of essentialist thinking in which forms of deviance are considered to be natural kinds, i.e. discrete, immutable, non-man-made groups. Psychologising occupies the middle ground, invoking mentalistic but causal and not fully intentional explanations for behaviour (Haslam, 2005). This model was validated in a study by Haslam and Levy (2005).

So what can this folk psychiatry tell us about stigma? The attribution theory approach to stigma clearly relates to the moralising dimension by its linking of the perceived self-controllability of mental illness to blame and anger, and renders sensible efforts to destigmatise mental illness by using biological/causal explanations, akin to the medicalising mode of explanation. The lack of success of such destigmatisation campaigns “reflect components of the essentialist mode of thinking hypothesised to underpin medicalising. Locating the disordered in a bounded category reflects the discreteness component [of natural kind thinking] and pessimism over recovery reflects immutability.” (Haslam, 2005).

The recommendations that researchers have made in the light of their results to reduce stigma vary from the firm line taken by Read and Harré (2001) that destigmatisation programs should primarily involve increasing the interaction between the mentally ill and the larger public, and placing the mentally ill person’s condition in the context of life events rather than biological/genetic factors, to more integrative models favoured by Phelan (2001, 2005) and Corrigan and Watson (2004). These researchers favour continuing to make use of biogenetic explanations in destigmatisation campaigns, given the importance of reducing blame and taking into account political considerations, such as the need to influence resource allocation. However, they believe that biogenetic explanations should be combined with psychosocial factors and information about the effectiveness of treatment and the actual likelihood of violence and other disturbing behaviour (Corrigan and Watson, 2004), and counteracting some of the misperceptions generated by genetic essentialist thinking (Phelan 2001, 2005).

And here's a list of references, so you know I'm not just quoting my imaginary friends:

Corrigan, P. W. and Watson, A. C. (2004). At issue: stop the stigma: call mental illness a brain disease. Schizophrenia Bulletin, 30(3), 477-479

Haslam, N. (2005). Dimensions of folk psychiatry. Review of General Psychology, 9(1), 335-47

Link, B.G. and Phelan, J.C. (2001). Conceptualising stigma. Annual Review of Sociology, 27, 363-385

Levi, M and Haslam, N (2005). Lay explanations of mental disorder: a test of the folk psychiatry model. Basic and Applied Social Psychology, 27(2), 117-125

Mehta, S and Farina, A. (1997). Is being “sick” really better? Effect of the disease view of mental disorder on stigma. Journal of Social and Clinical Psychology, 16(4), 405-419

Phelan, J. C. (2002). Genetic bases of mental illness – a cure for stigma? Trends in Neuroscience, 25(8), 430-431

Phelan, J. C. (2005). Geneticization of deviant behaviour and consequences for stigma: the case of mental illness. Journal of Health and Social Behaviour, 46 (December), 307-322

Read, J and Harré, N. (2001). The role of biological and genetic causal beliefs in the stigmatisation of ‘mental patients’. Journal of Mental Health, 10(2), 223-235