Rae Pass | 20 FEB 2017
If you haven’t already, read my related article ‘Perceptions of mental illness: The media and mental health’.
Over the last few years there has been a drive in mental health research to find biological explanations for mental illnesses, both to better understand the disorders themselves and to counteract the associated stigma. The hope is that if we can demonstrate that these conditions arise from faulty biology, people would be more understanding and compassionate, and the associated stigma would diminish. Logically, why would you blame someone for something they cannot control?
At first glance, this approach seems promising. A meta-analysis of studies, conducted over the last 20 years, into the beliefs and attitudes of the general population found that increased public understanding of biological explanations lead to greater acceptance of those seeking professional treatment (Schomerus, G. et al., 2012). When mental health disorders are framed as ‘brain diseases’, due to faulty genetics and biology, people tended to blame the sufferer less (Kvaale, Gottdiener & Haslam, 2013).
Unfortunately, these positive findings are in the minority, as surprisingly it appears that biological explanations do not reduce stigma, and may potentially increase it. Although the public appeared more accepting of the need for professional treatment overall stigma endured. The social rejection of sufferers was persistent and attitudes towards them remained negative, including stereotyping them as dangerous (Schomerus, G. et al., 2012). However, this study was conducted in western cultures and so the conclusions cannot be applied to all countries due to different societal norms. For example in some African tribes mental illness symptoms are misinterpreted as witchcraft. Additionally, the studies included in the analysis examined long-term impacts at a national level and not the short term impacts of anti-stigma campaigns.
Anti-stigma campaign poster from Time to Change.
In 2014, a study explored the impact of the chemical imbalance hypothesis on the sufferer’s self-stigma. This dominant, but controversial, hypothesis of depression states it is the result of an imbalance of neurotransmitters. Participants currently suffering, or who had previously suffered, a depressive episode were told their cause of the depression using a bogus test. Some were told their illness was caused by a chemical imbalance. Those given this biological explanation showed no reduction in blame (self-stigma), and an increased prognostic pessimism and worsened perceived self-efficacy (Kemp, Lickel & Deacon, 2014). This study demonstrates a surprising example where providing a biological explanation actually increased stigma, even if that stigma emanates from the victim themselves and not others. The study also found participants given the chemical imbalance theory viewed pharmaceutical intervention as more appropriate than therapy.
Biological explanations of mental illness seem to exacerbate the ‘us v them’ mentality, increasing distinction between ‘normal’ people and ‘abnormal’ sufferers (Lebowitz & Ahn, 2014). Additionally it increases avoidance of sufferers, who are portrayed as dangerous and not in control. A genetic cause may dehumanise sufferers by implying they are defective and distinct from others. It can also lead to stigmatisation of the entire family (Phelan, 2002) as family members are labelled as at risk or carriers, and potential partners may not want to pass on a genetic predisposition to their children. A Canadian survey in 2008 found that 55% people asked wouldn’t marry someone suffering from a mental illness. Even clinicians, the very people trying to help sufferers, appear to display decreased empathy for those suffering from a mental disorder when the patient’s disorder is described in biological terms (Lebowitz & Ahn, 2014).
Overall, a greater understanding of the biological causes of mental health conditions did lead people to blame the sufferer less for their condition, but reactions towards sufferers remained negative. Additionally, the sufferers themselves were more pessimistic about their recovery. It increased deterministic thinking which is extremely unhelpful, and untrue. Certain mutations guarantee you will develop a disease, as in Huntington’s disease, but this is rare. Other mutations do not always result in disease, but do significantly increase your risk: those who inherit two copies of the APOe4 allele are 10 fold more likely to develop Alzheimer’s disease, whilst those inheriting one copy have a 3 fold risk.
Genes do not act in isolation, and you will not develop schizophrenia because you have the ‘schizophrenia gene’: there is no such thing. Instead, it will be the interaction of different risk factors, both biological and environmental, that may result in you developing the disease. The interaction between different genes, and your environment, influences your responses to life events. A leading hypothesis in depression research focuses on the involvement of serotonin, the so called ‘happy chemical’. Serotonin is a chemical often believed to be at abnormal levels according to the chemical imbalance theory mentioned earlier. The gene SERT regulates how much serotonin is produced in your brain but its role is more complicated than simply not producing enough. A study published in 2015 found that a variation in the SERT gene moderated the development of depression in people abused as children (Nguyen et al., 2015). Only those with a specific version of SERT and had suffered abuse developed depression, whilst those with the same version but had not been subjected to abuse were reported to be the happiest participants.
This interaction highlights how a combination of factors collude to cause psychiatric diseases, and so the ideal method of treatment combines medication and therapy. Medication alleviates symptoms and allows patients to benefit from psychotherapy, which facilitates learning of more healthy coping methods. Unfortunately, this is not always a viable option available to people, due to costs of services and difficulties accessing them. If patients are given a biological explanation for their illness they are more likely to view drugs as their best treatment option, and may not seek therapeutic help. This is despite the fact that pharmacological treatment can have a limited impact on their condition. No psychiatric drug works for all sufferers, potentially due to individual variation in disease diagnosis and symptoms, and thus response to treatment. Around 40% of depression is considered drug resistant and the negative symptoms of schizophrenia (e.g. social withdrawal, apathy) aren’t currently treatable with drugs. Indeed, medication is not a cure but a symptomatic treatment as patients relapse if they stop taking them, and the side effects are often debilitating.
A campaign poster from an American mental health association. Image source.
Another consideration, easily overlooked by well meaning scientists and clinicians, is not everyone with a condition considers themselves ‘diseased’ and may not want to be ‘cured’. These beliefs will vary between individuals and so it is important to take people’s own beliefs surrounding their conditions into account. Defining them by their disease is akin to defining a disabled person by their disability; defining them by what they cannot do. When it comes to mental health clinicians and researchers must avoid only thinking in pathological terms, and failing to consider the whole person. If not we risk perpetuating an unconscious us v them stigma, between those studying the disease and those living with it. Someone who has fully embraced her condition and sought to change how people think of it is Touretteshero. She is informative, delightfully hilarious and her website should definitely be checked out.
Clearly, emphasising the biological causes above all else is not the way to reduce stigma. Only focusing on these causes may actually increase stigma, and it ignores the fact that the environment is also crucial in mental health. That is not to say biology is not involved-it is! These conditions would not run in families if it was not. But, the environment you grow up and live in is also hugely influential.
Classic graph depicted % risk of developing schizophrenia first published in Gottesman, 1991. Image source.
A good example to end on is schizophrenia. This is often held up as a largely genetic based mental health condition. The classical illustration above depicts increasing likelihood for developing schizophrenia, as demonstrated by increased risk with increased genetic similarity. If you identical twin has schizophrenia your risk for also developing it is almost 50%. Clearly, however, this genetic risk it is not 100%. Environmental factors will also hugely influence your risk, such as viral infection during the second trimester or suffering abuse as a child. In order to understand psychiatric diseases we need to consider the interaction of our environment and our biology. Only with better understanding of all aspects which interact and result in these diseases, rather than focusing on specific contributions, will we have a solid basis from which to combat mental health stigma.
Edited by Jonathan Fagg
- Kemp, J., Lickel, J., & Deacon, B. (2014). Behav Res Ther, 56, 47-52.
- Kvaale, E., Gottdiener, W., & Haslam, N. (2013). Soc Sci Med, 96, 95-103.
- Lebowitz, M., & Ahn, W. (2014). PNAS, 111 (50), 17786-17790.
- Nguyen, T., et al. (2015). British Journal of Psychiatry, 1 (1), i104-109.
- Phelan, J. (2002). Trends Neurosci, 25 (8), 430-1.
- Schomerus, G., et al. (2012). Acta Psychiatrica Scandinavica, 125 (6), 440-452.