Frauds, fear of failure and finances: The mental health problem in academia

Lauren Revie | 10 OCT 2019

Mental health is a hot topic at the moment – and it is about time. Around 1 in 6 adults will experience anxiety or depression (Mental Health Foundation, 2016), with the number of people recognising suicidal thoughts increasing drastically (McManus et al., 2016). However, as a response to this growing problem, we have also seen a rise in the formation and support for mental health charities and research into different mental health and psychiatric conditions. More and more people are beginning to talk about our mental health openly; how we feel, what is affecting our mental health, and seeking support for problems we might be experiencing. Mental health awareness and advocacy is gaining momentum, and everything *seems* to be heading the right way in working towards normalization of sharing our feelings, emotions and mental state. 

But what about the researchers behind the mental health statistics and the breakthroughs? There is  growing evidence of a mental health epidemic that is often hidden behind academic success, with almost half of PhD students and graduates in academia struggling with mental health. Approximately 41% of PhD students demonstrate moderate to severe symptoms of anxiety and depression – almost threefold that of the general public – meaning mental health issues are rife in researchers (Evans et al., 2018). 

Perhaps, then, we may attribute this to the ‘type’ of person who is attracted to pursuing a career in academia – highly motivated, a perfectionist, and maybe a little hard on themselves. However, research by Levecque et al (2017) compares the incidence of these problems within PhD students to their highly educated counterparts in industry. The findings indicate that one in two PhD students experience psychological distress, and one in three is at risk of developing a common psychiatric disorder – findings which are significantly higher than those within the comparison group.

But why might this be? Why would seemingly driven, motivated and highly successful young individuals be battling with these staggeringly high rates of mental health problems? Levecque and colleagues (2017) attribute these statistics to the effect of their research on work-family life, and found strong predictors of poor mental health to be job demands, lack of job control, and supervisor’s leadership style. Others have attributed these rates to workplace ‘bullying’ of doctoral students (English, Flaherty & English, 2018) and a feeling of disconnection from the research community due to unfamiliar topics or long isolated work (Reeve & Patridge, 2017). 

Academics and postgraduate students alike attribute mental health problems and feelings of being overwhelmed to lack of support and isolation. Further research by Belkhir et al (2018) followed a group of young academics and early career researchers over four years.  It was reported that feelings of loneliness came from social isolation due to workplace culture, meaning individuals weren’t able to make meaningful relationships with those in their immediate groups. In addition to this, they also reported that they felt unable to participate in conversations with their peers and others in their field, as they felt they lacked both cultural and technical knowledge. 

This leads us on to an issue that many postgraduates and early career researchers can related to, known as the ‘Imposter syndrome’. Clance and Imes (1978) first coined the term ‘Imposter syndrome’ in a bid to collectively define the traits of high-achievers who were struggling to accept and internalize their own success. Often, someone struggling with imposter syndrome will claim to be a fraud, or underestimate their own knowledge, attributing their success to luck or circumstance. ‘Imposters’ will often compare themselves to others, and reject praise, leading to anxiety, stress and in some cases, depression. Positive correlations have been observed between imposter syndrome and academic success, neuroticism and perfectionism – all strong traits of a postgraduate student or early career researcher. And it isn’t just them! Many senior faculty members wake up believing they will one day be ‘found out’ Whilst the syndrome is not exclusive to academics, it is rife amongst university staff and students, and is a huge contributor to declining mental health in post graduate education. Watson and Betts (2010) attribute feelings of imposter syndrome to three main themes in an early career researcher’s experience: fear, family and fellowship. The researchers assessed email conversations of graduate researchers, in which a fear of being discovered as a fraud appeared to be one of the main factors driving feelings of imposter syndrome. In addition, this was further exacerbated by feelings of being drawn away from family responsibilities, and a lack of peer support or fellowship during study. 

There are a number of reasons why researchers and students may feel like imposters. Firstly, academia is a competitive world. Postgraduate study attracts the best of the best, and fairly often, those surrounding you are intelligent and also over-achieving. Partnered with the constant pressure to ‘publish or perish’, and the need to justify your project and area of expertise, this can result in stress, anxiety and often burnout (Bothello & Roulet, 2018).

Other factors which may also contribute to poor mental health in academia include difficulty in time management, organizational freedom (van Rijsingen, 2018) and perception of career perspectives, funding opportunities and financial problems. The struggle to manage your own work, produce innovation and progress whilst being largely self-taught can often come at the price of mental health issues. It is suggested that stress may stem from insecurity within this sphere – be it financial insecurity, or insecurity concerning ‘unwritten rules’ within the lab or school – and also from frequent evaluation, and a seemingly unmanageable workload (Pyhalto et al., 2012). 

All in all, the consensus seems to be that postgraduate researchers and academics alike are struggling in the University environment. This issue is beginning to be addressed more readily, however the phenomenon is not new. McAlpine and Norton (2006) note that the calls for action to rectify this growing problem have generally been ad hoc rather than theory driven (ironically!). As such, research which has been conducted has not been broad enough to integrate factors which could influence outcomes in a University context. And so the cycle continues. 

If you have been affected by anything in this article, please talk to a trusted friend or family member, or access help on

www.nhs.uk/conditions/stress-anxiety-depression/mental-health-helplines/

www.mind.org.uk

www.samaritans.org

References:

  • Bothello, J., & Roulet, T. J. (2018). The imposter syndrome, or the mis-representation of self in academic life. Journal of Management Studies, 56(4), 854-861.
  • Clance, P.R., & Imes, S. A. (1978). The impostor phenomenon in high achieving women: Dynamics and therapeutic intervention. Psychotherapy: Theory, Research, and Practice, 15(3), 241-247. 
  • English, S., Flaherty, A., & English, A. (2018). Gaslit! An examination of bullying on doctoral students. Perspectives on Social Work, 20.
  • Evans, T. M., Bira, L., Gastelum, J. B., Weiss, L. T., & Vanderford, N. L. (2018). Evidence for a mental health crisis in graduate education. Nature biotechnology, 36(3), 282.
  • Levecque, K., Anseel, F., De Beuckelaer, A., Van der Heyden, J., & Gisle, L. (2017). Work organization and mental health problems in PhD students. Research Policy, 46(4), 868-879.
  • McAlpine, L., & Norton, J. (2006). Reframing our approach to doctoral programs: An integrative framework for action and research. Higher Education Research & Development, 25(1), 3-17.
  • McManus, S., Bebbington, P., Jenkins, R., & Brugha, T. (2016). Mental Health and Wellbeing in England: Adult Psychiatric Morbidity Survey 2014: a Survey Carried Out for NHS Digital by NatCen Social Research and the Department of Health Sciences, University of Leicester. NHS Digital.
  • Mental Health Foundation. (2016). Fundamental Facts about Mental Health 2015. Mental Health Foundation.
  • Pyhältö, K., Toom, A., Stubb, J., & Lonka, K. (2012). Challenges of becoming a scholar: A study of doctoral students’ problems and well-being. ISrn Education, 2012.
  • Reeve, M. A., & Partridge, M. (2017). The use of social media to combat research-isolation. Annals of the Entomological Society of America, 110(5), 449-456.
  • van Rijsingen. (2018), E. Mind Your Head# 1: Let’s talk about mental health in academia.
  • Watson, G., & Betts, A. S. (2010). Confronting otherness: An e-conversation between doctoral students living with the Imposter Syndrome. Canadian Journal for New Scholars in Education/Revue canadienne des jeunes chercheures et chercheurs en éducation, 3(1).

The Neuroscience of Mindfulness: What Happens When We Meditate?

Joseph Holloway | 3 APR 2017

Joe is a guest writer for The Brain Domain, and is currently pursuing an MSc in Mindfulness-based Cognitive Therapies and Approaches, as well as an MA in 18th Century Literary Studies, at the University of Exeter.

‘Mindfulness’ is a word that has gathered momentum over the last decade. It has grown beyond associations of yoga and alternative therapies and moved into the realms of corporate culture, education, and mental health. Mindfulness has become such a prevalent aspect of our culture that there was even a Ladybird Books for Grown-Ups dedicated to it. When a phenomenon becomes this prominent and when it enters such fundamental spheres of our lives it is good to review its evidence base. What is Mindfulness meditation? How is it employed in a therapy context? What happens in the brain when we meditate? What evidence do we have that it is effective? This article attempts to answer these questions.

A Brief History of Mindfulness and Therapy

Firstly, what is Mindfulness? The term has an interesting history of development (Analayo, 2006, pp. 15-41) that is beyond the scope of this article, but a commonly accepted contemporary definition is: “moment-to-moment awareness” (Kabat-Zinn, 1990, p.2). Participants deliberately pay attention to thoughts, feelings, and sensations in the body, bringing their mind back to the task at hand when it wanders. This form of meditation is entrenched in many of the oldest religions and can be traced back to early canonical buddhist texts such as the Satipaṭṭhāna-sutta and the Mahāsatipatṭhāna Sutta. Contemporary Western understandings of Mindfulness meditation are a repackaging of the teachings of these texts in a secular context. They focus on the insights about the workings of the mind and the teachings on how to reduce the amount of distress that we cause ourselves.

A key example of such repackaging was Jon Kabat-Zinn’s Mindfulness Based Stress Reduction (MBSR) course originally developed at MIT in the 1970’s. This is an 8 week group course teaching participants how to engage with Mindfulness meditation and is open to all that feel (i) that they have too much stress in their lives, or (ii) that they are not relating to their stress healthily. In the 1990’s Mark Williams, John Teasdale and Zindel Segal combined Kabat-Zinn’s successful model with Beck’s Cognitive Behavior Therapy (CBT) to create a more specialised programme called Mindfulness-based Cognitive Therapy (MBCT). This programme is specifically designed to treat recurrent depression, and largely only open to those referred by their primary medical consultant. These two arms, the general MBSR and the specific MBCT, are the constituents of the Mindfulness-based interventions available on the NHS in the UK and through other providers around the world. They are widely used both as complementary and sole treatments for a variety of mental and physical health diagnoses including depression, generalised anxiety disorder, post-traumatic stress disorder, insomnia and eating disorders.

What evidence is there that Mindfulness is effective?

The effectiveness of Mindfulness-based interventions has been demonstrated through longitudinal studies, tracking the same people over time. An important early example found depressive participants in the MBCT programme to have half the amount of relapses one year after treatment compared to depressive participants that had treatment as usual (Teasdale et al, 2000). This finding was reinforced by the replication trial (Ma and Teasdale, 2004) concluding that there is ‘further evidence that MBCT is a cost-efficient and efficacious intervention to reduce relapse/recurrence in patients with recurrent major depressive disorder’ (ibid, p. 39). In these studies, the pool of participants in recovery from depression were randomly allocated into either the experimental or the control group. This was done by an external statistician and participants were matched for ‘age, gender, date of assessment, number of previous episodes of depression, and severity of last episode’ (ibid, p. 32). The results were important confirmation for the effectiveness of Mindfulness-based Interventions as therapy.

Whilst this was great news, it wasn’t until 2008 that Mindfulness-based interventions were compared to the gold standard for treatment of recurrent depression (Kuyken et al, 2008). This is maintenance antidepressive medication (m-ADM), requiring the participant to take antidepressive medication even when there are no indications of a relapse. Importantly, the 2008 study found that patients treated with MBCT were less likely to relapse than those treated with the gold standard after 15 months (47% compared to 60% of the m-ADM group). This was also replicated in a follow up study (Segle et al, 2010) where MBCT was compared against m-ADM and also against a placebo. Once participants were in remission they were given either MBCT, m-ADM or discontinued their active medication and given a placebo. Participants for all groups were randomly distributed by an external statistician, ensuring a close control on factors not being investigated. The MBCT and m-ADM group here showed the same levels of prevention from recurrence (73%), both much higher than the placebo group. Over a short term (15 months) Mindfulness-based interventions were thus shown to be better than m-ADM, and equally effective over an even longer period. In addition, it is arguably cheaper to administer Mindfulness-based interventions than m-ADM, there are no issues with drug tolerance, and unlike many antidepressants Mindfulness meditation can be utilised whilst pregnant or breastfeeding.

How does Mindfulness work?

When the brain is not responding to any particular task and is ‘at rest’, areas collectively known as the Default Mode Network (DMN) are activated (Berger, 1929), (Ingvar, 1974), (Andreasen et al, 1995).  This was found to be closely associated with mind wandering (Mason et al, 2007). It was also found it to be consistent with “internally focused tasks including autobiographical memory retrieval, envisioning the future, and conceiving the perspectives of others ” (Bruckner, 2008, p. 1). When our mind is wandering and not focused on a task we are normally either lost in personal memories or running through a scenario in our head, predicting, anticipating or worrying.

More frequent and more automatic activation of this network is associated with depressed individuals (Greicius et al, 2007); (Zhang et al, 2010) (Berman et al, 2011). Regularly wallowing in old memories or worrying about the future are perfect foundations for conditions that may lead to depression. These two functions, conducive to ‘living on autopilot’’, are the exact opposite to the definition of Mindfulness meditation given above: “moment-to-moment awareness.” Indeed, studies have shown that activation of the DMN can be regulated by Mindfulness meditation (Hasenkamp et al, 2012). Participants were observed meditating, and whenever they noticed their mind wandering they had to press a button. Immediately before this action the participants were unconsciously mind wandering. When the participants noticed that their mind had wandered, (indicated by the button press) the researchers regularly observed a deactivation of the DMN. The act of practising mindfulness-meditation was here regularly associated with a deactivation of the DMN.  A correlation between self-reported meditation experience and lower levels of DMN activation was also observed (Way et al, 2010).

Of course, the brain is never ‘doing nothing’ and a counter-network was regularly activated when participants weren’t mind-wandering: when they were paying attention to a task. This network in part consists of the anterior cingulate cortex (ACC), which is known to be instrumental in task monitoring (Carter et al, 1998). Activation of the ACC is closely associated with ‘executive control’ (Van Veen & Carter, 2002, p. 593) which detects incompatibilities or conflicts between a predicted outcome, and the observed reality. In this way the ACC functions as error-reporting or quality management. The ACC does not attempt to remedy the situation, but instead highlights it to other areas of the brain. This all happens before the subject is cognitively aware that there is a conflict.

Crucially, an association has been shown between meditation and activation of the ACC. A positive correlation between AAC thickness and meditation experience (Grant et al, 2010) and between mindfulness meditation and activation of the ACC (Zeidan et al, 2013), has been demonstrated. Mindfulness meditation is reliably shown to activate the ACC and improve the relative ease and likelihood of it being activated. Activation of the ACC prevents the mind from wandering, and prevents activation of the DMN. Mind wandering and activation of the DMN is related to depressive symptoms either developing or recurring. This is how Mindfulness-based interventions are thought to help those at a neurological level.

Conclusions

Mindfulness meditation has been around for 3500 years. It has been utilised in the West for nearly 40 years. We have had good evidence that it works for nearly 20 years but we are only just starting to explore how it works. The recent findings above help outline the process of change that the brain goes through whilst a regular Mindfulness-meditation practise is established, but they are by no means the full picture. We are also investigating how Mindfulness meditation facilitates people to more regularly respond instead of instinctively react. We are investigating how Mindfulness meditation enables decentering, and how it reduces the connectivity to the emotional areas of the brain. Research into the nuts and bolts of Mindfulness has never been so intense, and exciting results just like those depicted in this article are sure to arise soon.

Joe teaches a 10 week course devised by the Mindfulness in Schools Project (see details here). He teaches all levels and abilities, from College to University, and finds that it has had an overwhelmingly positive impact on level of well-being, achievement, and attendance of his students. If this is something that interests you, he can be contacted at joseph.c.holloway@gmail.com is now taking bookings for autumn term 2017, and for 2018.

Edited by Jonathan Fagg and Rachael Stickland

References:

  • Analyo (2003). Satipaṭṭhāna: The Direct Path to Realisation. Birmingham: Windhorse Publishing
  • Andreasen, N. et al. (1995). Remembering the past: two facets of episodic memory explored with positron emission tomography. Annals of the Journal of Psychiatry, 152, (1), pp 1576- 1585.
  • Berger, H. (1929). Über das elektrenkephalogramm des menschen. Archiv für Psychiatrie und Nervenkrankheiten, 87, (1), pp 527-570.
  • Berman, M. et al. (2011). Depression, rumination and the default network. Social Cognitive & Affective Neuroscience, 6, (1), pp 548-555.
  • Bruckner, R. (2008). The brain’s default network: anatomy, function, and relevance to disease. New York Academy of Sciences, 1124, (1), pp 1-38.
  • Carter, C. et al. (1998). Anterior cingulate cortex, error detection, and the online monitoring of performance. Science, 280, (1), pp 748-749.
  • Greicius, M. (2007). Resting-state functional connectivity in major depression: abnormally increased contributions from subgenual cingulate cortex and thalamus. Biological Psychiatry, 62, (5), pp 429-437.
  • Grant, J. et al. (2010). Cortical thickness and pain sensitivity in zen meditators. American Psychological Association, 10, (1) pp 43-53.
  • Hasenkamp, W. (2012). Mind wandering and attention during focused meditation: a fine-grained temporal analysis of fluctuating cognitive states. NeuroImage, 59, (1,) pp 750-760.
  • Holzel, B. et al. (2011). Mindfulness practise leads to increases in regional brain grey matter density. Psychiatry Research, 191, (1), pp 36-43.
  • Ingvar, D. (1974). Patterns of brain activity revealed by measurements of regional cerebral blood flow. Copenhagen: Alfred Benzon Symposium.
  • Kabat-Zinn, J. (1990). Full Catastrophe Living. New York: Dell Publishing.
  • Kuyken, W. et al. (2008). Mindfulness-Based Cognitive Therapy to prevent relapse in recurrent depression. Journal of Consulting and Clinical Psychology, 76, (6), pp 966-978.
  • Ma, S. & Teasdale, J. (2004). Mindfulness-Based Cognitive Therapy for depression: replication and exploration of differential relapse prevention effects. Journal of Consulting and Clinical Psychology, 72, (1), pp 31-40.
  • Mason, M. et al (2007). Wandering mind: the default network and stimulus-independent thought. Science, 315, (19), pp 393-395.
  • Teasdale, J. et al. (2000). Prevention of relapse/recurrence in major depression by Mindfulness-Based Cognitive Therapy. Journal of Consulting and Clinical Psychology, 68 (4), pp 615-623.
  • Segle, Z. et al (2010). Antidepressant monotherapy vs sequential pharmacotherapy and Mindfulness-Based Cognitive Therapy, or placebo, for relapse prophylaxis in recurrent depression. Archives of General Psychiatry, 67, (12), pp 1256-1264.
  • Van Veen, V. & Carter, C. (2002). The timing of action-monitoring processes in the anterior cingulate cortex. Journal of Cognitive Neuroscience, 14, (4), pp 593-602.
  • Way, B. et al (2010). Dispositional mindfulness and depressive symptomatology. Correlations with limbic and self-referential neural activity during rest. Emotion, 10, (1), pp 12-24.
  • Zeidan, F. et al. (2013). Neural correlates of mindfulness meditation-related anxiety relief. Social Cognitive and Affective Neuroscience, 9, (6), pp 751-759.
  • Zhang, D. et al. (2010). Noninvasive functional and structural connectivity of the human thalamocortical system. Cerebral Cortex, 20, (1), pp 1187-1194.

Perceptions of mental illness: Do biological explanations reduce stigma?

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.

stigma

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.

facebook-ads-kenneth2-1024x536

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.

gengraph

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

References:

  • 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.

Perceptions of mental illness: The media and mental health.

Rae Pass | 6 FEB 2017

You wouldn’t blame someone with breast cancer or cystic fibrosis for their disease, would you? We know they are caused by impaired biological mechanisms. Lifestyle choices can exacerbate risk but there is less stigma associated with suffering from a ‘physical’ rather than mental illness.  With both types of illness stigma stems from a lack of understanding. If someone walks down the street arguing with themselves you avoid them and think “that person is crazy”. You can’t help it, you avoid their gaze and hurry on by, you don’t want to get involved with something so out of the ordinary. But why? Why should we assign blame to people for something that is not their fault when we wouldn’t do it for other diseases?

The way mental health conditions are portrayed in the media reinforces our mistrust and negative reaction to sufferers. Time and time again they are depicted as evil, deceitful and intending harm, despite this rarely being the case. Empathising with people who suffer from mental illness and commit crime doesn’t detract from what they do, but understanding why they may have behaved in that way is vital to preventing it happening again.

In 2015 a pilot crashed a passenger plane in the Alps in an apparent suicide. It later came out that he had been battling depression for a long time. The majority of the coverage painted him as devious for hiding his illness and, in some reports, just waiting for the opportunity to harm others. What he did was horrible, and heart-breaking for those who lost loved ones, and it reinforces our aversion to dealing with someone with suicidal tendencies. Despite our gut reaction to this we must look at why he was suffering and whether he was he receiving suitable help. This will help us understand why he did it, if it could have been prevented and to stop anyone else from doing it again. The pressure of his job may have played a role in his depression and subsequent suicide. It has been highlighted how stressful a pilot’s life can be, on top of all the usual stresses people deal with, and how difficult and career ending it can be to seek help. If society were more accepting of mental health disorders and there was less attached stigma to a diagnosis people may be more willing to seek help, thus reducing the chance of something like this occurring.

Should we prevent someone doing a job simply because they have a mental health condition? You wouldn’t do the same for someone with a physical illnesses.  There will be some instances where it just isn’t feasible for them to carry out a job, but blanket banning someone from a career due to a mental health diagnosis is unreasonable. This is especially pertinent as although many disorders are given one name they often describe a spectrum of conditions and symptoms. Therefore, not everyone with a condition will behave in the same manner, and those who are more able to cope socially may be penalised for having a related condition. Discounting a proportion of society based on the actions of one person is detrimental to everyone. Cases like this flight, with such negative coverage and discussion of his diagnosis of depression, further fuels mistrust and suspicion. This it in turn makes it harder for those suffering to seek help, increasing the likelihood of it happening again.

Imagine if you were made redundant, or that you just lost someone close to you. You don’t think you cope anymore and all you want to do is stop but it has been drummed into you by friends, family and the media that being depressed, or needing help is weak and pathetic so you try to struggle by alone. It becomes easy to see how people end up in terrible situations, possibly even taking their own life. It will take time to change the public’s opinion but the media could be so powerful in changing our attitudes towards mental health, especially through social media campaigns such as Time to Change and Rethink Mental Illness. The media has been used to provide insight into the lives of sufferers before. A collaboration between Bryan Charnley and a journalist set out to illustrate his experiences of schizophrenia through self-portraits, whilst taking varying degrees of medication. Tragically, it ended with Bryan taking his own life, but his haunting, and increasingly distressing paintings, live on.  Increasing our exposure to messages of support, reminding people that they are not alone and that there is no shame in suffering from mental health conditions, and providing them with information on how to get help is a vital step forward in reducing stigma.

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IMAGE SOURCE.

So why is our gut reaction to mental health generally so negative? Is it purely due to misinformation and fear portrayed by the majority of the media coverage? Can we combat the stigma with our rapidly increasing understanding of the biological basis of these diseases?

If these questions interest you, read on to my next article Perceptions of mental illness: Do biological explanations reduce stigma?’ 

Edited by Jonathan Fagg