I have serious reservations about beginning the report with this introduction: “Imagine going to bed tonight & having to lock your bedroom door out of fear - fear that you might be attacked in your sleep by your own child.” - way to help the cause of the schizophrenic, ABC. No wonder those with a psychotic disorders are generally met with fear & suspicion: this is the media image they have to contend with. The rest of the video is quite interesting though…
“Everything great that we know has come to us from neurotics. They alone have founded our religions and created our masterpieces. Never will the world be aware of how much it owes to them, nor above all what they have suffered in order to bestow their gifts on it.”—Marcel Proust
“Humans expect positive events in the future even when there is no evidence to support such expectations. For example, people expect to live longer and be healthier than average, they underestimate their likelihood of getting a divorce, and overestimate their prospects for success on the job market. We examined how the brain generates this pervasive optimism bias. Here we report that this tendency was related specifically to enhanced activation in the amygdala and in the rostral anterior cingulate cortex when imagining positive future events relative to negative ones, suggesting a key role for areas involved in monitoring emotional salience in mediating the optimism bias. These are the same regions that shown irregularities in depression, which has been related to pessimism. Across individuals, activity in the rostral anterior cingulate cortex was correlated with trait optimism. The current study highlights how the brain may generate the tendency to engage in the projection of positive future events, suggesting that the effective
integration and regulation of emotional and autobiographical information supports the projection of positive future events in healthy individuals, and is related to optimism.”—Sharat et al (2007): Neural mechanisms mediating optimism bias
The popular perception of creative thinkers and artists is that they often also have mental disorders—the likes of Vincent van Gogh or Sylvia Plath suggest that creativity and madness go hand in hand. Past research has tentatively confirmed a correlation; scientific surveys have found that highly creative people are more likely to have mental illness in their family, indicating a genetic link. Now a study from Sweden is the first to suggest a biological mechanism: highly creative healthy people and people with schizophrenia have certain brain chemistry features in common.
A research team at the Karolinska Institute in Stockholm studied 13 mentally healthy, highly creative men and women. As noted in the paper published in May in PLoS ONE, other scientists had previously found that divergent thinking, or the ability to “think outside the box,” involves the brain’s dopamine communication system. The Swedish research team used PET scanning to determine the abundance of a particular dopamine receptor, or sensor, in the creative individuals’ thalamus and striatum, areas that process and sort information before it reaches conscious thought—and that are known to be involved in schizophrenia. The team found that people who had lower levels of dopamine receptor activity in the thalamus also had higher scores on tests of divergent thinking—for instance, finding many solutions to a problem.
“You enter the brain through the eye, march up the optic nerve, round and round the cortex, looking behind every neuron, and then before you know it, you emerge in the daylight on the spike of a motor nerve impulse, scratching your head and wondering where the self is.”—
This guy is brilliant. Thoroughly recommended reading, especially on qualia.
Congruent with their high prevalence rates, I’ve had some really interesting submissions from those with schizophrenia, generalized anxiety disorder & depression. They’ve been super interesting & well-written accounts - thank you to their authors.
However, I want the zine to represent all kinds of mental health.
Do you have a specific phobia / social phobia / PTSD / OCD / eating disorder / personality disorder? I would love to hear from you.
When did you realise you needed help? Did someone realise for you? How do you cope? Have you undergone treatment? How does it affect your life?
Click here to submit. You can log out of tumblr & make up an e-mail address if you want to remain anonymous. Your account will be saved & put in the published zine in (hopefully) February. If at any time before now & then you would like to retract your account, just drop me a line to let me know.
“It is proposed that happiness be classified as a psychiatric disorder and be included in future editions of the major diagnostic manuals under the new name: major affective disorder, pleasant type. In a review of the relevant literature it is shown that happiness is statistically abnormal, consists of a discrete cluster of symptoms, is associated with a range of cognitive abnormalities, and probably reflects the abnormal functioning of the central nervous system. One possible objection to this proposal remains—that happiness is not negatively valued. However, this objection is dismissed as scientifically irrelevant.”—Bentall (1992): J Med Ethics. 1992 Jun;18(2):94-8.
“A recent survey of attitudes conducted by Rethink found that 29% of the people surveyed would not be happy to live next door to a person with mental health problems, but this went up to 47% when asked about living next door to a Muslim person with mental health problems”—MIND report on the mental health of South Asian communities in Britain.
“White feminists may have provided valuable and challenging research literature on gender in, among other areas, caring for the sick, the masculinisation of medicine, the journey of being a mother and the sexist nature of medical sociology, but these have routinely excluded the Black women’s perspective.
African-Caribbean women bring distinctive insights and experience to both feminism and anti-racism. However, they frequently find that they have to struggle against sexism and racism not only within society generally but also against racism within White feminist movements and sexism within anti-racist movements. Moreover, race equality initiatives tend to benefit mainly Black men, and gender equality initiatives mainly White women.”—MIND report on BME mental health.
Mind Over Matter zine: The little things that keep me sane...
Mindovermatterzine are not just interested in those diagnosed with a psychiatric disorder, but also how people sustain their mental health. What are the little things that get you through the day and bring you happiness and mental wellbeing?
Reblog with your thoughts if you’d like them to be included!
Thanks, new followers! I am getting so excited reading submissions. There’s some really eloquent writers out there, and no amount of text book reading about signs & symptoms of psychiatric disorders can match hearing first person what it’s like to be schizophrenic, bipolar, anxious etc.
When a surgeon cut into Henry Molaison’s skull to treat him for epilepsy, he inadvertently created the most important brain-research subject of our time — a man who could no longer remember, who taught us everything we know about memory. Six decades later, another daring researcher is cutting into Henry’s brain. Another revolution in brain science is about to begin.
Is Depression caused by a lack of Serotonin in the brain, or are we being conned?
In the 1950s, scientists accidentally discovered that increasing levels of the monoamines (serotonin, dopamine and noradrenaline) in the brain was associated with increased positive mood, and the hypothesis was made that depression is due to decreased levels of neural monoamines, particularly serotonin. To what extent is this correct and to what extent are we being deceived by ‘Big Pharma’?
The pharmaceutical industry is estimated to be worth over $600 billion and, of this, over $3.1 billion is due to sales of the antidepressant Zoloft – the seventh best selling drug in the world. Arguably, it is in the best interests of this industry not to highlight and even to suppress the efficacy of other drugs which do not conform to the depleted serotonin hypothesis which has served drugs like Zoloft so well, for not doing so would mean remarketing their stance on the cause of depression, branding a new drug, and advertising it to the public – all of which are costly endeavours.
Hundreds of studies have demonstrated that antidepressant administration increases mood, affects cognition & reduces fear responses in the depressed & the healthy, but why do they not work in all people? Although antidepressants which serve to increase monoamine levels are effective, their immediate chemical effects take weeks to be translated into increased positive mood (average 6 weeks) - surely if depression was due to not having enough serotonin, we would all be happy as soon as we took an antidepressant pill, as they increase serotonin levels immediately.
Latency aside, some recent studies have proposed that the antidepressants currently on the market are not as effective as pharmaceutical companies would have us believe. Kirsch et al (2002) found, through analysis of all antidepressant clinical trials submitted to the FDA for approval, that the antidepressant response was matched by 80% of the placebos used, and in 57% of the trials there was no significant difference between antidepressant and placebo. Let’s just consider that for a second: 8 out of every 10 placebos they used worked just as well as antidepressants - that’s a huge number. Is simply being told you are taking something which will make you happier enough to make you happier? Lacasse and Leo (2002) contrast this with trials concerning insulin imbalance in studies aiming to find relevant medications for diabetics. In these trials, they claim, there is no such modest efficacy or high placebo response…so why should antidepressants be approved by the FDA with less evidence for their efficacy? Perhaps what they are hinting at is that although antidepressants have mild side effects such as dry mouth, anxiety, constipation and weight gain, incorrect adjustment of blood sugar levels can lead to coma and even death; so drug companies can successfully market antidepressants - even though the research to support their efficacy is not as well replicated as one would desire – because the negatives of doing so are less than for other disorders and medications.
Also troublesome are the findings of the efficacy of drugs which do not directly target the serotonergic system. For example, bupropion, reboxetine, and even St. John’s Wort have performed as well as or even better than SSRIs in recent randomised controlled studies. Most interesting perhaps is tianeptine, which is actually a selective serotonin reuptake enhancer. This actually reduces the available serotonin in your brain, so it would make you more sad, right? - Wrong: it has found to be clinically efficacious in the treatment of depression, with few side-effects. It even alleviates comorbid anxiety without sedation. This is an advantageous property, considering the high comorbidity of anxiety and depression (as high as 50%).
Regardless of whether we should be looking to increase or decrease serotonin, the question remains: can biology ever truly be a cause? Given that biological factors don’t necessarily lead to depression (they often provide only a vulnerability which must be ‘triggered’ by environment), it is too hasty for drug companies to claim that depression is caused by a lack of serotonin.
So why have antidepressants and a serotonin explanation come to the forefront in advertising literature and the minds of medical professionals and the general public if there are other plausible candidate mechanisms at play in depression? Turner et al (2008) highlighted a ‘publication bias’ prevalent in the scientific literature by comparing published and unpublished outcomes of 12 antidepressant studies involving 12,564 patients submitted to the FDA. 31% (3449 patients) were not published, and this was significantly associated with study outcome: out of 74 studies, 37 with a positive result were published as opposed to only 1 with a positive result that was not published. It therefore appeared, according to the published literature, that 94% studies were positive. However, when they returned to all the available literature, including the studies that were refused publication, only 51% were positive. That’s no better than chance! We cannot determine whether the bias observed resulted from a failure to submit manuscripts on the part of authors and sponsors, from decisions by journal editors and reviewers not to publish, or both. What does seem clear, though, is that there is a publication bias prevalent in the FDA and academic journal system, which may have skewed evidence more towards the pharmaceutical companies’ opinions.
Another important aspect at play here is journalism and the media, which Leo & Lacasse (2008) recognised in their study in which they looked to the media for support of their hypothesis that, whilst the cause of mental disorders such as depression is unknown, “the idea that neurotransmitter imbalances cause depression is vigorously promoted by pharmaceutical companies and the psychiatric profession at large”. They received responses from multiple sources, including practicing psychiatrists, clients, and a major pharmaceutical company. The evidence offered was “not compelling”, and several of the cited sources flatly stated that the proposed theory of serotonin imbalance was known to be incorrect. When they asked one particular journalist about why she had said in an article that depression was due to a “chemical imbalance”, ”the author mentioned that: psychiatrists would be the best people to talk with about chemical imbalances; mental illnesses have been linked to chemical imbalances; psychiatrists are trained to figure this out through a variety of tests; and that “numerous studies have been done” and “the research is definitely available.” We pointed out to her that, if there are “numerous studies” which are “definitely available,” then it should be relatively easy to cite at least one article. She did not reply.” In this way, journalists are the main link between scientific researchers and the general public, and careless writing can easily influence common thought about this disorder.
In summary then, I do not dispute that there is indeed convincing and statistically significant evidence within studies to support the hypothesis that a lack of serotonin has a role to play in depression, but rather I wish to show that such evidence may have been shown favouritism both in the media and in publication biases present in many of the most prominent scientific journals. I am drawn to agree with the recent literature, which suggest that the view of the cause of depression as a “chemical imbalance” is oversimplified at best: we have insufficient evidence to view it as a cause and, until we can, this may even be detrimental to patient recovery. As proponents of Cognitive Behavioural Therapy would argue, viewing oneself as the passive ‘victim’ of one’s own biology may even be detrimental to recovery.