Does Our Current Model of Mental Illness Need Rebooting?
Author: Sahana Hegde
Edited by: Tanvi Sheth
If you're the type of person who spends a lot of time thinking about mental illnesses, I'm sure you've noticed that there are a lot of different ways to do it - which, in and of itself, should tell you something. (If you're not the type of person who spends a lot of time thinking about mental illness, you may be on the wrong blog.) It wasn’t too long ago - maybe about ten years - that raising awareness around mental health meant combating the idea that mental illnesses were all made up and no realer than Harry Potter, and that conversation is still perfectly relevant in a lot of circles. Then there are more sub-school of thought even once one accepts the existence of psychological illness; the purely psychological and philosophical model a la Freud, behaviourism at the other end of the spectrum, diathesis-stress, and what is currently one of the most influential conceptualizations: the biomedical model.
Based heavily on the medical model for other diseases - such as, say, malaria or diabetes, this model conceptualises mental illness as, well, an illness; a result of a malfunctioning organ, most commonly the brain (other occasional offenders include gut bacteria and hormonal glands). Along with its gain in traction, though, the (purely) biomedical model of mental illness has garnered some flack as well in recent years.
It is undeniable that this approach has made several strides in the field of psychopathology. It has positive effects when used as the basis for treatment, and it also lends psychology and even psychiatry a level of legitimacy that isn’t as universal as it should be, especially in the Indian population. That said, a fair question to ask at this juncture is whether or not the biomedical model alone is sufficient as a conceptualization of mental illness.
The aspects of this model that I will be focusing on are twofold: one, the concept of discrete syndromes, and second, the idea that these syndromes are identified by rigid criteria/symptoms and are rooted solely and entirely in neurobiology and neurochemistry.
The most mainstream example of the BM model is probably the DSM (or the ICD), which faces some very heavy and very valid criticism, chiefly for its rigid, reductive approach and the way it claims to be objective in spite of being historically steeped in bias. Examples abound: the fact that homosexuality was considered a mental disorder until 1973, the fact that a BMI of below 17.5] is still one of the diagnostic criteria for anorexia nervosa. It’s clear that this leads to people getting ‘care’ they don’t need, or worse, not getting care they do need. (actually, it might be worse. Given the state of psychiatric care, wards especially, it’s hard to say who was better off. The point, though, is that it’s a miserable question to have to ask in the first place).
Similarly, the primary criticism of the biomedical model, which posits that mental illness is simply a cause of neurobiological malfunction, is that it is overly reductive. Deacon, one of the most outspoken critics of this model, goes so far as to claim that the mental health outcomes of this model aren’t as heartening as one might think, and that psychoactive drugs are not sufficiently effective at treating them (2013). A full discussion of that last one is somewhat out of the ambit of this post; however, it is clear that there is still some contention regarding drug-based treatments, specifically, for mental health issues.
Then again, it’s not as if psychoactive drugs are the be-all and end-all of the biomedical approach. Like I said earlier, the cornerstone of this model lies in the conceptualization of mental illness as resulting from biological malfunction. And, as we’ll see, with very good reason.
The neural correlates of several mental illnesses, from depression to schizophrenia, have been well documented. A number of forays have even been made into mapping specific symptoms to brain malfunctions; BPD, for instance, is associated with increased activity in the amygdala, which would fit with the high emotional reactivity and dysregulation that one sees in patients of the disorder. The thing is, though, that fifteen other disorders and their dog all exhibit increased activity in the amygdala. This is explained (in part) in modern psychology by the term comorbidity, which is exactly as grim as it sounds; essentially, a term describing the buy-one-get-three-free nature of mental illnesses. If you hit the BMI benchmark and get diagnosed with anorexia, the stats say you probably also have anxiety, and/or depression, maybe a personality disorder and bad fashion sense as well (you can’t see me, but I’m gesturing vehemently at myself as I write this). Which would make sense if there’s overlap in neural correlates as well, of course.
This is an extension of what some call ‘discrete syndrome theory’ - which is to say, the idea that each psychological disorder is, well, a discrete syndrome, each with a nametag and a list of symptoms and a cutoff point for how many symptoms Hahana Segde (name changed to protect privacy) needs in order to meet diagnostic criteria. Remember when we talked about the issues with diagnostic criteria for psychopathology? Yeah.
(Interestingly, Clark Keyes in 2005 published a paper arguing that this mental illness/mental health model was flawed because it didn’t sufficiently account for a spectrum of illness; he pointed out that many people who are free of psychopathology can nevertheless not be described as well; thereby making the argument that not only mental illness but also mental wellness becomes oversimplified under discrete syndrome theory.)
RDoC, or Research Domain Criteria, is a framework for investigating - not diagnosing - mental illness that is less susceptible to those pitfalls. While it’s certainly adherent to the biomedical model of disease, it eschews discrete syndrome theory in favour of seeing it as a ‘matrix of elements’, currently modelled on six major spheres of human functioning.
A related newer, shinier proposed alternative is what’s called network theory. Network theory views these common symptoms - such as impulsivity, or the aforementioned emotional dysregulation - as bridges, a term that is not only more cheerful but also slightly more complex. The idea is that we see disorders as less venn diagrams and more flowcharts, in essence. Common symptoms are connected across conditions and could act as bridges between them. This theory is augmented by neuroscience; Martin proposes that functional networks and connectivity patterns in the brain could hold the key to understanding how these symptom networks work. This would call for essentially doing away with discrete syndrome theory entirely, and reworking how we talk about, diagnose, and treat mental illness.
TL:DR: it is not true that the biomedical conception of mental illness is wrong - far from it. Nor is it the case that the psychological symptoms outlined in the DSM are inaccurate. The way forward is instead for both of these approaches to not only be even further integrated but also for them both to be further complicated. I'll be the first to admit that we don't have all the answers right now as to what exactly that would look like. But it might turn out to be a much more accurate, effective approach.