I was asked on Twitter:
When did depression stop being an emotion and start being a mental illness? #seriousQuestion
This is a really important question, and topical too, given the ever-increasing prescriptions for antidepressants written and filled throughout much of the world, and recent studies casting doubt on the efficacy of those medications (there are problems with those studies, and the breadth of their conclusions – even though there might be a kernel of truth to them).
So what is depression?
Depends who you talk to, and the context of the conversation. We all feel sad at various times, and when we so, might even say “I’m so depressed”. While sadness is an unpleasant state, it’s none of my business as a psychiatrist unless it is accompanied by the trappings of psychiatric illness…. So what does that mean then? The easy, pat, concrete and simplistic answer would be to refer you to the criteria for Major Depressive Disorder as set out in the DSM IV- TR, or the ICD-10. The Diagnostic and Statistical Manual of the American Psychiatric Assoiation, and the International Classification of Diseases (UK/Europe) contain lists of criteria for specific diagnoses, with the goal of increasing the number of things US psychiatrists can charge HMOs and insurance companies for standardising diagnostic practice, and thereby enhancing treatment through better comparisons and research.That wouldn’t be a particularly helpful answer though – and it would be one you could have got yourself, without reading my ramblings.
When is depression an illness?
Shouldn’t we all just pull our socks up and get on with it? Are we just big sooks? Are psychiatrists simply making a mint out of pathologising normal human experience? Well … Not really – overall at least. Sadness is one of the basic human emotions, and as such must serve a purpose. It’s been suggested that being sad about being in a bad situation might act as a spur to change that situation for the better, for example. Someone with major depressive disorder however might be rendered, by the magnitude of their symptoms, quite incapable of making the changes they should. Their depression might also overtake them completely without external precipitants – so there’s no situation to be changed, and no adaptive purpose to the mood shift.So there are both quantitative (the number and severity of symptoms) and qualitative (the kind of symptoms) differences between sadness, and what we as shrinks want to identify and poke our noses in on – which we call major depressive disorder (and dysthymic disorder: lower symptom burden, but chronic – 2 years+).
As you can see if you google or wiki the DSM and ICD criteria for depression, they’re quite similar. Broadly there’s stuff about pervasiveness and duration of symptoms, physical changes that accompany the low mood, and characteristic patterns of thinking (sometimes even psychotic). These patterns, which define the syndromes we call illnesses, have been developed by examining what symptoms cluster together, and what happens to people who display those symptom clusters.
So, we know everything now, right?
… Right??? Nope. Many of these symptoms are shared with various medical (physical) illnesses, and with symptoms of stress (when stressed we are all likely to feel unhappy, to lose our sleep and appetite, to not concentrate as well, and so on). What we have with these lists of criteria is a communication too. It makes sure we’re all speaking the same language; that when a colleague tells me he or she has seen a patient with a major depressive disorder, I have a pretty good idea of the sort of things that are likely to be going on – not the things specific to that individual, but the broad brush symptomatic stuff.
It also is meant to ensure that when we gather a research population it is fairly homogenous, so we can be reasonably confident we’re studying one problem, rather than an aggregation of a whole lot of different problems that look the same. Unfortunately that probably doesn’t follow 100%, but these are the best tools we have currently.
So why does it matter whether someone is sad or depressed anyway? Aren’t antidepressants just placebos – or at least no more effective? That was the result trumpeted around the world from a meta-analysis by Kirsch et al. A meta-analysis is a type of study that involves gathering all the relevant studies that have been done on a particular question, analysing them and putting the data together, to end up with in effect one much larger study. Sounds good, but is fraught in a number of ways. Despite seeming like the last word in evidence, it’s only as good as the studies it includes – and the search strategy used to find them. For example, Kirsch et al’s study used only data submitted to the FDA to get licensing for 3 antidepressants. The studies weren’t representative of the sort of studies done later (they were simply aimed at getting the drug licensed), and with only 3 antidepressants (all of one type) it’s not really generalisable. They then reanalysed their data and announced that for severe depression the pills were in fact better than placebo, but mild to moderate depressions didn’t respond any better to drug than placebo.
Another meta-analysis has been published in the Journal of the American Medical Association. The authors are very confident in their assertions that indeed antidepressants are no better than placebo except for the most severe depressions. Do I have a problem with this, given that they searched “PubMed, PsycINFO, and the Cochrane Library databases … from January 1980 through March 2009, along with references from meta-analyses and reviews.” 30 years of research. SOunds good. SOunds thorough. They also talk about doing a “patient-level” meta-analysis, meaning that instead of just aggregating results of trials, they aggregated data from the individual patients, to create one big sample. Sounds awesome, right?
Well, I have one thing to say:
Because of their decision to only include trials from which they could get data on individual patients, they ended up with 6 trials, of 2 antidepressants, involving just 718 patients. From. 30. Years. Of research. Pleh, and again pleh. And if you want more than just ‘pleh’ Richard Friedman MD in the New York Times wrote a very nice article discussing this latest meta-analysis.
But are they right anyway?
Well, maybe. In spite of themselves, I think they might have at least a kernel of truth there. As an analogy, ECT is our most powerful antidepressant treatment. It actually works better, the more severely ill the patient is. We use ECT in patients with severe depression, psychotic depression, melancholic depression … all likely markers of a serious underlying biological illness, rather than sadness and life stress. I wonder if in these meta-analyses, the severity is acting as a proxy for patients with a more biological illness, and – unsurprisingly – those patients respond better to antidepressant medication than do the less severely ill, who probably consist of a much greater proportion of people with less biological illness – and could reasonably be hypothesised to respond less well to biological treatment (i.e. pills – or ECT).
Now the picture says “science content” so in the spirit of science, that hypothesis needs to be tested. Unfortunately at this point we have no lab test, no physical investigation to differentiate depressed from non-depressed (possibly because our study groups, defined as they are syndromally, are not homogenous enough to give any clear or consistent results of that nature. I don’t really know off the top of my head what to do about that.
Professor Gordon Parker from the Black Dog Institute in Sydney, Australia, has a compelling model for separating depression by presence or absence of melancholic symptoms (the prototypical depressive picture, as described as far back as the ancient Greeks), and then by presence or absence of psychotic symptoms…. but I’ve not seen anything to validate that, other than clinical experience and anecdote. It has good face validity, but that’s no more than a starting point.
In essence …
In any case, Kristie, I think I’ve got wildly tangential to your initial question. I guess the guts of my answer would be about severity, the nature of symptoms associated with major depression and not (to the same degree) with sadness, and the implications for what to do about it (sadness = address situation, depression = active treatment – of one sort or another; pills aren’t the only things). We’re not here to stop people feeling sad – even very sad – unless that sadness has the trappings of illness: a cluster of duration, pervasiveness, physical changes (to sleep, appetite, energy etc), and characteristic thought patterns – in which case it’s reasonably likely to respond to a range of interventions we can bring into play to get that person back to normal function.
I often tell my depressed patients that are facing serious real stressors, that I’m not aiming to lift their mood and make them happy; I’m aiming to improve the function of their bodies and brains so they can do what they need to to cope with or fix their circumstances.