Following a Guardian article by Ed Bullmore, I tweeted today asking why psychiatry allows and encourages speculation about depression being an inflammatory disorder. As I've said before (eg. see previous post), it’s non-sensical to believe that depression is a form of inflammation. Yet, as in the article by Bullmore, such speculation is promoted as a “new frontier” which could lead to “breakthroughs” in the treatment of depression, with the “potential to transform our thinking about illness more broadly”. Exciting stuff apparently! But why the hype?
Of course part of the reason is to encourage participants to express an interest in the NIMA ATP trial. More fundamentally, the real problem is that depression is not always easy to treat (see previous post). We always need hope that there might be simpler and more effective treatments (see eg. previous post). I don't want to appear pessimistic about the treatment of depression. There can be spontaneous improvement over time. People have considerable personal resources and resilience to be able to overcome and adapt to their difficulties.
Of course psychiatry is merely responding to our idealistic wish for a simple, quick, cheap, painless and complete cure for depression. It does this for psychological therapy as well as medication (eg. see previous post). But promoting myths that depression is due to inflammation does not justify deflecting from the hard work required to help people recover from their depression.
First of all, DSM5 major depression is so watery, poorly defined and inclusive, no one will ever find a glaring independent variable. It's never going to be cigarette smoking and lung cancer. The article talked about observational associations in some forms of depression. They didn't say all depressions are inflammatory. There are plenty of studies that indicate that certain types of depression with high levels of inflammatory markers improve with control of chronic inflammation and correlate with reduction of CRP or cytokines. That may be secondary to physical improvement, but so what if it works? Secondly, it is well known that interferon treatment is highly associated with depression so this is not an unreasonable theory, and there's a lot more going on here than ever existed for serotonin. Thirdly, we do have evidence of inflammatory/endocrine dysregulation in melancholia for forty years. Any observational data on correlation should rightly be grounds for further research. Furthermore, the demographic increase in depression and dementia does closely correlate to the increase in sugar and the pro-inflammatory diet promoted since the eighties and other inflammatory diseases. Your rheum comparison fails because there are seronegative rheum diseases and antibody markers in rheum diseases are not as cut and dry as you have indicated.
I would think that critical psychiatry should embrace research into this area. Unlike SSRIs, chronic inflammatory control would have no side effects and many possible collateral positive effects, such as improved cardiovascular or orthopedic status as well as mitigation of dementia. I'm not a fan of SSRIs and agree with many of your takes, but I think you're swatting at straw men here.
PS, when I talk about chronic inflammatory control in this context I'm not referring to steroids, but control of inflammation through the gut biome and diet.
And what is the significance of a depression with higher inflammatory markers, James?
I already answered that question.
Your position here seems to be nihilism and throw in the towel on all research because there is no obvious independent variable. You and I agree on the reason for this. It's basically because MDD isn't really a disease. DSM ruins everything it touches. But depression is still a symptom and a problem. DSM idiocy and lack of an obvious independent variable that doesn't mean that research into potential causes of some forms of depression should come to a halt. Furthermore, in someone with depression and inflammatory markers (many of these are subtypes with somatic features( there is no downside and potentially a lot of upside to reducing inflammation through diet. They make feel mentally better because they feel physically better but that's a win.
This is something critical psychiatry should embrace because it doesn't involve pharma money and the downsides of medication.
BTW reflexive dismissal of any correlations study is not criticism, it's gainsaying, to paraphrase a famous Monty Python sketch (RIP Terry Jones). Correlation is not causation, but it's not necessarily nothing either.
Yes, but the correlation is likely to be non-specific to depression (rather stress, or similar). Not sure if you really answered my question. Why should some depressed people have raised inflammatory markers and some don't?
Just curious, is there ANY field of psychological or psychiatric research that you consider worthwhile?
Why should some people with rheum disease have greatly elevated markers and some be seronegative?
Why should some nonsmokers get lung cancer?
Why do some people with ApoE4,4 not get dementia?
Markers and independent variables are seldom absolute or perfect. That's pretty basic science.
Fair enough, but as you know, depression is a functional illness
I think you're right that more money will be put into research of this sort, but the point of the blog was to encourage more thought about why and ideally restrict this to the highest quality such research, so that there isn't too much money wasted on a pointless project as envisaged (although possibly something useful might be found out along the way).
Fair enough. But look at the other possible benefits. Cardiovascular is obvious. The other psychiatric would be related to dementia which is related to inflammation. Gut biome is a promising area anyway since it is the source of inflammation and so little is known about it. Diet is an obvious target for depression research, since intuitively the standard American diet is horrible and depression as a symptom is worsening with increased sugar consumption.
Depression is a functional illness (did you mean symptom? It's too nebulous in my mind to be just one illness), but we've known since Kandel that functional changes lead to structural changes at some level.
I'm certainly not a fan of using COX-2 inhibitors in depressed people, or God forbid, Prednisone.
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