Discussion in 'Latest ME/CFS Research' started by Firestormm, Feb 26, 2014.
Full paper: http://www.dovepress.com/getfile.php?fileID=19143
This study is an anology of which came first, the chicken or the egg.*There is no predictive value since it's retrspective as well as no control group!
This is basic study design that most here already know.
I call foul!
*It's the egg.
In other words, two of the most common symptoms in ME/CFS (fatigue and cognitive impairment) are directly related, in terms of severity of symptoms.
In other words, as patients become more ill, various symptoms increase in severity, and vice versa.
Self-efficacy is also adversely affected as symptoms increase in severity. No surprise there.
As for depression, we know that most depression measures are inappropriate for ME/CFS patients.
In this study they used the CES-D Scale.
Questions on this scale include:
I did not feel like eating; my appetite was poor.
I felt that everything I did was an effort.
My sleep was restless.
I felt lonely.
I could not get "going".
What a waste of time.
I have to say, that - and admittedly I have not yet read the full paper - I was disappointed.
Bansal is involved with IiME and the Rituximab 'Trial' (either the pre-trial study or the trial itself - I forget which), and helped with selection I think for their Microbiome project (the details of which are still hard to come by e.g. number of patients and controls and what exactly they will be doing).
But Bansal is also involved in a study for the ME Association*, and is scientific advisor to this research charity: http://www.mesolutions.org.uk/who-we-are/
I must say that I had hoped for more and was a bit shocked when I saw his name attached to this paper, but like I said, I am being pre-judgmental perhaps and not in full possession of the details.
Perhaps someone more able than me (@Simon ?) can, like, Bob have a read through the paper at the top of this thread (http://www.dovepress.com/articles.php?article_id=15953) and provide some more objective opinion. Many thanks.
I don't know much about Bansal, but his name is the last name on the list of authors. This often means that the person has simply been consulted about a specific issue in relation to the study, or has contributed to a specific area of the study, such as recruitment. (However, I believe that anyone who puts their name to a study has to accept ownership of it.)
The positive thing about the study is that they suggest that depression is caused by the "neurobiological effects of ME/CFS", rather than depression being the cause of symptoms.
I don't find the conclusions offensive, but the study seems weak, and a waste of time.
Agree completely. I am not sure what to expect from future work. Are we now heading for some amalgamation of ME/Depression etc. as all being caused by similar 'neurobiological' effects? And what the heck are 'neurobiological'? Is that a more acceptable term now, like 'biomedical'?
It suggests a definite physiological or anatomical cause of neurological symptoms. This terminology is probably being used to clearly separate it from the "neuropsychological" nonsense which seems to be something of a fad among certain researchers who are fond of twisting meanings in the name of opposing dualism while engaging in actual dualism.
Once upon a time, simply saying "neurological" would have been sufficient to indicate a biological etiology, but the warping of the definitions of plain terminology has made that impractical.
Yeah but it's all bollocks isn't it Val?
I mean. Everything is a biological process of some description when you get down to it. It is the notion that we are to blame that is really behind people's animosity - that our 'behaviour' is responsible for our disability.
As patients we want to have it proved that we aren't the cause of this situation, we want a test to say 'You are not to blame. It is not something you have invented. Or a figment of your imagination. Or something you could have simply put right if you thought in a different way or pushed on through with a bit of exercise.'
But all these terms really make be laugh - and it's all down to the names of the disciplines who are involved and how they categorise them. Doesn't matter if depression has a biological cause - which it does - you will still be seen by a therapist who will try to get you to better manage the condition by adapting your behaviour to it - along with some drugs probably... is it any different really for someone with epilepsy? I don't think so.
Megan Arroll is the psychologist with an interest in the cognitive side of CFS/ME. But I agree here as well, Bansal has his name on it, and it remains bothersome to me.
I'd disagree - the cause should be hugely important in deciding the treatment. If I'm depressed due to psychosocial factors, then it makes the most sense to remedy those factors. If I'm depressed due to neurotransmitter imbalance, then taking a drug to address that imbalance is likely to be more effective than talking about my feelings. If I'm depressed because my psychologist is an asshole, then the best solution is probably to avoid that psychologist. If I'm depressed because life is hard and I don't know how to cope with it, then it makes sense to get a therapy involving practical advice.
I'm not going to take a pill because my psychologist is an asshole, or because some doctors treat me like crap. All the advice in the world won't solve a severe neurotransmitter problem or brain damage. Hence the cause of the depression is of great importance, in my opinion. Unfortunately there often isn't a perfect pill or psychological treatment or piece of advice to solve a case of depression, but at least it gives guidance on where to start and what sort of improvements to expect.
I do like the cut of your jib, Val
However.... we are all human. We go to the doctor and sit in front of him, and he (or we) try and determine from our expressed symptoms (or visible symptoms and - let's face it - behaviours), what might be the problem. This involves much interpretation on the part of patient and doctor, and on anyone else's specialty part if we are referred.
So. How to determine if someone who is - for arguments sake - presenting with symptoms of depression, has a 'psychosocial' cause or a biological one? Indeed, I would argue that even a psychosocial 'cause' involves a stressor that antagonises a biological response by way of a defense mechanism perhaps.
For some (many?) antidepressants can help relieve some of the symptoms - but unless the cause is identified and treated successfully the problem will remain - as will any susceptibility. Antidepressants (stupid name) are also prescribed to relieve similar symptoms for conditions or symptoms unrelated to depression - biological causes as well as - if you chose to delineate - psychosocial ones.
Who is to say if there is not something 'deeper' behind any presenting symptoms? Only by a 'suck it and see' approach can even modern medicine hope to get to the root cause. Of course for many patients this isn't enough. They would rather face a battery of tests, and even if those tests are interpreted as meaning very little, they will seek even more. Sometimes - hopefully - a test or several will determine a cause. And that cause can be treated. And the symptoms will resolve.
But for many people with e.g. depression, there does seem to be this susceptibility. Does that come from a genetic component, an inability to cope as well as others, or something else? Is it 'really depression'? Or is depression really something else?
Replace depression with any condition you choose, including ME. It is I think the interpretation that causes the problems and seeing many doctors or specialists doesn't always lead to a determining cause or successful treatment and a resolution of the symptoms, disability and return to full function.
You know, I watched Lipkin's Oxford presentation recently, and he was talking about something I have mentioned in jest with Bob before now. This Star Trek gadget that they use on the show to scan and diagnose a patient. Lipkin was saying how something similar will likely be seen in hospitals enabling quicker diagnosis from the bedside. But the gadget still requires programming by humans and using human knowledge and... interpretation.
A little known fact (at least among the general population) is that antidepressants act on the immune system. As far as I'm aware, they all have this in common.
What are the psychosocial factors involved in the development of a psychiatrist's career that makes them deny the reality of proper science in favour of psychobabble?
My currently-being-treated with Citalopram depression is caused by having ME, the life I have lost because of it, being housebound and grubby, unable to do all the things I want to do and being treated with nothing but contempt and antidepressants by the medical profession.
Fix those "biopsychosocial" factors, and I won't be depressed any more!
For depression or pretty much anything else with an unclear cause, investigation of the cause would be the most obvious answer. If there's not a very obvious psychosocial trigger, or if there are additional neurological symptoms, etc, then it would make sense to assess neurotransmitter function, or check for brain damage (presumably this would have already been done after head trauma), etc.
Instead, the trend is to assume any neurological symptoms are psychological, and throw some antidepressants at it, with or without symptoms of a mood disorder. If that doesn't work, the next step is to try a different antidepressant, and another, and another. It's not even a matter of some doctors not looking for the supposedly rare "zebras" ... they're assuming that almost every problem is a very specific breed of horse that they happen to fancy, and missing out on obvious and common alternative diagnoses.
On a slightly more serious note, one bout of depression I had was caused by being bullied by my line-manager at work. He had sacked me (wrongly) for my alcohol problems, just as I went into rehab.
When I was completely sober and well again, I was immediately reinstated on appeal. He didn't like that and so when he got the chance, he doubled my workload and then criticised the quality of my output. He set me up to fail. He would have little meetings with me in his office, but refused to let me have anybody in at the same time, to observe how he treated me.
My union guy told me that there was absolutely nothing in any legislation that said I should expect to be treated with any normal, common or garden humanity in the workplace.
If I couldn't cope with the work politics, that was my failing.
I eventually get depression when I am being bullied by somebody who has power over me. It has always been an external "social" source over which I have no control, which has precipitated it.
Before depression sets in, I go manic trying to get things right, it becomes obsessive, I talk to myself, my anxiety increases and increases, before the final wallop of full anhedonia hits.
Sometimes, there is absolutely nothing that can be done about the source of the depression.
I've just read the full paper.
I would have found this paper much more interesting if they had measured actual cognitive functioning. What they actually measured was self-reported impairments, which may not be the same thing:
It doesn't seem that surprising that one might find relationships with self-efficacy, for example. If you're not confident in your ability to do things (low self-efficacy) one may report more cognitive failures. Similarly if one reports more cognitive failures, one might report less confidence in one's ability to do things. Basically, there seems to be a big risk that one isn't really measuring completely separate things: a lot of what one is measuring depends on what people tell you.
I'm does sceptical of claims like:
What one might say with more confidence is that such programs might lead to patients reporting better cognitive functioning, which isn't necessarily the same thing.
I found the paper reasonably sympathetic: it tended to tie in the sort of problems seen in ME/CFS with other "physical" conditions e.g. multiple sclerosis.
However, the last paragraph is sort of odd. Usually the last paragraph is a summary of what was said before but these points weren't really raised (that I recall).
It has the feel of something stuck in later. One reason this happens is a point raised by a reviewer. Anyway, I think it's good that it's in it.
I don't know why they didn't do it in this case. Seemed odd. But they did get a good response rate at 63%:
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