ANOTHER PERSPECTIVE: IS THERE REALLY MORE PSYCH COMORBIDITY IN THE CANADIAN AND INTERNATIONAL CRITERIA FOR M.E.?
Posted in response to
http://www.cortjohnson.org/blog/201...elect-for-more-psychiatric-patients/#comments
ARE WE ASKING THE RIGHT QUESTIONS?
Cort, you’ve written a very thought-provoking piece. But I can’t help thinking we need to flesh this topic out, and also ask some tougher questions. I’m having a rare “OK” day, so will make hay while the sun shines and perhaps contribute a related perspective.
1) ISSUE #1: IF WE TREAT THE OSTENSIBLE PSYCH COMORBIDITY, WILL IT RETURN US TO FUNCTION?
For me as a patient, all I ultimately care about is: “What do we have to treat, to restore patients to a modicum of functionality?” And the answer to this question has EVERYTHING to do with whether psychiatric comorbidity (if present) is primary, i.e. integral to M.E. as a disease; or secondary, i.e. a natural sequela to profound disability.
Why is this important? Because if we perseverate on the possibility of profoundly ill patients being depressed, for example, and if we’re sloppy in our assumptions, we can put ourselves in exactly the position that the UK is, where CBT and GET are positioned (despite a lot of arm-waving by the psychs) as the be-all and end-all for ME and CFS patients. I.E. The Psych perspective is being positioned as a fix-all for ME and CFS. To whit, the endemic refusal of biomedical testing, to better understand the biomedical underpinnings of ME and CFS – much less biomed treatment.
I submit that any time psych comorbidity is raised, we have to be meticulous about identifying whether, if we treat that psych comorbidity, that will address the core pathology of ME or CFS, and return the ME or CFS patient a significant measure of functionality. Or whether said psych treatment will just help patients cope better. (And I don’t for a moment believe that treating “false illness beliefs” or graded exercise are safe, much less helpful in ME, even for coping). Consider the number of Rituxan or Ampligen patients who have been able to return to work after treatment – versus those in the PACE trial, which has been consistent in its INABILITY to return patients to work. And this is a big deal, considering – as Dr Unger stated last week about the patients her multi-site research, “What was consistent, was that 75 percent were not working.”
How many of us, for example, have been prescribed antidepressants, only to find them less than useless in affecting our level of disability, much less our abilty to do self-care, or return to work?
And how many of us have been lucky enough to get some biomedical treatment which returned us, dramatically, to a measure of our former lives? I’ve had a small number of blessed but TOTAL remissions on IVIg – unfortunately formulations that are no longer available to me. But I’ve experienced it – from a few days to a week after treatment, spontaneously waking up refreshed in the morning, BOUNCING out of bed, clear of mind, with to-do lists bubbling up with joy; being able to go for walks with the family; able to make meals; tolerating standing up; being cognitively clear enough to dream up all kinds of fun things to do. And being “myself” again, for as long as 3 months after these treatments. With no PEM nor angina. It was like the movie “Awakenings”. Pure joy. Did this affect my mental state? Darn right it did. I felt like myself again.
ISSUE #2: WE NEED TO DIG DEEPER TO UNDERSTAND “HOW” THEY ARE DEFINING PSYCHIATRIC COMORBIDITY
I would also argue that any time someone says that psych issues are comorbid, we need to go to their assumptions – i.e. the tools they are using – to see if those are in fact appropriate to our disease or spectrum of diseases. Specifically, we need to know if these tools can differentiate between a depressed patient, and someone who is naturally responding as a result of profound disability.
If you take a peek at Valentijn’s posts at this link:
http://forums.phoenixrising.me/inde...n-questionnaires-in-me-cfs.21578/#post-329074 , he provides examples of common depression inventories such as the Multidimensional Fatigue Inventory, the SF36, and the Zung Depression Scale, where a so-called diagnosis of depression could in fact be merely an assertion of significant biomedical disability.
For example, how many ME patients would respond affirmatively to the following – not because they’re depressed, but because they have lost a massive chunk of their quality of life, and have had to contract their life to prevent relapses? Here are just a few of the questions that would peg ME patients as “depressed”:
- “I have a lot of plans”
- “I still enjoy the things I used to do”;
- “I expect my health to get worse”
How many of us expect our health to get worse – not because we’re pessimists, but because we are realistically extrapolating from our past health trajectory, and factoring our slim hopes for imminent treatment? Given how widely used depression inventories are, that have lousy specificity and sensitivity, we must be vigilant about such assumptions about “psychiatric comorbidity”, when applied to a serious multisystem and chronic illness such as ME.
3) MULTISYSTEM SIGNS AND SYMPTOMS CONFLATED WITH SOMATIZATION PAR EXCELLENCE?
Next, while many psych instruments make the assumption that more physical symptoms = somatization (and indeed this skewed assumption is becoming entrenched in psych practice – witness the bastardization of the DSM), anyone with a complex multisystem disease knows differently. But as we saw this year, simply having multiple symptoms, and being concerned about them, will increasingly be taken by the DSM folks as signs of somatization. It’s all in the definition, even if it isn’t supported by science.
Bottom line, I would offer that we need to dig deeper, whenever we see people conflating ME with psychiatric comorbidity, with the ultimate questions always foremost in our minds: “Just how do they arrive at this conclusion of psych comorbidity?”, and “If we treat the so-called psych comorbidity, will this restore the patient to function?”. Proof of principle, in reverse.
4) WHICH ASPECTS OF DEPRESSION – IF PRESENT – ARE FEATURED?
Another consideration is that we need to tease out specifically which aspects of depression – if that is the issue – are coming up as positive in an ME or CFS population. I found it fascinating that at last week’s FDA meeting, Dr Unger made a point of saying that it’s NOT the Role Emotional or mental health that are coming up in her multi-site study of “ME/CFS” patients. Now, even Dr Unger is saying that not all instruments have been validated in CFS, and even she is breaking some paradigms, by saying that Mental Health and Role Emotional are PRESERVED in CFS. Very, very interesting stuff. As she said (from the preliminary transcript on PR):
“In the SF36 … you can see that the bars are all very low except for two of them. And … those two relatively high scores are on … mental health and (role) emotional indicating those areas of function are preserved in CFS and that again is pretty consistent across all of the clinics.” (WOW, just wow… what a change of tune. I thought it was STUNNING to hear the CDC, of all entities, say this)
And more from Dr Unger: “This is also giving us a hint that measures themselves may be limited in their ability to distinguish robust phenotypes and/or robust subgroups, and that’s why we’re proposing to expand this study to some other measures. And it could very well be that other biologic correlates will be needed in order to better define subgroups. The other study — other factor is that the data from these kinds of studies will allow us to evaluate how well these questionnaires work. For example, the MFI general fatigue scale in this population really from a specialty clinics did — was limited by its already reaching the maximum in 40 percent of the patients.”
5) A CARDIAC EXAMPLE – THE WOMEN’S ISCHEMIA SYNDROME EVALUATION (WISE study)
There’s another example of assumptions-gone-wild in the Women’s Ischemia Syndrome Evaluation, a massive NIH initiative looking at women with chest pain, but often clear-as-a-bell coronary arteries. These women nevertheless present with cardiac ischemia; and these women are at TEN TIMES the risk of cardiovascular events (death, myocardial infarction, stroke, etc) from those without chest pain. As it turns out, this population is heavily represented by multiple comorbidities, with chronic pain conditions such as FM, “CFS”, IBS, interstitial cystitis, migraine, and Raynaud’s – exactly the constellation of comorbidities associated with “ME/CFS”. In other words, ME and CFS are likely well represented in this WISE population of women who are dying prematurely from heart disease. And indeed, that’s what the work of Dr Newton and her team at the U of Dundee would suggest (
http://www.meresearch.org.uk/research/studies/2012/endofunction.html ).
This makes one finding from the WISE study stand out: the WISE researchers found that, “Anhedonia Predicts Major Adverse Cardiac Events and Mortality in Patients 1 Year After Acute Coronary Syndrome (ACS)” (
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058237 )
“Depression is a consistent predictor of recurrent events and mortality in ACS patients, but it has 2 core diagnostic criteria with distinct biological correlates—depressed mood and anhedonia… anhedonia and MDE (Major Depressive Episode) were significant predictors of combined Major Adverse Cardiac Events (MACE)/ All Cause Mortality (ACM), BUT DEPRESSED MOOD WAS NOT.”
“… Anhedonia identifies risk for MACE/ACM beyond that of established medical prognostic indicators. Biological correlates of anhedonia may add to the understanding of the link between depression and heart disease.”
IMO, the most pressing “biological correlate” of anhedonia that I can think of in this population, heavily represented by “chronic pain conditions” such as ME and CFS, is Post-Exertional Neuro-Immune Exhaustion – mislabeled as “anhedonia”. In other words, the WISE researchers need to start cross-pollenating with “ME/CFS” research, and start measuring for NK cell dysfunction, RNase-L abnormalities, cytokine profiles, etc.
This is an assumption about depression, among the massive team of WISE researchers that so far has gone unchecked.
6) THE KEY MESSAGE: WE NEED TO CHALLENGE GRATUITIOUS ASSUMPTIONS ABOUT COMORBIDITY
So will there be psych comorbidities in any chronic illness, particularly one with neurocognitive involvement? Absolutely? But let’s be aware that entrenched forces have a tendency to overstate that linkage in ME and CFS.
Specifically, let’s come back to this subgroup of CBT/GET practitioners whose “business is rehabilitation” (Wessely’s comment from this BMJ Group Podcast
http://www.bmj.com/podcast/2010/03/05/chronic-fatigue-syndrome – see 11 minute, 15 seconds for his quote). It needs saying that this is an all-out war for market share and credibility, and for the psychiatric paradigm of “CFS”, this tenuous hold on credibility requires that they keep the largest and most expansive definition of the disease(s). We feed into this grab for market share, if we don’t ask tough enough questions, whenever psych comorbidity is conflated with ME or even CFS. Just how are they arriving at this linkage?
I do find it deeply worrisome that so many people are comfortable making the implied leap that just because there is a hint that significantly disabled patients despair at times, that the treatment must equal psychiatric. It is a massive leap of logic that is not justified by science. True, there are other neurocognitive aspects of this disease that might blur into psych domains. But we need to be precise when discussing this.
All I’m sayin’ is that we need to probe a little deeper, and DEMAND treatment that “fixes” us – not window dressing. And this starts with dissection of the assumptions that drive our historically limited treatment options.
Now to throw a spanner in the works. In my earlier life, I used to research corporate health outcomes, and saw – in insurance payouts – the impact of psychosocial factors on health cost and health outcomes. For example, in workplaces where employees had poor control over how they did their work, and high demands, combined with high effort and low reward (“high stress workplaces”), we saw an increase in colorectal cancer by a factor of 6; back pain by a factor of 3; injuries and infections by a factor of 2-3, and so on. So I DO believe that psychosocial factors can drive and influence health outcomes – I’ve seen it in the corporate health numbers. BUT never in a million years, however, would I support that any disease precipitated, influenced, or exacerbated by psychosocial factors – aka epigenetic changes – have its treatment LIMITED to psych therapy. That’s just silly.
Just think how ludicrous it would be to tell a colorectal cancer patient that they are going to receive ONLY GET and CBT, AND no more biomedical testing nor treatment because psychosocial factors may have precipitated or worsened their disease. But somehow society has allowed this runaway train, especially in the UK, to run amok, and to make this grandiose and unsupported leap of logic, where it pertains to ME and CFS. This, we have to stop. And a first step might be in demanding precision, whenever psych issues are conflated with ME/CFS. “Just how are you defining this?” “What are your underlying assumptions”?
We need to dig deeper.
Parvofighter