Is Cognitive Change Necessary to Alleviate Symptoms in Patients With Functional Somatic Syndrome?, 2021, Maroti and Johansson

Andy

Retired committee member
Introduction

What has been included under the umbrella term “Functional somatic syndromes” (FSS) has varied over the years. Diagnoses such as “somatoform” and “somatic symptom disorders,” as well as “medically unexplained symptoms,” have been included in FSS (1). Although there is no complete consensus, FSS usually comprise of conditions such as fibromyalgia, irritable bowel syndrome (IBS), and chronic fatigue syndrome (CFS) (2). A characteristic of FSS is persistent physical symptoms that lead to impairment or disability and that disrupt the capacity to take part in daily life. Although FSS are believed to be caused by a complex interaction of biological and psychosocial factors (3), the conditions are not medically explained in terms of well-Understood or established pathophysiological mechanisms.

Cognitive behavioral therapy (CBT) has become the gold standard psychological treatment for FSS. Several meta-analyses have shown a small to moderate effect in patients with FSS (47). Even though the small to moderate effect is robust, in the sense that results have been replicated both within and across conditions, there is limited research on treatment mechanisms (8). That is, CBT has an effect, but why the effect takes place is not firmly established.

Traditional CBT rests on the idea that changing cognitions and behaviors in FSS will decrease somatic symptoms (9). Specifically, changing so-called dysfunctional illness beliefs “are of paramount importance for treatment (success)” (10). According to a review of Windgassen et al. (11), there is a “clear indication” that “cognitive change is important for reducing symptom severity.”

Put simply, a patient who, for example, believes that “something is wrong with my body” or claims a physical attribution such as “I have a chronic infection, that is why I feel fatigued,” will not easily get well. There are some merits to this position. In a review of CBT for IBS, four out of five studies found cognitions to mediate the effect of treatment on symptom severity (11). In another review of CBT for CFS, three different types of illness perceptions (fatigue as something aversive, activity as potentially dangerous to health, and a symptom preoccupation with fatigue) were found to potentially perpetuate CFS symptoms (12).

Although there is a value in the position that changing cognition is of “paramount importance” to reduce symptoms in FSS, we argue that this idea is a simplification and leaves several questions unanswered. In the following, we provide two major arguments against this position.

Open access, https://www.frontiersin.org/articles/10.3389/fpsyt.2021.781083/full
 
Put simply, a patient who, for example, believes that “something is wrong with my body” or claims a physical attribution such as “I have a chronic infection, that is why I feel fatigued,” will not easily get well. There are some merits to this position. In a review of CBT for IBS, four out of five studies found cognitions to mediate the effect of treatment on symptom severity (11). In another review of CBT for CFS, three different types of illness perceptions (fatigue as something aversive, activity as potentially dangerous to health, and a symptom preoccupation with fatigue) were found to potentially perpetuate CFS symptoms (12).
So much arbitrary causal attribution to unpack. Still can't tell their correlates from their causes.
 
From the discussion section:

In this article, we have argued that while CBT produces a robust small to moderate effect in FSS, it is less clear if altered dysfunctional illness beliefs form the most important vehicle of change in all patients with FSS or to all improvements in symptoms in patients with FSS. We have provided two major arguments for why altered dysfunctional illness beliefs might not be of “paramount importance” for treatment success. They could be summarized as (1) patients with FSS hold complex illness beliefs or attributions and not simply dysfunctional illness beliefs, (2) patients can get better even if there is no change in illness attributions. These two arguments highlight difficulties with the idea that changing dysfunctional illness beliefs is necessary for patients with FSS to reduce somatic symptoms. Arguments such as these have previously been raised by other authors (20).

To be fair, some of the CBT models of, for example, CFS do not explicitly state that cognitions are the causative agent of fatigue. Instead, cognitions are believed to be related to behavior, which in turn influences somatic symptoms (21). Nevertheless, some proponents of CBT still stress that cognitions should be the target of change in treatment (22).

Most researchers would argue that various mechanisms, and not just cognitions, are important in the treatment of FSS. One is, as previously discussed, behavioral avoidance (19). Another potential mechanism is that of emotional processing. In a study of Emotional Awareness and Expression Therapy for FSS patients, a mediation analysis distinguished two emotional processes that were associated with reductions of somatic symptoms (23). One was “impoverished emotional experience,” which is similar to the concept of alexithymia. The other process was “signs of unprocessed emotions,” where memories and emotions feel fragmented and intrusive. The mediation analysis showed an association between the ability to identify and make better sense of emotions without finding them intrusive and a reduction in somatic symptoms. This research suggests that there are other possible mechanisms of change in the treatment of FSS besides cognitions.

This attempt at objective analysis is bizarre given the authors remain oblivious to the design flaws in the research evidence they rely on (ie the use of subjective outcomes in unblinded trials), to the fact that they have no real evidence that what they regard as ‘dysfunctional illness beliefs’ are either dysfunctional or irrational/inaccurate and they display, as @Sean points out, a confusion between association and causality.

If you are building on sand, making your constructions ever more elaborate does not compensate for the lack of any solid foundation.
 
"...fatigue as something aversive"

1) why is this a problematic belief?

2) in my pre-ME life I was very busy, and experienced fatigue; it was no big deal, except when I became hypothyroid, when even walking felt like moving through molasses

3) for me there is a big difference between fatigue from Cross country skiing for hours (pre-ME), and the fatigue with ME

4) and, to correct these researchers, it's not just fatigue!

In my case, as I don't wish to speak for others, it's universal muscle pain, weakness, feeling lightheaded and brain fogged, especially with upright positions, etc., and yes fatigue. A paralyzing kind of fatigue. The kind that takes an act of will to move one's body.

When will this be understood?!
 
Although these authors do not seem to be up to speed on evidence they do seem to have the right idea in some ways.

They are questioning the validity of the false belief paradigm and the idea that treatment has to address beliefs.

Their final conclusion is pretty sensible:
To establish which mediating variables are of importance, two different treatment protocols with their own distinctive mechanism would ideally be compared.

This is what PACE should have done - compare to different protocols both of which would count as 'active test' treatments but with different putative modes of action. If one worked better than the other then that would hint at mechanism. The problem with PACE was that the two 'active test' treatments were really the same thing under different names, with the same theory behind them. So unsurpisingly there was no difference. And since the other comparison groups were not 'active' controls we don't know if there was any effect at all.

They actually quote some quite useful evidence against the beliefs theories.
Just a pity they had not noticed that CBT doesn't work anyway.
 
“That is, CBT has an effect, but why the effect takes place is not firmly established”

They just don’t want to admit that their model doesn’t work, it is frequently discussed in psych literature that just the act of sitting down in a room for an hour, therapist qualities and rapport with client (and not doing CBT) with a patient has a treatment effect.
 
About Maroti et al's alexithymia study:

https://www.s4me.info/threads/patients-with-chronic-fatigue-syndrome-do-not-score-higher-on-the-autism‐spectrum-quotient-than-healthy-controls-2018-bileviciute‐ljungar-et-al.4090/#post-71683
Alexithymia study said:

Clinical implications
Alexithymia has been associated with poor outcomes in psychodynamic therapy and supportive therapy [...] Moreover, difficulties in emotional awareness capacity have been shown to be a strong moderator of treatment effectiveness in both CBT and psychodynamic psychotherapy (Beutel, Scheurich, Knebel et al., 2013).

Given that existing CBT treatments for CFS have a moderate effect (White, Goldsmith, Johnson et al., 2011) and that CFS patients both report and have a hampered emotional awareness capacity, an increased focus on emotional awareness could enhance treatment outcome (Chalder & Hill, 2012; Moss- Morris, 2005).

Simply adding two 30-minute psycho-educative sessions of emotional awareness training to standard medical treatment led to a more decreased pain intensity for patients with Irritable Bowel Syndrome
(Edited to add quote.)
 
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That is, CBT has an effect, but why the effect takes place is not firmly established.
Nor that the effect is genuinely beneficial, as opposed to it being merely due to a range of known biases and confounders, which are not only typically inadequately controlled for in these kind of studies, but often actively promoted and arbitrarily re-labelled as genuinely beneficial therapeutic effects.

Hard to take seriously any paper which makes this sort of claim.
 
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I don't remember coming across the statement that people with cfs have 'hampered emotional awareness capacity'. Given that comes from Chalder and Moss-Morris, I guess I shouldn't be surprised. No doubt the source is their dodgy interpretation of some equally dodgy questionnaires.
 
Yes, I worry about anything that mentions alexithymia which is just depression that did not reach a high enough score on the questionnaire!

It is very easy to answer these questionnaires in such a way that they take the physical symptoms of disease as signs of emotional disease. It is difficult to be excited about anything when you are struggling to sit up.
 
It is difficult to be excited about anything when you are struggling to sit up.
Exactly. Its not just ME that needs objective diagnostics, its all of psychiatry as well. At least we have thousands of objective abnormalities in the literature. We just don't understand how it all fits together. Psychiatry has found things in some cases but they still seem to love their questionnaires.
 
Nor that the effect is genuinely beneficial, as opposed to it being merely due to a range of known biases and confounders, which are not only typically inadequately controlled for in these kind of studies, but often actively promoted and arbitrarily re-labelled as genuinely beneficial therapeutic effects.
See also: "lie detectors". They detect something. It's an actual objective measurement. Does it detect lies or honesty? Of course not. An effect is irrelevant, it's easy to have "an effect". "The book moved on its own" is an effect that can be argued to be a ghost. Means nothing at all, people just want to see what they hope to see and it's sad that in medicine no one seems to care where the psychiatry exemption is applied.
 
It would be great if psychiatry had more objective diagnostics. Unfortunately most are imaging and not sensitive enough to see what pathways are being used. I think I saw one person in 20 years of community psych in NZ that I thought alexithymia met the criteria of being a personality trait i.e. marked dysfunction and was a problem with respect to helping them with their depression. I think the BPS crowd have used this term too loosely and there is no strong evidence for this to be used as a goal of treatment.
 
It would be great if psychiatry had more objective diagnostics. Unfortunately most are imaging and not sensitive enough to see
This is the problem. The brain is a black box and we are still making guesses. Advances in medicine occur with advances in technology. I don't think we yet have the technology to get this right.

The lack of diagnostic tests is only part of the problem. There is too much acceptance that psychiatric hypotheses are proven fact. Not all psychiatrists fall into this trap, and its the same for psychologists and the general public, but far too many either do accept it and/or don't acknowledge the issues.

Diabetes and MS advanced with the right technologies. We made rapid advances in Covid vaccine research because of newer technologies. Lack of the right technologies in psychiatry means nearly all of it is tentative, starting with diagnoses. We need to treat most of it as working hypotheses at best. How can we trust even a pharmacological trial in psychiatry when we cannot be sure what the diagnosis should be? This whole thing is difficult, psychiatry is probably the most difficult area in medicine, but that is no excuse for lax standards or for irrational conduct. Pragmatic compromises are what we can do, but we need to acknowledge the vast scale of uncertainty.
 
This whole thing is difficult, psychiatry is probably the most difficult area in medicine, but that is no excuse for lax standards or for irrational conduct.
If anything it should be the contrary. A lack of hard knowledge should demand much higher standards of safety and caution, much larger margins of error.

One thing psychiatry has proven beyond doubt is how unreliable and potentially dangerous subjective judgements are, no matter how carefully considered and well intentioned. Multiply that by being built on several layers of subjective judgement, and it is a very serious risk to patients.
 
@Sean absolutely.

The point I was heading toward is that you can compensate for uncertainty by adopting both honesty and caution. Acknowledge it, do not lie to patients about it (even a benevolent lie though there are cases where that is in the patient's best interest but it seems far too overused), and most importantly do not hide the issues from other psychiatrists. Indeed, the level of uncertainty can be a barometer for the level of awareness and caution necessary.
 
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