A reexamination of the cognitive behavioral model of chronic fatigue syndrome, 2018, Madison Sunnquist, Leonard A Jason

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http://onlinelibrary.wiley.com/doi/10.1002/jclp.22593/full

A reexamination of the cognitive behavioral model of chronic fatigue syndrome


Author Madison Sunnquist, Leonard A Jason


  • First published: 19 February 2018
DOI: 10.1002/jclp.22593

Abstract
Objective
The cognitive behavioral model of chronic fatigue syndrome (CFS) suggests that cognitions and reduced activity level perpetuate the fatigue and impairment that individuals with CFS experience. The two empirical evaluations of this model resulted in conflicting findings. The current study examines the influence of case definition fulfillment on the applicability of this model to CFS.

Method
A moderated mediation analysis was conducted on 990 individuals with CFS to reexamine the behavioral pathway of this model. Case definition fulfillment was entered as a moderator.

Results
Findings were generally inconsistent with the cognitive behavioral model of CFS. Case definition fulfillment significantly moderated the relation between activity level and physical impairment (β = –0.08, p = 0.03); individuals who met more stringent case definitions demonstrated a weaker relation between activity level and impairment.

Conclusions
This model may not accurately represent the experience of individuals with CFS, particularly those who fulfill more stringent case definitions.
 
http://onlinelibrary.wiley.com/doi/10.1002/jclp.22593/full

A reexamination of the cognitive behavioral model of chronic fatigue syndrome

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Conclusions
This model does not accurately represent the experience of individuals with CFS, particularly those who fulfill more stringent case definitions.

Fixed! ;)

How 'tired I feel' does not stop me from wanting to and/or undertake activities. An abnormal
rate of fatigability induced by even the most trivial levels of mental and/or physical activity, to the point that I have no further energy available to do any further activity, until I recover sufficiently well, is what stops me in my tracks. On this latter point, my ability to recover, even from trivial levels of activity, is severely impaired at my worst, and has no relationship to 'false illness beliefs', 'fear of exercise' or deconditioning.

Subjective fatigue questionnaires, in the absence of objective data, e.g. appropriate physical and neurological examinations/investigations noted over different time points in response to mental and physical activity, just doesn't cut it. Far too many patients have been caused serious harm by the 'scandalous' research undertaken by the BPS adherents, and how this so-called research has been used to inform the 'treatment' of PwME the world over, and is now being extended to other illnesses - the risks of serious harm with GET, directive CBT/GAT have been dismissed and ignored by far too many health professionals, and so many others. Far too many opportunities to pick up comorbidities and/or misdiagnoses have been missed, as well as benefits, care support needs, and health insurance claims wrongly denied.

Rant over, and back to the paper in question .. it was not until I read the ICC criteria in 2011, that I was able to develop some understanding of ME, and its relevance to my own health issues, experienced since September 2008. I recognise from my time online in the 'other place' and here, that 'consensus' criteria is not to everyone's liking. That said, I do think that it is a useful document, which can aid diagnosis and inform research practice, particularly in regard to identifying potential sub-groups of PwME.

My thanks to the authors for this paper.

Wishing everyone improved health and every happiness. John :)
 
Far too many patients have been caused serious harm by the 'scandalous' research undertaken by the BPS adherents, and how this so-called research has been used to inform the 'treatment' of PwME the world over, and is now being extended to other illnesses - the risks of serious harm with GET, directive CBT/GAT have been dismissed and ignored by far too many health professionals, and so many others.
My personal feeling is that this has been surreptitiously fostered by one of the most powerful forces there is - the political determination to cut financial costs, no matter what the human costs.
 
In addition, the Vercoulen et al. (1998) study's sample size may have been too small for SEM. Though no firm sample size guidelines exist for SEM, some literature recommends an absolute minimum of 100 cases (Kline, 2011), and evidence from simulated data indicates that a higher sample size to parameter ratio is associated with more accurate fit statistics (Jackson, 2003). The Vercoulen et al. (1998) study applied SEM to a sample of 51 individuals. Although the article did not explicitly state whether error covariances were estimated, the final model consisted of at least six parameters, or approximately 8.5 cases per parameter. This ratio is lower than ideal (Kline, 2011); thus, the model may lack robustness.

Finally, the Vercoulen et al. (1998) study stated that utilizing SEM allowed the relationships in the final model to be interpreted as causal. In describing the final model, the articles states, “Attributing complaints to a somatic cause produced low levels of physical activity, which in turn had a causal effect on fatigue severity.” Though SEM could be used as a tool to demonstrate causality in a highly controlled, prospective, longitudinal experimental design, the Vercoulen et al. (1998) study does not demonstrate three requisite tenets of causality: temporal precedence of cause from effect, covariance of cause and effect variables, and rejection of all plausible alternative causes for the effect (Shadish, Cook, & Campbell, 2002).
 
As the two extant data-driven studies of the cognitive behavioral model of CFS reported discrepant results, the current study seeks to reexamine the Vercoulen et al. (1998) model using a sample of 990 individuals with CFS and determine whether case definition fulfillment influences results. This study will specifically investigate the model's “behavioral pathway”: causal attribution's relation to activity level and activity level's relation to fatigue and impairment (see Figure 1). This pathway is used as justification for the prescription of graded exercise therapy (GET) to individuals with CFS (Bavinton, Darbishire,&White, 2004).
 
3.2 Moderated mediation analysis

As hypothesized, causal attribution did not significantly predict activity level ( = 1.48, t[2, 987] = 1.75, p = 0.08); thus, activity level did not mediate the relation between causal attribution and impairment. Contrary to the study's hypothesis, causal attribution predicted impairment ( = 5.22, t[5, 984] = 5.22, p < 0.001), such that individuals who reported a physical illness etiology were more physically impaired than those who reported some psychological etiology. As hypothesized, activity level was significantly related to impairment ( = 0.64, t[5, 984] = 8.61, p < 0.001), and case definition fulfillment moderated the relation between activity level and impairment ( =−0.08, t[5, 984]=−2.15, p = 0.03), such that individuals who met more stringent case definitions evidenced a weaker (though still significant) relation between activity level and impairment. Coefficients and significant levels for the full model are displayed in Figure 2. Figure 3 displays a graphical representation of the moderating influence of case definition fulfillment on the relation between activity level and impairment. Table 4 displays the means and standard deviations of activity level and impairment by case definition group.
Results weren't as clear-cut as I would have liked. A result with p=0.08 is borderline in my view.
 
The significant moderation effect of case definition fulfillment suggests that the most impaired individuals are overexerting themselves compared to what would be predicted by the deconditioning hypothesis. Among severely impaired individuals, this overexertion may result from the need to complete basic activities of daily living (e.g., personal hygiene tasks, preparing meals, etc.) or respond to illness demands (e.g., attending medical appointments).
This is an interesting interpretation. Though I am not sure it is the only one possible.

Sunnquist 2018 figure 3.png

To evaluate activity level, participants reported the average number of hours per week they spent on household, social, family, and work related activities over the past month.
 
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Though activity level and impairment were significantly correlated, this result may simply demonstrate that these represent indicators of illness severity, as opposed to implying that activity reductions cause individuals’ impairment. In order to establish causality, researchers would need to demonstrate covariance between cause (i.e., activity level) and effect variables (i.e., impairment and fatigue). Proving covariance (i.e., changes in activity level lead to changes in impairment and fatigue), requires an experimental design. Neither the Vercoulen et al. (1998) nor the current study utilized an experimental design; thus, conceptualizing these variables as indicators of a latent construct may be more methodologically appropriate, as individuals with greater illness severity likely have lower activity level, greater impairment, and more severe fatigue. Individuals who grapplewith debilitating illnesses are less able to engage in activity and experience more severe symptomatology. Cross-sectional studies of individuals who have had ME and CFS for many years cannot statistically or methodologically justify claims that reduced activity levels cause greater impairment and symptom severity.
Regarding the bolded bit, I would expect that activity level and impairment would correlate. I was surprised when the authors predicted they wouldn't.
 
One of the current study's hypotheses was unsupported. Contrary to prediction, causal attribution was associated with impairment; individuals who attributed their illness to physical causes reported greater impairment than those who attributed their illness to both physical and psychological factors. Though not originally hypothesized, this finding suggests that individuals hold valid perceptions related to factors that contribute to their symptoms.
The last sentence seems sympathetic though I'm not sure it is the only possibility.

The measure of impairment utilized in this study assessed only physical impairment. Individuals who attributed some of their illness to psychological causes may have evidenced greater mental health or emotional impairment.
An interesting suggestion. But it is only (fairly wild?) speculation at this stage.
 
Despite the large, heterogeneous sample, too few participants reported that their illness derived from “definitely psychological” or “mainly psychological” causes to allow for analysis of these categories.
 
A prospective, experimental study that collects pre-illness data and systematically requests post-illness activity alterations would allow for a more robust examination of the cognitive behavioral model of CFS; however, if cost or time constraints preclude this type of experimental design in future research, the results of the current study suggest that investigators should document and utilize the most updated, stringent case definitions.
 
Concluding paragraph, but as I said I don't find the results that clear-cut.
Despite the current study's limitations, its results have implications for the treatment and management ofME and CFS. This study, along with the Song and Jason (2005) study, was another attempt to replicate the Vercoulen et al. (1998) model, and both replication attempts were inconsistent with the original model. Findings suggest that individuals’ activity level is unrelated to perceptions about illness etiology. These results are inconsistent with cognitive behavioral theories of CFS that presume that individuals’ symptoms stem from deconditioning and maladaptive illness beliefs. The current study indicates that caution should be exercised when prescribing treatments, such as CBT or GET, that presume a relation among illness beliefs, activity, and impairment, particularly when working with individuals who fulfill more stringent case definitions forME and CFS. A recent meta-analysis of CBT treatments found a null effect (Smith et al., 2015), and investigators are now contesting the results of the largest GET intervention study to date (Marks, 2017), with some suggesting that GET interventions may be harmful to individuals with ME and CFS (e.g., Kindlon, 2017). In contrast to GET strategies, energy envelope and pacing interventions encourage individuals with ME and CFS to monitor their level of available energy to avoid over- and under-exertion (Jason et al., 2013). A review of energy envelope studies suggested that these interventions have resulted in modest gains in physical functioning (Jason et al., 2013); however, these treatments are not curative, and future research should continue to search for effective treatments for ME and CFS.
 
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