Does the PACE trial represent professional misconduct?

#PACEtrial Psychiatry is much worse than #DiederikStapel psychology: Two great articles about the seriously flawed PACE trial

Two great articles about the seriously flawed PACE trial

  Editorial: On PACE by Trevor Butterworth, Mar 21, 2016: "And the thing about patients who either suffer from a rare disease, or a more common and inexplicable one as with ME/CFS, is that they are usually a formidable resource—a network of distributed experts who have sifted and weighed the scientific research with the kind of avidity you would expect, given that their lives depended on it. In pharmacology, rare disease patient groups are highly respected and are seen as partners in research rather than just subjects and consumers of studies."

  MORE @ stats.org

  AND

  PACE: The research that sparked a patient rebellion and challenged medicine by Professor Rebecca Goldin, Mar 21, 2016 :

  "The results from PACE (including these) have been published in prestigious journals and influenced public health recommendations around the world; and yet, unraveling this design and the characterization of the outcomes of the trial has left many people, including me, unsure this study has any scientific merit. How did the study go unchallenged for five years? And how could journalists have recognized the problems before reporting unqualified, but unjustified, good news?"

  MORE @ stats.org

Echocardiography objectifies Central nervous system dysfunction responsible for good and bad days in Myalgic Encephalomyelitis

Original Article, Heart and Vessels, pp 1-7 First online: 15 September 2015:

 
  Variability of postural orthostatic tachycardia in patients with myalgic encephalomyelitis and orthostatic intolerance
  Kunihisa Miwa 
  Author information
  Department of Internal Medicine, Miwa Naika Clinic, 1-4-3 Shintomicho, Toyama, 930-0002, Japan,
  info@miwa-naika.com

  Abstract
  Central nervous system dysfunction with myalgic encephalomyelitis (ME) has been suggested as the main cause of chronic fatigue syndrome. Fluctuation of the symptom severity and hierarchy is a characteristic feature in ME patients.

  The characteristics of the sympathetic activation may differ between the “good days” and “bad days” in them. Twenty-four ME patients with orthostatic intolerance underwent a conventional 10-min active standing test and echocardiography both on a “good day” and a “bad day”, defined according to the severity of their symptoms.

  The mean heart rate at rest was significantly higher on the “bad days” than on the “good days”. During the standing test on a “bad day”, 5 patients (21 %) failed to maintain an upright posture for 10 min, whereas on a “good day” all the 24 patients maintained it. Postural orthostatic tachycardia (POT) (increase in heart rate ≥30 beats/min) or severe POT (heart rate ≥120 beats/min) was observed on the “bad days” in 10 patients (43 %) who did not suffer from the severe tachycardia on the “good days”, suggesting the exaggerated sympathetic nervous activation.

  In contrast, POT did not occur or severe POT was attenuated on the “bad days” in 5 patients (21 %) who developed POT or severe POT on the “good days”, suggesting the impaired sympathetic activation.

  Echocardiography revealed significantly lower mean values of both the left ventricular end-diastolic diameter and stroke volume index on the “bad days” compared with the “good days”.

  In conclusion, in ME patients with orthostatic intolerance, the exaggerated activation of the sympathetic nervous system while standing appears to switch to the impaired sympathetic activation after the system is loaded with the additional accentuated stimuli associated with the preload reduction.

Exercise physiologist Prof Keller: it is intellectually embarrassing to still suggest that ME is a psychological illness

This statement was sent to Patricia Carter by Prof. Betsy Keller:

Response to Lancet Psychiatry article from Prof. Betsy Keller, Ph.D., Ithaca College:

What is at issue with both the primary and secondary analyses of the PACE Trial is

1) The fundamental misrepresentation of ME patients as being individuals defined by the archaic and non-specific Oxford criteria, and

2)The tacit assumption that a statistically significant reduction in “fear avoidance beliefs” tracks with a meaningful decrease in functional impairment, the latter of which was not measured in the Pace trial.

Regarding diagnosis, use of the Oxford criteria for participant selection makes it likely that a portion of the study sample suffered from non-specific fatigue only. Further, participation in the PACE Trial necessitated a moderate to high level of function, without representation from those who are severely ill. While this is not uncommon in most studies, it is a major limitation so that conclusions should be fairly characterized with this fact in mind.

With respect to fear avoidance, I have yet to evaluate an adult-onset ME patient who did not want to recover their pre-illness level of function. Many such patients still persist in overreaching on those ‘good days’ in hopes that they will miraculously not fall prey to a dreaded post-exertion symptom rebound that they have experienced many times before.

In contrast, the pediatric-onset ME patient typically learns early on that activity overreaching exacerbates symptoms, and absent the institutional memory of a prior ‘healthy’ life, they soon become ‘activity avoiders’. However, if you ask, these children will tell you that they also wish to be like other healthy kids. For ME patients, activity overreaching equals symptom exacerbation, including decreased functional capacity. It’s a predictable action and reaction that is borne out by numerous and replicated physiological studies.

Given what we have learned in the past eight years about this illness, it is intellectually embarrassing to suggest that ME is a psychological illness. Likewise, to suggest that some with Me may not benefit from ‘support’ (CBT, support group or other) may rob patients of the opportunity to develop management (not healing) strategies that could be helpful. However, with regard to GET, there are very, very few individuals in the world who truly understand the hairline trigger created by the aerobic metabolism pathology in these patients.

A statement proclaiming the efficacy of GET for those with ME must be founded on actual physiological evidence of positive physiological adaptation and no symptom exacerbation, and should not incude words such as “suggest” or “might” when encouraging therapists to promote more physical activities amongst their ME patients. To state, as the authors have done, that the results of the PACE Trial provide sufficient evidence for therapists to couple CBT with GET is irresponsible and harmful. Notwithstanding the large sample size of the PACE Trial, outcome measures were simply not chosen to allow for such a conclusion regardless of the statistical power.

The Economist (1/17/15), not typically regarded as a foremost scientific or medical journal, reminded us in an article about the PACE analysis that the link between a healthy mind and healthy body has been well established for centuries. So it is not surprising that helping one to understand their symptoms and learn supportive strategies to manage profound exhaustion, post-exertion symptom exacerbation, cognitive impairment, unrefreshing sleep, and often pain and dysregulated autonomic nervous system functions (orthostatic intolerance, POTS, GI symptoms and more), may be beneficial to a ME sufferer. However, as The Economist also pointed out, the healthy mind-body ink is “…by no means the same as saying something is all in the mind.”

Betsy Keller, Ph.D. Ithaca, NY ( Betsy Keller: Professor, Department of Exercise and Sport Sciences)

# Exercise physiologist prof Keller: ME/CFS patients will respond abnormally to 2-day cardiopulmonary exercise

Emergency CBT 4 professor Simon Wessely as the NIH wants to retire the Oxford criteria

Professor, What The Hell Is POTS?