Journal of IiME Volume 6 Issue 1 (June 2012) 2004 A study of immunological aspects of ME/CFS by Wessely School psychiatrist Professor Peter White et al deserves particular attention: this is because he was Chief Principal Investigator (PI) of the PACE Trial and despite his prior knowledge of the immune abnormalities associated with exercise in ME/CFS patients, the PACE Trial did not use that evidence but instead focused on attempting to prove that correction of patients’ “aberrant illness beliefs” and graded exercise could “cure” ME/CFS. “We designed this pilot study to explore whether the illness was associated with alterations in immunological markers following exercise. Immunological abnormalities are commonly observed in CFS…Concentrations of plasma transforming growth factor-beta (TGF-) (antiinflammatory) and tumour necrosis factor-alpha (TNF-) (pro-inflammatory) have both been shown to be raised….Abnormal regulation of cytokines may both reflect and cause altered function across a broad range of cell types…..Altered cytokine levels, whatever their origin, could modify muscle and or neuronal function. “Concentrations of TGF-1 (anti-inflammatory) were significantly elevated in CFS patients at all times before and after exercise testing. “We found that exercise induced a sustained elevation in the concentration of TNF- (proinflammatory) which was still present three days later, and this only occurred in the CFS patients. “TGF- was grossly elevated when compared to controls before exercise (and) showed an increase in response to the exercise entailed in getting to the study centre. “These data replicate three out of four previous studies finding elevated TGF- in subjects with CFS. “The pro-inflammatory cytokine TNF- is known to be a cause of acute sickness behaviour, characterised by reduced activity related to ‘weakness, malaise, listlessness and inability to concentrate’, symptoms also notable in CFS. Invest in ME (Charity Nr. 1114035) “These preliminary data suggest that ‘ordinary’ activity (i.e. that involved in getting up and travelling some distance) may induce antiinflammatory cytokine release (TGF), whereas more intense exercise may induce proinflammatory cytokine release (TNF-) in patients with CFS” (Immunological changes after both exercise and activity in chronic fatigue syndrome: a pilot study. White PD, KE Nye, AJ Pinching et al. JCFS 2004:12 (2):51-66). 2004 “Many patients with (ME)CFS have symptoms that are consistent with an underlying viral or toxic illness. Because increased neutrophil apoptosis occurs in patients with infection, this study examined whether this phenomenon also occurs in patients with (ME)CFS. Patients with (ME)CFS had higher numbers of apoptotic neutrophils, lower numbers of viable neutrophils, and increased expression of the death receptor, tumour necrosis factor receptor-1 on their neutrophils than did healthy controls. These findings provide new evidence that patients with (ME)CFS have an underlying detectable abnormality in their immune cells” (Kennedy G et al. J Clin Pathol 2004:57(8):891-893). Commenting on this paper, Dr Neil Abbot, Director of Operations at ME Research UK, noted: “The new paper by Dr Gwen Kennedy (MERGE Research Fellow) and colleagues reports evidence of increased neutrophil apoptosis (programmed cell death) in ME/CFS patients. Neutrophils represent 50-60% of the total circulating white blood cells and are fundamental to the functioning of an intact immune system. The data presented in this report are consistent with the presence of an underlying, detectable abnormality in immune cell behaviour of many ME/CFS patients, consistent with an activated inflammatory process, or a toxic state” (Co-Cure RES MED 30th July 2004). Also commenting on this paper, Dr Charles Shepherd of the UK ME Association said: “The BMJ doesn’t normally show any interest in research which supports a physical cause for ME/CFS. However, today’s edition does refer to some www.investinme.org Page 67 of 108
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