Journal of IiME Volume 6 Issue 1 (June 2012) Maria A Vera (University of Miami), together with Professors Mary Ann Fletcher and Nancy Klimas, noted that Metabolic Syndrome (MetSd) is a known risk factor for cardiovascular and cerebrovascular disease, and that previous studies have shown that patients with (ME)CFS were twice as likely to have metabolic syndrome as controls. They set out to compare cytokine levels in patients with (ME)CFS with and without metabolic syndrome. They concluded that the prevalence of metabolic syndrome in an (ME)CFS population was 26%, and that similarly to their previously reported findings in (ME)CFS, patients with both (ME)CFS and metabolic syndrome had abnormalities in pro-inflammatory, Th2, Th1 and IL-8 compared with healthy controls and were biased towards a Th2 cytokine pattern, accompanied by autoantibody production. The investigators recommend that large longitudinal studies should be performed to determine the contributing factors to this increased risk. Professors Mary Ann Fletcher and Nancy Klimas (Miami) looked for biomarkers in (ME)CFS. Prospective biomarkers included NK cell cytotoxicity (NKCC), T lymphocyte proliferation in vitro in response to mitogen (LPA), lymphocyte activation markers (CD26, CD38), 16 plasma cytokines and neuropeptide Y. The results provided credible biomarker status for NKCC, LPA, and markers of lymphocyte activation in (ME)CFS. A significant elevation in the relative amounts of four of five pro-inflammatory cytokines in peripheral blood plasma of patients with (ME)CFS was found when compared with the controls. Both IL-4 and IL-5 were elevated in (ME)CFS. The anti-inflammatory cytokine IL-3 was significantly lower (15% lower) in (ME)CFS patients. IL-12 was significantly elevated (120% higher) and IL-15 decreased 15% in cases compared with controls. IL-8 was 42% lower in the (ME)CFS patients. The stress hormone NPY was elevated in plasma of (ME)CFS patients and positively correlated with perceived stress. The authors concluded that fifteen useful biomarkers were identified in their studies, and that the differences in these markers compared with controls give important information regarding the pathophysiology of (ME)CFS. The association of low LPA response, elevated proportion of activated CD4 and CD8 T cells, defective NKCC, elevated Th2 cytokines in (ME)CFS cases suggests Invest in ME (Charity Nr. 1114035) that T cells are metabolically limited in performing their helper function. All but one of the inflammatory cytokines were elevated, as was the stress hormone NPY, supporting the hypotheses that inflammation and abnormal stress responses are important components in the pathophysiology of (ME)CFS. Ekua Brenu et al (Bond University, Queensland) studied the effects of vaccination on immune function in (ME)CFS. Noting patients’ inability to tolerate certain toxins and their hypersensitivity, they set out to examine the effects of routine vaccination on immune function in patients with (ME)CFS. They concluded that their findings suggest a potential role of vaccines in the pathophysiology of (ME)CFS. It is notable that Dr Daniel Peterson is on record in relation to the above study at Bond University saying on 14th October 2011 that the investigators assessed immune functioning before and after people with (ME)CFS were vaccinated and they found evidence that vaccinations may be significantly affecting immune functioning (http://forums.phoenixrising.me/content.php?490 -Dr-Peterson-Talks-On-Diagnosing-Treatin-XMRVCFS-MECFS-chronic-fatigue-syndrome ). This may tie in with the AISA syndrome (autoimmune/inflammatory syndrome induced by adjuvants in vaccines) noted by Rosenblum et al in Infectious Diseases of North America mentioned above. It is further notable that on 23rd March 2012 neurosurgeon Dr Russell Blaylock was reported as saying in an interview that vaccines switch the immune system to Th2 and that they suppress immunity rather than boosting it by confusing the immune system and altering the way it responds to viruses and bacteria: “We found that, in fact, (vaccination) causes the immune system to switch to what we call Th2-type cytokine production which inhibits immunity. And your major protection against viruses…is your cellular immunity. Well, vaccines don’t stimulate cellular immunity at all, in fact they suppress it” (http://tv.naturalnews.com/v.asp?v=DFBE7C32CB DBF43B7342333B7D827EB0). 2011 “There is evidence that inflammatory pathways and cell-mediated immunity (CMI) play an www.investinme.org Page 93 of 108
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