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Br J Radio, E-Pub Nov 29, 2011, "Regional grey and white matter volumetric changes in myalgic encephalomyelitis (chronic fatigue syndrome): a voxel-based morphometry 3-T MRI study," Puri et al.
These London researchers wanted to prove there was structural brain damage in CFIDS/ME and they did. Their science supported neuroanotomic changes of "reduced grey matter" in the right and left occipital lobes as well as two other areas of the brain. This study also explains why "impaired memory… is common in this illness" as well as visual processing and how it can affect movement.

J Am Soc Hyperten, E-Pub Nov 29, 2011, "Autoantibody activation of beta-adrenergic and muscarinic receptors contribute to an 'autoimmune' orthostatic hypotension," Yu et al.
In the mid-90's, Steeten et al proved those with CFIDS/ME had some type of orthostatic hypotension although not always the exact same type. In 2008, Hokama et al proved CFIDS/ME was an autoimmune disease. Now researchers from the University of Oklahoma have provided "new insights into the pathophysiology" of why those with neurological autoimmune diseases have an abnormal response to upright posture.

J Intern Med, E-Pub Nov. 2011, "Chronic fatigue syndrome: acute infection and history of physical activity affect resting levels and response to exercise of plasma oxidant/antioxidant status and heat shock proteins," Jammes et al.
Yet another study that found excercise was harmful to those with CFIDS/ME. This study from France found two markers of oxidative stress (HSP27and HSP70) were found to be abnormal in patients following exercise.

Psychosom Med, E-Pub Dec 31, "Differences in Metabolite-Detecting, Adrenergic, and Immune Gene Expression After Moderate Exercise in Patients With Chronic Fatigue Syndrome, Patients With Multiple Sclerosis, and Healthy Controls," White et al.
CFS patients had more postexercise fatigue and pain than found in MS as well as more ion channel and other problems although both had adrenergic receptor problems.

Disabil and Rehab, E-Pub Dec. 2011. "Pacing as a strategy to improve energy management in myalgic encephalomyelitis/chronic fatigue syndrome: A consensus document," Goudsmit et al.
Although many adademic articles have found exercise to be harmful and pacing to be beneficial, this is the first one to describe various versions of pacing that have been evaluated for CFIDS/ME.

Bulletin IACFS, 2011:19(2), "Reporting of Harms Associated with Graded Exercise Therapy and Cognitive Behavioral Therapy in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome," Tom Kindlon.
"Harms" is a technical term for adverse effects that is seen in the most frequently advised "therapy" by our own CDC as well as England. The adverse results seen from both GET and CBT are often ignored by others but are carefully exposed in this paper. There are several forms of CBT but the one that has been shown to be the most harmful is that which increases daily activity however slowly. In one study, 51% had adverse reactions. The British PACE (pacing combined with CBT and GET) trial said this was "effective" but Kindlon, a volunteer co-head of the Irish ME/CFS Association, spent a great deal of time carefully reporting data that showed the opposite was true and that the PACE trial did not have any longterm follow-up. The lenghy paper highlights the harm such as this report: "… when I went to the hospital I could walk 100 yd., feed, wash and dress myself. when I left I could not weight bear at all, had no leg muscles to speak of, and needed two people to transfer me on and off the toilet and in and out of bed. I had little use of my hands and was totally bed bound. I could not tolerate sitting upright aginst the pillows, conversation was beyond me, and I could barely manage to feed myself by picking up food in my hands — cutlery was out of the question. Nine years later I have improved, but I'm still bed bound."

J Intern Med, 2011 (doi: 10.1111), "Gene expression alterations at baseline and following moderate exercise in patients with Chronic Fatigue Syndrome and Fibromyalgia Syndrome," Light et al.
"No gene expression changes occurred following exercise in Controls. In 71% of CFS patients, moderate exercise increased most sensory and adrenergic receptor's and one cytokine gene's transcription for 48 hours. These post-exercise increases correlated with behavioral measures of fatigue and pain… the other 20% of CFS patients, alpha-2A receptor's transcription was decreased at all time points after exercise… FM only patients showed no post-exercise alterations…" The researchers found orthostatic intolerance significally worsened with those showing alpha-2A transcription decreases. The healthy controls were age and gender matched.

Eur J Clin Invest, Feb 2012:42(2), "Loss of capacity to recover from acidosis on repeat exercise in chronic fatigue syndrome: a case-control study," Jones et al.
Yet another study on why exercise is harmful to CFIDS/ME patients from the UK exploring muscle bioenergetic function. They conclude, "when exercising to comparable levels to normal controls, CFS patients exhibit profound abnormality… Although exercise intervention is the logical treatment for patients showing acidosis, any trial must exclude subjects who do not initiate exercise as they will not benefit. This potentially explains previous mixed results in CFS exercise trials."

J Virol, Jan 2012, "Restricted Replication of Xenotropic Murine Luekemia Virus-Related Virus in Pigtailed Macaques," Del Prete et al.
Twenty one authors collaborated including some from the National Cancer Institute and Tufts University. Two macaques were injected with XMRV and found, after following them, the retrovirus did not cause any immune dysfunction such as is found in CFIDS/ME and had limited or no spread to the prostate as has been found in male patients. Because similar proteins are found in macaques, the results would be the same in humans.

Psychosomatics, Jan 2012, "Conditions comorbid with chronic fatigue in a population-based sample," Dansie, et al.
As part of the twin study in Seattle, they investigated "conditions concurrent with a CFS-like illness" but never stated what diagnostic criteria was used. The study included no real science and relied on self reporting finding "cormorbid chronic widespread pain, irritable bowel syndrome and/or major depressive disorder" were "frequent" which really tells us nothing.

Eur J Clin Invest, Feb: 42(2), "In the mind or in the brain? Scientific evidence for central sensitisation in chronic fatigue syndrome," Nijs et al.
Central sensitisation in CFIDS/ME contributes to hyperresponsiveness of the central nervous system and this review of the science is from a group from Belgium. Stressors worsen this such as "exercise and noxious heat pain" which explains why psychological influences are reported. It is brought on by immune dysfunction, infectious agents and a dysfunctional HPA axis.

Transfusion, Feb: 52(2), "The scientific method at work: xenotropic murine leukemia virus-related virus is neither a cause nor a threat to the blood supply," Karatin, Stramer.
The title says it all. The work is by Johns Hopkins University and the American Red Cross.

Clin Cardiol, Dec. 2011, 34/12, "Small Heart With Low Cardiac Output for Orthostatic Intolerance in Patients With Chronic Fatigue Syndrome," Kunihisa, Fujita.
These Japanese researchers began with an hypothesis: "Small heart is associated with OI (orthostatic intolerance) in patients with CFS" and then proved it! The small heart results in less cardiac output and these researchers demonstrated this fact by testing patients with and without OI finding the problem was in all but worsened in degree and led to OI over time. A smaller heart is also found in all patients with OI regardless of causation although no person is born that way.

Psysiol Meas, E-Pub Jan 2012, "Chronic fatigue syndrome and impaired peripheral pulse characteristics on orthostasis - a potential diagnostic biomarker," Allen et al.
A new technique of assessment was used to measure the ear fingers, toes and ear pads in a noninvasive way followed by a tilt table. While the healthy group had no significant changes, the patients had great changes. Autonomic nervous system dyfunction was proven many years ago by Dr. David H. P. Streeten (Orthostatic Disorders of the Circulation, NY, Plenum, 1987) and his testing method has been available from the NCF since our inception along with one of his medical journal articles spefically on CFIDS/ME.

J Psychosom Res, Feb 2012; 72(2), "Validation of the three-factor model of the PSQI in a large sample of chronic fatigue syndrome (CFS) patients," Meriman et al.
The PSQI (Pittsburgh Sleep Quality Index is supposed to measure sleep quality but these authors found it had "limited usefulness". Of course, the more scientific studies of the sleep phases deficient in CFIDS/ME shown by Moldovsky many years ago proved this and explained nonrestorative sleep was the main problem.

NMR Biomed. E-Pub Jan 27, 2012, "Increased ventricular lactate in chronic fatigue syndrome. lll. Relationships to cortical glutathione and clinical symptoms implicate oxidative stress in disorder pathophysiology," Shungu et al.
This report, the final of three already published, begins, "Chronic fatigue syndrome (CFS) is a complex illness, which is often misdiagnosed as a psychiatric illness." These researchers from Cornell University's medical school, from their ongoing study, conclude, "Collectively, the results of this third independent study support a pathophysiological model of CFS in which increased oxidative stress may play a key role in CFS pathophysiology." The article did not highlight the word, "may" but this points to a lot of money that funded researchers who could not prove anything that hasn't already been found by many. One of the research teams that found oxidative stress in CFIDS/ME was from Australia and reported on it in 2000 and they were far from the first (Redox Rep, 5(1)). The funding the most recent one was provided by the CAA.

Nature Prec, E-Pub 1/2012, "Oxidative Stress and Mitochondrial Injury in Chronic Multisympton Conditions: From Gulf War Illness to Autism Spectrum Disorder," Golumb.
This paper shows consequences of GWI and and overlapping conditions which "advances understanding of GWI, health conditions attending GWI at elevated rates; and overlapping conditions like CFS and ASK, providing prospects for vulnerability assessment… with implications germane to additive and excessive environmental oxidative stressor exposures in the civilian setting."

The Lancet, E-Pub Feb, 2012, "XMRV — the sad end of a story," Britton.
The saga of the retrovirus is told that ended with the retraction of the original paper. "In the past, several infectious agents have been associated with CFS but none of these could be confirmed in subsequent studies, leaving the field and patients in the same state of uncertainty as before." Replication of Stat-1depletion, funded by the NCF, illustrates why this happens.

Neurogastroenterol Motil, E-Pub Feb 2012, "Role of Lactobacillus acidophilus loaded flouting beds in chronic fatigue syndrome: behavioral and biochemical evidences," Singh et al.
The inclusion of this one from India is merely to demonstrate that there are many medical journal articles that are meaningless. This one used rats that they forced to swim until the rodents were exhausted and, thereby, had "chronic fatigue syndrome" that met no criteria and certainly did not test for any known and proven abnormalities. We actually felt sorry for the rats in this case!

QJM, E-Pub Feb 2012, "Lyme disease (LD) in a British referral clinic," Cottle et al.
Overdiagnosis of Lyme Disease has been documented in the US and in the UK yet this study found over 1/3 of the patients diagnosed with LD had "CFS". No diagnostic criteria was mentioned in the article which makes this report fairly useless since they may have been relying on the Oxford criteria which is akin to the US's Empirical criteria.

BMC Gastrointerol, 2012, 12:13, "Chronic fatigue syndrome after Giardia enteritics: clinical characteristics, disability and long-term sickness absesnce," Naess et al.
After a waterborn outbreak of laboratory confirmed giardia infection, over 20 of the over 1200 patients developed CFS in Norway. The trigger, as we know, can be multiple infections both viral and bacterial. These authors found no illness behavior nor did they find any depression in these patients.

Labeled Immunoassays & Clin Med, 2011/2, "Expression of Lymphocyte Subsets and CD25-+ Regulative T Cells in Peripheral Blood of Patients with Chronic Fatigue Syndrome," Ding-hau et al.
Higher levels were found in this study from China using flow cytometry.

Curr Opin Gastroenterol, E-Pub Feb 2012, "Carnitine derivatives: clinical usefulness," Malaguarnera.
This article mentions "chronic fatigue syndrome" but this is another example of how many medical articles are far from new. The NCF has offered a chapter about carnitine for CFIDS/ME for many years.

Lancet, Feb 2012, "Effectiveness of internet-based cognitive behavioral treatment for adolescents with chronic fatigue syndrome (FITNET): a randomised controlled trial," White, Chalder.
Two famous "psychobabblers, one of whom continues to be an advisor for the CDC's CFS division, used "self-rated results for several outcomes" despite the usual care gropu reporting "surprisingly poor". The participant teens did not need any medical diagnosis which makes their "improvement" reported by the authors useless.

Eur J Pharmacol, 2012 in press, "Chrysin improves cognitive deficits and brain damage induced by chronic cerebral hypoperfusion in rats," Xiau-Li He et al.
Hypoperfusion has been shown in CFIDS/ME. These Chinese researchers found chrysin helpful. (See Information Materials Available-NEW)

Cell Proliferation, 2011,44, "Resveratrol enhances the cytotoxic profile of docetaxel and doxorubicin in solid tumour cell lines in vitro," Al-Ahd et al (incl. El-Shemy).
This supplement was found helpful in work done when the NCF provided funding and markers with which the researchers built a what they termed a "leukemic cell line" although no patient yet had been diagnosed with leukemia. (See Information Materials Available-NEW)

Curr Medicinal Chem, 2010.17, "Antitumor Properties and Modulation of Antioxidant Enzymes' Activity by Aloe Vera Leaf Active Principles via Supercritixcal Carbon Dioxide Extraction," El-Shemy et al.
These researchers from Egypt, Saudi Arabia and Japan, working on markers provided by the NCF, found this supplement helpful although not curative. (See Information Materials Available-NEW)

J Enzyme Inhib & Medicinal Chem, E-Pub 2011, "Anti-cancer characteristics of mevinolin against three different solid tumor cell lines was not solely p53-dependnt," Mahmoud et al (incl. El-Shemy).
These researchers from Egypt and the U.S. found mevinolin (MVN) clinically helpful "for the treatment of hypercholesterolemia with very good tolerance by patients." (See Information Materials Available-NEW)

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