Saturday, January 2, 2010

"CBT: Chalder's Brush Therapy ..."


Anonymous said...

...and while she and her daft as a brush chums are grabbing all the research funding and giving us only psychobabble in return, people with M.E. are dying prematurely:

Why myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) may kill you

Neuro Endocrinol Lett. 2009 Dec 30;30(6). [Epub ahead of print]

Why myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) may kill you: disorders in the inflammatory and oxidative and nitrosative stress (IO&NS) pathways may explain cardiovascular disorders in ME/CFS.
Maes M, Twisk FN.

Maes Clinics, Antwerp, Belgium.

There is evidence that disorders in inflammatory and oxidative and nitrosative (IO&NS) pathways and a lowered antioxidant status are important pathophysiological mechanisms underpinning myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS). Important precipitating and perpetuating factors for ME/CFS are (amongst others) bacterial and viral infections; bacterial translocation due to an increased gut permeability; and psychological stress. Recently, Jason et al (2006) reported that the mean age of patients with myalgic encephalomyelitis/chronic fatigue syndrome dying from heart failure, i.e. 58.7 years, is significantly lower than the age of those dying from heart failure in the general US population, i.e. 83.1 years. These findings implicate that ME/CFS is a risk factor to cardio-vascular disorder. This review demonstrates that disorders in various IO&NS pathways provide explanations for the earlier mortality due to cardiovascular disorders in ME/CFS. These pathways are: a) chronic low grade inflammation with extended production of nuclear factor kappa B and COX-2 and increased levels of tumour necrosis factor alpha; b) increased O&NS with increased peroxide levels, and phospholipid oxidation including oxidative damage to phosphatidylinositol; c) decreased levels of specific antioxidants, i.e. coenzyme Q10, zinc and dehydroepiandrosterone-sulphate; d) bacterial translocation as a result of leaky gut; e) decreased omega-3 polyunsatutared fatty acids (PUFAs), and increased omega-6 PUFA and saturated fatty acid levels; and f) the presence of viral and bacterial infections and psychological stressors. The mechanisms whereby each of these factors may contribute towards cardio-vascular disorder in ME/CFS are discussed. ME/CFS is a multisystemic metabolic-inflammatory disorder. The aberrations in IO&NS pathways may increase the risk for cardiovascular disorders.

PMID: 20038921 [PubMed - as supplied by publisher]

Anonymous said...

Magical Medicine: How to make a disease disappear.

Professor Malcolm Hooper and Margaret Williams

Spring 2010

Anonymous said...

MEA-funded study published into severe risk factors for ME/CFS
Sunday, 03 January 2010 11:30

Pheby D and Saffron L. Biology and Medicine (2009); 1 (4): 50 - 74

This very comprehensive questionnaire based research study was carried out by Dr Derek Pheby and colleagues at the Unit of Applied Epidemiology, University of the West of England.

The research was funded by The ME Association's Ramsay Research Fund.

The conclusions were obtained using information from questionnaires that were given to 124 people with severe ME and 619 people with less severe ME, who acted as the controls. The questionnaires were completed by members of The ME Association, the 25% Group, CHROME, and by people attending the National ME Centre in Essex and the Wiltshire ME service.

A key conclusion to the study is that the standard of early management appears to be the most important determinant of severity. Having a mother with ME was an additional risk factor – a finding that is consistent with an illness causing mitochondrial dysfunction.

Of particular importance is the fact that no evidence was found to indicate that conscientiousness, neurotic traits or personality traits are risk factors in the development of severe ME.


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