Patient organisations in ME and CFS seek only understanding

BMJ 2004; 329 doi: https://doi.org/10.1136/bmj.329.7457.112-b (Published 08 July 2004) Cite this as: BMJ 2004;329:112

Dr. De Meirleir's work supports Dr. Marshall's hypothesis - CFS - Th1

It is my opinion that Dr. Marshall's hypothesis has significant merit
for chronic fatigue syndrome. The work and research of Dr. Kenny De
Meirleir, who is considered an expert in the CFS community, supports Dr.
Marshall's theory quite a bit.

For example, Dr. De Meirleir proposed that mycoplasma infections are
capable of causing the 83 kDa RNase L proteolysis and dysfunction which
has been consistently found in CFS patients. Mycoplasma can activate
monocytes, neutrofils and T-cells. To bring about their phagocytic
activity, monocytes, neutrofils and activated T-cells produce elastase
which is one of the primary findings by Dr. De Meirleir and was recently
revealed by the National CFIDS Foundation. Dr. De Meirleir holds a
worldwide patent on his discovery. Subsequently, in the CFS community,
patients tested for human leukocyte elastase (HLE) by R.E.D. Laboratories
have consistently shown higher levels of elastase corresponding with the
RnaseL proteolysis and dysfunction which clearly could be involved in
systematic inflamation and numerous symptoms associated with CFS.

Once the 83 kDa RNase L cleavage has occurred, cell apoptosis
(programmed cell death) is initiated. Apoptosis in turn enhances the
activity of pro-apoptotic and pro-inflammatory proteases including both
elastase and calpain, each of which is capable of high molecular weight
RNase L proteolysis..

A vicious cycle is initiated by the cell-wall deficient bacteria
species (mycoplasma, lyme) and numerous opportunistic infections take
advantage of the impaired immune system in CFS patients. Cytokine
responses are clearly involved in this process.

Dr. De Meirleir's work defintely supports Dr. Marshall's hypothesis
that CFS is indeed a Th1 immune disease most likely caused by "stealth"
bacteria without cell walls that can evade and disrupt the immune
response. In my opinion it is likely there is a genetic or other co-factor
in CFS patients. For example, women have considerably higher rates of CFS
in the general population (and other autoimmune diseases) than men. It
isn't clear why chronic fatigue syndrome and other autoimmune diseases
affect women more than men but the answer could likely lead to a greater
understanding of the immune system.

I highly recommend reading Dr. De Meirleir's work and all the
research papers that he has been an investigator in. After reading them,
along with Dr. Marshall's research papers, it is fairly clear that there
is a common factor that almost every CFS researcher has found - and Dr.
Marshall's hypothesis brings it together for a clear understanding of the
cause and treatment for chronic fatigue syndrome and possibly other
autoimmune conditions.

Competing interests:
None declared

Competing interests: No competing interests

26 July 2004
Jason L Breckenridge
CFS Researcher / NCF Volunteer
Syracuse New York, 13209