Charlotte CFS/ME/FM Support Group Newsletter

for June 6, 2013


Hi Everyone,

Below are some articles that I think you may find interesting. Our June meeting will feature Jennifer Watson demonstrating Tai chi.  She is a physical therapist with Arthritis Services. There will be more details in my reminder newsletter. You'll receive that on or around June 16th.


Upcoming Meetings:


June 20 - Jennifer Watson - Tai chi, physical therapist with Arthritis Services

July 18 -   Daytime Lunch at Panera's in Pineville (details forthcoming)

August 15 - Daytime Lunch at Panera's in Matthews (details forthcoming)

September 19 - Dr. Charles Lapp

October 17 - Dr. Nancy Waring - Learning How to Live with Chronic Illness

November 21 - TBA

December 19 - Annual Christmas Party



Dr. Peterson Calls for “Therapeutic Strategy” to Develop Drugs for ME/CFS

By Cort Johnson • • May 22, 2013

 Source: Simmaron Neuroimmune Research Foundation

“We’re Ready”

After 30 years of treating approximately 9,000 patients and tired of the ‘therapeutic stagnation’ in this disease, he called on the FDA to ‘execute a therapeutic strategy’ that would pave the way for drug development. No doubt speaking not just to the FDA but to drug company reps listening, he gave them good pragmatic reasons to do so; 1,000,000 sick people in the US, a $9 billion hit to our economy yearly, a market for a diagnostic marker yielding potentially $250 million a year, a drug therapy possibly bringing in billions….

“I implore the esteemed committee to develop a therapeutic strategy for ME/CFS” Dr. Dan Peterson to FDA

Listen to Dr. Peterson at minute 92:00 of this VIDEO.  (Link Below)

To read the rest of this article by Cort Johnson for ProHealth, go to:



Redefining ME/CFS?  CDC Chief Reveals First Fruits of  Multi-Center Doctor study at FDA StakeHolder Meeting

By Simon McGrath on May 11, 2013

 (Are different ME/CFS doctors seeing different types of ME/CFS patients. Would closely examining those patients reveal the elusive subsets researcher have been talking about for decades? At the FDA Workshop on April 26, Dr Elizabeth Unger, head of the CDC’s Chronic Fatigue Syndrome programme revealed the initial results of their multi-clinic study assessing ME/CFS patients. Please welcome Simon McGrath to Health Rising as he digs deeper into the first fruits of this fascinating study).  To read those initial results go to

Things are changing at the CDC. Previously known for it’s insularity, the CDC set up a collaboration with the top ME/CFS clinics in the States to look at patients in detail (and even collaborated with the clinics on designing the study protocol ). The goals were to see if and how patients differed between clinics, to gather hard data to help address the issue of case definition, and to find the best ways of measuring this illness.


ME/CFS Physicians Take the Lead in Deciding Who Has ME/CFS

To read further, go to:

Redefining ME/CFS? CDC Chief Reveals First Fruits of Multi-Center Doctor Study at FDA Stakeholder Meeting


Note from Nancy:  This article comes to us thanks to the dedication of a fine advocate, Cort Johnson, whose blog is available at . 

Dr. Nancy Klimas (Institute for Neuroimmune Research, Nova Southeastern, Ft. Lauderdale, FL

You have to go back, way back – over twenty years – to find Dr. Nancy Klimas’s first contribution to ME/CFS research. With a nice career in HIV research underway, Dr. Klimas – in a move that must have left some of her colleagues shaking their heads- took a chance on a controversial disease early in their career.

Dr. Klimas and her research partner, Dr. Mary Fletcher, have played significant roles in uncovering the immune abnormalities, particularly natural killer cell dysfunction, present in this disorder. Their first paper on natural killer cell dysfunction appeared in 1990. Now believed to be major player in ME/CFS pathophysiology, the Fletcher/Klimas research has spurred researchers from across the US, including the CDC, and now Australia to tackle natural killer cell research. and has continued on and off for over 20 years.

To continue reading this article, go to:



From Co-Cure - An article from "Frontiers in Physiology"

Front. Physiol., 05 April 2013 | doi: 10.3389/fphys.2013.00063

Caught in the thickness of brain fog: exploring the cognitive symptoms of Chronic Fatigue Syndrome

Anthony J. Ocon*

  • Departments of Physiology/Medicine, Center for Hypotension, New York Medical College, Valhalla, NY, USA

Chronic Fatigue Syndrome (CFS) is defined as greater than 6 months of persistent fatigue that is experienced physically and cognitively. The cognitive symptoms are generally thought to be a mild cognitive impairment, but individuals with CFS subjectively describe them as “brain fog.” The impairment is not fully understood and often is described as slow thinking, difficulty focusing, confusion, lack of concentration, forgetfulness, or a haziness in thought processes.

Causes of “brain fog” and mild cognitive impairment have been investigated. Possible physiological correlates may be due to the effects of chronic orthostatic intolerance (OI) in the form of the Postural Tachycardia Syndrome (POTS) and decreases in cerebral blood flow (CBF). In addition, fMRI studies suggest that individuals with CFS may require increased cortical and subcortical brain activation to complete difficult mental tasks.

Furthermore, neurocognitive testing in CFS has demonstrated deficits in speed and efficiency of information processing, attention, concentration, and working memory. The cognitive impairments are then perceived as an exaggerated mental fatigue. As a whole, this is experienced by those with CFS as “brain fog” and may be viewed as the interaction of physiological, cognitive, and perceptual factors.

Thus, the cognitive symptoms of CFS may be due to altered CBF activation and regulation that are exacerbated by a stressor, such as orthostasis or a difficult mental task, resulting in the decreased ability to readily process information, which is then perceived as fatiguing and experienced as “brain fog.” Future research looks to further explore these interactions, how they produce cognitive impairments, and explain the perception of “brain fog” from a mechanistic standpoint.


From Co-Cure

Date:    Fri, 12 Apr 2013 10:45:06 -0500
From:    kelly <kellylatta66@GMAIL.COM>
Subject: RES: Immunostimulation in the treatment for chronic fatigue syndrome/myalgic encephalomyelitis

Immunol Res. 2013 Apr 11. [Epub ahead of print]

Immunostimulation in the treatment for chronic fatigue syndrome/myalgic

Proal AD, Albert PJ, Marshall TG, Blaney GP, Lindseth IA
Autoimmunity Research Foundation, 3423 Hill Canyon Ave, Thousand Oaks, CA,
91360, USA.


Chronic fatigue syndrome (CFS)/myalgic encephalomyelitis (ME) has long been
associated with the presence of infectious agents, but no single pathogen
has been reliably identified in all patients with the disease.

Recent studies using metagenomic techniques have demonstrated the presence
of thousands of microbes in the human body that were previously undetected
and unknown to science. More importantly, such species interact together by
sharing genes and genetic function within communities.

It follows that searching for a singular pathogen may greatly underestimate
the microbial complexity potentially driving a complex disease like CFS/ME.
Intracellular microbes alter the expression of human genes in order to
facilitate their survival.

We have put forth a model describing how multiple species-bacterial, viral,
and fungal-can cumulatively dysregulate expression by the VDR nuclear
receptor in order to survive and thus drive a disease process.

Based on this model, we have developed an immunostimulatory therapy that is
showing promise inducing both subjective and objective improvement in
patients suffering from CFS/ME.  Copy and paste this to get to the rest of this article.




Date:    Mon, 13 May 2013 21:06:53 -0500
From:    Tate Mitchell <>
Subject: RES: In (ME/CFS), increased autoimmune activity against 5-HT is associated with immuno-inflammatory pathways and bacterial translocation

In myalgic encephalomyelitis/chronic fatigue syndrome, increased autoimmune activity against 5-HT is associated with immuno-inflammatory pathways and bacterial translocation.

Michael Maes a, b, c, Karl Ringel d, Marta Kubera e, George Anderson
f, Gerwyn Morris g, Piotr Galecki h, Michel Geffard i
a Maes Clinics @ TRIA, Bangkok, Thailand
b Department of Psychiatry, Chulalongkorn University, Bangkok, Thailand
c Department of Psychiatry, Deakin University, Geelong, VIC, Australia
d Immunologischen Laboratorien, Aachen, Germany
e Department of Experimental Endocrinology, Institute of Pharmacology,
Polish Academy of Sciences, Krakow, Poland
f CRC, Rm 30, Glasgow, Scotland
g Tir Na Nog, Pembrey, Llanelli, UK
h Department of Adult Psychiatry, Medical University of Lódź and
Babinski Memorial Hospital, Lódź, Poland
i Association Institute for Research & Development in Human Pathology
and Therapy, Talence, France

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is
accompanied by activation of immuno-inflammatory pathways, increased
bacterial translocation and autoimmune responses to serotonin (5-HT).
Inflammation is known to damage 5-HT neurons while bacterial
translocation may drive autoimmune responses. This study has been
carried out to examine the autoimmune responses to 5-HT in ME/CFS in
relation to inflammation and bacterial translocation.

We examined 5-HT antibodies in 117 patients with ME/CFS (diagnosed
according to the centers for disease control and prevention criteria,
CDC) as compared with 43 patients suffering from chronic fatigue (CF)
but not fulfilling the CDC criteria and 35 normal controls. Plasma
interleukin-1 (IL-1), tumor necrosis factor (TNF)α, neopterin and the
IgA responses to Gram-negative bacteria were measured. Severity of
physio-somatic symptoms was measured using the fibromyalgia and
chronic fatigue syndrome rating scale (FF scale).

The incidence of positive autoimmune activity against 5-HT was
significantly higher (p<0.001) in ME/CFS (61.5%) than in patients with
CF (13.9%) and controls (5.7%). ME/CFS patients with 5-HT autoimmune
activity displayed higher TNFα, IL-1 and neopterin and increased IgA
responses against LPS of commensal bacteria than those without 5-HT
autoimmune activity. Anti-5-HT antibody positivity was significantly
associated with increased scores on hyperalgesia, fatigue,
neurocognitive and autonomic symptoms, sadness and a flu-like malaise.

The results show that, in ME/CFS, increased 5-HT autoimmune activity
is associated with activation of immuno-inflammatory pathways and
increased bacterial translocation, factors which are known to play a
role in the onset of autoimmune reactions. 5-HT autoimmune activity
could play a role in the pathophysiology of ME/CFS and the onset of
physio-somatic symptoms. These results provide mechanistic support for
the notion that ME/CFS is a neuro-immune disorder.



 Editor’s Comment: Sicca, or dry eyes and mouth, is included in both the Canadian and International case definitions for CFS/ME. In 1996, researchers in Japan found that fully one-third of the CFS/ME patients met the diagnostic criteria for Sjögren's. 

Novel aspects of Sjögren’s syndrome in 2012

By Angela Tincani et al. 


Sjögren’s syndrome (SS) is a systemic progressive autoimmune disease characterized by a complex pathogenesis requiring a predisposing genetic background and involving immune cell activation and autoantibody production. The immune response is directed to the exocrine glands, causing the typical ‘sicca syndrome’, but major organ involvement is also often seen. 

The etiology of the disease is unknown. Infections could play a pivotal role: compared to normal subjects, patients with SS displayed higher titers of anti-Epstein-Barr virus (EBV) early antigens, but lower titers of other infectious agent antibodies such as rubella and cytomegalovirus (CMV) suggest that some infections may have a protective role against the development of autoimmune disease. 

Recent findings seem to show that low vitamin D levels in patients with SS could be associated with severe complications such as lymphoma and peripheral neuropathy. This could open new insights into the disease etiology. 

The current treatments for SS range from symptomatic therapies to systemic immunosuppressive drugs, especially B cell-targeted drugs in cases of organ involvement. Vitamin D supplementation may be an additional tool for optimization of SS treatment.

Source: BMC Medicine 2013, 11:93 doi:10.1186/1741-7015-11-93. Angela Tincani, Laura Andreoli2, Ilaria Cavazzana1, Andrea Doria, Marta Favero, Maria-Giulia Fenini, Franco Franceschini, Andrea Lojacono, Giuseppe Nascimbeni, Amerigo Santoro, Francesco Semeraro, Paola Toniati and Yehuda Shoenfeld. 


Our Support Group Leader and Board Members:

-  Kebbie Cannon is our Support Group Leader (704) 843-1193 at or Asst. Support Group Leader, Maggie Reed at

- Medical Advisor Dr. Charles Lapp, Hunter Hopkins Clinic in Charlotte. You can visit Dr. Lapp's Web Sites at where there is ample info about his clinic and making an appointment if you need.

- Treatment - Another site by Dr. Lapp and others, which is primarily directed toward helping your doctors treat these disorders, is:

- Treasurer is Leslie Vann at

- Newsletter Editor is Nancy Henson at

- Publicity Chairman is Howard Honeycutt at

- Visit our web site at