Monday, December 22, 2008

ME/CFS Blood Test On The Horizon

14 December 2008

The Whittemore Peterson Institute for research and treatment of Neuroimmune Diseases located in Nevada USA has announced it is approximately only 12 months away from the clinical establishment of a blood test for ME/CFS.

The major benefit of a blood test that will accurately distinguish even one sub-type of the amorphous and vague CFS illness construct is that scientist can begin to research homogeneous groups of patients all with the same disease. Since 1988 when the US CDC introduced the vague 'fatigue' oriented concept of CFS, and more recently the even less specific Empirical Definition of CFS, advances in understanding of the disease has been severely hindered by research carried out on mixed groups of patients, many of whom most likely didn't or don't have ME/CFS.

The institute's website can be viewed at

Tuesday, December 9, 2008

CFIDS Association Research Grants Raise Hope

The Following Article Was Taken From The ME/CFS Society of WA's Website

By: PR Newswire
Dec. 3, 2008 03:00 PM

CHARLOTTE, N.C., Dec. 3 /PRNewswire/ -- The four million Americans who suffer from chronic fatigue syndrome (CFS) have new reason for hope today with the announcement of an unprecedented research program to help identify biomarkers for the illness and improve diagnosis and treatment of CFS. The announcement was made by the CFIDS Association of America, which is funding the program, called the Accelerate CFS Research Initiative.

As part of this initiative, the CFIDS Association also announced today research grants totaling $647,940 to six research teams in the U.S. and Canada.

"These awards represent a new approach to CFS research," said Suzanne Vernon, PhD, the CFIDS Association's scientific director. "Instead of each investigator working in isolation, we are building a network of researchers and a framework for data sharing and collaboration not only among researchers who receive grants from the CFIDS Association, but among scientists worldwide."

Vernon, a microbiologist who helped pioneer the application of genomics to CFS, is now working to pioneer this new CFS research network and to direct the Accelerate CFS Research Initiative. "We were very impressed with the number and caliber of grant proposals we received this year, which signals a heightened level of interest in CFS research," said Vernon. "CFS, once shied away from by some researchers, is now considered a legitimate and challenging field of scientific inquiry."

The grant recipients are:
-- Gordon Broderick, PhD, of the University of Alberta in Canada, who will study the immune and endocrine response in adolescent patients who became ill with CFS after contracting infectious mononucleosis, which is caused by the Epstein-Barr virus. By studying patients from the time they get infectious mononucleosis to the development of CFS and through the first 24 months of illness, the researchers hope to identify disease progression biomarkers, including those essential for early diagnosis.

-- Kathleen Light, PhD, of the University of Utah Health Sciences Center, who will investigate the mechanisms involved in chronic pain that afflicts 40%-70% of CFS patients. This study will determine whether receptors located on blood cells are increased and overactive in people with CFS and associated with increased pain sensitivity. Light theorizes that increases in specific receptors following exercise may be blood-based biomarkers for CFS and could lead to a medical test to identify CFS patients.

-- Marvin Medow, PhD, of New York Medical College, who will investigate how orthostatic intolerance, seen in many CFS patients, affects brain function. This study will examine if CFS patients have increased pooling of blood in the abdomen that results in reduced cerebral blood flow. Medow will also investigate physiologic and oxidative stress changes associated with disturbance in blood flow. These results will help determine if alterations in blood flow affect brain metabolism.

-- Bhubaneswar Mishra, PhD, of the Courant Institute of Mathematical Sciences at NYU, who will use state-of-the-art bioinformatics and computational biology tools to create a computational model of CFS-a kind of "Google for CFS" that will be part database, part knowledge-base, part research network. This new resource will provide a "systems view" of CFS that accumulates published CFS literature and experimental data to
disentangle complex relationships among reported findings and discover causes of CFS.

-- Sanjay Shukla, PhD, of Marshfield Clinic Research Foundation, who will use metagenomics to determine if the ratio of good to bad intestinal bacteria in CFS patients is altered, and whether this imbalance in gut bacteria may be responsible for triggering CFS symptoms. Recent advances in metagenomics have demonstrated the significance of altered gastrointestinal bacteria in illnesses like HIV, diabetes, Crohn's disease, inflammatory bowel disease and ulcerative colitis. Shukla theorizes that CFS patients also have an imbalance of good and bad intestinal bacteria, resulting in enhanced intestinal permeability-called leaky gut-allowing bacteria to move across the protective intestinal barrier and causing chronic inflammation and immune activation in CFS patients. This study will contribute to our understanding of the relationship between the human microbiome and CFS. It may also lead to new treatment options, including the use of probiotics.

-- Dikoma Shungu, PhD, of Weill Medical College of Cornell University, who will use a brain scanning technique called magnetic resonance spectroscopy to confirm earlier findings that brain fluid of CFS patients contains significantly elevated levels of lactate, a substance important in metabolism. Shungu's team will also investigate the reason for this phenomenon, exploring whether lactate levels are higher in CFS patients because their brains contain high levels of toxic compounds that cause a condition called oxidative stress (which could implicate chronic inflammation), or because mitochondrial dysfunction is causing malfunctions in the production of brain energy. If this study is successful, brain lactate levels could provide an objective diagnostic biomarker for CFS.

The Accelerate CFS Research Initiative was made possible by the successful completion of a yearlong, million-dollar fundraising campaign, the largest research campaign for CFS to date in the United States. The CFIDS Association has funded more than $5.4 million in CFS research since 1987, making it second only to the federal government in CFS research spending.

"This was a real grassroots campaign, with most contributions coming not from major corporations or foundations, but from ordinary people whose lives have been affected by the illness," said Kimberly McCleary, president and CEO of the CFIDS Association. "Patients, their family, friends and doctors stepped up to give donations large and small to fuel the research initiative."

"While support from individual American citizens is vital for research progress," McCleary noted, "more funding from the government, from biotech firms and from the pharmaceutical industry is desperately needed. CFS affects more Americans than many other well-known diseases, but receives far less research funding."

About the CFIDS Association of America

The CFIDS Association was founded in 1987 to stimulate high-quality CFS research, improve the ability of health care professionals to diagnose and manage the illness, provide educational information for patients and their families, and build widespread public awareness of CFS. The organization has invested more than $26 million in research, education and public policy and is the largest charitable funder and advocate of CFS research in the U.S.

Saturday, November 1, 2008

Create A Story II

From our games board - The Three Word Story - If you'd like to participate it's as easy as joining up and posting!

"In the Beginning, there was a tiny little house with a red little hat and a giant brick chimney. Sometimes, it blew a big spiraling poof of lightly rainbow flavored lollipops. The big chimney was twisted and contorted in loop de loops of great complexity and incredible flexibility. This allowed for two very important messengers from a totally different dimension!"

Wednesday, October 29, 2008

Serum antioxidants and nitric oxide levels in fibromyalgia: a controlled study.

Taken from here

Serum antioxidants and nitric oxide levels in fibromyalgia: Rheumatol Int. 2008 Oct 14. [Epub ahead of print] Sendur OF, Turan Y, Tastaban E, Yenisey C, Serter M.

Department of Physical Medicine and Rehabilitation, Adnan Menderes University Medicine School Hospital, Aydin, Turkey. PMID: 18853166

We proposed to assess antioxidant status and nitric oxide in fibromyalgia (FM) patients in comparison to healthy controls. Additionally, the association between the serum antioxidant levels and clinical findings in FM patients was also investigated.

Thirty-seven FM patients and 37 healthy controls were enrolled in this study. Severity of fatigue and pain were determined by Visual Analogue Scale. Functional capacity in daily living activities was evaluated by fibromyalgia impact questionnaire. Serum NO, catalase and glutathione were measured.

Serum glutathione and catalase levels were significantly lower in FM patients than controls. However, no significant difference was seen in serum NO levels between the two groups. A significant correlation was evident between serum NO level and pain. Additionally, the correlation between glutathione level and morning stiffness was found to be significant.

These findings support other studies, we assume that these two antioxidants might have impact on the pathogenesis of FM disease.

Saturday, October 11, 2008

Create A Story I

From our games board - The Three Word Story - If you'd like to participate it's as easy as joining up and posting!

The little spider had hairy legs that made squeaky noises like tiny out-of-tune violins.
From atop the largest building in the whole world he decided to do a backflip and trail webbing all about the tower's shiny glass viewing windows, next to the open stellar wormhole leading all the pixies to the fantastic plastic yellow submarine sinking into oblivion.

Thursday, September 25, 2008

Hypothesis: ME/CFS caused by dysregulation of hydrogen sulfide metabolism

Article source

Chronic fatigue syndrome (CFS), which is also known as myalgic
encephalomyelitis (ME), is a debilitating, multi-system disease
whose etiology is unclear, and for which there are as yet no reliable
treatments. Here the hypothesis is advanced that the multi-system
disturbances in CFS/ME are caused by disturbances in the homeostasis
of endogenous hydrogen sulfide (H2S) and result in mitochondrial

Research on H2S -- the gas that causes the characteristic smell of
rotten eggs -- dates to the 1700‚s and has shown a remarkable
range of effects in both animals and humans. At high concentrations,
H2S has a variety of biological toxicities including being
instantaneously deadly; at low concentrations some evidence suggests
that H2S has beneficial effects and can act as an endogenous
biological mediator the third such gaseous mediator discovered
(after nitric oxide and carbon monoxide). The brain, pancreas and
the gastrointestinal tract produce H2S. Endogenous H2S plays a role
in regulating blood pressure, body temperature, vascular smooth
muscle, cardiac function, cerebral ischemia, and in modulating
the hypothalamus/pituitary/adrenal axis. It even has been called
a "master metabolic regulator."

Recent research has demonstrated that at low, non-toxic doses,
exogenous H2S produces a reversible state of hibernation-like deanimation
in mice, causing a decrease in core body temperature,
an apnea-like sleep state, reduced heart and respiration rates,
and a severe metabolic drop [1]. These characteristics are not unlike
the symptoms and extreme "de-animation" experienced by
CFS/ME patients. Moreover, H2S affects biological networks that
are disrupted by CFS including neurologic, endocrine and immunologic
systems. Therefore, a plausible etiology of CFS is an increase
in the activity of endogenous H2S, thereby inhibiting mitochondrial
oxygen utilization.

H2S and Mitochondria
In this view, fatigue and the other CFS/ME symptoms could be
due to diminished physiological and cellular energy due to reduction
in the capacity of mitochondria to utilize oxygen and synthesize
ATP. Specifically, H2S binds to the mitochondrial enzyme
cytochrome c oxidase, which is part of Complex IV of the electron
transport chain, and attenuates oxidative phosphorylation and ATP

Consistent with this finding, recent research on low levelH2S toxicity
points to increased formation of free radicals and depolarization
of the mitochondrial membrane, a condition that would
decrease ATP synthesis [2]. If poisoning renders mitochondria inefficient,
one would expect cells to shift to anaerobic mechanisms, a
shift that has been reported for CFS patients. Also consistent with
this hypothesis is the fact that mitochondria are organelles descended
from ancient eukaryotic sulfur-utilizing microbes. Thus, it
is not surprising that they show a very high affinity for sulfide.
Of course, H2S or sulfide may not directly affect mitochondria
by binding to them. Genomic changes could mediate some of the
effects of H2S. Some studies have found evidence for the involvement
of the cytochrome c oxidase gene in CFS/ME. Also, investigators
have found CFS abnormalities in genes related to fatty acid
metabolism, apoptosis, mitochondrial membrane function, and
protein production in mitochondria. Given a predisposing genetic
background, H2S may lead to genomic instability or cumulative
mutations in the mitochondrial DNA [3].

Alternatively, the effects of H2S could be initially mediated by
changes in the redox potential of cells or changes in their sulfur
metabolism, especially in glutathione. Another possible mechanism
is a direct effect of H2S on the immune system. Recent research
indicates that exogenous hydrogen sulfide induces
functional inhibition and cell death of cytotoxic lymphocyte subsets
of CD8 (+) T cells and NK cells.

Finally, H2S plays a pivotal role in both aerobic and non-anaerobic
organisms as a signaling molecule. Bacteria in the gut both produce
H2S and utilize it as a substrate alternative to oxygen. This is of
particular relevance in the gastrointestinal tract, where unusually
high levels of gram-negative bacteria, which increase intestinal permeability,
have been found in patients with CFS/ME [4]. In addition
to bacteria, yeast, mold and other fungi also emit H2S.
CFS/ME is a model disease for multisystem disturbance. It is my
hypothesis that mitochondria, organelles required by every cell to
sustain life, are unable to adequately utilize oxygen. This mitochondrial
disturbance could be due to the combined effects of
anaerobic conditions known to occur in CFS and associated low-level
H2S toxicity. This increase in H2S alters fine signaling necessary
for body homeostasis, and causes CFS. Understanding the role of
H2S in the body, and, in particular, in mitochondrial function,
may provide a unifying lens through which to view the diverse
manifestations of this complex disease.

[1] Blackstone Eric, Morrison Mike, Roth Mark B. H2S induces a suspended
animation-like state in mice. Science Magazine 2005;308(5721):518.
[2] Eghbal MA, Pennefather PS, O‚Brien PJ. H2S cytotoxicity mechanism involves
reactive oxygen species formation and mitochondrial depolarisation.
Toxicology 2004;203(13):6976. PMID: 15363583.
[3] Attene-Ramos MS, Wagner ED, Gaskins HR, Plewa MJ. Hydrogen sulfide induces
direct radical-associated DNA damage. Mol Cancer Res 2007 [PMID: 17475672].
[4] Maes M, Mihaylova I, Leunis JC. Increased serum IgA and IgM against LPS of
enterobacteria in chronic fatigue syndrome (CFS): indication for the
involvement of gram-negative enterobacteria in the etiology of CFS and for
the presence of an increased gut-intestinal permeability. J Affect Disord
2007;99(13):23740. PMID: 17007934

Friday, September 5, 2008

Announcment: Live Chat Session

Blue Butterflies is having a live chat session this weekend. For now it is members only so if you would like to participate please sign up!

If you are interested but don't wish to sign up until you get to know what we are about better then let us know. If there is enough interest we may hold a public live chat session.

Following are the times but if you don't see your timezone and would like to participate either leave a comment here or log into the forum and post in this thread

The live chat times are;

Cananda (Toronto) Sunday 7th at 7:30pm
US (St Paul) Sunday 7th at 6:30pm
Syd/Melb Monday 8th 9:30am

Thursday, August 21, 2008

Zombie Science In ME/CFS

From 15/8/08

Mental health researchers at The Institute of Psychiatry (London) are
currently undertaking a study of "social cognition". The project seeks to
find out whether "the processing of social information" is affected in
people with anorexia nervosa and whether or not people with anorexia can
recognise complex emotions in other people.

The anorexia group will be compared with healthy controls and also with
people who have "CFS", the latter being recruited through outpatient
services of The South London and Maudsley NHS Foundation Trust.

The project was announced in 2007 just before the publication of the NICE
Guideline on "CFS/ME".

Recruitment for this "research" will run until the end of 2008 and the
project will be completed in 2009.

( )

The study literature states: "The comparison with CFS will allow
(researchers) to gauge whether any social cognition deficits are unique to
anorexia, or reflect more global symptoms of psychiatric illness with marked
physical symptoms".

So there we have it in black and white: according to researchers at the IoP
(the home of stalwart supporters of CBT and GET for "CFS/ME" Professors
Simon Wessely and Trudie Chalder), "CFS" is "a psychiatric illness with
marked physical symptoms".

The background to the project states: "Anorexia nervosa and chronic fatigue
syndrome are classical psychosomatic disorders where response to social
threat is expressed somatically (e.g. Hatcher & House, 2003; Kato et al
2006; Schmidt et al 1997). Other similarities between these disorders
include strong female preponderance and overlapping personality
characteristics, such as being introverted and avoidant. Aberrant emotional
processing is a strong candidate as a maintaining factor for these disorders
(Schmidt & Treasure 2006)".

Is it by chance alone that this "research" coincides with the publication of
the NICE Guideline and that the only "evidence" upon which the NICE
Guideline Development Group relied is that of the Wessely School, whose
assumption about the nature of "CFS/ME" is that it is a psychosomatic
disorder and whose model and management recommendations are based on "fear
avoidance" and "deconditioning"?

It is surely remarkable that the beliefs of the Wessely School about
"CFS/ME" (in which they unequivocally include "ME/CFS") remain uninfluenced
by the ever-mounting biomedical evidence which proves their beliefs to be
seriously misinformed.

A possible explanation has been put forward by Professor Bruce Charlton,
Editor-in-Chief of Medical Hypotheses; Emeritus Professor of Public Policy
at the University of California and Reader in Evolutionary Psychiatry at the
University of Newcastle (UK).

Charlton is well-known for his campaign to breathe new life into academic
medicine in order to capture issues that matter to patients and which would
make a difference to their lives.

In a compelling Editorial (Zombie science: A sinister consequence of
evaluating scientific theories purely on the basis of enlightened
self-interest. Medical Hypotheses, 26th July 2008) Charlton debunks the
ideal of impartial and objective science. The following quotations apply
with particular resonance to the current ME/CFS situation in the UK:
"In the real world it looks like most scientists are quite willing to pursue
wrong ideas - so long as they are rewarded for doing so with a better chance
of achieving more grants, publications and status".

"This is 'enlightened self-interest' a powerful factor in scientific
evaluation because the primary criterion of the 'validity' of a theory is
whether or not acting upon it will benefit the career of the scientist;
'enlightened' because the canny career scientist will be looking ahead a few
years in order to prefer that theory which offers the best prospect of
netting the next grant, tenure, promotion or prestigious job opportunity".

"When a new theory is launched, it is unlikely to win converts unless (they)
are rewarded with a greater chance of generous research funding, the
opportunity to publish in prestigious journals and the hope of increased
status exemplified by admiration and respect from other scientists".

"Theories may become popular or even dominant purely because of their
association with immediate incentives and despite their scientific

"Even the most conclusive 'hatchet jobs' done on phoney theories will fail
to kill, or even weaken, them when the phoney theories are backed up with
sufficient economic muscle in the form of funding. Scientists will gravitate
to where the money is so long as the funding stream is sufficiently deep and

"Classical theory has it that a bogus hypothesis will be rejected when it
fails to predict 'reality', but (this) can be deferred almost indefinitely
by the elaboration of secondary hypotheses which then require further
testing (and generates more work for the bogus believers)".

"That the first theory is phoney, and always was phoney, is regarded as
simplistic, crass (and) a sign of lack of sophistication".

"And anyway, there are massive 'sunk costs' associated with the phoney
theory, including the reputations of numerous scientists who are now
successful and powerful on the back of the phoney theory, and who now
control the peer-review process (including the allocation of grants,
publications and jobs)".

"False theories can therefore prove very long-lived".

"The zombification of science (occurs) when science based on phoney theories
is serving a useful but non-scientific purpose (so it is) kept going by
continuous transfusions of cash from those whose interests it serves".

"For example, if a branch of pseudo-science based on a phoney theory is
valuable for political reasons (e.g. to justify government policies) then
real science expires and 'zombie science' evolves".

"(This) can be explained away by yet further phoney theoretical
elaborations, especially when there is monopolistic control of information".

"In a nutshell, zombie science is supported because it is useful propaganda
(and) is deployed in arenas such as political rhetoric, public
administration, management, public relations, marketing and the mass media
generally. Indeed, zombie science often comes across in the mass media as
being more plausible than real science".

"Personal careerist benefits seem easily able to overwhelm the benefits of
trying to establish the 'real world' of truth".

"In current science, there seems to be a greater possibility that large
scale change may be fashion rather than progress, and such change may be
serving propagandist goals rather than advancing scientific understanding".

"Modern science may have a lumbering pace, and its vast bulk means that once
it has begun to move in a particular direction, trying to deflect its path
is like stopping a charging rhinoceros".

"Perhaps funders co-operate, co-ordinate and collude, and therefore should
be regarded as a cartel".

To halt this raging rhinoceros, Charlton says: "Individual ambition should
ensure a sufficient supply of debunkers to keep the gardens of science
weeded of bogus theories, and to banish the zombies of science to the
graveyards where they belong".

The ME/CFS community can have no doubt that Charlton has hit the nail on the

For how much longer must these desperate people be sacrificed on the defiled
altar of zombie science?

Tuesday, August 19, 2008

Antiviral Drug Under FDA Review For ME/CFS

An interesting piece of news I came across on - Original Article

FDA accepts antiviral drug AmpligenR for review as first-ever ME/CFS therapeutic

After 30 years in development and testing, the experimental “antiviral/immune modulatory” drug Ampligen has been accepted by the FDA for review as potentially the first prescription drug approved in the U.S. for treatment of ME/CFS – specifically for certain patients with severe ME/CFS.

Delivered intravenously, typically twice weekly over a year or more, Ampligen (AMPLified GENetic activity) has been available in Belgium and Canada for ME/CFS and HIV treatment since 1996.

Ampligen (polyI:polyC12U) - still allowed only in specific clinical trial settings conducted under U.S. governmental authorization - is termed “a nucleic acid drug,” designed to “modulate” the body’s immune system. Its mechanism of action in ME/CFS “is not entirely clear,” but it is thought to act on two enzyme systems so as to help the immune system destroy viral RNA and speed the death of virus-affected cells. In particular it may “downregulate” an anti-viral pathway which research suggests has become “upregulated” in certain ME/CFS patients (the 2-5 Synthetase/RNase L anti-viral pathway).

The drug’s maker – Philadelphia-based Hemispherx Biopharma, submitted a New Drug Application to the FDA in 2007, and had been asked to answer a series of questions. The FDA’s acceptance of the drug for safety/efficacy review was based on receipt of the requested data. The maker reportedly suggests it is also researching oral delivery of the drug.

A "Who's-Who" of the world’s leading ME/CFS specialists have participated in Ampligen trials over the years

Saturday, August 16, 2008

What Is Fibromaylgia?

(As I'm pretty sure that I mentioned in the previous post I'm pretty bad at explaining illnesses so here's something that explains it better then I could have)

Taken from the Athritis Victoria website

Fibromyalgia is a name given to a group of symptoms marked by generalised pain and muscle stiffness. These symptoms can be felt in all different areas of the body. Extreme fatigue (tiredness) and sleep problems are also common in fibromyalgia. Fibromyalgia does not cause inflammation or damage to the painful areas, but seems to be due to an overactive pain system. Fibromyalgia is different to polymyalgia rheumatica, a type of arthritis that causes inflammation in the muscles.

If you'd like to learn more - symptoms, cause, managment etc - I highly recommend checking out the website. Follow the link at the top of this entry. It's all on the one page.

Wednesday, August 6, 2008

First Post & What Is ME/CFS

I think the first post is always the hardest and I myself always have a hard time starting it so I guess maybe dispensing with the small talk this time round might be best.

I've started this blog as a compliment to the Blue Butterflies Forum. The forum I started over a year ago. It's an alternative get together for sufferer's of ME/CFS & FM. I have had ME/CFS, since 2005, and I'm a bit of an alternative person.

What do I mean by alternative?

Well when it comes down to it I'm an atheist but I like to call myself an open minded atheist. I dabble in a bit of Buddhism, crystal work and other alternative healing, spirituality and paganism. All that jazz is what I mean by "alternative". So if you're a pagan, spiritualist, atheist or just open minded and curious you might like the forum. If it's not your cup of tea then that's fine, you can still read the blog of course!

As for the whole ME/CFS & FM question...

For all my writing skills I'm terrible at explaining exactly what Myalgic Encephalomyelitis or Fibromyalgia (I try to avoid having to explain it) is let alone writing it up so I'm going to take a piece from another site that has it so well written out I am beyond impressed.

This is for the Myalgic Encephalomyelitis (Chronic Fatigue Syndrome). Fibromyalgia will be the next post.

What Is ME/CFS?
Taken from the WA Society Website

ME/CFS is a complex chronic disease affecting multiple body systems/organs. The disease is characterised by abnormal persistent or relapsing fatigue, post-exertional malaise/fatigue, sleep dysfunction, cognitive dysfunction, muscle/joint pain and headaches. Post-exertional malaise/fatigue, which is a hallmark of the disease, describes the worsening of symptoms and incapacitating malaise/fatigue experienced by those affected following physical or mental exertion, sometimes even of a trivial nature.

Individuals may also experience their own unique constellation of accompanying symptoms which may include impaired concentration and memory, swollen lymph nodes, recurrent feverishness, food intolerance, nausea, disorientation and cognitive and sensory overload amongst others (see Symptoms).

The severity of the disease and symptoms vary from one individual to another and can in very rare instances be fatal (see Severity). It is frequently known to develop following infection or may have a more gradual onset and has the potential to cause devastating and possibly lifelong disability in those affected.

Although the disease is generally referred to as ME/CFS, ME and CFS are not identical. To understand the differences between ME and CFS and the confusion and misunderstanding this has caused see Brief History.

If you'd like to learn more please follow this link

Thanks for reading