Blue Butterflies

Blog Has Been Moved

2009-09-27T19:19:00.001+10:00

The Blue Butterflies blog has now been moved to a wordpress one. From now on if you'd like to catch up with all the blog posts, please follow the blog at our new address.

bluebutterflies.wordpress.com

All public readers can also comment on that blog as well and if you'd like a link to your blog to be added to it please either leave a comment on the new blog.

Thank you.

Chiropractic Treatment Insufficient For Fibromyalgia

2009-08-20T15:48:00.003+10:00

Evidence of Chiropractic Treatment Insufficient For Fibromyalgia
Original article

There is no evidence to suggest chiropractors are effective in treating people with fibromyalgia, according to a new review of existing literature on the subject.

Professor Edzard Ernst of the Peninsula Medical School at the Universities of Exeter and Plymouth, carried out the study.

"Many patients use chiropractic as a treatment of fibromyalgia and many chiropractors seem to be convinced that it is effective for that condition," he explained in the medical journal Clinical Rheumatology.

"The aim of the study was to conduct a systematic review of randomised clinical trials testing the effectiveness of chiropractic care for fibromyalgia."

Professor Ernst reviewed three previous research articles on the effect of chiropractic treatment for the condition, which were found through six electronic searches through online databases.

The three studies were judged to have "poor" methodological quality and they "generated no evidence to suggest that chiropractic care is effective for fibromyalgia".

"Currently, there is insufficient evidence to conclude that chiropractic is an effective treatment for fibromyalgia," Professor Ernst concluded.

Fibromyalgia is also known as chronic widespread pain and occurs mainly in women. The disease affects the muscles, and the intense pain, fatigue and depression associated with the condition make it distressing for sufferers, many of whom may find that they cannot continue with their daily activities.

At present, there is no known cure for fibromyalgia, though patients are advised to exercise, seek counselling if they are depressed and discuss medication to improve symptoms with their GPs.

The Arthritis Research Campaign is currently carrying out a major clinical trial to find out if a combination of exercise and cognitive behavioural therapy improves the symptoms of chronic widespread pain, which includes fibromyalgia.

How Does ME Affect My Life - By Jodi Bassett

2009-08-14T19:03:00.004+10:00

The creator of the sight A Humming Birds Guide speaking about having ME and how it has affected her life.

ME: Proof That It Isn't All In The Mind?

2009-06-08T11:46:00.002+10:00

Source - UK Daily Telegraph

Belgian doctors, Professor Kenny De Meirleir and Dr Chris Roelant, have developed a simple test that, they claim, solves the mystery of 'yuppie flu'.

Anna's deterioration was rapid and unrelenting. One moment the pretty, young Scandinavian woman was at the peak of youthful vitality, newly married and excited about the future. The next, that future was much diminished, her life limited to the environs of her bedroom, and dictated to by the illness that had overwhelmed her.

It had started with persistent fatigue, muscle pain, and a growing sensitivity to light after a honeymoon trip to Mexico in the summer of 2006. By December, she was in a wheelchair. Three months later she was bedridden, her face pale, her features shrunken, barely able to move or talk, and being fed through a naso-gastric tube.

Anna – not her real name as her identity is being protected at the request of her family – was the subject of a short film shown at a conference in London last week. Her case, according to Professor Kenny De Meirleir of the Vrije Universiteit Brussel, Belgium, illustrates the worst ravages of myalgic encephalomyelitis/encephalopathy or ME, also known as chronic fatigue syndrome or post viral fatigue syndrome.

Once it was derided as "yuppie flu" because, following its emergence in the early Eighties, its "typical" victim was, supposedly, a high-achieving young professional. ME was also assumed by many doctors, and much of the public, to be psychosomatic in origin – if it existed at all.

In more enlightened times, ME is now accepted by the World Health Organisation, and Britain's medical royal colleges, as a complex, chronic disease of varying severity characterised by a complex set of symptoms. (In addition to extreme fatigue, and general malaise, there are musco-skeletal symptoms, especially muscle pain, brain and central nervous symptoms, evidence of immune system dysfunction, mood swings, depression etc.) According to the ME Association, there are 250,000 sufferers in Britain.

The debate about the cause of ME continues to flourish at conferences, in journals and on websites: are the symptoms a physical manifestation of a problem in the brain such as a chemical imbalance; is sustained stress or exertion to blame; or is ME the result of abnormal physiological functioning, with an organic cause, such as a viral or bacterial infection, or exposure to a toxic agent?

The answer is crucial because it determines the direction of research funding which has, according to Prof De Meirleir, for too long been skewed in favour of a psychiatric approach. He hopes to change that. After more than 20 years of investigation, and having assessed and treated thousands of patients in Europe and America, Prof De Meirleir, who is an internist at the Himmunitas Foundation in Brussels (a non-profit organisation specialising in chronic immune disorders), believes he has identified a mechanism to explain the development of ME that opens up new treatment options.

In addition, he and his fellow Belgian, Dr Chris Roelant, Chief Operating Officer of the diagnostics company Protea biopharma, have developed a self-diagnosing urine test for ME. If they are correct – and that must be determined by scrutiny of their research and use of the test by other scientists and doctors – then it marks an encouraging breakthrough. The symptoms of ME are wide-ranging and occur in a number of other conditions, so a diagnosis of ME is currently reached only after eliminating other causes. "This test will tell patients that it is not a problem between their ears, but a real physiological problem," insists Dr Roelant.Prof De Meirleir and Dr Roelant have, somewhat controversially, opted to go public with their findings before publication in a peer-reviewed journal. They say this is because of the implications of their research, especially for severely debilitated ME patients. At the Invest in ME conference in London last Friday they also raised the possibility of "transmissability" of the illness in this group of patients – another controversial claim.

Prof De Meirleir has never believed that ME is an "illness of the mind". Exercise physiology was his initial area of expertise and it was in this capacity that he was asked by a psychiatrist to assess some of his patients who were suffering from a mystery illness characterised by extreme fatigue.

"One of them was a banker who started work at 9am and had to finish at 11am because he was so exhausted," says Prof De Meirleir. "He did not appear to be suffering from any psychiatric disorder."

The case ignited the young doctor's interest. During a six-month sabbatical at the University of Pennsylvania in 1990, he heard about the "Lake Tahoe epidemic". In 1984, hundreds of people living in a small town on Lake Tahoe in California succumbed to a flu-like illness. The symptoms, including fatigue, neurological and immunological symptoms, persisted in just under 10 per cent of the population (about 300). This was followed by numerous reports of outbreaks of a similar illness around the world, and persuaded Prof De Meirleir of the likelihood of a causative agent being involved in ME, a fact that has heavily influenced his research interests. Since the early 1990s, he has built up a large clinical practice in Brussels where he sees around 2,000 new patients a year. Antibiotics are a cornerstone of his therapeutic approach, as dictated by his research.

In recent years, and in collaboration with a microbiologist, Dr Henry Butt, and his team at the University of Melbourne, Prof De Meirleir has focused on bacteria in the gastro-intestinal tract. "This is an obvious place to start since 80 per cent of immune system cells are located here," he says. A healthy, functioning gut is colonised by "good" bacteria that aid digestion and contribute to our wellbeing. Many ME patients suffer from multiple intestinal symptoms, and Prof De Meirleir believes that an overgrowth of "bad" bacteria, including enterococci, streptococci and prevotella, is to blame. These bacteria are normally present in very small quantities in a healthy gut, but can initiate a sequence of events leading to the multifarious symptoms of ME if they proliferate. (This research will be published in the journal In Vivo, in July).

These "bad" bacteria produce hydrogen sulphide (H2S)– a gas naturally occurring in the body, where it has several functions – in minute quantities. However, in larger quantities, it is a poisonous gas that suppresses the immune system, and damages the nervous system, according to Prof De Meirleir. (Hydrogen sulphide is produced by some animals in preparation for hibernation because it "shuts down" the body which, in effect, is what occurs in ME.) In addition, Prof De Meirleir described how he believes the gas reacts with metals, including mercury, introduced in minute amounts as contaminants in food. The form of mercury produced after reacting with hydrogen sulphide also disrupts the normal production of energy (known as the Krebs Cycle) by individual cells, and this, he says, would explain the energy shortfall experienced by ME patients.

Normal cellular functioning is inhibited and, over time, this generates damaging free radicals, highly reactive molecules that distort the structure of key proteins, such as enzymes and hormones, necessary for chemical reactions. This results in what Prof De Meirleir calls "aberrant" proteins (or prions), which lead to further symptoms as the body is increasingly compromised, and which he says may play a role in the transmissibility of ME.

The urine test, developed by Prof De Meirleir and Dr Roelant in their privately funded research, detects the presence of hydrogen sulphite metabolites, which they say confirm the presence of abnormal quantities of hydrogen sulphide-producing bacteria. The intensity of the colour change in the urine indicates the severity of the disease progression.

Not every ME patient progresses to its most severe form, says Prof De Meirleir, but the varying symptoms can all be explained by this proposed mechanism for the disease. In the worst cases of ME, he says it can be shown that there is an almost complete eradication of "good" bacteria (such as E. coli), the presence of a high number of "bad" bacteria in stools, metal deposits in tissues, and the presence of aberrant proteins in saliva. "What we have shown is that these patients have an organic disease involving one of the most toxic substances [H2S] that exist," he says.

So what causes the proliferation of harmful bacteria in the first place? There are, he says, many potential triggers ranging from food- borne bacterial (eg salmonella) infections, viruses, and toxins, or mental stress. He says many ME sufferers have a history of gut disorders including gluten and lactose intolerance, which may predispose them to colonisation by enterococci and streptococci.

Anna, the 28-year-old Scandinavian patient, is typical in this respect, he claims; she had gut problems in the past, including possible food poisoning while in Mexico. Her treatment focuses on short courses of antibiotics to decrease the numbers of bad bacteria, treatment with probiotic supplements to help restore the good bacteria, plus vitamin and mineral supplements. "She is improving," says Prof De Meirleir.

ME support groups and the medical profession are now considering Prof De Meirleir's work. However, Sir Peter Spencer, chief executive of Action for ME, welcomed the findings, albeit with a caveat: "It is always heartening to see new developments that might bring hope to the 250,000 people in the UK affected by this horrible illness.

"We look forward to seeing Professor Meirleir's findings published in a peer-reviewed journal so that we can develop a better understanding of this research."

Prof De Meirleir says that helping patients like Anna, of whom he has known many, is what has brought him to this point. "This has preoccupied me for more than 20 years. I told [the psychiatrists] we would find a cause, and I believe we have." There are many ME patients and their families who must hope that he is right.

Awareness About Fibromyalgia Needed

2009-05-18T09:54:00.005+10:00

Taken from ShrevePort Times
Provided by Member Susana
Originally Posted May 12th

Today is the sixth annual National Fibromyalgia Awareness Day. The first Walk of F.A.M.E. (Fibromyalgia Awareness Means Everything) was held in 2008. This year the National Fibromyalgia Association has changed the Walk of Fame to include virtual walkers since some Fibromyalgia sufferers simply can't participate in an organised walk or run. Their symptoms simply don't allow them to exert themselves physically.

Fibromyalgia is a disorder characterised by chronic, body-wide pain, persistent fatigue, chronic headaches, cognitive or memory impairment, low blood pressure, blurred vision, gastrointestinal disorders and non restorative sleep. Instigators include trauma, neurological conditions, neurohormonal changes, autoimmune irregularities and myofascial pain. More than 6 million Americans, 90 percent of them female, suffer with Fibromyalgia, affecting relationships with family members, friends and employers. There is no cure. Effective treatment consists of concerted efforts of educated patients and physicians.

I've joined the cause this year. I was diagnosed with Fibromyalgia in 1989 and have spent some years since in debilitating fashion and some in relative remission. The past seven months have probably been the most difficult for me with Fibromyalgia. The disorder is exacerbated by stress, and I've had quite a bit in the past short while. My husband's grandfather passed away in August, followed by our house burning down in October. A total loss, including losing one of our precious dogs, our boxer, Baby, who saved our lives. Our company's been bought out, and adapting is hard, in addition to fear of downsizing.

I am usually a positive person; I think all my friends would say that I'm one of the most positive people they know, always laughing, always finding the bright lining in things. It is because of this that many people who suffer from Fibromyalgia are misunderstood and believed to be "fine." Many of us don't let the trials and tribulations, the pains of every day, and the impossible fatigue stop us on most days.

The Lyrica commercial leaves much to be desired. It portrays a person who has Fibromyalgia as "not one to lay down and quit" only if they take Lyrica. This is a bad commercial and a bad portrayal of the many of us who suffer from this disorder. Most of us don't lay down and quit any time; on the contrary, we fight to function normally and be considered normal. It's those times when we can't that really get us down, in addition to the perception that we are "fine" because there are no outward signs of the disorder.

Please join me in supporting the cause: Contribute to research at www.fmaware.org. Even if you can't or don't desire to contribute, you can still make a difference by recognising the limitations of those of us who have Fibromyalgia. A little understanding goes a long way.

Disability Pensioner Numbers 'Will Rise'

2009-04-10T11:49:00.001+10:00

The global financial crisis is likely to lead to an increase in the number of people accessing the disability support pension, the federal government says.

Parliamentary secretary for disabilities Bill Shorten says growth in the number of people accessing the disability support pension has been greater than in any other pension category in the 10 years to 2007.

Between 1996 and 2007, the number of disability support pensioners increased from 499,000 to about 725,000, he said.

"In these difficult economic circumstances, yes, I think it will go up again," he said following an address at the National Press Club on Wednesday.

The government wants to develop a national plan to get more people with disabilities into the workforce and off the pension.

But Mr Shorten said there was concern that workers with disabilities could be the first to lose their jobs during the financial crisis.

"Maybe's there a temptation amongst some employees to say, 'well people with disabilities should be the first to be, metaphorically, thrown overboard'."

"That's not appropriate," he said.

Mr Shorten said jobs for people with disabilities in areas like gardening and manufacturing were at risk, as well as services provided by the not-for-profit sector, which relies heavily on grants from the business sector.

Sean Fitzgerald, a 38-year-old quadriplegic, has helped businesses access the necessary technology to employ disabled workers for years.

He wants businesses to be required to take on a percentage of disabled workers, and adequate government funding to make this possible.

"People with a disability provide more than just productivity and a bum in a seat in a business, they provide a level of diversity and understanding," he told AAP.

"It is very difficult for an employee to spend their life bitching about the boss when they're sitting next door to someone who has obviously got so much more to deal with in life."

The federal government took delivery two weeks ago of a review of pensions by the head of the Families Department, Jeff Harmer.

Details of the review are yet to be released, but Families Minister Jenny Macklin earlier this week guaranteed disability support pensioners, as well as some other pensioners, would receive a boost in their fortnightly payments in the May budget.

Disability support pensioners receive up to $569.80 a fortnight. It's expected that will be lifted by up to $30 a week.

Source - Sydney Morning Herald

Found by Member: Gypsy

Probiotic May Ease Fatigue Syndrome Anxiety

2009-04-09T14:39:00.000+10:00

Taking a daily probiotic supplement appears to improve anxiety in patients with chronic fatigue syndrome, new Canadian research suggests, a finding that might one day impact how depression and other mental disorders are treated.

The researchers, led by A. Venket Rao of the University of Toronto, found that giving patients with chronic fatigue syndrome (CFS) a probiotic for two months not only boosted so-called "good" bacteria in their stomachs, it also led to a significant decrease in their anxiety symptoms.

A probiotic is a dietary supplement, most often in pill or powder form, that contains live bacteria such as Lactobacillus or Bifidobacteria. These bacteria help maintain gut flora, microbes in the stomach that perform a variety of functions, including aiding digestion, boosting the immune system and warding off harmful bacteria. "We were quite excited with the fact that these were positive results and we felt that probiotics truly have a role to play in the management of neurophysiological disorders such as anxiety, such as depression and other symptoms associated with that," Rao told CTV News. "Rather than going into medications, which may result in side effects, it's a safe, it's a very easy way to manage problems such as that."

The findings are published in the journal BMC Gut Pathogens. Patients who are diagnosed with CFS often experience a broad range of symptoms, the most significant being persistent fatigue.

Nearly all CFS patients also experience neuropsychological problems, such as cognitive dysfunction, sleep disturbances, anxiety and depression. In fact, according to the researchers, about half of all CFS patients meet the diagnostic criteria for an anxiety disorder or major depressive disorder. As well, CFS patients often complain of gastrointestinal problems and many are diagnosed with digestive disorders such as irritable bowel syndrome. Tests show that they often have lower levels of so-called "good" bacteria in their stomachs, which can regulate digestive activity.

All of this has led researchers to begin probing a link between gut bacteria and mental disorders and early findings suggest that bacteria levels may influence behaviour related to anxiety and depression. Researchers believe that probiotics "crowd out" the more toxic stomach bacteria that are linked to an increase in depression and other mood disorders, study co-author Dr. Alison C. Bested told CTV News.

For this study, Rao, Bested and their team gave 39 CFS patients either a daily dose of Lactobacillus casei or a placebo for two months. They found that 73 per cent of subjects taking the probiotic experienced an increase in levels of Lactobacillus and Bifidobacteria in the gut, which corresponded with a significant decrease in anxiety symptoms.

In the placebo group, only 37.5 per cent showed an increase in Bifidobacteria, while only 43.8 per cent showed an increase in Lactobacillus bacteria. The researchers found no statistically significant change in anxiety symptoms among this group. According to Bested, Bifidobacteria appears to increase levels of tryptophan in the brain, a chemical that "helps people feel better." Patients taking the probiotic also showed a marked improvement in their digestion, experiencing less bloating and gas and a reduction in inflammation. The findings are "huge," Bested said. "(Subjects) felt less anxious, they felt calmer, they felt better able to cope with their illness, they were sleeping better, had less heart palpitations and less symptoms of anxiety," she said. "We were pleasantly surprised, that people who were taking probiotics were able to lower their anxiety." Rao explained that the good bacteria produce "compounds that get to the brain and help the brain to manage problems associated with behavioural and mood problems, such as anxiety and depression."

He said the findings open "a door to a whole new field, and that is the relationship of gut micro flora, or gut bacteria, to many disorders - mental disorders being one of them. So it opens a door to many future research and applications in this area."
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(c) 2009 Bell Canada

Source

Forum URL Change

2009-03-30T10:01:00.002+11:00

Recently Proboards (the people who host the forum) have upgraded the forum's url by taking out the number

So instead of the old url with the number in it - cfsandfmshelp.proboards84.com

It is now cfsandfmshelp.proboards.com so if you have the forum bookmarked or are linked to it from your website/blog it would be best to upgrade it. The old url should redirect you to the new one but it's best to update it just in case.

Bonnie

Neuropsychological Performance in Persons With ME

2009-03-28T10:57:00.000+11:00

Neuropsychological Performance in Persons With Chronic Fatigue Syndrome: Results From a Population-Based Study

Objective: To examine the neuropsychological function characterised in subjects with chronic fatigue syndrome (CFS) at the same time controlling for relevant confounding factors. CFS is associated with symptoms of neuropsychological dysfunction. Objective measures of neuropsychological performance have yielded inconsistent results possibly due to sample selection bias, diagnostic heterogeneity, co-morbid psychiatric disorders, and medication usage.

Method: CFS subjects (n = 58) and well controls (n = 104) from a population-based sample were evaluated, using standardised symptom severity criteria. Subjects who had major psychiatric disorders or took medications known to influence cognition were excluded. Neuropsychological function was measured using the Cambridge Neuropsychological Test Automated Battery (CANTAB).

Results: Compared with controls, CFS subjects exhibited significant decreases in motor speed as measured in the simple and five-choice movement segments of the CANTAB reaction time
task. CFS subjects also exhibited alterations in working memory as manifested by a less efficient search strategy on the spatial working memory task, fewer % correct responses on the spatial recognition task, and prolonged latency to a correct response on the pattern recognition task. A significantly higher percentage of CFS subjects versus controls exhibited evidence of neuropsychological impairment (defined by performance 1 standard deviation below the CANTAB normative mean) in tasks of motor speed and spatial working memory. Impairment in CFS subjects versus control subjects ranged from 20% versus 4.8% in five-choice movement time (p = .002) to 27.8% versus 10.6% in search strategy on the spatial working memory task (p = .006).

Conclusions: These results confirm and quantify alterations in motor speed and working memory in CFS subjects independent of co-morbid psychiatric disease and medication usage.

For a more in depth read of the research click here (PDF)
Source - Co-Cure.org

Lower Ambulatory Blood Pressure in ME/CFS

2009-03-23T19:49:00.004+11:00

Journal: Psychosom Med. 2009 Mar 17. [Epub ahead of print]
Authors: Newton JL, Sheth A, Shin J, Pairman J, Wilton K, Burt JA, Jones DE.
Affiliation: Institute for Cellular Medicine, University of
Newcastle, Newcastle-upon-Tyne, United Kingdom.
NLM Citation: PMID: 19297309

Objective: To examine blood pressure circadian rhythm in subjects with chronic fatigue syndrome (CFS) and appropriate normal and fatigued controls to correlate parameters of blood pressure regulation with perception of fatigue in an observational cohort study. The cause of CFS remains unknown and there are no effective treatments.

Methods: To address whether inactivity was a confounder, we performed a 24-hour ambulatory blood pressure monitoring in the following three subject groups: 1) CFS patients (Fukuda Diagnostic criteria) (n = 38); 2) normal controls (n = 120); and 3) a fatigue comparison group (n = 47) with the autoimmune liver disease primary biliary cirrhosis (PBC). All patients completed a measure of fatigue severity (Fatigue Impact Scale). In view of the different demographics between the patient groups, patients were age- and sex-matched on a case-by-case basis to normal controls and blood pressure parameters were compared.

Results: Compared with the control population, the CFS group had significantly lower systolic blood pressure (p < .0001) and mean arterial blood pressure (p = .0002) and exaggerated diurnal variation (p = .009). There was a significant inverse relationship between increasing fatigue and diurnal variation of blood pressure in both the CFS and PBC groups (p < .05). Conclusion: Lower blood pressure and abnormal diurnal blood pressure regulation occur in patients with CFS. We would suggest the need for a randomized, placebo-controlled trial of agents to increase blood pressure such as midodrine in CFS patients with an autonomic phenotype.

Source: Co-Cure.org
Posted @ Forum by Upnorth

A Sudden Ilness by Laura Hillenbrand -Edited

2009-02-26T10:45:00.006+11:00

*due to brain fog I gave the author the wrong name, this post has been rectified

How My Life Changed

We were in Linc's car, an aging yellow Mercedes sedan, big and steady, with slippery blond seats and a deep, strumming idle. Lincoln called it Dr. Diesel. It was a Sunday night, March 22, 1987, nine-thirty. Rural Ohio was a smooth continuity of silence and darkness, except for a faintly golden seam where land met sky ahead, promising light and people and sound just beyond the tree line.

We were on our way back to Kenyon College after spring break. Linc, my best friend, was driving, his arm easy over the wheel. My boyfriend, Borden, sat behind him. I rode shotgun, a rose from Borden on my lap. Slung over my arm was a 1940s taffeta ball gown I had bought for $20 at a thrift shop. I was 19.

The conversation had dropped off. I was making plans for the dress and for my coming junior year abroad at the University of Edinburgh. My eyes strayed along the right shoulder of the road: a white mailbox, the timid glint of an abandoned pick-up's tail-light. The pavement racing under the car was gunmetal gray. We were doing 50 mph or so. A balled-up bag from a drive-through burger joint bumped against my ankle.

A deer.

At first, he was only a suggestion of an animal, emerging from the darkness by degrees: a muzzle, a sharp left eye. Then the headlights grasped him.

He was massive -- a web of antlers over his head, a heavy barrel, round haunches lifting him from the downward slope of the highway apron. Briefly, his forehooves rested on the line between the shoulder and the highway. I saw his knee bending, the hoof lifting: he was stepping into the car's path.

In the instant that I spent waiting for the deer to roll up over the car's hood and crash through the windshield I was aware of my body warm in the seat, Linc's face lit by the dash, Borden breathing in the back, the cool sulfur glow of the car's interior, the salty smell of the burger bag. I watched the deer's knee and waited for it to straighten. I drew a sharp breath.

The bumper missed the deer's chest by an inch, maybe two. The animal's muzzle passed so close that I could see the swirl of hair around his nostrils. Then he was gone behind us.

I blinked at the road. My eyes caught something else. A brilliant light appeared through the top of the windshield and arced straight ahead of the car at terrific speed. It was a meteor. It burned through the rising light of the horizon and vanished in the black place above the road and below the sky.

My breath escaped in a rush. I turned toward Linc to share my amazement. He was as loose as he had been, his eyes slowly panning the road, his long body unfolding over the seat. I looked back at Borden and could just make out his face. They had seen nothing.

I was about to speak when an intense wave of nausea surged through me. The smell from the bag on the floor was suddenly sickening. I wrapped my arms over my stomach and slid down in my seat. By the time we reached campus, half an hour later, I was doubled over, burning hot, and racked with chills. Borden called the campus paramedics. They hovered in the doorway, pronounced it food poisoning, and left...more

Laura Hillenbrand is the author of Seabiscuit (eventually made into a movie). Thanks for fellow butterfly Upnorth for finding the link and sharing it.

Problems Accessing The Forum

2009-02-06T13:49:00.002+11:00

I don't know how long this has been going on but I have noticed this isn't rare lately.

Earlier I tried to access another forum (on the same server) and rather then going directly to it I was shown an Invalid URL page. Something I thought was a tad odd seeing as I'd only been on the forum about an hour beforehand.

I've checked out the Proboards Support forum to see if anyone else had the same problem and apparently they have. I don't know if it has anything to do with updates to the servers etc but I found a solution.

If you ever have this problem try the address without the number. Have it as http://cfsandfmshelp.proboards.com instead of with the 84. Works fine after that.

If at any time you have trouble accessing the forum please let me know by either leaving a message here or emailing me at bluebutterflyforum@gmail.com

Otherwise if you have any questions and can access the forum there is a thread to post in.

Thank you
Bonnie

ME/CFS and mitochondrial dysfunction

2009-01-22T14:33:00.004+11:00

Source Link

PDF Warning for foggy, spoon (energy) limited individuals - this is a long research piece (16 pages). Warning for you to prepare, rather then opening it, seeing how big it is and being turned off.

In the meantime I will try to find if there is somewhere it is online for those who can't download PDFs.

Abstract: This study aims to improve the health of patients suffering from chronic fatigue syndrome (CFS) by interventions based on the biochemistry of the illness, specifically the function of mitochondria in producing ATP (adenosine triphosphate), the energy currency for all body functions, and recycling ADP (adenosine diphosphate) to replenish the ATP supply as needed. Patients attending a private medical practice specializing in CFS were diagnosed using the Centers for Disease Control criteria. In consultation with each patient, an integer on the Bell Ability Scale was assigned, and a blood sample was taken for the “ATP profile” test, designed for CFS and other fatigue conditions. Each test produced 5 numerical factors which describe the availability of ATP in neutrophils, the fraction complexed with magnesium, the efficiency of oxidative phosphorylation, and the transfer efficiencies of ADP into the mitochondria and ATP into the cytosol where the energy is used. With the consent of each of 71 patients and 53 normal, healthy controls the 5 factors have been collated and compared with the Bell Ability Scale. The individual numerical factors show that patients have different combinations of biochemical lesions. When the factors are combined, a remarkable correlation is observed between the degree of mitochondrial dysfunction and the severity of illness (P<0.001). Only 1 of the 71 patients overlaps the normal region. The “ATP profile” test is a powerful diagnostic tool and can differentiate patients who have fatigue and other symptoms as a result of energy wastage by stress and psychological factors from those who have insufficient energy due to cellular respiration dysfunction. The individual factors indicate which remedial actions, in the form of dietary supplements, drugs and detoxification, are most likely to be of benefit, and what further tests should be carried out.

Co-enzyme Q10 distribution in blood is altered in patients with Fibromyalgia

2009-01-14T10:20:00.001+11:00

Source

OBJECTIVE: Co-enzyme Q10 (CoQ(10)) is an essential electron carrier in the mitochondrial respiratory chain and a strong antioxidant. Signs and symptoms associated with muscular alteration and mitochondrial dysfunction, including oxidative stress, have been observed in patients with fibromyalgia (FM). The aim was to study CoQ(10) levels in plasma and mono nuclear cells, and oxidative stress in FM patients.

METHODS: We studied CoQ(10) levels by HPLC in plasma and peripheral mono nuclear cells obtained from patients with FM and healthy control subjects. Oxidative stress markers were analysed in both plasma and mono nuclear cells from FM patients.

RESULTS: Higher level of oxidative stress markers in plasma was observed respect to control subjects. CoQ(10) level in plasma samples from FM patients was doubled compared to healthy controls and in blood mononucleosis isolated from 37 FM patients was found to be about 40% lower. Higher levels of ROS production was observed in mono nuclear cells from FM patients compared to control, and a significant decrease was induced by the presence of CoQ(10).

CONCLUSION: The distribution of CoQ(10) in blood components was altered in FM patients. Also, our results confirm the oxidative stress background of this disease probably due to a defect on the distribution and metabolism of CoQ(10) in cells and tissues. The protection caused inmononuclear cells by CoQ(10) would indicate the benefit of its supplementation in FM patients.

Normalisation of leaky gut in ME/CFS

2009-01-04T13:28:00.001+11:00

Article Source

Normalisation of leaky gut in chronic fatigue syndrome (CFS) is accompanied by a clinical improvement: effects of age, duration of illness and the translocation of LPS from gram-negative bacteria.
Journal: Neuro Endocrinol Lett. 2008 Dec 29;29(6). [Epub ahead of print]
Authors: Maes M, Leunis JC.
Affiliation: M-Care4U Outpatient Clinics, and the Clinical Research Center for Mental Health, Belgium. NLM Citation: PMID: 19112401

BACKGROUND: There is now evidence that an increased translocation of LPS from gram negative bacteria with subsequent gut-derived inflammation, i.e. induction of systemic inflammation and oxidative & nitrosative stress (IO&NS), is a new pathway in chronic fatigue syndrome (CFS).

METHODS: The present study examines the serum concentrations of IgA and IgM to LPS of gram-negative enterobacteria, i.e. Hafnia Alvei; Pseudomonas Aeruginosa, Morganella Morganii, Pseudomonas Putida, Citrobacter Koseri, and Klebsielle Pneumoniae in CFS patients both before and after intake of natural anti-inflammatory and anti-oxidative substances (NAIOSs), such as glutamine, N-acetyl cysteine and zinc, in conjunction with a leaky gut diet during 10-14 months. We measured the above immune variables as well as the Fibromyalgia and Chronic Fatigue Syndrome Rating Scale in 41 patients with CFS before and 10-14 months after intake of NAIOSs.

RESULTS: Subchronic intake of those NAIOSs significantly attenuates the initially increased IgA and IgM responses to LPS of gram negative bacteria. Up to 24 patients showed a significant clinical improvement or remission 10-14 months after intake of NAIOSs. A good clinical response is significantly predicted by attenuated IgA and IgM responses to LPS, the younger age of the patients, and a shorter duration of illness (< 5 years).

DISCUSSION: The results show that normalization of the IgA and IgM responses to translocated LPS may predict clinical outcome in CFS.

The results support the view that a weakened tight junction barrier with subsequent gut-derived inflammation is a novel pathway in CFS and that it is a new target for drug development in CFS. Meanwhile, CFS patients with leaky gut can be treated with specific NAIOSs and a leaky gut diet.

ME/CFS Blood Test On The Horizon

2008-12-22T20:11:00.002+11:00

Source
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 http://www.wpinstitute.org/.

CFIDS Association Research Grants Raise Hope

2008-12-09T20:18:00.003+11:00

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.

Create A Story II

2008-11-01T12:02:00.002+11:00

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!"

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

2008-10-29T15:39:00.001+11:00

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.

Create A Story I

2008-10-11T10:52:00.004+11:00

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.

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

2008-09-25T20:12:00.001+10:00

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
dysfunction.

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
production.

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.

References
[1] Blackstone Eric, Morrison Mike, Roth Mark B. H2S induces a suspended
animation-like state in mice. Science Magazine 2005;308(5721):518.
doi:10.1126/science.110858.
[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

Announcment: Live Chat Session

2008-09-05T10:50:00.006+10:00

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

Zombie Science In ME/CFS

2008-08-21T02:00:00.001+10:00

From mecfswa.org.au 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.

(http://www.b-eat.co.uk/Supportingbeat/MediaResearch/Socialcognitioninanorexianervosa )

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
weaknesses".

"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
sustained".

"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
head.

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

Antiviral Drug Under FDA Review For ME/CFS

2008-08-19T10:41:00.003+10:00

An interesting piece of news I came across on Immunesupport.com - 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

What Is Fibromaylgia?

2008-08-16T20:09:00.004+10:00

(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.

First Post & What Is ME/CFS

2008-08-06T12:10:00.005+10:00

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
Bonnie