Hope for CFS

If you have CFS, please don’t think things look entirely hopeless.

Doctors will tell you "no treatment, no cure", but they’re only half-right ... there’s no FDA-approved treatment, but there are things that they can do to help you. First, they need to address your symptoms with appropriate medication. If you’re vomiting, then anti-nausea medication; if you’re dizzy, then anti-vertigo medication, etc.

My first relapse was Thanksgiving 1987. By late Spring 1988, I was back to work full-time, and stayed at work full-time till February 2000. I won’t say it was easy – there were a lot of times that all I did was work/commute/sleep, but a doctor who knew what he was doing was able to get me back to work full-time for 12 years. That was 12 extra years to build up the monthly amount of my Disability benefits, 12 extra years to save for retirement, 12 extra years of not being stuck in the house 99% of the time.

His theory was that if you improved the quality of sleep, the body would begin to heal itself and then you could see what symptoms remained to be treated pharmaceutically.

Although CFS is not caused by insomnia, like any other health problem it can be made worse by not sleeping well. If you’re having trouble sleeping because of pain, then pain pills and/or sleeping pills will improve the quality of your sleep. Instead of drifting in light Stage 1 sleep for 20 hours, which is the "unrefreshing sleep" most patients complain of, you’ll get down to deep Stage 4 sleep, where healing occurs. After several months on effective sleeping pills, I suddenly developed a 101 fever. After a week, I was concerned that it didn’t go away and asked a friend who’s a nurse practitioner. She responded "Congratulations, you have an immune system again!" Good sleep had strengthened my immune system to the point that it could attack the virus. I ran a fever for six months, and when it was over, I felt better than I had in a long time. Although I backslid when I could no longer get those sleeping pills and was no longer sleeping well, I never got as bad as I had been before, because I now have a functioning immune system again to keep the virus in check.

Dr. Montoya at Stanford is having good luck with an anti-viral medication, but the stuff he’s using costs over $1000 a month. A member of my support group talked to her doctor about it, who suggested that Valtrex is almost the same thing, for only $200 a month, try that first, and if it doesn’t work, then move up to the more expensive stuff. Just like Dr. Montoya’s patients, she had a period of feeling even worse for several weeks, as the medication did its work, and then started to improve – she’s now back to work!

Dr. St. Amand has a popular therapy for fibromyalgia, which would seem to make sense for CFS, too. His theory is that guaifenesin (the stuff in cheap cough syrup and Mucinex) releases the toxins from the tissues. Like Dr. Montoya’s therapy, you’ll feel worse at first, with all those loose toxins running around looking for a way out.

Personally, I combined guaifenesin with triple-digit days and my grandfather’s old-fashioned sweat therapy: take a hot bath at bedtime, immediately followed by chugging a hot beverage (he preferred mulled wine, I used hot tea to wash down my guai pills), then immediately wrap up in every blanket in the house and sweat it out. And, boy, did I ever. Do laundry right before you start this ... I woke up every morning with my sleep shirt stinking to high heaven. I couldn’t stand to leave it on for one minute more than necessary. It wasn’t a good clean healthy sweat smell: it reeked nauseatingly, which indicated to me that those nasty toxins really were coming out as promised, and in massive quantities. Every night, I had to put on a different sleep shirt because I couldn’t wear the same one a second night, and the sheets needed changing a lot more often than usual, but the end result was worth it.

Dr. Murphree (www.DrRodger.com) told me that for every year of deterioration, you need at least one year of recuperation. So, don’t get frustrated if you’re not up to running marathons right away; at the earliest, I should expect to reach maximum improvement in 2010-2012 (and, no, I didn’t run marathons when I was well, so I don’t expect to be able to run one in 2015 – I don’t need to be SuperCrip, I just want to get back to work in the career I loved).

Nonetheless, compared to where I was in 2000-2002, when no one was giving me any useful treatment, I can see that I’ve made big strides: I’m no longer spending 24 hours a day lying in the middle of the bed hoping that I won’t pass out. I can sit up without immediately getting dizzy and needing to lie down. I can go out a couple hours two days a week without making myself worse (but three days is too much), a vast improvement when a quick trip to the doctor 4 blocks away sent me to bed the rest of the week. The digestive problems that used to plague me on a daily basis are now down to a couple times a week – still annoying, but no longer overwhelming: my life doesn’t revolve entirely around running to the bathroom. I can work more hours, more reliably – we’re a long way from the end of 2000 where I could manage only 5 minutes per hour.

Knowing what was recommended to my friend with polio for hand/arm problems from overuse, I tried the same thing: it’s not "use it or lose it" but "conserve to preserve". My hands work better if I don’t do too much. Whether it’s stitching/knitting/typing/chopping vegetables, I know when to stop and take a break so that I don’t reach the point of complete muscle failure. You don’t need a doctor for that quick-fix, only your own sense of observation of how much is too much.

In addition, there have been great strides made in research. While some government-funded researchers are still clinging to the disproven notion that the problem is entirely psychological, privately-funded research has found genetic abnormalities, a virus that’s also found in MS patients, and similarities to polio. Once they know what causes it, they can quickly work on a test, and a cure (or at least a treatment to minimize the symptoms).

Until then, find a doctor open-minded enough to experiment and think outside the box. The physician assistant I’m now seeing has a brother with MS; he sees the same symptoms, unlike someone who has only read about them in a book he knows I’m not exaggerating about how severe they can be, and prescribes for me what the MS specialist is prescribing to his brother for the same symptoms. Problem solved.

Media Information on Invisible Illness Awareness Week

Links to share with your favorite media people -- think about who you know who works in radio, TV or print journalism and send them a personalized note.

 

Dear Media Representative:

Thank you for taking the time to find out more about National Invisible Chronic Illness Awareness Week (NICIAW).We hope you will find helpful information to write your article, conduct your interview. If you have a specific question for our readers, we are happy to refer people to you.

For further information, please contact Lisa directly at: lisa@invisibleillness.com . She's happy to answer your questions or point you toward additional resources or information.

NEWS RELEASES Who Hates to Hear They Look Great? Over Half of the Chronically Ill! Our Site | Distribution site Word documents to alter/send to others: Regular release | Christian slant AUGUST 2007 (#1) The Chronically Ill Are Tired of Casseroles: New Book shares 505 ways to encourage a chronically ill friend Our site | Distribution site

• Fact Sheet about Chronic Illness & Rest Ministries, the week's sponsor
• Read more about Lisa Copen, founder of NICIAW, radio programs she has been on, books she has authored, and more.
• Download print-quality logo (high, med and low resolutions)
• Download general 5.5 x 8.5 postcard "brochure" - view card (pdf)
• Download poster (5.5 x 8.5)
• NICIAW Week promotional items
• See "articles to read"

Other dates to be aware of:
September is Pain Awareness Month -Visit the Partners for Understanding Pain portal, available on the American Chronic Pain Association’s web site at www.theacpa.org

• National Courtesy Month; September; 702-386-9115
• National Shut-in Visitation Day; October 13; 215-374-2930
• Make a Difference Day; October 21; 703-276-6445
• Sweetest Day (act of unselfishness); October 21; 810-362-3223
  

Other resources of interest:

• 2002 US Census Bureau- Americans With Disabilities: 2002
• Easing the Burden of Chronic Illness for Communities of Color: 20 pages
• Chronic Care in America: A 21st Century Challenge Revised in September 2004, it provides an overview of chronic health conditions in the United States and the impact of these conditions on individuals and their caregivers, as well as on the U.S. health care system. 68 pages
• Cornucopia Of Disability Information - Including Statistics

Invisible Illness Awareness Week 9/8-14

http://www.sbwire.com/news/view/20924

Invisible Illness Awareness Week Unites Thousands Who Get it

Posted: Wednesday, August 27, 2008

Living with an invisible illness can cause heartache and bitterness when one
feels no one understands the significance of the illness. Invisible Illness
Week provides that validation that people with invisible diseases often
seek.


San Diego, CA -- (SBWIRE) -- 08/27/2008 -- While we assume that most people
are generally healthy, you may be surprised to find out that an alarming
nearly 1 in 2 people in the United States live with a chronic illness. So
why is it that most of us don't even know when a friend or co-worker is
dealing with diabetes, heart disease, lupus, or chronic fatigue syndrome?
Because, according to the U.S. Census, about 96% of people have invisible
illnesses.

National Invisible Chronic Illness Awareness Week is being held this year,
September 8-14, 2008. It's a secular event sponsored by Rest Ministries, the
largest Christian organization that serves the chronically ill. Visit the
invisible illness awareness campaign's web site at
www.invisibleillnessblog.org  . You can be encouraged through dozens of
articles, including daily guest bloggers, find ideas to get involved in the
outreach, and goodies to help promote awareness, from silicone bracelets to
brochures. Tired of those looks when you park in a handicapped spot? Be sure
to pick up a license plate or bumper sticker.

The focal point of the awareness campaign is September 8-12 (M-F) during
which 20 telephone seminars will be held on a variety of topics and are open
to anyone. Topics may also be of interest to those with loved-ones who have
an illness. Some seminars include:

- Assess Yourself: Find the Job You Desire and Can Do Despite Illness
Limitations

- The Civil Rights of Patients with Invisible Chronic Illnesses

- Overcoming Self-Defeating Behaviors

- Secrets of Paying for Medical Care

How to Get Paid to Blog

- After the Diagnosis: The Journey Beyond

The theme this year is "Hope Can Grow From The Soil of Illness."

Lisa Copen, 39, began National Invisible Chronic Illness Awareness Week in
2002 as she continuously witnessed hundreds of people emotionally hurting
just because they felt as though no one "got it." Lisa has lived with
rheumatoid arthritis and fibromyalgia for fifteen years and understands how
validating it can be to just have one friend who you don't have to explain
everything to.

"Though there are hundreds of illnesses represented, and large differences in symptoms and pain levels, none of that matters more than feeling like someone understands you. When our best friends and family members are skeptical about our disease, it can be that last straw that sets us off into a spiraling depression."

She says, "We plan to unite the millions of people who live with chronic
pain and illness by offering an oasis of hope and understanding, as well as
helpful information and practical tools to live the best life possible."

Through the guest bloggers of Invisible Illness Week, to 20 seminars that
supply tools to ensure that one is cared for--both body and soul--National
Invisible Chronic Illness Awareness Week is succeeding in meeting that goal.


Find out more information and receive daily updates at
http://www.invisibleillnessblog.org


Media Relations Contact
Lisa Copen
Director
National Invisible Chronic Illness Awareness Week
888-751-7378
http://www.invisibleillness.com


Related Links
Action Web Link Description
Visit National Invisible Chronic Illness Awareness Week's Press Room
http://www.restministries.org/invisibleillness/invisibleillnesshome.htm
        

Severe ME

Severe ME in Britain by Greg Crowhurst

(May be Reposted)

Dominated by the overarching influence of the psychosocial model of the illness, which emphasises "beliefs, coping styles, and behaviours" , this "elephant in the room", according to Neil Abbot, Director of ME Research UK (2007) colours the perception of Myalgic Encephalomyelitis (ME) right across the board in the UK from the 2007 NICE Guideline, to the policy of government agencies such as the Department of Work and Pensions and NHS Plus, leading to wrongful assumptions such as :

Cognitive Behaviour Therapy (CBT) and Graded Exercise are an effective cure for ME.

that those unable or refusing to participate in inappropriate psychiatric "treatment" regimes or who are not getting better following them, are somehow inadequate and at fault.

or that people with ME do not have the right thought processes or the correct attitude to getting better/returning to work.

Severe ME patients are simply dismissed or abandoned without support (Hooper et al 2005), for there is no appropriate biomedical NHS treatment facility anywhere for patients in the UK.

A national survey, conducted by the author for the 25% Severe ME Group and presented at the Gibson Parliamentary Inquiry (2006) "presented shocking evidence of the abuse of severe ME patients at the hands of the UK "psychiatric lobby". Members reported being locked in secure psychiatric wards or AIDS units and their lack of response to "treatment" being taken as an indication of their misguided thinking". (Greg and Linda Crowhurst 2007)

Crawford, Aitken and McCagh (2008) recently found that UK nurses still respond more positively to patients with Multiple Sclerosis and Rheumatoid Arthritis than patients with ME/CFS, which they are more likely to wrongly view as a psychological disorder. Nurses also report low levels of training and confidence in their skills when working with patients who have ME/CFS.

Background

The disease, which can occur in both sporadic and epidemic forms (Jenkins 1991) has been described in the medical literature for about 70 years. Over 4,000 papers have been published, documenting the biomedical abnormalities found in ME/CFS (CDC 2006) There are an estimated 62, 500 people with severe ME/CFS in the UK receiving "seriously inadequate health care" according to the Chief Medical Officer (DH 2002).

Since 1969 ME/CFS has been classified as a neurological disorder by the World Health Organisation. ME/CFS was recognised as a specific disease entity by The Royal Society of Medicine in 1978 and as an organic disorder by the Department of Health in 1987 (Hansard 1987). ME is included in the National Service Framework (DH 2004) as a long-term neurological condition. The terms 'fatigue' and 'chronic fatigue' were not associated with this disease at all until the name was changed from ME to Chronic Fatigue Syndrome (CFS) in 1988 in the US . In 1988, following a spectacular increase in cases in the US, the term "chronic fatigue syndrome" (known as "CFS") was introduced and doctors were encouraged to lump together all cases of "chronic fatigue" of whatever origin and to regard them as one syndrome. The Fukuda criteria drawn up in 1994 by the United States centre for Disease Control and Prevention (CDC), has become internationally accepted. However the CDC criteria, were primarily intended for research purposes and not for clinical definition. Because the CDC emphasises fatigue as the sole compulsory criterion, it has attracted criticism for allowing disparate fatigue conditions, for example post-traumatic stress disorder, depression and conditions that improve with exercise to be diagnosed as ME; the CDC definition is increasingly viewed as being too broad and indistinct to be useful.

Few of the 18 members who drew up the CDC criteria had either looked at an epidemic of the illness (there have been over seventy around the world) or examined any patients with the illness. The three most experienced members of the board refused to sign the final document. With very few exceptions the remaining members never published on ME/CFS again.

A common misapprehension is to confuse ME with Chronic Fatigue and then treat them both as mental health conditions. ME/CFS, a neurological condition should not be confused with Chronic Fatigue. Chronic Fatigue is classified by the World Health Organisation in ICD-10 as F48 (a mental disorder), whereas ME/CFS is classified as an organic neurological disease under ICD code G93.3. Despite fatigue being seen in mental health disorders, it is important not to confuse ME as a mental health disorder. Hyde (2003), for example, found that less than 5% of ME/CFS sufferers "have any significant psychiatric illness. " There is no published evidence whatsoever, as opposed to opinion, that ME (as distinct from chronic fatigue) is a psychiatric disorder. (Williams 2004). Unlike somatisation disorder, M.E. is not ‘medically unexplained.’ M.E. is a multi-system disease with many organ and bodily systems affected, producing a myriad of symptoms [and] many aspects of the pathophysiology of the disease have, indeed, been medically explained in volumes of research. (ME Society of America) ME/CFS, the neurological condition, differs from the mental illness Chronic Fatigue in:

The epidemic characteristics

The known incubation period

The acute onset

The associated organ pathology, particularly cardiac.

Infrequent deaths with pathological central nervous system (CNS) changes.

Neurological signs in the acute and sometimes chronic phases.

The specific involvement of the autonomic nervous system.

The frequent subnormal patient temperature.

The fact that chronic fatigue is not an essential characteristic of the chronic phase of ME. (Hyde 2003)

Cheney, Bassett (2004) found that in dual chromatography analyses, many ME/ICD-CFS patients actually had more derangement of the brain, on a biochemical level, than Parkinson's or Alzheimer's patients.

ME/CFS is not "cured" by Cognitive Behavioural Therapy (CBT) and Graded Exercise (GET). CBT and GET are potentially harmful to anyone with neurological ME. The Chief Medical Officer (2002) has warned that exercise-based regimes advocated for less severely affected patients tend not to have been studied among those most severely affected. Cycles of severe relapse are common in ME as are further symptoms developing over time. "Substantial improvement is uncommon and is less than 6%" (Anderson et al. 2004); and, "Full recovery... is rare" (Cairns & Hotopf, 2005). The aetiology and pathogenesis of ME/CFS are not fully understood (Crowhurst 2005) Although there is as yet no single test which can diagnose the condition, there is, as Bassett (2004) explains, "an abundance of research which shows that it is an organic illness which can have profound effects on many bodily systems and many aspects of the pathophysiology of the disease have, indeed, been medically explained in volumes of research articles.

The Experience of Severe ME/CFS

It is not 'fatigue' or 'tiredness' that is the one essential characteristic of ME/CFS but central nervous system (CNS) dysfunction (Bassett 2006). Bell (1995) describes the word "fatigue" as: 'A very inappropriate term for what patients experience. It's not really fatigue at all, which is defined as a normal recovery state from exertion and that is precisely what does NOT happen in this illness". Everyday life for the severe ME sufferer is a perpetual struggle. As Owen (2007) points out the most severely affected may not be able to speak, eat, swallow, open their bowels. They may not be able to sit up or move themselves, they may be too exhausted to dress or wash . The sound of running water may be too much for them to bear, they may not be able to open their mouth to brush their teeth. Crowhurst L. (2007) describes how : "Having severe ME is unimaginable; the experience is so different, intense and unremitting than anything I have ever experienced before. I am never unaware of the range of symptoms that rage through my body, and are dominated by intense never ending pain in every millimetre of my skin and muscles, over and throughout my whole body; head, shoulders, back, front, arms, legs, hands, feet, toes, fingers, eye lids, scalp, the soles of my feet, the tip of my nose, my eyebrows even. They all burn, throb, tingle, itch, and hurt in ways indescribably unbearable, along with other unusual sensations"

Politics of ME in the UK.

The ME community in the UK has for many years suffered, perhaps uniquely, from the corporate takeover and denial of their illness, for the Medical Insurance Industry, since the mid-1980's has lobbied hard to take over the UK Health market, under the auspices of a prevailing market fundamentalism.

Since 1999, business–friendly NHS initiatives like : Payment by Results ; Choose and Book; Independent Sector Treatment Centres, Integrated Clinical Assessment and Treatment Services ; tenders for the commissioning function of Primary Care Trusts; Alternative Provider of Medical Services ; Unbundling, Private Finance Initiatives and Practice-based commissioning; have led to a great fear that commercialism, competition, patronage and fear are undermining the NHS.

New Labour’s Welfare Reform Act, based upon an understanding that the sick and disabled can be talked "into believing they can lead normal lives", was passed in May 2007. Features of the Reform are familiar from other policy areas, argues Ravetz (2008), in that they involve the demonisation of a needy or vulnerable group;"

As far as people with ME are concerned "it cannot be denied that powerful forces are at work to deny the validity of ME/CFS."(Williams 2008), by giving ME a false psychogenic attribution, even though there is not a single shred of evidence that ME is a psychiatric, behavioural condition.

According to Professor Pall (2007), psychogenic advocates typically ignore "crucial genetic, physiological and biochemical evidence inconsistent with their views, they substitute emotional terminology for sound argument. They often use flawed logic. They rarely make any clear testable predictions that may be used to distinguish their views from those of physiological explanations, a cardinal sin in science."

In what other neurological disease would psychiatric interventions, designed to convince the patient there is nothing wrong with them, be advocated as first-line/core treatments?

Williams (2008) states that it is " irrefutable that certain UK psychiatrists, all deeply involved with the medical insurance industry, have worked unceasingly to deny the nature of ME/CFS."; the results have been devastating, as one patient, surveyed by the author (Crowhurst 2007) explains :

"It is soul destroying to have a World Health Organization recognized illness that neurologists are not interested in even exploring or validating. The neurological symptoms can be extremely frightening and severe . I don't have the energy or the physical ability to cope with being insulted and demoralised on top of being dismissed, when I have extreme paralysis, spasms, all over body numbness, facial palsy - things not to be dismissed lightly and not to be left to get on with by yourself. Abandoned and left to get on with it, living in constant fear of misunderstanding, medical abuse and withdrawal of benefits; this summarizes the current state of affairs here in the UK, for severe ME sufferers.

References

Abbot N (2007) Research Challenges in ME/CFS, Interaction, December 2007

Bassett J (2004) updated July 2005. What is ME/ICD-CFS? A Medical and Political Overview. http://www.ahummingbirdsguide.com/whatisme.htm

Carruthers et al (2003) "Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocols" which appeared in the Journal of Chronic Fatigue Syndrome, Vol. 11(1) 2003, pp. 7-115, )

Crawford J, Aitken S, McCagh J (2008) A comparison of nurses attitudes towards people with Myalgic Encephalomyelitis / Chronic Fatigue Syndrome, Multiple Sclerosis and Rheumatoid Arthritis. Liverpool Hope University.. British Psychological Society Conference I, Dublin 2-4th April 2008. Book of Abstracts ; Poster Presentation 0o7,( page 227) : http://www.bps.org.uk/downloadfile.cfm?fileuuid=294D335D-1143-DFD0-7E3E-511853853E27&ext=pdf  

Crowhurst G (2005) Supporting People with Severe myalgic encephalomyelitis, Nursing Standard, 19, 21, 38-43

Crowhurst G, Crowhurst L A Critical Response to the Inquiry into the Status of CFS/ME and Research into Causes and Treatment by the Group on Scientific Research into Myalgic Encephalomyelitis (ME) : The ‘Gibson Report’ Greg & Linda Crowhurst February 1st 2007 http://www.25megroup.org/Campaigning/Gibson%20Inquiry%20Information/A%20Critical%20Response%20to%20the%20Inquiry%20into%20the%20Status%20of%20CFS.doc.

Crowhurst G (2007) A Survey of Severe ME Patients in Norfolk and Suffolk www.metrainingco.org.uk Department of Health (2002) Annexes to the Report of the Chief Medical Officer of an Independent Working Group, London, The Stationary Office)

Hooper, M. & Montague S 2001 Concerns about the forthcoming UK Chief medical officer's report on Myalgic Encephalomyelitis (ME) and Chronic Fatigue Syndrome (CFS) notably the intention to advise clinicians that only limited investigations are necessary http://www.meactionuk.org.uk/CommentsonadvicegivenbyamemberoftheKeyGroup.htm  

Hooper, Williams (2006) ) A synopsis for the UK Parliamentary Enquiry 18th Aug 2005, http://www.meactionuk.org.uk/ME-WHYNOACCOUNTABILITY.htm )

Hyde B (2003) The Complexities of Diagnosis, Handbook of Chronic Fatigue Syndrome, John Wiley & Sons Inc

Marshall E et al (2001) What is ME/What is CFS? Information for Clinicians and Lawyers.www.meactionul.org/WhatIsMEWhatIsCFS.htm) The ME Society of America website, [Online], Available: http://www.cfids-cab.org/MESA/framework.html  

Pall ML (2007) Explaining Unexplained Illnesses, Disease Paradigm for Chronic fatigue Syndrome, Multiple Chemical sensitivity, Fibromyalgia, Post-traumatic Stress Disorder, Gulf War Syndrome and Others" Harrington Park Press, New York and London pp189/90.

Ravetz A (2008) Is Labour abolishing illness? New Statesman, 01 May 2008 www.newstatesman.com/politics/2008/05/work-benefit-claimants-reform  

Williams 2008 More Zombiefication of ME/CFS? http://www.meactionuk.org.uk/MoreZombieficationofMECFS.htm

* * *

The first doctor I saw in 1987 dismissed me as a hypochondriac because I was dragged to the ER in response to my husband recognizing my symptoms in a magazine article (I hadn’t read it; anyway, how could an article produce symptoms months before it was published?).

The doctor who made the diagnosis in 1988 listened to me complain (as Linda Crowhurst does half a world away) "even my hair hurts", and knew that I could not be inventing that symptom: it had not been published yet. If I knew to say that, then he knew I was truly experiencing the symptoms and not quoting from a magazine article.

No matter what the detractors may say, this is not psychiatric or hypochondria, immense amounts of research have shown viral damage and neurological abnormalities that cannot be imagined into being. Anyone who continues to maintain that we’re simply lazy or crazy is themselves delusional; too closed-minded to consider any evidence that they are wrong. No trained counselor, psychiatrist or psychologist has ever found any sign of mental illness in me: they all felt my symptoms were consistent with a physical illness like the flu. I worked against the odds for years after diagnosis, so I’m not too lazy to work. I’m simply at this point too sick to be employable, probably because I struggled so hard to keep working.

Treating Chronic Fatigue states as a disease of the regulation of energy metabolism

Source: Medical Hypotheses Preprint http://www.sciencedirect.com/science/journal/03069877

Treating Chronic Fatigue states as a disease of the regulation of energy metabolism

William Bains(*) Delta G Ltd, 37 The Moor, Melbourn, Royston, Herts SG8 6ED, UK * Corresponding author. Tel. +790 4931369. E-mail address: william@delta-g.com

Abstract

Chronic Fatigue Syndrome is a physiological state in which the patient feels high levels of fatigue without an obvious organic cause, which affects around 1 in 400 people in the developed world. A wide range of causes have been suggested, including immune or hormonal dysfunction, viral or bacterial infection, and psychological somatization. It is likely that several causes are needed to trigger the disease, and that the triggers are different from the mechanisms that maintain fatigue over months or years. Many treatments have been tested for CFS, with very limited success - a programme of combined CBT and graded exercise shows the most effect. I suggest that patients with CFS have a reduced ability to increase mitochondrial energy production when exertion requires it, with fewer mitochondria that are each more efficient, and hence nearer to their maximum energy output, than normal. A range of indirect evidence suggests that the renin-angiotensin system stimulates mitochondrial responsiveness and reduces mitochondrial efficiency: chronic under-stimulation of this system could contribute to CFS aetiology. If correct, this means that CFS can be successfully treated with RAS agonists (eg angiotensin mimetics), or adrenergic agonists. It also suggests that there will be a positive link between the use of adrenergic- and RAS-blocking drugs and CFS incidence, and a negative link between adrenergic agonist use and CFS.

Background

Chronic Fatigue Syndrome is a physiological state in which the patient feels high levels of fatigue without an obvious organic cause. Abnormal fatigue is known to be a pathological feature of many diseases. In a set of syndromes together called Chronic Fatigue Syndromes (CFS) fatigue is a defining symptom, and does not have an obvious organic cause, such as physical exertion or the metabolic effects of another disease process [1,2]. Clinical diagnosis emphasises the presence of symptoms of fatigue and the absence of obvious causes [3-5]. For reasons of social acceptability, CFS is often called Myalgic Encephalomyelitis (ME) in the non-technical literature [2].

'Fatigue' in this context is not the same as 'weakness'. CFS patients usually have normal muscle strength [6-8] (although a few studies find loss of muscle power in CFS patients, possibly an effect of 'deconditioning', ie being 'out of shape' from prolonged lack of muscle use [9,10]), so CFS is caused neither by a failure of muscle power or a failure of motivation. It is also not caused by failure of the cardiovascular system to support muscle physiology [10] (although see [11] who finds some cardiovascular deconditioning). The chronic fatigue found in chronic heart failure patients is also metabolic rather than due to haemodynamic effects[12,13]. Rather, CFS is an inability to apply that power to sustained effort. This is usually taken to mean physical effort, but mental effort seems to be similarly impaired, independent of any depressive or other psychiatric disease [14].

CFS can be severely disabling [15]. The disease can last for years, while some patients recover on their own, others show resistance to recovery over a decade or more [16]. This variability of outcome, as well as the variability of symptoms and different diagnostic criteria, make comparison between studies and therapeutic approaches very hard [17].

Typical prevalence estimates suggest around 1/400 people are suffering from CFS at any one time [2,18 ­25]. Some studies have found lifetime risk of suffering prolonged, inexplicable fatigue as high as 33% [26].

CFS causes and treatments

Most studies show that no single factor is necessary and sufficient to trigger CFS, and that a combination of triggering factors applies, such as allergy and psychological factors [27], heavy exercise and viral infection [28] or other muscle damage [29,30], or CNS and immunological factors [31]. Consequently, there has been little progress in finding a cure.

Several meta-studies of the trials literature show that graded exercise programmes and Cognitive Behavioural Therapy (CBT) are the only approaches which shows a consistently good track record of benefit in clinical trials [17,32,33]. There is no effective pharmacological treatment for CFS [33,34], although this is not for lack of searches - Whiting et al analysed found 350 trials, and in a meta-analysis of 44 of them found 31 different interventions [17,32]. A major issue is that the trigger for CFS is believed to be different from the mechanisms that sustain the disease [1,35], so searches for, and treatments of, triggering factors may say little to how to treat or cure the disease once it is established.

Suggested etiologies for CFS generally fall in the category of psychological/psychiatric [1,36], immunological/viral, or hormonal [37]. The disease is at least partly psychological [1,26], and it is often comorbid with psychiatric disease, especially depression [1,38-41]. But antidepressants are generally considered ineffective against all but the psychological sequelae of CFS [37,42,43], and a large trial using treatments to enhance cognition [14] was not successful [44]. Association with immune and allergic disease and immune activation parameters [27,45] or abnormal immune regulation [46] has suggested immunological treatment, but these have not generally shown any objective value [47,48]. Anti-viral agents do not seem to help [2,49], and the symptomatic similarities to adrenal insufficiency are not supported by any more than mild impairment of the hypothalamic-adrenal axis [50-53], although these are the only consistent hormonal changes in CFS [52,54]. A wide range of other etiologies have been suggested for CFS (eg. [55-58]).

In part, the variability in trial outcome may be because 'CFS' is not one disease [2,4,59], or if a single disease (as Ciccone and Natelsson argue on epidemiological grounds [60]) that is has distinct sub-types [2]. So it is likely that, even if a treatment does work well for one sub-group of patients, it will not work as well for others.

Metabolism in CFS

There are no obvious metabolic 'problems' that could cause CFS, but a common finding is a reduced level of oxidative metabolism [61] and increase in lactate production [9,10], which these workers attribute to deconditioning - loss of muscle tone and power from prolonged lack of use. (Lactate elevation could also be related to the reduction in post-exercise delivery of oxygen to tissues observed by McCully and Natelson [62], although this reduction does not in itself seem to alter muscle metabolism [63]). Mitochondrial abnormalities and degeneration are frequently [64] although not always [10] found.

RAS, alarm response and CFS

A common (although not obvious) theme running through CFS is the involvement of the body's 'fight or flight' systems, and particularly the neurotransmitters and hormones of the sympathetic nervous system (SNS) and the renin-angiotensin system (RAS). Several indirect lines of evidence suggests that low RAS activation is related causally linked to CFS triggering or maintenance.

* Serum Angiotensin converting enzyme (ACE) is recognised as a marker for CFS [65].

* Gulf war veterans with the Tissue ACE gene I allele (high level expression) are less likely to be found to develop CFS as part of the 'Gulf War Syndrome' spectrum of disorders than veterans who carry the D allele. DD veterans are 8 times as likely to suffer chronic fatigue as the whole population [66].

* Chronic heart failure is often accompanied by CFS-like fatigue (which is not designated CFS because of the co-morbidity with heart failure). Haemodynamic parameters do not explain this. The principle difference between the two patient sets is the extensive dosing of heart failure patients with AT-II inhibitors, beta blockers and ACE inhibitors, usually in combination [12].

* Vasopressin levels have been reported to be lower in CFS patients, suggesting relative inactivity of all blood pressure control systems [67]. Oxygen delivery to muscles post exercise has been found to be reduced in CFS, which has been attributed to reduced autonomic control of vasodilation in CFS [62].

RAS, SNS and mitochondria

A mechanism for the effect of the RAS on fatigue is through mitochondrial efficiency and energy reserve. Several pieces of evidence suggest that RAS and SNS activation reduce the efficiency of mitochondrial energy production, and increase mitochondrial number.

* Beta-3 agonist induce UCP-1, through mechanism involving rB protein, in fat (turning white to brown fat) [68,69] and muscle [70]. Beta adrenorecetopr knockouts depress brown fat formation [71]. The same pathways stimulate mitochondrial biogenesis via CaMK and PGC-1 [72].

* AT-II antagonists increase the duration and energy of sperm swimming. Sperm are almost totally dependent on mitochondrial metabolism of externally supplied sugars for their energy. AT-II antagonists increase this power generation, ie increase the efficiency with which the sperm generate energy. [73,74].

* RAS blockade is associated with increased ability to build muscle mass. There are several pieces of evidence of this type, from cachexic patients, training athletes and high altitude moutaineers [75-77]. This may seem a contrary pieceof evidence. However, any body builder knows that muscle mass is best increased through intense anaerobic exercise, not through aerobic exercise. If RAS blockade reduces the ability of mitochondria to upregulate their energy generation, then a given level of activity would exhaust the aerobic energy generation capacity of low-RAS individuals before it exhausted the aerobic capacity of high-RAS individuals.

Consistent with this hypothesis (but with many others as well) is that CFS symptoms are increasingly being shown to be associated with, and possibly caused by, increased oxidative stress [78], which would be expected of long-term loss of adequate mitochondrial function as other systems took up the task of balancing muscle redox balance [79,80].

RAS, SNS and mitochondrial responsiveness in CFS

Why should the same hormonal system increase mitochondrial number yet decrease mitochondrial efficiency? I hypothesise that this is due to an inverse correlation between mitochondrial efficiency and the ability of mitochondria to increase energy output on demand, and that this links the same systems to CFS.

For rapid response to shock or stress (such as caused by psychological shock, such as activates the SNS, or haemodynamic shock such as activates the RAS), mitochondrial energy production must be capable of being upregulated in seconds. One of the more common ways of enabling metabolic pathways to respond rapidly to changes in control, and to provide greater response than feedback inhibition and substrate activation mechanisms can allow, is to use substrate cycles at key points in the metabolic pathway concerned [81]. Such a cycle in mitochondria would have the effect of making the mitochondria 'inefficient', ie causing it to oxidise substrate to H2O and CO2 without generating maximal energy. Uncoupling proteins allow precisely this to happen: other mechanisms can also be imagined to achieve this in oxidative phosphorylation.

The physiological benefit of such cycles is that the body can respond rapidly to increased energy demand. The downside is that you need more mitochondria at rest (because each is less efficient), and some resting energy is 'wasted', ie dissipated as heat.

The paradoxical effects of RAS and the SNS can therefore be seen as the cell's response to chronic stimulation from hormonal systems that alert the body to the need for immediate, substantial energy demand, through increasing mitochondrial number and mitochondrial responsiveness. Blockade of these systems signals a reduction in stress demand and hence the need for fewer, more efficient and less potentially responsive mitochondria. This relates to muscle mass because mitochondrial cycling is not something that can be switched on and off on a matter of minutes - protein synthesis, and creation of new mitochondria take hours or days. If a patient has their RAS chronically blocked, genetically or pharmacologically, then the number of mitochondria will fall and their ability to rapidly increase energy output will fall. When such muscle is exercised, it will rapidly reach its limit of oxidative phosphorylation and move into a glycolytic metabolism, typical of sprint rather than marathon training regimes. This will result in more muscle build-up, as it does in more conventional training. For patients suffering severe muscle wasting (cachexia), even everyday tasks would become sprint training tasks, resulting in muscle build-up (or slowing of muscle decline).

Hypothesis: chronic lack of ras/sns stimulation maintains CFS

My hypotheses is that the failure of CFS patients to maintain power output in physical or mental activities is due to an inability of their metabolism to deliver increased energy in response to increased demand. This is a key component of the maintenance of CFS. Any event that causes the patient to reduce their exertion to a low level might trigger the state: the likelihood that it did so would be influenced by other physiological and genetic factors. Once the capacity to increase energy production on demand has been reduced, any exercise will be 'felt' to be like heavy exertion, and will rapidly cause the muscle to become hypoxic, generating lactic acid, and sometimes causing muscle damage more normally associated with over-exercise. Depending on other physiological and psychological factors, this may be sufficient to deter the individual from exercising, maintaining a vicious cycle. This is illustrated in Figure 1. This means that treating the initial, triggering causes of CFS - viral infection, injury, inflammation, depression ­ are very unlikely to be cure the disease: this is found to be the case. The only two approaches likely to be effective are i. increasing physical activity: this is the only therapeutic approach presently shown to have an effect ii. increasing mitochondrial mass and responsiveness

I propose to treat CFS through the second of the two options above. The pharmacology for doing this could include use of stimulants of the renin-angiotensin system, or sympatheticomimetic agents, especially beta adrenergic agonists such as salbutamol, thiotropium or ephedrine. In practice, because of the redundancy of biological circuitry and the need to avoid unwanted pharmacological effects, combinations of low doses of these compounds are likely to be the best approach.

I note that this is unlikely to be a 'universal cure'. In some groups of patients other factors than cell-level power generation may be a dominant maintaining factor, and in particular in some defects in neuromuscular transmission or inappropriate psychological attitudes are strongly suspected to be important in the disease [59]. However it is plausible to suggest that this approach will be of some use to a lot, maybe a majority of patients, and as it is very easy to administer and should have a rapid effect, if proven successful it could be used as a 'first line' treatment, with more costly and time-consuming psychological and exercise approaches being brought in subsequently.

Predictions and tests

Testable predictions flow from this hypotheses. Most obviously, it suggests that a suitable combination of RAS and adrenergic agonists will be an effective treatment for CFS. However proving this is a long-term prospect. In the more immediate term, the following experimental tests are available.

* In any cycling system, as flux through the pathway is increased, back flux through the cycle becomes less a factor in the overall flux (although it never reaches 0). One would expect that the 'efficiency' of mitochondria in cells that were being energetically exercised would be higher than the same cells under resting conditions. This could be tested with cultured muscle cells.

* Tissue (specifically muscle) in chronically-RAS- stimulated or RAS-blocked animals would be expected to have more or less mitochondria per unit mass than average, respectively, and less or more efficient mitochondria respectively.

* Other agents associated with the 'fight or flight' response might be expected to have similar effects: The effect of a-adrenergic agonists would be interesting in this regard, as the a-adrenergic system does not activate RAS: in this respect I note that Naschitz et al [82] report that Midodrine, an a-adrenergic agonist, was effective in one case of CFS.

* Other agents associated with tissue growth, and with muscle bulk, such as growth hormone or IGF, would however not be expected to have these effects. * Other agents associated with the clinical control of blood pressure, but acting other than through the RAS, such as the thiazide diuretics, would not have these effects.

The measurement of mitochondrial number can be done by electron microscopy. Mitochondrial mass may be estimated from assay of any one of several mitochondrion-specific enzymes, or measuring relative amount of mitochondrial DNA [83,84]. 'Efficiency' can be measured by three approaches - measuring the net amount of oxygen and glucose consumed by resting cells (assuming that drug treatment has not altered the cells' energy requirements), measuring intracellular ATP pools compared to oxygen and glucose consumtion, and measuring mitochondrial membrane potential. This last is most direct, and can be achieved by using dyes such as rhodamine 123 [85] or JC-1 [86].

In addition, there is a clear epidemiological prediction of the logic above, that patients treated with RAS or SNS antagonists will be more prone to develop long-term, disabling fatigue than patients treated for the same diseases with other classes of drugs. The obvious comparison is in cardiovascular disease, where the sequelae of the use of ACE inhibitors, AT-II antagonists, and beta-blockers can be compared to those arising from use of diuretics, Ca2+ blockers, cardiotonics, or nitrates. Conversely, patients treated with adrenergic agonists might be expected to have a lower than normal level of fatigue syndromes. Asthmatics are an interesting case here, being treated with inhaled beta adrenergic agonists that act primarily topically but which do have a low level of systemic penetration [87-89]. Very extensive academic databases of cardiovascular medicine treatments and outcomes have been compiled over the last two decades. These databases could be tested by suitable 'data mining' of these patient and clinical trial databases for these predicted outcomes.

CONTINUED

CFS and Energy Metabolism -- Part 2

Acknowledgements

I am very grateful to Dr Aubrey de Grey (Cambridge), and Johanna Busch, David Hampton, Charles Conrad Uy and Ponarul Palanisamy (Cambridge M. Phil in Bioscience Enterprise programme) for their comments and contributions.

 

 

Figure caption

Figure 1

Cartoon of the mechanism of the proposed hypothesis(A wide range of insults can result in a patient reducing activity over a substantial period of time (weeks or months). This leads to reduced RAS and sympathetic activity, and hence to an decrease in mitochondrial number and increase in efficiency which leads to an inability to sustain high power output levels, and hence exertional pain on even mild exercise).

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Obstructions for quality care experienced by patients with chronic fatigue syndrome (CFS) - A case s

Source: Patient Education and Counseling May 15, 2008 http://www.sciencedirect.com/science/journal/07383991

Obstructions for quality care experienced by patients with chronic fatigue syndrome (CFS) - A case study

Ann Marit Gilje(a), Atle Soderlund(a), Kirsti Malterud(b,*) a Department of Public Health and Primary Health Care, University of Bergen, Bergen, Norway b Research Unit for General Practice, Unifob Health, Kalfarveien 31, N-5018 Bergen, Norway

* Corresponding author. Tel.: +47 55 58 61 33; fax: +47 55 58 61 30. E-mail address: kirsti.malterud@isf.uib.no  (K. Malterud).

Abstract

Objective

To explore obstructions for quality care from experiences by patients suffering from chronic fatigue syndrome (CFS).

Methods

Qualitative case study with data drawn from a group meeting, written answers to a questionnaire and a follow-up meeting. Purposeful sample of 10 women and 2 men of various ages, recruited from a local patient organization, assumed to have a special awareness for quality care.

Results

CFS patients said that lack of acknowledgement could be even worse than the symptoms. They wanted their doctors to ask questions, listen to them and take them seriously, instead of behaving degrading. Many participants felt that the doctors psychologized too much, or trivialized the symptoms. Participants described how doctors' lack of knowledge about the condition would lead to long-term uncertainty or maltreatment. Even with doctors who were supportive, it would usually take months and sometimes years until a medical conclusion would be reached, or other disorders were ruled out. Increased physical activity had been recommend, but most of the informants experienced that this made them worse.

Conclusion

Current medical scepticism and ignorance regarding CFS shapes the context of medical care and the illness experiences of CFS patients, who may feel they neither get a proper assessment nor management. Practice implications CFS patients' reports about patronizing attitudes and ignorance among doctors call for development of evidence based strategies and empowerment of patients, acknowledging the patients' understanding of symptoms and the complexnature of the disease. The NICE guidelines emphasize the need of patient participation and shared decision-making.

Table

Table 1. CDC 1994 case definition of CFS [2]

Clinically evaluated, medically unexplained fatigue of at least 6 months duration that is

New onset (not life long)

Not result of ongoing exertion

Not substantially alleviated by rest

A substantial reduction in previous level of activities

The occurrence of four or more of the following symptoms

Subjective memory impairment

Sore throat

Tender lymph nodes

Muscle pain

Joint pain

Headache

Unrefreshing sleep

Postexertional malaise lasting more than 24 hours

Exclusion of all relevant differential diagnoses.

References

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(c) 2008 Elsevier Ireland - ScienceDirect B.V.

Complete text in next two posts....

Obstructions to Care -- Part 2

Complete text of article

Obstructions for quality care experienced by patients with chronic fatigue syndrome (CFS) - A case study

1. Introduction

Chronic fatigue syndrome (CFS) is a disabling condition characterized by a profound, persistent fatigue, which is typically worsened by minimal physical or mental exertion [1,2]. Pain, cognitive impairment, sleep problems and other additional symptoms usually occur (Table 1). The etiology is still uncertain, but a variety of possible disease mechanisms including the immune system, adrenal/pituitary axis, and psychological stress, have been proposed [3]. The patients suffer from debilitating subjective symptoms, while consistent, objective findings are lacking. No single diagnostic test can confirm diagnosis, which is made on clinical grounds, requiring the presence of the specific fatigue with associated features and exclusion of alternative medical and psychiatric disorder [4]. No universal treatment has yet been identified, but cognitive behavioral therapy (CBT) has shown benefit in several studies [5]. Doctors and patient may hold opposing explanatory models about the nature of the condition [6,7].

CFS is not the only condition where patients present with symptoms for which no physical pathology can be found. This kind of problems are often labelled as the medically unexplained disorders or physical symptoms (MUPS) [8,9]. MUPS challenge the traditional biomedical framework, where a disease is supposed to have a structural origin, caused by an agent or event which can be traced by a diagnostic test, and treated by counteracting the cause. The biomedical conceptualization of disease fits some disorders, such as streptococcal pharyngitis or other infectious diseases, while more complex conditions with multicausal background or individualized treatment response are less adequately incorporated by this model.

As a consequence, a broad range of chronic, disabling health problems cannot be adequately understood by means of the biomedical framework alone. Doctors and patients work hard with the subsequent uncertainty in different ways, and tensions emerge when they meet. General practitioners report skepticism towards CFS [10]. Doctors even say explicitely that they feel uneasy when the biomedical ideals do not fit with the clinical reality [11,12]. They struggle when their professional authority shall be managed under what is perceived as scientific uncertainty [7]. The consequence is not beneficial for the patient. Women with chronic pain presented accounts of being met with scepticism and lack of comprehension, feeling rejected, ignored, and being belittled, blamed for their condition [13]. Patients with CFS are often dissatisfied with the quality of medical care they receive [14]. They report experiences of stigmatization related to the unclear symptomatology of the disorder, especially before receiving a diagnosis [7,15].

A functioning doctor-patient relationship is essential for quality care for patients with any chronic, disabling health problem, including the process of diagnosis, treatment, and support. Previous research has demonstrated some of the challenges which may appear in encounters between doctors and patients with CFS. After several encounters with distressed CFS patients in the last author's practice, we felt a need to learn more about the perspectives and needs for health care in this group of patients. We therefore conducted a study to explore obstructions for quality care from experiences by patients suffering from CFS.

2. Methods

2.1. Design, data, analysis

This is a case study based on analysis of data from multiple sources - a group meeting, a questionnaire, and a follow-up meeting. The study was approved by the regional committee for medical research ethics (Health Region West, Norway) and The Norwegian Data Inspectorate. Participants in the group meeting were recruited from the local patient organization, which we considered as a purposive sample of people who might be especially aware of questions related to quality care. Ten women and two men aged 22 ­54 years (mean 41) attended the meeting. All had suffered from CFS for at least 1 year, one of them the last 20 years. Their diagnoses had been confirmed by various doctors, and all the informants were on disability or rehabilitation pension. None of the participants belonged to the practice of the third author.

We conducted a group interview during the meeting according to focus group principles [16]. The moderator (KM) invited the participants to share their experiences from encounters with health care providers, and to describe episodes from everyday life where the symptoms made a difference as compared to life before illness onset. Findings regarding the latter have previously been presented [17]. The conversation was audiotaped, transcribed, and supported by field notes. Qualitative analysis was conducted with systematic text condensation inspired by Giorgi [18,19]: (a) reading all the material to obtain an overall impression and bracketing previous preconceptions; (b) identifying units of meaning, representing different aspects of participants' experiences of health care and coding for these; (c) condensing the contents of each of the coded groups; and (d) summarizing the contents of each code group to generalize descriptions and concepts concerning health care experiences.

The questionnaire, intended to complement the interview, was designed by the organization. Roughly it contained similar issues as the interview, expressed as open-ended questions, and also some quantitative issues such as duration of illness. Questions beyond the scope of this study were also included, such as beliefs about etiology. Due to the limited amount of time, these matters were not introduced in the interview, and were omitted from analysis.

The follow-up meeting 1 year later was attended by 5 of the 12 participants, all of them women. The major findings from the initial analysis were then presented and discussed in depth. Fieldnotes from this meeting and the questionnaires were used to clarify and supplement issues from the group interview.

3. Results

CFS patients said that lack of acknowledgement could be even worse than the burden of symptoms. They wanted their doctors to ask questions, listen to them and take them seriously, instead of behaving degrading or patronizing. Many participants felt that the doctors psychologized too much, interpreting the exhaustion as depression or trivializing the symptoms. The participants described how doctors' lack of knowledge about the condition would lead to long-term uncertainty or maltreatment. Even with doctors who were supportive and believed in the patients, it would usually take months and sometimes years until a medical conclusion would be reached, or other disorders were ruled out. Increased physical activity had been recommended, but most of the informants experienced that this made them worse. These findings are elaborated below.

3.1. Lack of acknowledgement can be even worse than the burden of symptoms

Several participants remarked that although the symptoms were terrible, even worse was not being believed by their doctors. When all tests came out as normal, they would become labelled as healthy, even though their level of functioning was deteriorating. Repeated stories referred to doctors who appeared to have more confidence in themselves than listening to the patients. Our participants wanted the doctor to ask questions, listen to them and take them seriously. Instead, there were many examples of events perceived as degrading by the patients:

'Sometimes you meet such an arrogant attitude that you get... you get scared of them.' (#4)

Yet, those who were satisfied with their GPs, told about doctors who during a long-term relationship had showed that s/he believed in them. Although few of these doctors had given a diagnosis, they were perceived as examining the patients thoroughly and loyally accepted their information. One participant told that the doctor had read an article about postviral fatigue syndrome and hypotension, and sent it to her. A woman explained her positive experiences:

'I guess I've been lucky, because my GP knew me from I was a kid. She knew that if I said I was ill, I was ill.' (#2)

Another woman had come to the emergency room due to pain she did not relate to CFS. When they heard that she was a CFS patient, she was sent back home. She felt she was rendered suspect because of her illness. After 2 days with severe pain she was operated in the uttermost moment. Many participants felt that the doctors psychologized too much. One woman got ill as a child. She was therefore automatically labelled as a victim of problems at home or in school. Another one met a doctor who believed that she tried to escape from her job situation through her symptoms. The exhaustion would quickly be interpreted as depression:

'And then I met a doctor who was convinced that I was depressed. He asked if I cried a lot. In fact, I didn't cry more than I laughed during that period. So crying was not a problem. Then I said: 'I can't do anything at all.' Well, then of course I was depressed because I didn't manage anything, or was in lack of initiative. But that was not the problem. I wanted to do all sorts of things, but as soon as I tried, I became exhausted and had to go to bed again.' (#6)

Generally, the participants felt that the doctors' interest for them and their illnesses diminished as time went by and no cause or treatment was found. One of them was told by his doctor that he would have been a lot more interesting if he had suffered from a heart disease. Another participant reported giving an article about CFS to his internist. A few weeks later he received a bill from the physician, who demanded a fee to study the article. One woman mentioned that when she gave her doctor some information material about CFS, he was not willing to study it: 'The doctor said: 'I don't think I have the time to study this'. You'll have to find another GP.' (#1)

Doctors were often perceived as inactive, wanting to get rid of the patient as quickly as possible. The participants wished to be taken seriously, even being women in their forties. The woman above added that she felt that her symptoms were trivialized:

'...they did not listen to me because I was of no interest. I was a typical housewife at a difficult age. Probably menopausal symptoms and things like that. Was a bit stressed and frustrated. Had grown-up kids and felt uncomfortable, and didn't find myself and so on.' (#1)

3.2. Lack of knowledge can lead to long-term uncertainty or maltreatment

A common impression among our participants was that their GPs held a low level of knowledge about CFS. Since they did not understand, they could not give any advice. Two women told about doctors who never examined them properly, even after having seen them for several years, claiming that they did no efforts at all to find out whether they were ill or not. Some of the participants were not even able to tell their doctor what was wrong with them before he gave them a prescription It seemed to represent an 'easy exit' for the doctors.

'First I came to the emergency room. I had two red eyes, I didn't manage my job, I couldn't remember what to do, I couldn't walk up hills. Everything was wrong. They looked me in the eyes and said: 'Nyeah, it's probably a virus. Here are eye drops if it is bacteria. Keep on working.'' (#6)

Even with doctors who were supportive and believed in the patients, it would usually take months and sometimes years until a medical conclusion would be reached, or other disorders were ruled out. In the meanwhile, the doctor hoped that the symptoms would disappear. A woman who felt well taken care of, said:

'When the doctor is so confused, it is important to refer people to specialists. What concerns this illness, they said to me at the university hospital: 'You have listed a whole lot of neurological symptoms. Now we'll take some tests, and then we'll exclude other things, other dangerous conditions. Exclude MS, cerebral tumour etc.'' (#8) Many of the GPs had more or less reluctantly referred their patients to specialists for investigation, and most of our participants had been seen by neurologists at a hospital department with a special interest in CFS. This was usually the place where the diagnosis had been concluded. The neurologists had also offered advice and guidance about diet and training. Similar levels of knowledge were called for among GPs:

'I don't believe that anything will happen before one day there is a sign at the door of a doctor: 'Specialist of ME.'' (#8)

Both specialists and GPs had recommended increased physical activity. The patients were encouraged to go to work, do exercise, and go out to see other people. Many of them had been advised to stretch their physical limits and referred to physiotherapists for exercise. However, most of the informants had experienced that this would worsen their condition. Some of them thought they would have been better today if they had not followed this advice. One participant was referred to a rehabilitation center, and this led to a total collapse. Still he was recommended to keep on training:

'I said: 'It's crazy! I have problems walking up a hill, and now I'm going to a center for physical training!' Ok, I'd try. So I went. And after two days I collapsed.' (#4)

(CONTINUED...)

Obstructions for Care -- Part 3

4. Discussion and conclusion

4.1. Discussion

4.1.1. Validity and transferability

This is a case study approaching experiences and associated attitudes of CFS patients who belong to a patient organization. Material from the interview and the questionnaire confirmed that all participants had undergone thoroughly diagnostic testing at the hospital. We conclude that our sample covers a sufficient content validity regarding the CFS diagnosis. We were interested in the stories from people with a special awareness for quality care, realizing that CFS patients who are members of an organization, may differ from other CFS patients. On one hand, they may represent the most serious and disabling stages of the disorder, on the other hand, they may be more active and articulate than patients who do not organize. Membership might represent a bias of bad health care experiences. We therefore took this as a challenge to look across the material for variations and nuances, and to acknowledge substantial wishes for improvement of health services, regardless of their quantity or distribution. We do not claim transferability of these experiences to all CFS patients, yet consider the phenomena described as relevant for any medical encounter where the patient suffers from a medically unexplained disorder. The better part of reality would probably be more precisely described by a different sample The moderator's initial dedication for improvement of health services for this group of patients may have facilitated trust and alliances with the participants by confirming an ethical commitment to their expressed needs.

The number of participants present in the group interview (more than we had expected!) limited the amount of information from each of them, and some remarked afterwards that it was too brief. However, the atmosphere was relaxed, and the associative creativity during the interview contributed to a rich and diverse material. Data collection was limited to one group meeting, which however presented a broad diversity of experiences. Our methodological approach was not aiming for saturation, since the study did not hold an ambition to describe all possible experiences. Concentrating on stories from members of the organization, we were fully aware that other groups may have yielded different data. The information obtained through the questionnaire and the follow-up meeting validated and complemented the main findings.

4.1.2. What is known from before - what does our study add?

Patients with persistent, subjective symptoms without objective findings, such as CFS and other MUPS, hold a low ranking in the medical hierarchy. While conditions like myocardial infarction, leukaemia and brain tumour are ranked highest by doctors, fibromyalgia and anxiety neurosis are among the lowest [20]. Such attitudes are reflected in the comment from the participant in our study, who said that she felt she was of no interest for her doctor. Edwards et al. have described patients' feeling of being let down and disbelieved when seeking help [21].

Our study also confirms previous studies about experiences of stigmatization in patients with CFS encountering health care [7,14,22]. Some doctors characterizes CFS patients by lacking stoicism, and use pejoratively stereotypes to describe certain personality traits supposed to cover the whole group of patients [10,12,23]. Patients perceive such attitudes as questioning their morality and credibility, asking whether they are really sick [12,22,24].

Yet, although acknowledgement of symptoms as well as person is necessary for quality care, it is not sufficient. The participants in our study challenge Deale and Wessely's understanding that medical care is evaluated less on the ability of doctors to treat CFS, and more on their interpersonal and informational skills [14]. Understanding the CFS condition itself is urgently called for by the participants in our study, who want their doctors to be better informed and less ignorant in order to provide adequate counseling. Within this field of experienced uncertainty, a stronger commitment to evidence based practice might improve the doctors capacity to give his or her patients adequate information about CFS [22,25,24].

Our participants emphasize the specific importance of reaching a diagnosis for coping [7] by sharing their experiences from the frustration appearing when time goes by and no conclusion regarding diagnosis or treatment has been achieved. Previous studies have emphasized patients' view on diagnosis [11,26,27], not only as legitimation of the condition, but also as a path to reconciliation and coping [7,28]. The NICE Guidelines recommend diagnosis to be reached within 4 months for adult patients [4]. Considering a CFS diagnosis as a provisional tool for understanding and reconciliation may support recovery for the patient, while attributing the diagnosis a warning about any physical activity would probably function counterproductively. The way the diagnosis is presented, is therefore crucial for quality care.

Our study adds to the knowledge base on doctors' uncertainty - when you do not know what to suggest, you therefore have nothing to offer [11]. Analysis revealed stories about doctors who lack knowledge but yet refuse being provided with information, and doctors who propose treatment which makes the patient feel worse. While physical activity is beneficial for a lot of health problems, the core symptom of CFS is actually postexertion fatigue and malaise [1]. Movement therapy based on carefully limited workload has shown promising results for CFS patients [29], and graded exercise therapy has been useful for some of these patients [1]. However, patients with this condition should not be advised to undertake vigorous exercise [4].

Our participants demonstrated some of the problems which can be experienced by patients when doctors do not know what to do. They demonstrate specific areas where quality of care can be improved by implementing evidence and guidelines among healthcare professionals. Special efforts would yet be needed to develop adherence to guidelines within a field where GPs seem to have strong opinions about the 'real' nature of the disorder [30,10,31].

4.1.3. Conflicting explanatory models on MUPS

Our findings indicate that quality care for CFS patients suffer from more than indifference and ignorance. The tensions arising from conflicting illness understanding seem to create serious obstacles in the interaction between doctors and patients with CFS. Conflicts may arise when the two parts have different beliefs about the nature and cause of the illness. According to Kleinman, explanatory models are 'the notions about an episode of sickness and its treatment' employed by all the persons involved in the clinical process, including beliefs about etiology, time and mode of onset of symptoms, pathophysiology, course of sickness, and treatment [6]. Some of the participants in our study felt that they were unduly labelled as depressed, perceiving this as a patronizing provocation, never having felt psychological problems, and being convinced of the bodily character of their symptoms.

We did not interview the doctors met by our participants, and hence do not know what actually took place. Nevertheless, the reported events correspond well with the sceptical viewpoints towards the diagnosis presented by doctors in other studies [10,12,31]. Previous research has described similar uncreative negotiations as 'the shame-blame-game', where all interaction concentrates on body-mind arguments about whether CFS is 'really' a psychological or a physical condition [24].

Burton turns down the idea that most MUPS are the result of a single process of somatization or mental distress. He concludes that in these conditions, there is good evidence for the impact of the interaction between physiology, personality, life experiences, health cognitions, and healthcare experiences [9]. Recent biopsychosocial models focusing feedback systems and homeostasis, such as The Cognitive Activation Theory of Stress (CATS) [32], transcend the dichotomous perseverance on classifying CFS as either body or mind [10]. Sustained activation has been suggested as the underlying mechanism for processes underlying subjective health complaints [33]. Within the framework of these models, even measurable bodily processes are accessible for cognitive input.

4.2. Conclusion

Our findings support a hypothesis that the current medical scepticism and ignorance regarding CFS shapes the context of medical care and the illness experiences of CFS patients, who may feel they neither get a proper assessment nor management. GPs need more knowledge and a broader understanding of the condition, making it possible to individualize the available strategies for diagnosis and management according to the patient's capacity and responses.

4.3. Practice implications

Being met with dignity and respect is especially important for people with chronic illness. However, doctors' feelings of helplessness and controversies about explanatory models may transform into behavior perceived as degrading by the patient [8,34], thereby obstructing quality care. The body-mind controversies arising from the biomedical model seems to be an especially important barrier for finding common ground between patients with CFS and their doctors. Development of comprehensive explanatory models which transcend the dichotomous explanatory models [32] can help doctors and patients to expand their understanding of the mechanisms underlying the complex symptomatology of CFS. Elaborating a diversity of strategies involved in the diagnosis and treatment plans of primary care problems that are uncertain and complex could also contribute to better care of CFS patients [35].

However, many doctors are not yet even prepared to acknowledge the CFS entity itself, but regards it as a dubious category [31]. Doctors' reluctancy towards giving this diagnosis is known from before [11,36], and confidence with making a diagnosis and management is low [37]. According to the British Chief Medical Officer Kenneth Calman (2002), chronic fatigue syndrome should be recognized as a real entity, which is distressing, debilitating, and affects a very large number of people [38].

To the patients the diagnosis may function as a tool that enables them to tell other people what is wrong with them [15,11]. Receiving a diagnosis was mentioned by our participants as a very important aspect, since the uncertainty during a period of increasingly debilitating symptoms may add strongly to the burden of suffering for the patient. Our findings indicate that GPs need to know more about why and how the diagnosis of CFS should be set. According to clinical guidelines, the CFS diagnosis can be concluded by the typical history of excessive, characteristic and lasting fatigue, when adequate differential diagnoses have been thoroughly excluded [4]. Often, a specialist referral is necessary. When diagnosis is clear, there is no apparent medical reason to withhold it from the patient. On the contrary, a diagnosis may constitute the starting point of a process of recovery and reconsiliation [39].

Intervention studies indicate that cognitive behavioral therapy and graded exercise therapy may be helpful for some CFS patients [5,40]. We still do not know how these modalities can provide the most benefit, and for whom. GPs need to learn how to offer evidence based treatment modalities such as cognitive behavioral therapy to patients with CFS without confining the disorder within the concepts of somatization or other kind mental diseases [9,41]. Our informants complained about the exercise recommendations which had seemed to make their symptoms worse. Since CFS per definition is a condition where postexertional malaise is one of the typical symptoms, undifferentiated physical exercise appears to be a questionable recommendation. However, the NICE Guidelines present a feasable program for individualized and tailored physical activity which could safely be offered to CFS patients under monitoring of effects and side effects [4].

The NICE guidelines emphasize the need of patient participation and shared decision-making [4]. CFS patients' reports about patronizing attitudes and ignorance among doctors call for development of evidence based strategies and empowerment of patients, acknowledging the patients' understanding of symptoms and the complex nature of the disease.

* * *

A Norwegian study which proves that the experiences I’ve complained about, with ignorant doctors unwilling to refer me to a specialist, preferring to give me the quick/easy (but erroneous) diagnosis of depression instead of seeking out the real cause of the problem, are not confined to the US. Like one of my doctors who never even asked me to take off my clothes so he could do a physical exam, because he thought my problem was depression and therefore nothing would be found on physical exam, some of the Norwegian patients made the same complaint of never getting a complete physical.

As Dr. Bell has stated, the abnormalities are subtle, but they are there. "On superficial examination, there are usually no abnormalities. However, on careful examination, ... patients have minor abnormalities. ... In general, the cranial nerves, mental status, and cognitive function are normal on routine exam. Detailed cognitive testing, however, may reveal abnormalities." The problem is, most doctors do only a superficial examination, and mental status testing is limited to only observing if the patient gives appropriate responses to simple questions, such as knowing their own name or what year it is. Never mind that I had psychiatrist-documented "severe cognitive and memory dysfunction", I wasn’t totally disoriented/demented, and therefore the MD wrote down that nothing at all was wrong with my mental status! (He later admitted that I would have had to say "butterscotch" in response to "good afternoon" for him to write down that there were any mental status abnormalities.)

Every doctor should have to read this article to see where they’re going wrong. Perhaps the CFS community would trust doctors more, if doctors proved themselves deserving of that trust.

"Previous research has described similar uncreative negotiations as 'the shame-blame-game', where all interaction concentrates on body-mind arguments about whether CFS is 'really' a psychological or a physical condition [24]" Not only are such arguments "uncreative" but they’re not helpful. They don’t do a thing to alleviate the patient’s suffering and, in fact, make the patient feel worse about it.

And those of us whorefuse to accept shame or blame for our condition are quickly written off as "uncooperative patients" because we won’t docilely accept the inappropriate treatment and medications, instead insisting that the doctor search for the biological cause of our biological ailment. My problems started with a 105 fever; I was not going to be browbeaten into accepting that there was nothing physically wrong, that I simply didn’t like being married – the doctor glossed over the reports that I’d had the symptoms for months before the wedding, when there was no husband to answer to, because that little "inconvenient truth" contradicted what he wanted to diagnose.

Another patient in this study complains "I said: 'I can't do anything at all.' Well, then of course I was depressed because I didn't manage anything, or was in lack of initiative. But that was not the problem. I wanted to do all sorts of things, but as soon as I tried, I became exhausted and had to go to bed again.'" Again, exactly the experience that I had. Whenever I said "I can’t", I was cajoled "you’ll be surprised what you can do if you try", and the subject was changed before I could point out that my statement that I "can’t" do certain things was based on empirical evidence, repeatedly trying and failing, and not by fear of failure. It wasn’t that I was afraid to apply for jobs and be rejected, but that in every interview that I successfully landed, the symptoms they saw persuaded the employers not to hire me. The paralytic muscle weakness in my hands made it impossible for me to exert enough pressure on the heavy-duty staple gun to secure the cover over the swamp cooler when winter approached; after three days of failed attempts I gave up in frustration and flung the stapler across the room. That definitely was not "I lack the initiative to get off the couch to winterize my home", that was a neurological problem that prevented doing what needed to be done, no matter how hard I tried to do it, and absolute frustration that I couldn’t do something so simple. (Eventually, I recalled what my friend with post-polio was told about overusing her muscles leading to such muscle failure, and when I stopped using my hands so much – watching more TV rather than holding a book upright or typing or doing needlework – I was again able to use my hands for chores requiring dexterity and hand strength. To this day, I’m limited in how many hours I can use my hands before I’m forced to stop ... and that limit is notenough hours to make me employable.)

Devin Starlanyl, doctor and patient, observes "Just because standard testing shows normal values does not always mean everything is fine. It may simply mean that the proper tests have not been run." There’s no readily-available test for whatever virus I have (some researcher somewhere, for some huge sum of money, might be willing to try to identify it, but my medical insurance won’t pay for that); we know I don’t have the half-dozen most popular viruses to test for. However, the C-Reactive Protein test, which proves there’s some form of infection/inflammation, was "off the charts", 10x what it should have been. So, even though some doctors will point to the virus-specific tests to claim "there’s nothing wrong", another doctor can look at the C-Reactive Protein test to say "there’s something very wrong, we just don’t know exactly what."