Saturday, January 24, 2009

Community Health Care Meeting Report Available Online

THIS MESSAGE MAY BE REPOSTED:

Just before Christmas, the Obama-Biden transition team asked the public to hold small living room "community meetings" on health care. The results were to be sent to Senator Tom Daschle, Secretary Designate of the Department of Health and Human Services (DHHS), where NIH, CDC, FDA, and public health are housed. The original deadline was December 31, 2008.

It soon became clear that an on-the-ground meeting was impossible for most of us.

The obvious answer was to hold a "meeting" via internet. By this point there wasn't much time to bring people together, throw out ideas, and come up with a report. Several could not be contacted in time.  Others who could be contacted could not participate. Three committee members were so sick they dropped out almost as soon as they joined. One was able at the last minute to read the report and make useful revisions. It took a lot of energy at a difficult period of time, but somehow we succeeded in putting together a report and getting it into the Obama-Biden transition team by the final deadline of January 4, 2009.

The committee included three members who asked that only their initials be used, plus Pat Fero, Steven Du Pre, Karen Campbell, Rik Carlson, Meghan Shannon, and myself.

The report discussed the fundamental inequity in treatment of patients with a CFS diagnosis at the DHHS agencies, and made the following recommendations:

1. The U.S. adopt the Canadian Consensus Document for diagnosing and treating ME/CFS, available online at
http://www.mefmaction.net/Portals/0/docs//ME-Overview.pdf;

2. The U.S. accept the World Health Organization's ICD-10 designation of CFS within the chapter on neurology, at G93.3, with M.E.

3. NIH and CDC focus on biomedical research instead of psychosocial;

4. GAO investigate NIH and CDC for the misapplication of funds; and

5. Secretary Daschle take seriously the existing Chronic Fatigue Syndrome Advisory Council to DHHS, along with the 11 recommendations of the CFSAC from 2004 (enclosed)

The Transition Team asked for personal stories; we were able to send eight.

The full report, including personal stories is available in html at the Vermont CFIDS Association's website:
     http://www.vtcfids.org/obama_biden_report.html

There is an index to the personal stories on the left of the website.

The report can also be found in pdf format at:
     Report alone: http://www.cfids-me.org/dhhs/simplereport.pdf
     Report plus personal stories: http://www.cfids-me.org/dhhs/longreport.pdf

The report by itself (including the appendix of 11 recommendations by the CFSAC), or the report plus the personal stories, may be referenced or downloaded (without changes) for any purpose that will help patients who share our disease.

Pat Fero, Steven Du Pre, Karen Campbell, Rik Carlson, Meghan Shannon, Carol O., PSB, Sue C., and Mary Schweitzer
"Ad Hoc Committee to Inform the Obama Transition Team About ME/CFS Issues"


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Non-Doctors

In light of the fact that more than 3/4 of CFS patients report unfavorable interactions with their doctors, I thought this bit of humor from Peter was apropos...
 
Non-Doctors

I would like to propose a new concept of 'Non-Doctor'.

In view some doctors activities and opinions regarding the serious
neurological illness, Myalgic Encephalomyelitis; I believe it accurate to
say that had some adopted a career as a plumber (no disrespect to plumbers
intended), the overall physical and mental health of the population of the
world would have been better by a significant degree.

With 'Non-Doctors' it is not a case of 'first, do no harm'; which is a nice
idea but an ideal that I believe could only be achieved by keeping any
doctor in a locked cupboard for 40 years.

My thought is that a 'Non-Doctor' is one whose activities cause more harm
than help, more illness than healing, more dischord than harmony in the
lives of their patients.

In view of the extensive training (which includes ethics) that doctors
undertake; it must be some sort of achievement when a doctor not only fails
to help the sick, but contrary to all reason and evading all safeguards,
they manage to increase and perpetuate illness; and at times even recruit
others to magnify their non-doctoring effect.

It seems a shame that such achievement goes mostly unnoticed except by the
patients and their families - who might tend to be biased and fail to
appreciate the eccentric genius of such initiative.

If you can think of the name of such a doctor, write their name on a piece
of paper, roll it into a ball and swallow it.  It will do you less harm than
going to see them (unless it is a very, very big piece of paper!).

Peter Kemp
 
 


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A TEST FOR CFS/ME!!! (Finally!!)


Dr Sarah Myhill MB BS, Upper Weston, Llangunllo, Knighton, Powys, LD7 1SL

Tel: 01547550331 Fax: 01547550339 E-mail: office@doctormyhill.co.uk  Website: www.doctormyhill.co.uk  

20 January 2009

PRESS RELEASE

A TEST FOR CHRONIC FATIGUE SYNDROME /

MYALGIC ENCEPHALOMYELITIS (CFS/ME)

The International Journal of Clinical and Experimental Medicine has published on line details of a biochemical test which measures energy supply to body cells and therefore fatigue levels in people with Chronic Fatigues Syndrome/Myalgic Encephalomyelitis (CFS/ME). The scientific paper entitled 'Chronic Fatigue Syndrome and Mitochondrial Dysfunction' is available here http://www.ijcem.com/files/IJCEM812001.pdf , Int J Clin Exp Med (2009) 2, 1-16

For treating the fatigue of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis, doctors have been hampered by the lack of a good test. This scientific paper clearly shows that the fatigue of CFS/ME is a symptom of mitochondrial dysfunction. Mitochondria are the biochemical engines within every cell in the body, which supply energy to that cell. What is shown by this paper demonstrates that the more fatigued the patient, the worse is the mitochondrial dysfunction and vice versa. This means that we now have an objective measure of energy supply and therefore a test for one immediate cause of CFS/ME

This test has resulted from the brilliant and pioneering work of the internationally recognised Dr John McLaren-Howard of Acumen laboratories. He has taken cutting edge research biochemistry and applied them to the clinical conundrums thrown up by the illness known as CFS/ME.

This test can help distinguish between those people fatigued because of a biochemical problem in their mitochondria and those who are fatigued for other reasons. Other reasons include dietary causes (allergy and carbohydrate intolerance), hormonal reasons (such as borderline thyroid and adrenal function), poor antioxidant status, chronic insomnia, psycho-social causes such as anxiety and other causes.

Many doctors are already using this test and hundreds of patients are already taking the necessary nutritional supplements to support mitochondria. Many of these doctors and patients have observed significant clinical improvements. For some their health is so much improved that they have been able to lead normal lives and return to the workplace.

Dr Myhill, one of the authors of the paper, says "This test represents a huge breakthrough in the diagnosis and management of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis. This illness has already been classified as a neurological disease by the World Health Organisation under ICD 10 G93.3, but many doctors continue to treat CFS/ME as if it were a psychological condition. This has been enshrined in NICE Guidelines for treating CFS/ME because their recommendations are for psychological treatments including antidepressants, cognitive behaviour therapy and graded exercise therapy. This is completely inappropriate for patients who have mitochondrial pathology and indeed is likely to make the mitochondrial pathology even worse.

"A useful analogy is to compare your body with your car. The mitochondria represent the engine of that car, the diet represents the fuel that goes in the tank, the thyroid gland represents the accelerator pedal and the adrenal gland the gearbox of that car. Using cognitive behaviour therapy or graded exercise to treat a patient with CFS/ME is akin to beating up the driver of the car when actually the car needs a re- conditioned engine, suitable fuel in the tank, resetting of the accelerator pedal, a new gear box or whatever. This test invalidates the psychological model of CFS/ME and clearly establishes this illness as having a physical basis. Sufferers of CFS/ME have known this for many years but now we have the biochemical basis to prove this.

"This study clearly shows that CFS/ME has a physical basis with the potential for correction through physical and biochemical interventions. Clinical experience has shown that the package of supplements to support mitochondrial dysfunction is effective and this will be the subject of further studies."

THE AUTHORS OF THE STUDY



Dr John McLaren-Howard is seen here receiving the Maberley Medal from the British Society for Ecological Medicine for his outstanding laboratory work in the field of Nutritional and Environmental Medicine. It is his brilliant work and skills which have made this research possible. He has developed many known biochemical research techniques and pioneered new tests for investigation of patients with fatigue syndromes and related disorders. These have proved vital in ascertaining the cause of disease. The ATP profile featured in this scientific paper is just one example of many cutting edge research tools which he has applied to establishing disease causation.

Dr Norman Booth is a retired physicist from Mansfield College, Oxford University. Dr Booth has been responsible for ensuring the necessary academic rigor to ensure publication in this scientific journal. He prepared all the necessary graphs and illustrations which clearly show the relationship between mitochondrial function and levels of fatigue

Dr Sarah Myhill is a clinical doctor with a special interest in the treatment of chronic fatigue syndrome/ME. She was responsible for collecting the original data from her patients, and from the biochemical tests, and noticing a relationship between the two.

We are all especially grateful to those CFS/ME patients and non-patients who all co-operated fully without whom none of this would have been possible.

- ENDS -

For further information, please contact

Dr Sarah Myhill, Telephone 0154755033 Email office@doctormyhill.co.uk  

Dr Sarah Myhill MB BS, Upper Weston, Llangunllo, Knighton, Powys, LD7 1SL

Tel: 01547550331 Fax: 01547550339 E-mail: office@doctormyhill.co.uk  Website: www.doctormyhill.co.uk  

NOTES TO EDITORS

The scientific paper entitled 'Chronic Fatigue Syndrome and Mitochondrial Dysfunction' is available here http://www.ijcem.com/files/IJCEM812001.pdf , Int J Clin Exp Med (2009) 2, 1-16

For more information about mitochondria and their clinical reference, see extract from the online book, free for anyone to download, written by Dr Sarah Myhill www.drmyhill.co.uk  

Mitochondria are the engine of the car - they supply energy to every cell in the body. When mitochondria goes slow, everything goes slow!

Dr Sarah Myhill writes:

I think this is one of the most important ideas I have come up with in terms of my understanding of CFS and what to do in order to recover! So please read this very carefully and several times over because for many sufferers it contains the keys to unlock their illness!

We are made up of lots of different cells - heart, blood, muscle nerve cells etc. All these cells are different because they all have a different job of work to do. To do this job of work requires energy. But the way in which energy is supplied is the same for every cell in the body. Indeed all animals share this same system. The mitochondria in my dog, my cat and my horse are exactly the same as mine. Mitochondria are a common biological unit across the animal kingdom. Energy is supplied to cells by mitochondria which I think of as little engines which power every cell in the body.

Chronic fatigue syndrome is the symptom caused by mitochondrial failure. The job of mitochondria is to supply energy in the form of ATP (adenosine triphosphate). This is the universal currency of energy. It can be used for all sorts of biochemical jobs from muscle contraction to hormone production. When mitochondria fail, this results in poor supply of ATP, so cells go slow because they do not have the energy supply to function at a normal speed. This means that all bodily functions go slow.

Chronic fatigue syndrome therefore is a symptom of mitochondrial failure and every cell in the body can be affected.



Mitochondrion

ATP (3 phosphates) is converted to ADP (2 phosphates) with the release of energy for work. ADP passes into the mitochondria where ATP is remade by oxidative phosphorylation (ie a phosphate group is stuck on). ATP recycles approximately every 10 seconds in a normal person - if this goes slow, then the cell goes slow and so the person goes slow and clinically has poor stamina ie CFS.

Problems arise when the system is stressed. If the CFS sufferer asks for energy faster than he can supply it, (and actually most CFS sufferers are doing this most of the time!) ATP is converted to ADP faster than it can be recycled. This means there is a build up of ADP. Some ADP is inevitably shunted into adenosine monophosphate (AMP -1 phosphate). But this creates a real problem, indeed a metabolic disaster, because AMP, largely speaking, cannot be recycled and is lost in urine.

Indeed this is the biological basis of poor stamina. One can only go at the rate at which mitochondria can produce ATP. If mitochondria go slow, stamina is poor.

If ATP levels drop as a result of leakage of AMP, the body then has to make brand new ATP. ATP can be made very quickly from a sugar D-ribose, but D-ribose is only slowly made from glucose (via the pentose phosphate shunt for those clever biochemists out there!). This takes anything from one to four days. So this is the biological basis for delayed fatigue.

However there is another problem. If the body is very short of ATP, it can make a very small amount of ATP directly from glucose by converting it into lactic acid. This is exactly what many CFS sufferers do and indeed we know that CFS sufferers readily switch into anaerobic metabolism. However this results in two serious problems - lactic acid quickly builds up especially in muscles to cause pain, heaviness, aching and soreness ("lactic acid burn"), secondly no glucose is available in order to make D-ribose! So new ATP cannot be easily made when you are really run down. Recovery takes days!

Worse than that, lactic acid has to be converted back to pyruvate - but this requires a lot of energy (ATP) to do this. So lactic acid hangs about for a long time causing pain.

The biological basis of treatment is therefore explained:

1. PACE - do not use up energy faster than your mitos can supply it.

2. FEED THE MITOCHONDRIA - supply the raw material necessary for the mitochondria to heal themselves and work efficiently. This means feeding the mitos correctly so they can heal and repair.

3. ADDRESS THE UNDERLYING CAUSES as to why mitochondria have been damaged. This must also be put in place to prevent ongoing damage to mitos. In order of importance this involves:

A- Pacing activities to avoid undue stress to mitos

B-Getting excellent sleep so mitos can repair

C-Excellent nutrition with respect to: taking a good range of micronutrient supplements, stabilising blood sugar levels, identifying allergies to foods

D-Detoxifying to unload heavy metals, pesticides, drugs, social poisons (alcohol, tobacco etc) and volatile organic compounds, all of which poison mitos.

E- Optimising gut fermentation - HYPOCHLORHYDRIA and PANCREATIC FUNCTION, GUT DYSBIOSIS

F-Addressing the common problem of hyperventilation


4. ADDRESS THE SECONDARY DAMAGE partly caused by mitochondrial failure such as immune disturbances resulting in allergies and autoimmunity, poor digestive function, hormone gland failure, slow liver detoxification.

The Perfect Test for Chronic Fatigue Syndrome

The central problem of chronic fatigue syndrome is mitochondrial failure resulting in poor production of ATP. ATP is the currency of energy in the body and if the production of this is impaired then all cellular processes will go slow. It is not good enough to measure absolute levels of ATP in cells since this will simply reflect how well rested the sufferer is. The perfect test is to measure the rate at which ATP is recycled in cells and this test has now been developed by the brilliant medical biochemist Dr John McLaren Howard. He calls it "ATP profiles". It is a test of mitochondrial function.

Not only does this test measure the rate at which ATP is made, it also looks at where the problem lies. Production of ATP is highly dependent on magnesium status and the first part of the test studies this aspect(A).

The second aspect of the test (B) measures the efficiency with which ATP is made from ADP. If this is abnormal then this could be as a result of magnesium deficiency, of low levels of Co-enzyme Q10, low levels of vitamin B3 (NAD) or of acetyl L-carnitine.

The third possibility (C) is that the protein which transports ATP and ADP across mitochondrial membrane is impaired and this is also measured.

The joy of the ATP profiles test is that we now have an objective test of chronic fatigue syndrome which clearly shows this illness has a physical basis. This test clearly shows that cognitive behaviour therapy, graded exercise and anti-depressants are irrelevant in addressing the root cause of this illness.

To get the full picture I recommend combining this test with measuring levels anti-oxidants such as Co-enzyme Q10, superoxide dismutase (SODase), and glutathione peroxidase together with NAD (an element in the process of energy production).

Cell free DNA is very useful because it measures severity of the illness. When cells are damaged and die, they release their contents into the blood stream - cell free DNA measures the extent of this damage. The levels which come back are similar to those from patients recovering from major infections, trauma, surgery or chemotherapy - so this test puts CFS firmly in the realms of major organic pathology. SODase is an important antioxidant which mops up the free radicals produced in all the inefficient chemical reactions in the cells. Dr McLaren Howard also looks at the genes which code for the different types of SODase! It is common to find blockage or polymorphisms typical of toxic stress.

In fact, all of these blood tests have now been combined as a MITOCHONDRIAL FUNCTION PROFILE (which combines the "ATP profiles" and tests of antioxidant levels) and can be ordered from my practice - see details below.

The two other important co-factors in the production of energy in cells are L-carnitine and D-ribose. The latter is used up so quickly by cells that measuring levels is unhelpful, but low levels of ATP imply low levels of D-ribose. Acetyl L Carnitine is supplemented as routine.

The cost of the Mitochondrial Function Profile, which will now include the mitochondrial function studies (ATP profiles), levels of Co-enzyme Q10, glutathione peroxidase, zinc copper SODase, manganese SODase and extracellular SODase together with NAD levels and cell-free DNA is £195, plus £50.00 for the letter of interpretation to the GP.

John McLaren Howard now has specialist equipment to refine these tests further, particularly in respect of oxidative phosphorylation.

Severe CFS is also low cardiac output secondary to mitochondrial malfunction

Two papers have come to my notice recently, which make great sense of both my clinical observations and also the idea that CFS is a symptom of mitochondrial failure. The two symptoms I am looking for in CFS to make the diagnosis is firstly very poor stamina and secondly delayed fatigue. I think I can now explain these in terms of what is going on inside cells and the effects on major organs of the body. More importantly, there are major implications for a test for CFS and of course management and recovery.

If mitochondria (the little batteries found inside every cell in the body) do not work properly, then the energy supply to every cell in the body will be impaired. This includes the heart. Many of the symptoms of CFS could be explained by low cardiac output because the heart muscle cannot work properly. Cardiologists and other doctors are used to dealing with low cardiac output due to poor blood supply to the heart itself. In CFS the low cardiac output is caused by poor muscle function and therefore strictly speaking is a cardiomyopathy. This means the function of the heart will be very abnormal, but traditional tests of heart failure, such as ECG, ECHOs, angiograms etc, will be normal.

Firstly MicroRespiratory studies which look at oxidative phosphorylation (conversion to ADP to ATP) in more detail. Secondly translocator protein studies which look in more detail at how well ATP and ADP move across mitochondrial membrane. The point is that the blood supply to the heart is fine (fuel and oxygen adequate) but the mitochondria cannot convert this to ATP which is the currency of energy for muscle contraction.

Research by Dr Arnold Peckerman www.cfids-cab.org/cfs-inform/Coicfs/peckerman.etal.03.pdf  shows that cardiac output in CFS patients is impaired. Furthermore the level of impairment correlates very closely to the level of disability in patients. Dr Peckerman was asked by the US National Institutes of Health to develop a test for CFS in order to help them to judge the level of disability in patients claiming Social Security benefits. Peckerman is a cardiologist and on the basis that CFS patients suffer low blood pressure, low blood volume and perfusion defects, he surmised CFS patients were in a low cardiac output state. To test this he came up with Q scores.

"Q" stands for cardiac output in litres per minute and this can be measured using a totally non-invasive method called Impedence Cardiography. This allows one to accurately measure cardiac output by measuring the electrical impedence across the chest wall. The greater the blood flow the less the impedence. This can be adjusted according to chest and body size to produce a reliable measurement (this is done using a standard algorithm). It is important to do this test when supine and again in the upright position. This is because cardiac output in healthy people will vary from 7 litres per min when lying down to 5 litres per min when standing. In healthy people this drop is not enough to affect function. But in CFS sufferers the drop may be from 5 litres lying down to 3.5 litres standing up. At this level the sufferer has a cardiac output which causes borderline organ failure.

This explains why CFS patients feel much better lying down. They have acceptable cardiac output lying down, but standing up they are in borderline heart and organ failure. CFS is therefore the symptom which prevents the patient developing complete heart failure. Actually, everyone feels more rested when they are sitting down with their feet up! The subconscious has worked out that the heart has to work less hard when you are sitting down with your feet up - so we do so because we feel more comfortable!

Low cardiac output explains the symptoms of CFS

The job of the heart is to maintain blood pressure. If the blood pressure falls, organs start to fail. If the heart is working inadequately as a pump then the only way blood pressure can be sustained is by shutting down blood supply to organs. Organs are shut down in terms of priority, i.e. the skin first, then muscles, followed by liver, gut, brain and finally the heart, lung and kidney. As these organ systems shut down, this creates further problems for the body in terms of toxic overload, susceptibility to viruses which damage mitochondria further, thus exacerbating all the problems of the CFS sufferer.

1. Effects on the Skin

If you shut down the blood supply to the skin, this has two main effects. The first is that the skin is responsible for controlling the temperature of the body. This means that CFS patients become intolerant of heat. If the body gets too hot then it cannot lose heat through the skin (because it has no blood supply) and the core temperature increases. The only way the body can compensate for this is by switching off the thyroid gland (which is responsible for the level of metabolic activity in the body and hence heat generation) and so one could get a compensatory under active thyroid. This alone worsens the problems of fatigue.

The second problem is that if the micro-circulation in the skin is shut down, then the body cannot sweat. This is a major way through which toxins, particularly heavy metals, pesticides and volatile organic compounds are excreted. Therefore the CFS sufferer's body is much better at accumulating toxins, which of course further damage mitochondria.

2. Symptoms in Muscles

If the blood supply to muscles is impaired, then muscles quickly run out of oxygen when one starts to exercise. With no oxygen in the muscles the cells switch over to anaerobic metabolism, which produces lactic acid and it is this that makes muscles ache and fatigue so much.

As well as the above problem, muscles in the CFS patient have very poor stamina because the mitochondria which supply them with energy are malfunctioning.

When we do translocator protein function tests it is common to find lactic acid stuck onto mitochondrial membranes - this illustrates one of the many vicious cycles in CFS - if TL protein is blocked by lactic acid, mitochondria work less efficiently and therefore one is more likely to switch into anaerobic metabolism and produce more lactic acid!

3. Symptoms in the Liver and Gut

Poor blood supply to the gut results in inefficient digestion, poor production of digestive juices and leaky gut syndrome. Leaky gut syndrome causes many other problems such as hypochlorhydria, allergies, autoimmunity, malabsorption, etc., which further compound the problems of CFS.

If liver circulation is inadequate, this will result in poor detoxification, not just of heavy metals, pesticides and volatile organic compounds, but also toxins produced as a result of fermentation in the gut again further poisoning the mitochondria.

4. Effects on the Brain

Last October I attended a conference sponsored by the late Dr John Richardson. A Canadian physician Dr Byron Hyde showed us some functional scans of the brains of CFS patients. If I had not known the diagnosis, I would have diagnosed strokes. This is because the blood supply to some area of the brain was so impaired. The default is temporary and with rest, blood supply recovers. However, this explains the multiplicity of brain symptoms suffered from, such as poor short term memory, difficulty multi-tasking, slow mental processing and so on. Furthermore brain cells are not particularly well stocked with mitochondria and therefore they run out of energy very quickly. Brain mitochondria are particularly dependent on blood sugar levels. Many brain symptoms are caused by HYPOGLYCAEMIA.

5. Effects on the Heart

There are two effects on the heart. The first effect of poor micro-circulation to the heart is disturbance of the electrical conductivity which causes dysrhythmias. Many patients with chronic fatigue syndrome complain of palpitations, missed heart beats or whatever. This is particularly the case in patients with poisoning by chemicals since the chemicals are also directly toxic to nerve cells.

The second obvious result is poor exercise tolerance. Heart muscle fatigues in just the same way that other muscles fatigue. Symptomatically this causes chest pain and fatigue. In the longer term it can cause heart valve defects because the muscles which normally hold the mitral valve open also fatigue.

THIS APPROACH TO TREATING HEART DISEASE IS EXACTLY THE SAME REGARDLESS OF THE CONVENTIONAL DIAGNOSIS. So patients with angina, high blood pressure, heart failure, cardiomyopathy, some valve defects as well as patients with cardiac dysrhythmias often also have mitochondrial problems and will respond in the same way to nutritional therapies and detox therapies.

6. Effects on Lung and Kidney

The lung and kidney are relatively protected against poor micro-circulation because they have the largest rennin-angiotensin system, which keeps the blood pressure up in these vital organs. Therefore clinically one does not see CFS patients with kidney failure or pulmonary hypoperfusion.

Explanation of the Fatigue Problems in CFS Patients.

Energy to the body is supplied by mitochondria, which firstly produce NAD (nicotinamide adenosine diphosphate) from Kreb's citric acid cycle and this is used to power oxidative phosphorylation which generates ATP (adenosine triphosphate). These molecules are the "currency" of energy in the body. Almost all energy requiring processes in the body have to be "paid for" with NAD and ATP, but largely ATP. The reserves of ATP in cells are very small. At any one moment in heart muscle cells there is only enough ATP to last about ten contractions. Thus the mitochondria have to be extremely good at re-cycling ATP to keep the cell constantly supplied with energy.

If the cell is not very efficient at re-cycling ATP, then the cell runs out of energy very quickly and this causes the symptoms of weakness and poor stamina. The cell literally has to "hibernate" and wait until more ATP has been manufactured.

In producing energy, ATP (three phosphates) is converted into ADP (two phosphates) and ADP is re-cycled back through mitochondria to produce ATP. However, if the cell is pushed (ie stressed) when there is no ATP about, then it will start to use ADP instead. The body can create energy from ADP to AMP (one phosphate), but the trouble is that AMP cannot be re-cycled. The only way that ADP can be regenerated is by making from fresh ingredients, but this takes days to do. This explains the delayed fatigue seen in chronic fatigue syndrome.

So to summarise, the basic pathology in CFS is slow re-cycling of ATP to ADP and back to ATP again. If patients push themselves and make more energy demands, then ADP is converted to AMP which cannot be recycled and it is this which is responsible for the delayed fatigue. This is because it takes the body several days to make fresh ATP from new ingredients. When patients overdo things and "hit a brick wall" this is because they have no ATP or ADP to function at all.

Implications for Treatment

Many patients I see get well with my standard work up with respect to vitamins and minerals, diet, pacing and sleep. All these things must be put in place to repair and prevent ongoing damage to mitochondria so allowing them to recover. For mitochondria to recover they need all the essential vitamins, minerals, essential fatty acids and amino acids to manufacture the cellular machinery to restore normal function. The mitochondrial function tests then allow us to identify lesions which can be corrected by attention to nutritional supplements, improving antioxidant status, detoxing, hyperventilation or whatever. CFS sufferers have limited reserves of physical, mental and emotional energy and this test allows us to direct those energies into the most fruitful line of approach.


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Friday, January 23, 2009

One-Page Fact Sheet

The usual disclaimer: in the US, CDC effectively eliminated your ability to get an ME diagnosis; only a very few activist doctors are willing to dispute their attempt to re-name it CFS by giving you the historic ME name for your condition.
 
 
*please repost* *please repost* *please repost* *please repost*

This is a one page fact sheet designed to get the basic facts across quickly
(especially to friends and family who don't understand why we are so limited
with being active).

Soon I'll be adding it to the end of lots of different papers on the site,
to serve as a summary. You can view and download it now, here:

www.ahummingbirdsguide.com/whatismesummary.htm

-------

Myalgic Encephalomyelitis: The simple facts by Jodi Bassett, January 2009

·         Myalgic Encephalomyelitis is a neurological disease that is very
similar to multiple sclerosis (M.S.) and polio (poliomyelitis). Earlier
names for M.E. were 'atypical multiple sclerosis' and 'atypical polio.'


·         The term Myalgic Encephalomyelitis was coined in 1956 (using
evidence from M.E. autopsies) and means: My = muscle, Algic = pain,
Encephalo = brain, Mye = spinal cord, Itis = inflammation.


·         Myalgic Encephalomyelitis has been recognised by the World Health
Organisation since 1969 as a distinct organic neurological disease with the
code G.93.3.


·         Myalgic Encephalomyelitis is primarily neurological, but also
involves cognitive, cardiac, cardiovascular, immunological,
endocrinological, metabolic, respiratory, hormonal, gastrointestinal and
musculo-skeletal dysfunctions and damage. M.E. also causes an inability to
maintain bodily homeostasis. M.E. affects all bodily systems. There are more
than 60 individual symptoms of M.E.


·         Myalgic Encephalomyelitis is an acute (sudden) onset, infectious
neurological disease caused by a virus. M.E. occurs in epidemics as well as
sporadically. There is ample evidence that M.E. is caused by the same type
of virus that causes polio; an enterovirus.


·         Myalgic Encephalomyelitis can be more disabling than MS, polio and
many other serious diseases. M.E. is one of the most disabling diseases
there is. More than 30% of M.E. patients are housebound, wheelchair-reliant
and/or bedbound and are severely limited with even basic communication.


·         Why are people with Myalgic Encephalomyelitis so severely (and
uniquely) disabled? To keep you alive, just at the most basic level, your
heart has to pump a certain amount of blood. Every time you want to do
something (other than lie completely still), the amount of blood your heart
needs to pump is increased. Every noise you hear, every word you speak,
every second you move or sit upright, and every word you read and every
thought you think... every little thing you do requires more blood to be
pumped.

      The problem is that the hearts of people with M.E. only pump just
enough for them to stay alive, with very little left over. This is why
people with M.E. are so severely limited with physical, cognitive and
orthostatic activity and sensory input.

      This cardiac insufficiency is why every conversation, light or noise,
every brief walk or sit can affect M.E. patients so much, and make them so
much more severely ill and disabled and cause such extreme extra suffering
for so long afterward.

      If activity levels exceed cardiac output by even 1%, death occurs. So
the activity levels of M.E. patients must remain strictly within the limits
of their reduced cardiac output, just for them to stay alive.


·         Myalgic Encephalomyelitis is a testable and scientifically
measurable disease that is not difficult to diagnose (within just a few
weeks of onset) using a series of objective tests (eg. MRI and SPECT brain
scans). Abnormalities are also visible on physical exam in M.E.


·         In some cases Myalgic Encephalomyelitis is fatal. (Causes of death
in M.E. include heart failure.)


·         Myalgic Encephalomyelitis is a long-term/lifelong disease that
affects more than a million adults and children worldwide.



Permission is given for this unedited document to be freely redistributed,
please redistribute this text widely.

------

(Of course the quote above leaves out a lot of what is happening with M.E.,
it is only a very brief and simple explaination designed to get the basics
facts through to non-M.E. patients, very quickly. It is also true that this
description (and this whole paper) is inaccurate with regard to those
non-M.E. patients who may merely qualify for a 'CFS' or 'ME/CFS'
misdiagnosis. This information is only relevant to M.E. and M.E. patients!)


Best wishes everyone,
Jodi Bassett
--
A Hummingbirds Guide to Myalgic Encephalomyelitis:
www.ahummingbirdsguide.com
--
"All that is essential for the triumph of evil is that good men do nothing"
Edmund Burke
-- 
 
 


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Newsletter and YouTube Videos from Hummingbirds Guide

Hello and welcome to the 'A Hummingbirds Guide to Myalgic Encephalomyelitis'
e-newsletter for January 2009

I hope this newsletter finds you and yours doing as well as possible and
that 2009 is treating you well, so far.

I have a quite a few new things to tell you about this month.

-----

A new paper is available: Who benefits from 'CFS' and 'ME/CFS'? by Jodi
Bassett and co-written/edited by Lesley Ben

"For whose benefit was 'Chronic Fatigue Syndrome' created, and for whose
benefit is it so heavily promoted despite its utter lack of scientific
credibility?

Who benefits from Myalgic Encephalomyelitis and 'CFS' being mixed together
through unscientific concepts such as 'CFS/ME' and 'ME/CFS' and Myalgic
'Encephalopathy'?

Who benefits from the facts of M.E. remaining ignored, obscured and hidden
in plain sight?"


This important new paper looks at all of these questions, and how we can
move forward from here (finally).

If you've ever thought 'WHY is this political and medical nightmare
happening?' and 'HOW is this mess/hell/injustice allowed to happen and how
did it come about?' or you aren't sure what to say/send when others ask you
similar questions.... then this paper is for you!

See: www.ahummingbirdsguide.com/whobenefitsfromcfs.htm

-------

Three new M.E. videos are available

The three new videos are:


1. 'Some facts about Myalgic Encephalomyelitis (and me)'  04:20

A brief description of some basic facts about M.E. and my experience with
having M.E. for the last 13 years.

See: http://www.youtube.com/watch?v=VGoeMZkrThc


2. 'What getting Myalgic Encephalomyelitis feels like (to me)' 07:24

Some brief comments on what it feels like to get M.E. This video also
highlights the importance of avoiding overexertion if you have M.E.

See: http://au.youtube.com/watch?v=lPKf6POuQSo


3. Treating Myalgic Encephalomyelitis: The basics 07:37 and 06:33

Some of the basics of how to live with, cope with and treat M.E.

Part 1: http://www.youtube.com/watch?v=X6yctpWL7uk
Part 2: http://www.youtube.com/watch?v=HrAYqzh9rk4


To download audio or text versions of these videos see:
http://www.ahummingbirdsguide.com/topicaudioandvideo.htm

-----

Two new updated papers!

1. Treating M.E. - The Basics has been updated and now includes more
information about the benefits of high-dose ubiquinol (reduced CoQ10) and
L Carnitine.

See: www.ahummingbirdsguide.com/treatingmethebasics.htm


2. What is M.E. - Summary has been updated and now includes a new one page
'ME: The basic facts' section added onto the end, which just sums up the
basic facts about M.E. in simple language, using bullet points. An excerpt:

"Why are people with Myalgic Encephalomyelitis so severely (and uniquely)
disabled?

To keep you alive, just at the most basic level, your heart has to pump a
certain amount of blood. Every time you want to do something (other than lie
completely still), the amount of blood your heart needs to pump is
increased. Every noise you hear, every word you speak, every second you move
or sit upright, and every word you read and every thought you think... every
little thing you do requires more blood to be pumped.

The problem is that the hearts of people with M.E. only pump just enough for
them to stay alive, with very little left over. This is why people with M.E.
are so severely limited with physical, cognitive and orthostatic activity
and sensory input.

This cardiac insufficiency is why every conversation, light or noise, every
brief walk or sit can affect M.E. patients so much, and make them so much
more severely ill and disabled and cause such extreme extra suffering for so
long afterward.

If activity levels exceed cardiac output by even 1%, death occurs. So the
activity levels of M.E. patients must remain strictly within the limits of
their reduced cardiac output, just for them to stay alive."

See: www.ahummingbirdsguide.com/whatismesummary.htm

(Of course the quote above leaves out a lot of what is happening with M.E.,
it is only a very brief and simple explaination designed to get the basics
facts through to non-M.E. patients, very quickly. It is also true that this
description (and this whole paper) is inaccurate with regard to those
non-M.E. patients who may merely qualify for a 'CFS' or 'ME/CFS'
misdiagnosis. This information is only relevant to M.E. patients!)


Feedback and constructive criticism is welcome, as always. This new summary
paper will be added to many other papers on the site, in time.

------

New author pages and articles

1. A new featured author section is availible, featuring links to selected
writings by the very talented Lesley Ben.

Highly recommended is of course 'Who benefits from 'CFS' and 'ME/CFS'?' plus
Lesley's great article on the 'Lightning therapy' scam as well as her
comments on MERGE, Cheney and antioxidants and her great quotes that I've
used in several papers already!

See: www.ahummingbirdsguide.com/wlesley.htm


2. A new featured author section is availible, featuring selected writings
by Criona Wilson, mother of Sophia Mirza (who tragically died of severe
M.E.).

A link to a new video featuring Criona is also available. It goes without
saying that Criona is one of our real M.E. super heroes. She is an amazing
woman, and we need far more like her. (We may finally get somewhere then!)

See: www.ahummingbirdsguide.com/wcriona.htm


2. A new featured author section is availible, featuring selected
writings/letters by the wonderful Dr John H. Greensmith whose great letters
to newspapers about the true facts of M.E. make so many of us so happy to
see on such a regular basis.

See: www.ahummingbirdsguide.com/waauthors.htm


3. A new article is available by LK Woodruff: ICD-10-CM (USA) ready for
approval by USA Congress, Jan 2009

This article explains why it is more important than ever for us to separate
M.E. and 'CFS' and to stop using confusing and misleading terms and concepts
such as 'CFS/ME' and 'ME/CFS' and so on; especially in the US.

See: www.ahummingbirdsguide.com/wlkwoodruffpapers.htm#310695314


4. A new video featuring Annette Barclay explaining how you can help improve
the chances of success of 'The NICE M.E. Guidelines Judicial Review' in the
UK is available, see: www.youtube.com/watch?v=uojoJ07OktE

-------

A new page is available: On the 'Lightning Process' scam and other related
scams aimed at M.E. patients

Psychologically based 'treatments' touted by some groups as being very
beneficial or even curative for 'chronic fatigue' (a term used
interchangeably with 'CFS' and 'ME/CFS' and even M.E. by these groups) such
as 'Reverse Therapy,' 'Mickel Therapy,' 'Emotional Freedom Techniques' (EFT)
and the 'Lightning Process,' may or may not be useful for those with fatigue
caused by various emotional or behavioural problems, but they simply cannot
improve authentic M.E. In fact they can often cause very severe relapse.

If family members are pressuring you to participate in scams such as the
Lightning process, Reverse therapy, Mickel therapy, EFT and so on, in the
mistaken belief that they are safe, useful and appropriate treatments for
M.E., see the new Comments on the 'Lightning Process' (etc.) scam page.

See: www.ahummingbirdsguide.com/lightning.htm

Note: This page has just got started, it will be expanded further over the
next few months. Please feel free to send me a copy of anything you feel
would be a useful addition to the page too.

-------

A new 'group comments' page is available

Some comments and discussions in the AHGs Yahoo groups have been so
wonderful and useful, that I feel like they would be enjoyed by other
members of the M.E.community, so I have reposted some of them on the site
(with permission).

The first discussion topic available is: Group comments on being told 'you
look well' (when you are very ill with M.E.) and on getting nasty comments
related to M.E.

See: www.ahummingbirdsguide.com/groupscomments.htm#291757430


-------

A translation update

Lotte Mayar has updated and improved her translation into Dutch of 'M.E.:
The Medical Facts'

See: www.ahummingbirdsguide.com/translations.htm

-------

A technical query: Can anyone help??

I'm thinking of:

a. Making my videos available to be downloaded from my site, so people can
burn their own DVDs of my films ot give to friends and family who perhaps
aren't online

b. Burning some DVDs myself with all my films on and making them available,
copyright free, and as cheapy and cost-priced as possible, to those who want
them.

If I do both these things, what do I need to be aware of? What formats
should the films be in? AVI? WMV? MP4? Which formats are the most compatible
and compact etc.? What about DVD types? Any help and advice gratefully
recieved.


------

That's it for this month.

Congratulations to all those who made it this far!

All the best, as always, in your ongoing battle with M.E. or your loved
one's battle with M.E., until next month,


Jodi Bassett
--
A Hummingbirds Guide to Myalgic Encephalomyelitis:
www.ahummingbirdsguide.com

Do not for one minute believe that CFS is simply another name for Myalgic
Encephalomyelitis (M.E.). It is not. The CDC 1988 definition of CFS
describes a non-existing chimera based upon inexperienced individuals who
lack any historical knowledge of this disease process. Any disease process
that has major criteria, of excluding all other disease processes, is
simply not a disease at all; it doesn't exist. M.E. and CFS should be
separated as definitions. They are not the same. Dr Byron Hyde MD 2006

Far too many Drs, researchers and even (often self-claimed) experts are
continuing to lump ME, a neurogenic illness classified by the WHO under
G93.3, with 'CFS' (Fukada, et al), which is based on 'fatigue' and is
referred to as 'ill-defined', etc. Understanding the significant differences
is not difficult, when one is familiar with ME and knows what to look for.
PLEASE do all that you can to rectify this untennable situation!! Please
share this information. Too many years have been wasted already...too many
lives already lost. YOU can do this, if you just decide to. LK Woodruff

"All that is essential for the triumph of evil is that good men do nothing"
Edmund Burke

-----------

A HUMMINGBIRDS GUIDE ELECTRONIC NEWSLETTER NOTES:

1. if you'd like to unsubscribe, just reply to this newsletter (or email me
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2. Permission is given for you to forward this email (unedited). Please
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But what IS it, really?

Rik received the follow from Ken Friedman:

In the view of all attendees of the meeting held yesterday at the NJ
State Department of Health and Senior Services, the meeting was a success.

We did obtain a commitment from representatives of both houses of the
NJ State legislature for the passage of resolution supporting the
concept of the Neuroendocrine Immune Institute to be established in
New Jersey and in particular at the New Jersey Medical School.

As you know, Chronic Fatigue Syndrome is homeless in the federal
government. The CDC program for CFS is housed under infectious, viral
borne illnesses (which CFS may or may not be). The NIH program is
housed in the Office of Women's Health which has no money to support
research programs and gives the false impression that CFS is an
women's illness (which it is not!).

The establishment of a Neuroendocrine Immune Institute would finally
give CFS a home along with related illnesses. It would also increase
the efficiency and synergy of research, patient care, and education by
having similar illnesses researched and treated under one roof. Any
advances made in the treatment or understanding of one of these
illnesses would be quickly (if not immediately) shared with
researchers and healthcare practioners of the related illnesses. And
that would be good news.

It would be appreciated if organizations and their members (as
individuals) would search their souls and see if they are willing to
support this initiative.

Many thanks,

Ken

Kenneth J. Friedman, Ph.D.
Associate Professor
Department of Pharmacology and Physiology
New Jersey Medical School
185 South Orange Avenue
Newark, NJ 07103


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More from Ellen Goudsmit on ME


To avoid patients finding that scientists demolish their arguments by
pointing out inaccuracies, therefore undermining their credibility and the
evidence for the existence of ME, I wish to note the following errors or
oddities in a previous post:

The term Myalgic Encephalomyelitis was coined in 1956 (using evidence from
M.E. autopsies)..."

The term was not based on autopsies, but on speculation, given the symptoms.
I have this from the individuals involved. Some of the symptoms which they
took into account, e.g palsies, are rare now.   "Myalgic Encephalomyelitis
is an acute (sudden) onset, infectious neurological disease caused by a
virus. M.E. occurs in epidemics as well as sporadically. There is ample evidence that M.E. is caused by the same type of virus that causes polio; an enterovirus."

Sadly, there is not sufficient evidence that ME is always caused by a virus.
The research we need has not been done. For example, during the epidemics in
the Uk in the mid 80s, sympathetic researchers identified raised antibodies
to enteroviruses but not in every individual. koch's postulates were not
met. According to Dr. Chia, this may well be because it is difficult to
measure this family of viruses accurately.  Idem ditto, there is
insufficient evidence that the virus  maintains the condition. It is
difficult to differentiate ME from post-viral fatigue syndromes triggers by
other viruses, e.g. CMV. We need more research and better criteria to reduce
heterogeneity.   "The problem is that the hearts of people with M.E. only pump just enough for them to stay alive, with very little left over."

There is no evidence for this as a universal abnormality. Research with
Halter monitors sometimes indicate problems, but not always. It is a moot
point whether that is related to cognitive deficits.  "If activity levels exceed cardiac output by even 1%, death occurs. So the activity levels of M.E. patients must remain strictly within the limits of their reduced cardiac output, just for them to stay alive."

I have seen no published evidence to support this statement. If it were
true, the death rate would almost certainly be higher.   "Myalgic
Encephalomyelitis is a testable and scientifically measurable disease that
is not difficult to diagnose (within just a few weeks of onset) using a
series of objective tests (eg. MRI and SPECT brain scans). Abnormalities are
also visible on physical exam in M.E."

There is no diagnostic marker for ME, partly because there has not been the
research on ME, partly because there are no consensus research criteria to
study ME (as opposed to more broadly defined, similar fatiguing states).  I
am aware of only one published study using SPECT on ME. The abnormality
found was also documented in more broadly defined patients with CFS using
PET. Abnormalities on brain scans are also found in psychiatric disorders.
Without agreed research criteria, it is hard to test anything. Those
criteria need to identify core symptoms, allowing doctors to differentiate
between, say, patients with ME and individuals with symptoms resulting from
chronic stress. The heterogeneity of the syndrome is one reason for the
inconsistent results.

"Myalgic Encephalomyelitis is a long-term/lifelong disease that affects more
than a million adults and children worldwide."

Happily, I and others have known people who have recovered to a significant
degree, with no or few residual symptoms. Given the lack of criteria, there
have been no epidemiological studies into ME. We can only guess at its
prevalence.  Moreover, as it may occur in epidemics, the prevalence of the
illness tends to fluctuate over time, with known peaks as in the mid 50s and
mid 80s.

My personal beliefs, that ME is a distinct entity, usually triggered by an
infection are based on gut instincts, but little scientific proof. I am
still waiting for that, and find the obsession with broad concepts such as
gradual onset, post-trauma CFS frustrating.
    ---------------------------------------------------------------------- 
Ellen M. Goudsmit PhD CPsychol AFBPsS
Chartered Health Psychologist
Visiting Research Fellow, School  of Psychology
University of East London E15 4LZ
For information on ME and CFS, see:
http://freespace.virgin.net/david.axford/melist.htm  
 
 
 


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Wednesday, January 21, 2009

Thesis available online

The psychological aspects and management of the chronic fatigue syndrome. Doctoral thesis. EM Goudsmit. 1996.

This thesis, which includes a discussion of myalgic encephalomyelitis and some of the differences between ME and other fatigue states, plus the results of three studies (qualitative analysis of the illness, attributions, coping strategies etc, quantitative assessment of various predictors of disability, anxiety and depression, as well as the effects of a pragmatic, clinic-based, multi-component programme)  is now available to download, free of charge, via  the Electronic Thesis Online System (Ethos). Correction of typos identified after submission are not included. 

The patients who participated in the three studies were diagnosed with stricter criteria than those devised by the CDC.  For example, the participants in study 2 were recruited from the microbiology clinic of Dr. Betty Dowsett.

Results of the findings have been submitted to journals, but as specialists are well aware, it is difficult at this time to get psychological research on ME accepted if it does not promote the CBT model of CFS. The title of the thesis was not chosen by the author but reflects a compromise.

Available via:  http://ethos.bl.uk/OrderDetails.do?did=1&uin=uk.bl.ethos.318425
Or use search facility: http://ethos.bl.uk/Home.do

  ----------------------------------------------------------------------
Ellen M. Goudsmit PhD CPsychol AFBPsS
Chartered Health Psychologist
Visiting Research Fellow, School  of Psychology University of East London
 
 


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Monday, January 19, 2009

Perpetuating Factors in CFS/FM

Source: Psychosomatics
Vol 49, #6, pp. 470-477
Date: November/December 2008
URL: http://psy.psychiatryonline.org/cgi/content/abstract/49/6/470


[Review Article]

Customizing treatment of Chronic Fatigue Syndrome and Fibromyalgia: the role
of perpetuating factors
----------------------------------------------------------------------------
Boudewijn van Houdenhove, M.D., Ph.D., Patrick Luyten, Ph.D.
- From Dienst Liaisonpsychiatrie, UZ Gasthuisberg, Herestraat 49, B-3000
Leuven, Belgium. Send correspondence and reprint requests to Dr. Boudewijn
Van Houdenhove. e-mail: boudewijn. vanhoudenhove@uz.kuleuven.ac.be

Received October 4, 2007; revised December 13, 2007; accepted January 2,
2008.


Abstract

Background
Syndromes characterized by chronic, medically unexplained fatigue, effort-
and stress-intolerance, and widespread pain are highly prevalent in medicine.

Results
In chronic fatigue syndrome (CFS) and fibromyalgia (FM), various perpetuating
factors may impair patients' quality of life and functioning and impede
recovery. Although cognitive-behavioral and graded-exercise therapy are
evidence-based treatments, the effectiveness and acceptability of therapeutic
interventions in CFS/FM may largely depend on a customized approach taking
the heterogeneity of perpetuating factors into account.

Conclusion
Further research should clarify the aim and outcome of different treatment
strategies in CFS/FM, as well as the underlying mechanisms of change,
including those facilitating neurobiological recovery.

- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -

Syndromes characterized by chronic, medically unexplained fatigue, effort-
and stress intolerance, and widespread pain are highly prevalent in medicine,
from general practice to several medical specialties. Such syndromes cause
much individual and family suffering, and are often associated with serious
physical, mental, and social/professional disability.1

Operational criteria have been formulated, defining these symptom-pictures as
chronic fatigue syndrome (CFS)2 and fibromyalgia (FM;3 Table 1). However,
since both syndromes largely overlap, some authors ("lumpers") argue that
CFS and FM should be merged under the broad umbrella of "functional somatic
syndromes," whereas others ("splitters") plead for maintaining CFS and FM as
discrete entities.4 Although the scientific literature on CFS and FM still
follows distinct paths, there are increasing tendencies toward an
integrative approach of these and other stress-related somatic syndromes.5-7
In this article, we will assume the "lumper" point of view by using the
abbreviation CFS/FM.

On the other hand, it has become evident that patients with a CFS/FM
diagnosis are a heterogeneous group. In this respect, different subgroups
have been proposed, for example, depending on type of onset (sudden or
gradual, initiating infection or not, etc.),8 activity patterns (passive or
relatively active),9 or putative biological mechanisms,10 but no consensus
has been reached on this issue.

Current evidence-based treatments for CFS/FM mainly consist of cognitive-
behavioral therapy (CBT) and graded-exercise therapy (GET).1 However, despite
positive results in randomized, controlled trials (see metaanalyses11-13),
the use of these treatments in routine clinical practice is still problematic
- as, for example, reflected on websites of patient-support groups.14
Moreover, many questions remain about the therapeutic aim, strategies, and
outcome, as well as mediating and moderating processes underlying mechanisms
of change in CFS/FM treatment.15,16 Also, little attention has been paid to
the role of perpetuating factors
in explaining heterogeneity among CFS/FM
patients and to the way in which this heterogeneity may influence treatment
results.

Hence, the main aim of this article is to clarify the rationale of CFS/FM
treatment in light of the heterogeneity of perpetuating factors. We will
first outline a biopsychosocial model of the etiology and pathogenesis of
CFS/FM. Subsequently, we will review recent empirical evidence about the
role of perpetuating factors in the illness. Finally, we will argue that, in
clinical practice, the effectiveness and acceptability of therapeutic
strategies in CFS/FM may largely depend on customizing interventions to the
patient's personal set of perpetuating factors.


THE BIOPSYCHOSOCIAL MODEL

Etiological Factors

Although the etiology of CFS/FM is still uncertain, various precipitating,
predisposing, and perpetuating factors have been identified, suggesting that
multiple pathways may lead to the causation and persistence of the illness
(Figure 1).1,17

More concretely, a whole range of physical and psychosocial stressors seem to
play a precipitating role; familial-genetic factors, traumatic experiences,
personality/lifestyle factors, and previous episodes of depression may
increase vulnerability to CFS/FM, and various physical, perceptual-cognitive,
affective, personality-related, behavioral, social, and iatrogenic factors
may perpetuate the illness.1,17


Pathophysiological Hypothesis

The exact pathophysiology of CFS/FM remains unclear, yet it has become very
probable that the illness has a neurobiological substrate including subtle
disturbances in physiological regulatory systems; notably, the neuro-hormonal
stress system, different neurotransmitter systems, the immune system, and the
central pain-processing system.
1,17

Most neurobiological findings point to a hypo(re)activity of the
hypothalamic-pituitary-adrenal (HPA) axis, which may not only impede a
normal stress response, but also foster abnormal inflammatory activity.17-19
Also, the widespread pain and pain hypersensitivity of CFS/FM patients
(allodynia) may be based on central sensitization, in which cytokine-mediated
inflammation, as well as genetically-determined disturbances in
neurotransmitter balance, lead to decreased central pain inhibition.17­20

Many questions remain, however, about the causal significance of these
neurobiological findings.1,21,22 Nonetheless, the illness-narrative of most
CFS/FM patients,23 as well as retrospective studies,1,17 suggest that a
dysfunction of the stress system may be the primum movens of the illness,
whereby, after a long period of overburdening, a "switch" from hyper- to
hypofunctioning might take place, which, in turn might provoke a cascade of
further neuronal, neurohormonal, and immunological dysregulations. This
hypothesis nicely fits within McEwen's "allostatic load" paradigm,24 and it
has recently received preliminary support from a metaanalysis25 and a
population-based study.26

Finally, perpetuating factors may - often via vicious circles - not only
reinforce symptoms and disability, but presumably also impede recovery by
interacting with the pathophysiological basis of the illness, and/or
negatively influencing the patient's associated illness-perceptions and
illness-behavior. These factors, listed in Table 2, will be discussed below.


PERPETUATING FACTORS

Physical Factors

Deterioration of CFS/FM patients' physical condition logically results from
their decreased activity due to fatigue and pain. In turn, loss of muscle
power and endurance (cardiopulmonary functioning) reinforces and perpetuates
symptoms and makes daily functioning still more problematic.27

However, research findings about the precise role of physical deconditioning
in CFS/FM are equivocal. Taken together, findings converge to suggest that
the degree of physical deconditioning varies significantly among patients and
that - in contrast with previous theories - this factor does not seem to play
a specific pathophysiological role in the illness
.27

Furthermore, persistent sleep problems may make symptoms and functional
limitations in CFS/FM patients worse, often also through circular
interactions.
Nonetheless, the perpetuating role of disturbed sleep in CFS/FM
and the contribution of perceptual factors in this respect remain
unclear.28-30

Also, some biologically-oriented researchers have proposed that CFS/FM
patients frequently suffer from opportunistic infections (e.g., chlamydia and
mycoplasma microorganisms), which may be at least partly responsible for the
persistence of some symptoms.10 At this moment, however, there is no evidence
either for the validity of this hypothesis or for the pharmacological therapy
based on it (see, for example, the results of a large antibiotic trial in
patients with Gulf-War syndrome who showed CFS-like symptoms.31)


Perceptual-Cognitive Factors

Many CFS/FM patients are badly informed about their illness or lose their way
in the labyrinth of diverse theories and opinions (for example, on the
Internet). This uncertainty not only causes much stress, but also makes
symptoms and disability worse, and hinders efficient coping.32 Some patients
focus excessively on even minimal signs of physical distress (somatic
hypervigilance).33 Others show a tendency toward rigid somatic attributions
while vigorously rejecting psychological or psychiatric explanations,1 or
remain preoccupied with their functional limitations or catastrophize about
the prognosis of their illness.34 Such perceptual-cognitive biases may play
an illness-perpetuating role by making patients feel helpless, leading to
decreased self-efficacy.


Affective Factors

Chronic pain and fatigue are frequently associated with depression and
anxiety, and there are indications of neurobiological and familial-genetic
links between these different sets of symptoms and syndromes.35-37 Most
frequent are feelings of demoralization and frustration, in response to the
loss of earlier capabilities, but some CFS/FM patients show manifest major
depression, panic disorder, or posttraumatic stress disorder.38,39

Although the relationship between depression and chronic physical illness has
been much studied
in recent years,40 the exact nature, prevalence, and
therapeutic implications of comorbidity between depression and CFS/FM are
still a matter of debate.40­42 Nonetheless, it can be assumed that additional
depressive symptoms in these patients may perpetuate the illness by
reinforcing symptoms and increasing the risk of patients' negatively
spiralling into more severe functional limitations.

To what degree fear of movement and associated activity-avoidance may play a
perpetuating role in CFS/FM is unclear, but it seems fair to state that only
a minority of patients are really "kinesiophobic."
43,44

Finally it should be mentioned that, particularly in patients with FM, not
only high levels of negative affect have been demonstrated,45 but even more
pronounced deficits in positive affects, increasing the risk of depression in
response to illness-related stressors.46


Personality Factors

The role of personality in CFS/FM is largely terra incognita. Experienced
clinicians have described CFS patients as conscientious, hard-working
,
somewhat "neurotic," and introverted individuals with high personal
standards, a strong wish for social acceptance, and a life-history that is
often characterized by exceeding physical limitations.23

However, systematic research on the role of personality in hampering
adaptation to the illness - and thus perpetuating it - is still in its
infancy.47 Interesting research topics in this context would be the
following: links between personality and comorbid depression in CFS/FM;48
emotion regulation related to alexithymia,49,50 including biological measures
such as salivary cortisol;51 the way in which some CFS/FM patients may create
their own stress, for example, by being too perfectionistic;52 and the role
such personality and lifestyle factors may play in the prognosis of CFS/FM
and other functional somatic syndromes.53


Behavioral Factors

CFS/FM patients who do not accept their limitations or have difficulty
adapting are not only more emotionally distressed but may unintentionally
perpetuate their illness. Indeed, as soon as they feel somewhat less
fatigued, they may engage in inappropriate activities
, putting their
disturbed stress mechanisms under severe pressure and making recovery less
probable. Patients with a history of an overactive lifestyle may be
particularly prone to this "boom-and-bust" activity pattern
.54

In chronic-pain patients55 as well as in patients with a CFS diagnosis,56 it
has been found that "nonacceptance" is correlated with lower quality of life
and more associated psychiatric symptoms, but whether this also results in a
less favorable outcome of CFS/FM remains to be studied.


Social Factors


Lack of recognition and understanding is a perpetuating factor that cannot be
overestimated. Concretely, many CFS/FM patients complain of a skeptical
attitude or even disbelief from their family members ("You don't look ill!"),
as well as from private or governmental insurance agencies ("[This illness]
does not exist!").57-60 Such reactions not only cause extra stress for the
patient and diminish his or her quality of life
, but may also encourage
illness-behavior: in the words of Hadler:61 "when you have to prove you are
ill, you cannot get well."

Some CFS/FM patients - like other chronically ill patients - welcome the
sickness status because it provides them with a range of advantages, such as
a solicitous partner.62 In classical terms, this has been called "secondary
gain," but this illness-reinforcing mechanism can also be formulated in terms
of operant conditioning.63

Opinions differ as to whether membership in a CFS or FM patient-support group
might play a role in the prognosis of the illness. Nevertheless, a recent
investigation found that active - as compared with nonactive - support-group
members had more serious symptoms and showed a less favorable illness
outcome.64


Iatrogenic Factors

A final perpetuating factor may be the inadequate treatment behavior of
doctors and therapists.65 Some practitioners seduce the patient into
undergoing various investigations (e.g., sophisticated immunological tests) or interventions with dubious benefit (among them, the replacement of dental amalgam fillings
or long-lasting treatment with antibiotics or nutritional
supplements). Others impose unfounded beliefs onto patients, making them
catastrophize even more ("Your immune system is a total loss!"). Such
messages may decrease patients' self-efficacy beliefs and active coping
efforts, which, as studies discussed below demonstrate, are crucial
requirements for recovery.


FROM PERPETUATING FACTORS TO THERAPY

Aims, Strategies, and Outcome

The rationale of current treatment interventions in CFS/FM can be formulated
as follows: since the pathophysiology underlying the illness cannot be
actively (e.g., pharmacologically) corrected, treatment should aim at
creating optimal conditions for "natural" stress-system recovery by tackling
illness-perpetuating factors.

In this respect, cognitive-behavioral therapy (CBT) and graded-exercise
therapy (GET) have shown moderate efficacy in CFS/FM via randomized,
controlled trials (RCTs).11-13 However, the effect sizes for individual CBT
are significantly higher than those for CBT-based group programs.66,67 This
may, at least partly, be due to the heterogeneity of perpetuating factors,
implying that individual treatment may be better able to address this
heterogeneity. Also, therapeutic effects are not always maintained in the
long-term, and drop-out rates are fairly high,11,68,69 which may also be
related to insufficiently individualized treatment. Furthermore, we cannot
ignore the resistance of some researchers and patient organizations to CBT
and GET - particularly when they follow a fixed protocol.10,14

It seems crucial, therefore, that the clinical application of CBT/GET should
not be based on a "one-size-fits-all" approach, but should be carefully
tailored to the patient's personal needs.1,68 The recently-published NICE
(British National Institute for Health and Clinical Excellence) guidelines
for CFS/ME, similarly, recommend a customized therapy.70

Finally, opinions differ as to what might be an attainable therapeutic
outcome in CFS/FM. Should these patients, in the first place, accept their
ailment and learn to cope optimally with symptoms and functional limitations,
or should they strive for real recovery? And, in the latter case, how should
"recovery" be defined? Should patients, after a symptomatic and functional
improvement, stop defining themselves as CFS or FM patients, or should they
take account of their - possibly lifelong - vulnerability? These are
questions for which no definitive answer has yet been given. (Several
investigators15,16,71 have offered more extensive discussions.)


THERAPEUTIC PROCESSES

There is a manifest lack of knowledge about factors that could account for
and predict successful treatment in CFS/FM.1,68 What are the core therapeutic
ingredients of CBT and GET in these patients? Is therapeutic success
initially dependent on correcting cognitive-perceptual errors and behavioral
adaptation, or are there more fundamental factors at work, such as changes in
emotional processing?72 Are some perpetuating factors more difficult to
influence than others? Are there contraindications for these treatment
strategies ? How can these treatments lead to enduring adjustments of
personality traits, lifestyle, and life goals - rather than producing only
temporary changes, such as a deactivation of maladaptive cognitive-affective
schemas that could easily be reactivated by new stressors?73

Such questions - which are crucial in view of individualizing therapy -
should be studied via process-outcome studies, focusing on putative
mechanisms of change. In this respect, the question "what works, and for
whom?"1,68 could be best addressed by using a conceptual framework
distinguishing between predictors, mediators, and moderators.74

Today, such studies are still scarce. In FM, cognitive behavior and exercise
treatments have been shown to be most effective in distressed patients in
which the disorder has had a high impact on their daily life.68 In CFS, some
of the perpetuating factors discussed above (such as membership of a
self-help group, receipt of sickness-benefits, low sense of control, strong
focus on symptoms, emotional problems, and passivity) have been found to
predict negative treatment-outcome of CBT,1 whereas a decrease in
symptom-focusing predicted a positive outcome for GET.75 These findings are
congruent with studies in chronic low-back pain showing that changes in
catastrophizing and self-efficacy/helplessness in part mediated the effects
of a multidisciplinary rehabilitation program.76-78

Finally, although it has been suggested that a favorable therapeutic outcome
in CFS/FM might be paralleled by positive changes in the neurobiological
substrate of the illness,1 in line with recent evidence that CBT and exercise
may increase resiliency of the HPA axis,79-81 no definitive proof of such
effects in CFS/FM patients has been given until now.


Therapeutic Practice

In the clinical setting, individualized treatment should consist of three
components: First, adequate therapy of possible comorbid depression, anxiety, and sleep disturbances, as well as optimal pain control, should be carried out, to minimize patients' emotional and physical distress.82 Although
antidepressants certainly have a role to play in this respect,35 it remains
controversial whether these medications might also lead to lower levels of
fatigue.42

Second, the patient should be offered a plausible illness theory that can be
the starting-point for translating the therapeutic rationale into concrete
practice. In accordance with the presumed pathophysiology of CFS/FM, a
formulation in terms of "loss of stress-system resilience" could be useful,
since it points to real, although subtle, biologically-based disturbances; it
links physical and psychological factors, and has a nonstigmatizing and
"nonpsychiatric" character, implying multiple "handles" for therapeutic
change.

Third, we should discuss with patients which perpetuating factors will be
concretely targeted during the therapy and what, in his or her particular
case, might be realistic objectives. For most CFS/FM patients, it will be
helpful to learn to pace their activities
, instead of periodically exceeding
their limits and provoking repeated set-backs manifesting as post-exertional
malaise.71 Also, some patients must be assisted to rebuild their physical
condition, by overcoming "fear of movement," while, at the same time,
respecting their dysfunctional recovery mechanisms.27 Other persons must be
confronted, for example, by means of a "Socratic dialogue," to abandon their
erroneous or unfruitful illness-beliefs that foster catastrophizing and
undermine self-efficacy, replacing them by more helpful approaches.1 For some
patients, stress-management techniques such as relaxation training may be
useful, as well as counseling focused on acceptance-based55,56,83 or
affect-regulation46,72 principles. Some patients should be treated together
with their partner in order to find a common modus vivendi adapted to
intended life-changes. Still others need active coaching in their efforts for
progressive professional reintegration or search for medical/social
compensation.84 Also, many CFS/FM patients may benefit from gaining insight
into personality and lifestyle factors that have contributed to their
illness, since a better understanding of the past can help keep future stress
levels within acceptable limits and help find a new equilibrium.52,72

It logically follows from the above that results of randomized, controlled
trials in CFS/FM (such as the current therapeutic trial in the U.K. comparing
CBT, GET, and pacing85) can guide, but never be simply translated into,
clinical practice.86 Thus, future process-outcome studies should randomize
different subtypes of CFS/FM patients to different treatment conditions that
should be customized in turn to individual patterns of perpetuating factors.

Finally, it may be expected that a more personalized therapeutic approach may
foster the openness of patients and researchers to a pragmatic management of
symptoms and functional limitations, and counteract perceptions of
psychological or rehabilitative treatments as being inflexible and
dogmatic.10,14


CONCLUSION

Next to precipitating and predisposing factors, various perpetuating factors
seem to play a role in CFS/FM by interacting with neurobiological dysfunction
and associated perceptual and behavioral disturbances.

From a therapeutic point of view, CBT and GET (as well as other
interventions) should start from a plausible illness theory and focus on
perpetuating factors in a tailored, patient-centered way. Under these
conditions, psychological and rehabilitative treatments may improve quality
of life and functioning in CFS/FM patients and optimize their chances of
recovery.

Nonetheless, many uncertainties remain about the therapeutic aim, strategies,
and outcome, as well as the mechanisms of change underlying the
above-mentioned treatments, particularly with regard to the recovery of
stress-system functioning. Long-term follow-up studies are needed to provide
answers to these unsolved questions.


Figure Caption

FIGURE 1.
Biopsychosocial Model of Chronic Fatigue Syndrome/Fibromyalgia


Tables

TABLE 1. Operational Diagnostic Criteria for Chronic Fatigue Syndrome
(CFS)2 and Fibromyalgia (FM)3
---------------------------------------------------------------------------
CFS

Medically unexplained, persistent fatigue, of new onset, not due to ongoing
exertion, not substantially relieved by rest, and significantly reducing
previous activity levels
Four-or-more additional symptoms, for at least 6 months, among which are
multiple muscle/joint pains
concentration/memory disturbances
non-refreshing sleep
headache (new onset)
sore throat
tender lymph nodes
post-exertional malaise
---------------------------------------------------------------------------
FM

History of widespread pain for at least 3 months
Pain in 11 of 18 tender point sites on digital palpation
---------------------------------------------------------------------------


TABLE 2. Potential Perpetuating Factors in Chronic Fatigue Syndrome (CFS)/
Fibromyalgia (FM)
---------------------------------------------------------------------------
* Physical Factors
- Physical deconditioning26
- Sleep disturbance27-29
- Opportunistic infections9
* Perceptual-Cognitive Factors
- Lack of information31
- Somatic hypervigilance/preoccupation32
- Rigid somatic attribution1
- Catastrophizing33
- Low self-efficacy1
* Affective Factors
- Depression34-40
- Anxiety disorders37,38
- Kinesiophobia42,43
- Problematic affect regulation44,45
* Personality Factors
- Perfectionism/dependency22,46,51
- Introversion46
- Alexithymia48-50
* Behavioral Factors
- Lack of adaptation/acceptance54,55
- Periodic overactivity53
* Social Factors
- Lack of understanding56-59
- Secondary gain/operant conditioning61,62
- Membership in patient-support group63
* Iatrogenic Factors64
---------------------------------------------------------------------------


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--------
(c) 2008 The Academy of Psychosomatic Medicine

* * *
I have repeatedly been told that the first step to treating CFS/FM is to address the sleep disturbance -- as with any other illness, sleep deprivation can make you sicker.

Unfortunately, there are many doctors who are so focused on purely psychological explanations that they refuse to prescribe anything for that problem, and then blame the patient when the wrong medication doesn't help.

Despite the fact that I reported that doing more made me sicker, I was advised to "try harder" , "do more", "go back to work", by doctors who couldn't get their heads around the notion that I lost my job because I was physically ill, not depressed because I had lost my job. I belonged in bed, not at the office, but had continued going to work long after I should have taken to my bed. It was an extreme insult to me, both personally and physically, to be ordered to do more because the doctor couldn't fathom that I was already pushing myself to my limits, and possibly beyond. And, sure enough, when I stopped listening to doctors urging me to prove that I wasn't merely lazy and made the decision to stay in bed more and do less, I stopped the rapid decline.

Doctors are not always right. There ARE "iatrogenic factors" that can perpetuate your illness, and they need to accept that pushing desperately sick patients to "do more" to "prove you're not too lazy to work" is a major perpetuating factor for many CFS patients.


CORRECTED URL FOR COMMENTS
The correct URL for this webpage is: http://meagenda.wordpress.com/2007/09/07/nice-cfs-me-guideline-statement-by-the-me-association-07-september-2007/

The authors of the paper and the Editor of the Journal of Psychosomatics have been informed. Senior Editor, Ms Elizabeth Stone, has confirmed that a data supplement has been added to the online version of the review article at: http://psy.psychiatryonline.org/cgi/content/abstract/49/6/470 and that an Erratum notice will be published in the March-April print issue of the Journal. ------------------- Concerning error in refererences to: Journal of Psychosomatics Vol 49, #6, pp. 470-477 November/December 2008 URL: http://psy.psychiatryonline.org/cgi/content/abstract/49/6/470



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