Research on Chronic Fatigue Syndrome

[robinson]

As you might expect, this mysterious and hard to understand Medical problem, CFS, is turning out to have many possible sources as well as treatments. I can remember well when my good friend came down with this, in the prime of life, and the incredible suffering and grief he went through, because Doctors didn't know what it was, they labeled him as mental. As well as refused to treat.

He was anything but crazy or delusional. The biggest problem was the amount of pain exercise caused. You know how much it can hurt if you over do it with exercise? The next day or two the muscles can hurt, and you can be overly tired. Well this poor bastard was like that every day if he did even light work. It was horrible.

But enough anecdotal stuff. I just read a blog that claims CFS is delusional, and lots of money has been wasted on researching it. I thought to myself, what quackery. And a quick search showed that not only are researchers getting more and more information, they may have valid treatments. The following is just a sampling of some recent and current Medical research. You know, Evidence based Medicine stuff.

Potential Drugs for Improving Chronic Fatigue Syndrome

Chronic fatigue syndrome (CFS) is the current name for a disorder Characterized by debilitating fatigue and several associated physical, constitutional, and neuropsychological complaints. Specific symptoms reported by CFS patients are fatigue, difficult concentration, headache, sore throat, tender lymph node, muscle ache, joint ache, feverishness, and allergies.

There are several hypotheses about its etiology, including postinfectious, immunological, neuroendocrine, neurological, and psychological ones. A CNS dysfunction brought about by abnormal cytokine release in response to antigenic challenge has been described. Substantial evidences show a pivotal role for proinflammatory Cytokines (e.g., interleukin1, interleukin6, and tumor necrosis factor-{alpha}) in induction of CNS mediated responses such as fever, somnolence, and sickness behavior in acute infections. A significant elevation in serum levels of interleukin-1, and tumor necrosis factor-{alpha} in the patient with chronic fatigue syndrome have been reported.

http://neuro.psychiatryonline.org/cgi/content/full/19/4/472

Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise.

CONCLUSIONS: The response of CFS patients to incremental exercise associates a lengthened and accentuated oxidative stress together with marked alterations of the muscle membrane excitability. These two objective signs of muscle dysfunction are sufficient to explain muscle pain and postexertional malaise reported by our patients.

http://www.ncbi.nlm.nih.gov/pubmed/...med.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus

Normalization of the increased translocation of endotoxin from gram negative enterobacteria (leaky gut) is accompanied by a remission of chronic fatigue syndrome.

There is now evidence that chronic fatigue syndrome (CFS) is accompanied by an increased translocation of endotoxins from gram-negative enterobacteria through the gut wall, as demonstrated by increased prevalences and median values for serum IgM and IgA against the endotoxins of gram-negative enterobacteria. This condition can also be described as increased gut permeability or leaky gut and indicates intestinal mucosal dysfunction (IMD). Here we report a case of a 13 year old girl with CFS who showed very high values for serum IgM against the LPS of some enterobacteria and signs of oxidative and nitrosative stress, activation of the inflammatory response system, and IgG3 subclass deficiency. Upon treatment with specific antioxidants and a "leaky gut diet", which both aim to treat increased gut permeability, and immunoglobins intravenously, the increased translocation of the LPS of gram negative enterobacteria normalized and this normalization was accompanied by a complete remission of the CFS symptoms

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Genetic evaluation of the serotonergic system in chronic fatigue syndrome.

Of the polymorphisms examined, three markers (-1438G/A, C102T, and rs1923884) all located in the 5-HT receptor subtype HTR2A were associated with CFS when compared to NF controls. Additionally, consistent associations were observed between HTR2A variants and quantitative measures of disability and fatigue in all subjects. The most compelling of these associations was with the A allele of -1438G/A (rs6311) which is suggested to have increased promoter activity in functional studies. Further, in silico analysis revealed that the -1438 A allele creates a consensus binding site for Th1/E47, a transcription factor implicated in the development of the nervous system. Electrophoretic mobility shift assay supports allele-specific binding of E47 to the A allele but not the G allele at this locus. These data indicate that sequence variation in HTR2A, potentially resulting in its enhanced activity, may be involved in the pathophysiology of CFS.

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Seven genomic subtypes of Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS/ME): a detailed analysis of gene networks and clinical phenotypes.

Genomic analysis revealed some common (neurological, cancer, immunological, inflammatory, haematological) and some distinct (metabolic, endocrine, dermatological, cardiovascular, connective tissue) disease associations among the subtypes. Subtypes 1, 2 and 7 were the most severe, and subtype 3 was the mildest. Clinical features of each subtype were as follows: subtype 1 (cognitive, musculoskeletal, sleep, anxiety / depression); subtype 2 (musculoskeletal, pain, anxiety / depression); subtype 3 (mild); subtype 4 (cognitive); subtype 5 (musculoskeletal, gastrointestinal); subtype 6 (postexertional); subtype 7 (pain, infectious, musculoskeletal, sleep, neurological, gastrointestinal, neurocognitive, anxiety / depression). It is particularly interesting that in these genomically derived subtypes, there were distinct clinical syndromes and that those which were most severe were also those with anxiety / depression, as would be expected in a disease with a biological basis.

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Attenuated Morning Salivary Cortisol Concentrations in a Population-based Study of Persons with Chronic Fatigue Syndrome and Well Controls.

Results There was a significant interaction effect, indicating different profiles of cortisol concentrations over time between groups, with the CFS group showing an attenuated morning cortisol profile. Notably, we observed a sex difference in this effect. Women with CFS exhibited significantly attenuated morning cortisol profiles compared with well women. In contrast, cortisol profiles were similar in men with CFS and male controls. Conclusions CFS was associated with an attenuated morning cortisol response but the effect was limited to women. Our results suggest that a sex difference in hypocortisolism may contribute to increased risk of CFS in women.

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Successful use of a primary care practice-specialty collaboration in the care of an adolescent with chronic fatigue syndrome.

We report on the successful collaborative care of an adolescent with chronic fatigue syndrome between a primary care pediatrician and an academic chronic fatigue syndrome specialist located in different cities. Regular telephone and e-mail communication and clearly defined patient-care roles allowed for timely management of symptoms and marked clinical improvement. We discuss ways to improve the collaboration of primary care and subspecialty physicians for patients with chronic fatigue syndrome and children with special health care needs.

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

As might be expected with such a bizarre disease, they are finding all kinds of reasons/causes behind it, as well as what was suspected early on, there may be multiple reasons, and not a specific pathogen involved.

Who knows? At least some Doctors could be bothered to research and find out, rather than just claiming it is "a shared delusion".

 

[CaptainManacles]

As you might expect, this mysterious and hard to understand Medical problem, CFS, is turning out to have many possible sources as well as treatments. I can remember well when my good friend came down with this, in the prime of life, and the incredible suffering and grief he went through, because Doctors didn't know what it was, they labeled him as mental. As well as refused to treat.

He was anything but crazy or delusional. The biggest problem was the amount of pain exercise caused. You know how much it can hurt if you over do it with exercise? The next day or two the muscles can hurt, and you can be overly tired. Well this poor bastard was like that every day if he did even light work. It was horrible.

But enough anecdotal stuff. I just read a blog that claims CFS is delusional, and lots of money has been wasted on researching it. I thought to myself, what quackery. And a quick search showed that not only are researchers getting more and more information, they may have valid treatments. The following is just a sampling of some recent and current Medical research. You know, Evidence based Medicine stuff.

Potential Drugs for Improving Chronic Fatigue Syndrome


http://neuro.psychiatryonline.org/cgi/content/full/19/4/472

Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise.


http://www.ncbi.nlm.nih.gov/pubmed/...med.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus

Normalization of the increased translocation of endotoxin from gram negative enterobacteria (leaky gut) is accompanied by a remission of chronic fatigue syndrome.


http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Genetic evaluation of the serotonergic system in chronic fatigue syndrome.

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Seven genomic subtypes of Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS/ME): a detailed analysis of gene networks and clinical phenotypes.

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Attenuated Morning Salivary Cortisol Concentrations in a Population-based Study of Persons with Chronic Fatigue Syndrome and Well Controls.

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Successful use of a primary care practice-specialty collaboration in the care of an adolescent with chronic fatigue syndrome.

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

As might be expected with such a bizarre disease, they are finding all kinds of reasons/causes behind it, as well as what was suspected early on, there may be multiple reasons, and not a specific pathogen involved.

Who knows? At least some Doctors could be bothered to research and find out, rather than just claiming it is "a shared delusion".

I didn't see much in those links to lend strong evidence to the existence of CFS. Really, the fact that there are so many "reasons/causes" behind it lends evidence to the notion that it's fake. Especially when one considers the "symptoms" are all classically very succeptable to self-delusion or could be more easily explained by the person not eating well, excersizing enough, or just having general depression/not getting out.

 

[sthomson]

Disclaimer: my father was diagnosed with Chronic Fatigue Syndrome after presented rather classic symptoms: excessive fatigue, sleeping more than 18 hours a day, skin sores, depression, mental fogginess, etc., etc. Furthermore, a marked decrease in immune response is very noticeable: he gets sick easily and often (despite the relative lack of exposure to other people), and is increasingly allergic to common pollen and pet dander. People who say that every case of CFS is a result of some sort of delusional hypochondria has never lived with someone who has had CFS.

Here's and abstract from a relatively old study from the University of Alberta that indicates that patients diagnosed with CFS can be independently differentiated from patients with either depression or with neither depression nor CFS.

The U of A study was the first of its kind to use electrodermal activity--electrodes were placed on each hand--to investigate the differences among CFS, depression patients and healthy controls. Using tone and light stimuli, the results showed that CFS can be discriminated from those with major depression by recordings of skin temperatures and electrodermal activity.

Moreover, the profile of CFS patients is clearly different from normal controls, suggesting there is a clear biological basis to the condition.

 

[sthomson]

The full text of that study.

 

[SteveGrenard]

I didn't see much in those links to lend strong evidence to the existence of CFS. Really, the fact that there are so many "reasons/causes" behind it lends evidence to the notion that it's fake. Especially when one considers the "symptoms" are all classically very succeptable to self-delusion or could be more easily explained by the person not eating well, excersizing enough, or just having general depression/not getting out.

EEG abnormalities are not delusionally possible insofar as I am aware. I have cross posted my personal observation from another thread based on 12 years of reading EEGs to stage sleep in a sleep lab:

I am no expert on fibromyalgia or CFS but one interesting thing I have noticed about it is that when people who have the symptoms of either term are tested in the sleep lab their EEG almost without exception demonstrates the relatively rare condition of alpha sleep and/or alpha (rhythm) intrusion during sleep. EEG alpha rhythm occurs at a frequency of 7 to 14 cycles per second and is NORMALLY found in a person who is awake with eyes closed.

So it is normally a wake rhythm but here it is occuring in a person whose EEG
otherwise indicates they are asleep. I am not sure of the significance of this but it is
certainly a true physical anomaly that has a high correlation with people with CFS and
fibromyalgia. It may very well be related to the statement above concerning the
hyperactivity of the serotonergic (5-hydroxytryptamine; 5-HT) system in the brain.
Increased serotonin (5-HT) levels predictably would produce this type of EEG.

 

[Molinaro]

I was 9 years old when I learned, from talking to friends, that not everyone feels that day after weightlifting pain every moment of every day, in every muscle. They don't see touch and pain as like 2 pees in a pod where one cannot exist without the other.

Took a long time to figure out what it was. Turns out for me it was Malignant Hyperthermia.

When I was 5, I was hit by a car [4 broken ribs, broken femur] and had surgery to fix the leg. Afterwords I nearly died, from what was then interpreted as an alergic reaction to an antibiotic called Illosone (no longer used). I had a dangerously high temperature.

Flash forward 20 years to when I had a skeletal muscle biopsy to test for MH, and was positive.

If someone with MH is given the commonly used anasthetics, they have an 80% chance of dying of a run-away high temperature.

If you live, your muscles are permanently damaged by constant microspasms of small bundles of muscle fiber. The spasms are so violent that the individual muscle fibres tear. This results in a network of scar tissue binding neighbouring fibres together, which then tears when the muscles are used.

And that hurts... all the time.

Doctors orders is to avoid letting my muscles warm up from use. That makes it worse. I found it hard to stay in shape under that advice, and actuly prompty ignored it and rode 100 to 150 miles a day as a bike courier for 6 years. I got in great shape, and much, much worse pain and fatigue.

Now 12 years later, I havn't found anything that helps with the pain. Well, except for that hour I was under a mix of valium/demerol while the doctors tried to yank my arm back into the socket. I felt no pain then.

I've had to learn not to care that I'm in pain, to make it so that I don't mind. That part at least is all in my head.

 

[SteveGrenard]

This study from 2007 confirms alpha sleep intrusion and is looking for a correlation between it and RNase L which could not be demonstrated. They feel it may be related to anxiety. Of course drugs that prevent the reuptake of serotonin, SSRIs, are used to treat depression and anxiety so the correlation to (untreated) depression these authors posit in their conclusion may, or may not be relevant.

Am J Med Sci. 2007 Feb;333(2):78-84. Links
Defining the occurrence and influence of alpha-delta sleep in chronic fatigue syndrome.
Van Hoof E, De Becker P, Lapp C, Cluydts R, De Meirleir K.
Department of Human Physiology, Vrije Universiteit, Brussels, Belgium. Van.Hoof@vub.ac.be

BACKGROUND: Patients with chronic fatigue syndrome (CFS) present a disordered sleep pattern and frequently undergo polysomnography to exclude a primary sleep disorder. Such studies have shown reduced sleep efficiency, a reduction of deep sleep, prolonged sleep initiation, and alpha-wave intrusion during deep sleep. Deregulation of the 2-5A synthetase/RNase L antiviral pathway and a potential acquired channelopathy are also found in a subset of CFS patients and could lead to sleep disturbances. This article compiles a large sleep study database on CFS patients and correlates these data with a limited number of immune parameters as it has been thought that RNase L could be associated with these sleep disturbances. METHODS: Forty-eight patients who fulfilled 1994 Centers for Disease Control and Prevention criteria for CFS underwent extensive medical evaluation, routine laboratory testing, and a structured psychiatric interview. Subjects then completed a complaint checklist and a two-night polysomnographic investigation. RNase L analysis was performed by gel electrophoresis using a radiolabeled 2',5'-oligoadenylate trimer. Basic descriptive statistical parameters were calculated. RESULTS: Patients experienced a prolonged sleep latency, showed a low sleep efficiency index, and had a low percentage of slow wave sleep. The present alpha-delta intrusion correlated with anxiety; no correlations appeared, however, between alpha-delta sleep and immunologic parameters, including RNase L. CONCLUSIONS: The main findings are 1) validation of sleep latency problems and other sleep disturbances as already suggested by several authors; 2) alpha-delta intrusion seems associated with anxiety; and 3) elevated RNase L did not correlate with alpha-delta sleep.

The study below, published in 1995, has findings which differ from mine and which may be related to the fact our lab has seen alpha intrusion over leads C3 and C4 (central cerebral) which may not be the location of the leads used in their observations. They admit the electrode placement they used may not be the correct one optimized for detecting this rhythm. There are not many refs in MedLine on this subject although there are many general CFS sites that mention alpha intrusion and alpha sleep (alpha-delta sleep) which I was not aware of before this evening.

Sleep. 1995 Oct;18(8):702-6. Links
Determination of observer-rated alpha activity during sleep.
Flanigan MJ, Morehouse RL, Shapiro CM.
Department of Psychiatry, University of Toronto, Ontario, Canada.
Patients suffering from chronic fatigue syndrome (CFS) have been described as having alpha intrusion into sleep. In a separate study of the relationship between depression and CFS, we investigated the sleep of CFS patients. We could not detect any observable alpha anomaly in our group of CFS patients. It is possible that there is a subgroup of CFS patients in whom no alpha anomaly is present. However, the sleep electroencephalogram (EEG) montage used in our study was different to that employed by previous researchers. This paper investigates the influence of electrode derivations on the outcome of observable alpha ratings. We compared simultaneous recordings of sleep EEG using three commonly employed montages. Our results indicate that use of the mastoid reference (montage 1) results in the highest observer-related alpha. This may suggest that data regarding alpha intrusion should always be collected using montage 1. However, there is a possibility that the mastoid electrode is not electrically silent and is contaminating the data of the referenced channels. The implications of these findings are discussed in relation to the validity of alpha intrusion measurement of CFS and fibromyalgia.

 

[quixotecoyote]

I was diagnosed with CFS in high school. In my (anecdotal) experience the diagnosis was used as a catch-all category for symptoms that didn't match up. Given that after I came back to school after missing a year, all the ******** who made my life miserable had graduated and I never had another symptom. I say it was psychosomatic depression in my case, but there could be accurate diagnoses out there I suppose..

 

[casebro]

CFS is a syndrome. A syndrome is a collection of symptoms held in common amongst patients. Could have many causes. Like the way that diabetes has a couple dozen genetic links.

My wrong diagnosis of fibromyalgia turned out to be a 'hereditary, congenital myopathy'. Like Molinaro's problem, proven by a muscle biopsy. Among other findings, my biopsy showed ragged red fibers, which is an indication of mitochondrial metabolism problems. At least now I understand all those maternally inherited diseases in the family- they are mitochondrial. After complaining of aching leg muscles my whole life. Ten doctors gave me wrong diagnoses.

I'd get lots of post exertional cramps, and occasionally 'peed blood'- dark urine due to muscle cells dying from lack of energy.

Actually, it's one of many 'muscular dystrophies'.

CoQ 10, plus Acetyl-L-Carnitine seem to help.

ETA: The crux of my true diagnosis was when a Neurologist checked my Aldolase and CKs. Both being high means muscle cell damage. And oh yeah, " high liver enzymes" may be from muscles, the same enzymes do the same thing within muscle as within livers. But damaged muscles also give of CKs.

 

[Iamme]

Do researchers know every reason what makes people who feel good, feel good? You could make a list a mile long as to all that has to be right with someone, to make them feel really really great.

Well, now reverse this. You'd have to identify every single thing that can cause a person to get out of balance. Once that happens a chain reaction could occur regarding psychological and physiological problems becoming intertwined.

For anyone to ridicule someone with such a claimed disorder would be fool hardy, to condemn when all the unknowns can't possibly be known. Especially by some lay person spouting off. *I* get mad at people who even spout off about morbidly obese people (since *I* could not become remotely obese myself if I tried).

I know this guy who can drink 18 beers a day (for real, NO exageration) and stagger back and forth across a 33 foot wide road to finally make his way home. The next day he can be up at the crack of dawn and feel fine. I am not making this up. How can THIS be? Who has the answer to THIS? If I have 3 beers I might wake up stiff for the next 3 days. People's chemistry is different.

 

[robinson]

I didn't see much in those links to lend strong evidence to the existence of CFS.

The links were to recent/current research on a Medical Condition, one being studied all over the world. To insist, or state their is no such thing, is blatant quackery, as well as insulting to both the Doctors treating people, as well as the patients suffering. I didn't know anybody was still beating that dead horse, until I read it on a blog. Along with some other misinformation, it stated -

... chronic fatigue, mental fogginess, muscle aches, and other symptoms but with no physical findings. (Ask any internist or family practitioner what percent of patients have those symptoms.) That was the germ of the chronic fatigue syndrome epidemic that resulted when millions of people who were feeling tired or depressed suddenly realized they could have a real disease, and bandwaggoned together to form a mass sociogenic illness of unprecedented volume.

http://www.sciencebasedmedicine.org/?p=30

What? Even the CDC has a defintion.
http://www.cdc.gov/ncidod/diseases/cfs/about/definition/case_def_abridged.htm


So when I read something like:
"the chronic fatigue syndrome epidemic that resulted when millions of people who were feeling tired or depressed suddenly realized they could have a real disease"

I can't believe the person who wrote that is really a Doctor. I'm glad they are not in charge of research.

People who say that every case of CFS is a result of some sort of delusional hypochondria has never lived with someone who has had CFS.

Obviously. Maybe it is a case of "If you can't see it, it must not be real."

Excuse me for a minute, I'm still steaming over the stupid here:

A characteristic of episodic, localized sociogenic illesses - sick building syndrome, schoolgirl fainting, etc. - is that they spread by line of sight. Interestingly, this current epidemic spreads locally via a line of sight surrogate - local TV reports and newspaper columns, and that the predominant reported early centers were all in English speaking countries.

http://www.sciencebasedmedicine.org/?p=30

Sheesh. Where do people get this stuff from? Do they just make it up? I notice the blog offers no references or scientific evidence to back up the claims. Meanwhile, back in the real world:

Chronic fatigue syndrome in children aged 11 years old and younger.
Davies SM, Crawley EM.

Gloucester Royal Hospital, United Kingdom.

AIM: To describe children who presented to the Bath paediatric CFS/ME service under the age of 12. Method: Inventories measuring fatigue, pain, functional disability, anxiety, family history and symptoms were collected prospectively for all children presenting to the Bath CFS/ME service between September 2004 and April 2007. Data from children who presented to the service under the age of 12 were described and compared to those who presented at age 12 or older. RESULTS: 178 children (under the age of 18) were diagnosed as having CFS/ME using the RCPCH criteria out of 216 children assessed. The mean age at assessment for children with CFS/ME was 14.5 years old (SD 2.9). 32 (16%) children were under 12 years old at the time of assessment, four children were under 5 years old and the youngest child was 2 years old. Children under 12 were very disabled with mean school attendance of just over 40% (average 2 days a week), Chalder Fatigue score of 8.29 (CI 7.14 -9.43 maximum possible score=11) and pain visual analogue score of 39.7 (possible range 0-100). Comparison with the children aged 12 or older showed that both groups were remarkably similar at assessment. 24/26 children with complete symptom lists, would have been diagnosed as having CFS/ME using the stricter adult CDC criteria. CONCLUSION: Disability in the under 12 age group was high, with low levels of school attendance, high level of fatigue, anxiety, functional disability and pain. The clinical pattern seen is almost identical to that seen in older children and the majority of children would also be diagnosed as having CFS/ME using the stricter adult definition.

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

You might think there is something going on, after reading that. But maybe all them Doctors are just deluded or something. I dunno...

While researching this topic, I found an interesting connection. The following excerpt is from a scientific paper. Like all good science, it lists sources and references.

These extrapyramidal symptoms are thought to be due to the inhibition of the acetylcholinesterase in the human extrapyramidal area. Psychosis, delirium, aggression, hallucination and depression, may also be seen during recovery from the cholinergic syndrome. Other types of delayed neurobehavioural effects are seen amongst people exposed to low dose of organophosphorous compounds for prolonged periods. Levin et al[27] found a high level of anxiety in commercial sprayers of insecticides but not in farmers. Behan et al[28] observed that clinical features of psychological syndromes occurring after chronic exposure to organophosphorous compounds had great similarity to chronic fatigue syndrome. A study of electrical activity of the brain of workers exposed to the organophosphorous compound 'sarin', showed that after one year of exposure, there were significant differences, as evidenced by increased beta activity, increased delta and theta slowing, decreased alpha activity and increase in the rapid eye movement during sleep when compared to normal controls. Kelly et al[29] have described a variety of behavioural and electroencephalographic changes in exposed persons. On electrophysiological examination, 'jitter' has been observed in those with chronic long term exposure to organophosphorous compounds. Defects in the perfusion have also been demonstrated using positron emission tomography which persist long after exposure to organophosphorous compounds.[30]

http://www.neurologyindia.com/artic...me=48;issue=4;spage=308;epage=13;aulast=Singh

I wonder what role organophosphorous compounds might play in CFS. The one thing that is true in the blog, is that it started in the Western world. While it is found all over the world, I wonder if it follows the same pattern as other industrial disease? Do isolated people free from western diet, life style and pollution have this problem? And if so, what does that mean?

While some might want you to think CFS is an imaginary disease of Americans, German Doctors have made great strides in treatment and research.
http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

I guess nobody told them it is just an imaginary American delusion.

 

[robinson]

Somebody needs to tell those crazy Italians that CFS is a delusion. They are not only finding genetic markers

RESULTS: There is a highly significant increase of TNF -857 TT and CT genotypes (p = 0.002) among patients with respect to controls and a significant decrease of IFN gamma low producers (A/A) (p = 0.04) among patients with respect to controls. CONCLUSIONS: We hypothesize that CFS patients can have a genetic predisposition to an immunomodulatory response of an inflammatory nature probably secondary to one or more environmental insults of unknown nature.

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

But doing research on animals with CFS!!

Retrospective analysis of immune dysfunctions found in 55 dogs and 62 cats diagnosed with Chronic Fatigue Syndrome (CFS), revealed leukopenia in 11% of dogs (n = 6) and 22.5% of cats (n = 14), lymphopenia in 14.5% of dogs (n = 8) and 10% of cats (n = 6), hypogammaglobulinaemia in 9% of dogs (n = 5) and 13% of cats (n = 8) and thrombocytopenia in 20% of dogs (n = 11) and 68% of cats (n = 42). All patients had creatine kinase enzyme levels above the normal range (CK = 5-100 IU/L) and carried micrococcus-like organisms on erythrocytes. Blood cultures proved positive for Staphylococcus spp. in 16 cases. After low-dosage arsenic-based therapy (thiacetarsamide sodium) all animals experienced complete clinical remission.

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

That is just crazy.

 

[CaptainManacles]

The links were to recent/current research on a Medical Condition, one being studied all over the world. To insist, or state their is no such thing, is blatant quackery, as well as insulting to both the Doctors treating people, as well as the patients suffering.

Cool, well, if you see anyone in this thread do that let me know. I'm just saying you're dumb and don't know what constitutes good evidence, and probably shouldn't be critisizing other people alongs those lines. That's a different claim then saying it doesn't exist.

 

[Elizabeth I]

I thought CFS had been shown to be a manifestation of Guillaume-Barre?

 

[luchog]

I thought CFS had been shown to be a manifestation of Guillaume-Barre?

That's one link that is being studied, but no conclusive evidence demonstrating an exclusive eitiology has ever been found. It's still believed that it may be one of many potential causes for the syndrome.

Personally, I'm very glad that they're finally getting some good, solid research done. I was diagnosed with CFS by two different doctors, and so far it's seemed like little more than a catch-all for a vaguely related constellation of symptoms that on one has any clue to the cause or causes of. And I do know that a number of people have been misdiagnosed with CFS; particularly those with certain autoimmune disorders (such as Hashimoto's disease, an autoimmune thyroid disorder).

Interestingly, in my case, I've decided to monitor my blood glucose levels and behaviour, since I know that I'm hypoglycemic, and in the last 7 or 8 years have been experiencing increasing CFS-like symptoms. What I've discovered is that there is something seriously wrong with the way my body processes glucose. Which makes me wonder if that's a causative factor in my case, or yet another symptom of whatever is causing the CFS.

 

[Professor Yaffle]

4 members of my family have been diagnosed with CFS, an in 3 cases they eventually found out that they had developed a food intolerance (gluten, yeast and milk). Removing the offending food cleared up their symptoms quick as you like. But only one of them had food intolerance suggested by their doctor, the other two had to figure it out for themselves. So I don't know if my family is an unusual case (we have a lot of allergies and intolerances generally), or whether there might be a lot more people out there suffering needlessly from CFS without a doctor even considering a food intolerance.

Also I would be careful of lumping together those who think it is imaginary, or delusional, with those who believe it has a psychological component, or believe that it is related to depression.

There are some doctors out there who think it is imaginary (my brother's doctor was one of these), but in my experience they are not the majority (at least in the UK).

 

[JJM]

You may find this interesting
http://www.sciencebasedmedicine.org/?p=30

 

[robinson]

You can't buy that kind of irony. I'm curious exactly how JJM could not get it. Oh wait, it's called "not reading a thread first syndrome".

Proteins in Spinal Fluid May Be Markers of Syndrome, Early Tests Show
By Miranda Hitti
WebMD Medical News

Dec. 1, 2005 -- Scientists may have found biological evidence of chronic fatigue syndrome.

Chronic fatigue syndrome involves severe, unexplained tiredness that lasts for at least six months and doesn't improve with rest.

Chronic fatigue syndrome often greatly interferes with patients' lives. But it hasn't been well understood from a scientific point of view, and its cause is unknown.

The new evidence lies in patients' spinal fluid. Tests show 16 proteins in the spinal fluid of people with chronic fatigue syndrome but not in healthy people, according to a study in BMC Neurology.

Chronic fatigue syndrome researchers offer physical evidence

"There are a number of medical professionals who don't believe that CFS exists in the first place," said Pazderka-Robinson. "The problem is, both CFS and depression are characterized by very similar profiles. Imagine a patient who approaches a doctor and tells him they feel depressed and tired all the time.

"Since depression shows a high co-morbidity with CFS, some CFS patients are often given antidepressants--that don't work or work poorly, since they do not address the underlying condition. Again, when these medications don't work, physicians sometimes jump to the conclusion that there isn't really anything, physically, wrong. Obviously, both misdiagnosis and the tendency for doctors to treat these patients as if they're not really sick can be extremely distressing. It can also undermine the patient's trust in the doctor and make them less likely to seek treatment if the condition worsens."

The most significant part of the research was to provide independent verification for CFS sufferers that these patients are different than normal controls and they're not "just depressed," said Pazderka-Robinson.

http://www.ualberta.ca/

Research Provides More Evidence That Chronic Fatigue Syndrome Is A Legitimate Medical Condition

ScienceDaily (Jan. 10, 2006) — Researchers at Georgetown University Medical Center have found that chronic fatigue syndrome (CFS) may be rooted in distinct neurological abnormalities that can be medically tested. Although the sample studied was small, this research provides objective, physiological evidence that the controversial disorder can be considered a legitimate medical condition.

Researchers might have found evidence that chronic fatigue syndrome is a real and legitimate neurological condition.

A pilot study published in the open access journal BMC Neurology reveals that patients with chronic fatigue syndrome (CFS) have a set of proteins in their spinal cord fluid that were not detected in healthy individuals. These proteins might give insight into the causes of CFS, and could be used as markers to diagnose patients with CFS.

 

[sthomson]

Professor Yaffle - in my father's case, a food sensitivity was discovered (in his case, corn), although I don't know how related that was to his CFS. It's difficult, in many cases of CFS, to determine what problems are causing/caused by CFS and which ones are ancillary. For my father, SSRI anti-depressants do help a little, as does a strict rice-tofu-broccoli diet (during food allergy elimination studies - that was a pretty bad period), as does cognitive therapy, as does strictly regulation of sleep time and activity time, as does avoiding "mental labor", and so on. But each change is so small, it's hard to tell whether that improvement is just due to time passing (as many CFS cases report gradual improvement over 5-10 years).

Of course, it's very important for docters to rule out viral, bacterial, immunological, and psychological causes before diagnosing CFS. But, when everything has been ruled out (as in my father's case), what's left? A daily struggle with symptoms that we've got to shoulder.

I'm actually glad that JJM brought up Morgellon's Disease (and I'm a bit disappointed that the article dismissed CFS without doing the research). The difference between Morgellon's disease and CFS is that CFS presents real, documentable symptoms that would be difficult for people to consciously or unconsciously create. Indeed, the initial reports of CFS did cause many more cases to come forward, but how does a doctor determine whether those were people who previously did not report symptoms, or whether those people created or exaggerated symptoms based on a news article or report? But when we look at modern cases, how can we attribute "line of site" causation when CFS is rarely or never reported? Indeed, in my father's case, he did not go to the doctor saying, "I think I have CFS" - he went to the doctor saying, "I'm sleeping all the time, I can't work, and you need to help me."