Figures and Tables at http://www.co-cure.org/Griffith.htm
The Primary Care Companion to the Journal of Clinical Psychiatry Vol. 10, #2, pp. 120-128
March 2008
http://psychiatrist.com/pcc/abstracts/abstracts.asp?abstract=pcc100206.htm
A systematic review of Chronic Fatigue Syndrome:
Don't assume it's depression
James P. Griffith, M.D., F.A.C.P., and Fahd A. Zarrouf, M.D. - From the Internal Medicine/Psychiatry Residency Program, West Virginia University, Charleston. - Corresponding author and reprints: Fahd A. Zarrouf, M.D., Medicine/ Psychiatry Residency Program, West Virginia University, 501 Morris St., 4 West, Charleston, WV 25326 fahdzarrouf@hotmail.com
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Abstract
Objective
Chronic fatigue syndrome (CFS) is characterized by profound, debilitating fatigue and a combination of several other symptoms resulting in substantial reduction in occupational, personal, social, and educational status. CFS is often misdiagnosed as depression. The objective of this study was to evaluate and discuss different etiologies, approaches, and management strategies of CFS and to present ways to differentiate it from the fatigue symptom of depression.
Study Selection and Data Extraction
CFS definitions, etiologies, differential diagnoses (especially depression) and management strategies were extracted, reviewed, and summarized to meet the objectives of this article.
Data Synthesis
CFS is underdiagnosed in more than 80% of the people who have it; at the same time, it is often misdiagnosed as depression. Genetic, immunologic, infectious, metabolic, and neurologic etiologies were suggested to explain CFS. A biopsychosocial model was suggested for evaluating, managing, and differentiating CFS from depression.
Conclusions
Evaluating and managing chronic fatigue is a challenging situation for physicians, as it is a challenging and difficult condition for patients. A biopsychosocial approach in the evaluation and management is recommended. More studies about CFS manifestations, evaluation, and management are needed.
"She is depressed," her physician wrote when referring Ms. A, a 65-year-old married woman, for a psychiatric consult. "She has been feeling tired for more than a year and described being exhausted most of the time, with headaches, joint pain, and problems with her concentration and memory. Her fatigue is frustrating for her and for her family; she cannot function well even in the morning. She denied being depressed, and does not have any previous mental or medical illnesses. Every lab I checked was normal. I still think that she is hiding her depression and manifesting it with all these somatic complaints."
Prolonged fatigue is defined as self-reported, persistent fatigue of 1 month or longer.1 Chronic fatigue syndrome (previously known as myalgic encephalomyelitis2 or neurasthenia3) is characterized by profound, debilitating fatigue and a combination of symptoms resulting in substantial reduction in occupational, personal, social, and educational status1,2,4-7 (see Table 1). Diagnosis of the chronic fatigue syndrome (CFS) can be made only after alternate medical and psychiatric causes of chronic fatiguing illness have been excluded.
At least 1 million Americans have CFS,1,8 more than have lung cancer or multiple sclerosis
; yet more than 80% go undiagnosed. In the primary care setting, the prevalence of CFS ranges from 3% to 20% and from 80% to 90% at the end of life.9,10 There are no ethnic or racial differences. Previous reports have mentioned a female:male ratio of 1.3:1,6 but a recent report by the U.S. Centers for Disease Control and Prevention (CDC) showed a female:male ratio of 4:1. It occurs most often in the 40- to 59-year age group and in the geriatric population.1,9,10Although the concept of neurasthenia was introduced in 1869 by George Miller Beard,3 CFS was defined in 1988 by the CDC, and while more than 3000 research studies have been done in this field, there is still some debate about the existence of this syndrome.1,11,12 The uncertainty about its existence and the lack of a specific laboratory test or marker to identify it, associated with hesitancy about making a diagnosis without knowing exactly how to treat it, all act as barriers to the diagnosis and treatment of CFS by primary care practitioners and psychiatrists.
Unlike the uncertainty about its existence, there is strong certainty about the impact of CFS. CFS patients, by definition, are functionally impaired and as disabled as patients with multiple sclerosis, heart disease, end-stage renal disease, and similar chronic conditions. The annual economic impact of CFS in the United States is estimated to be $9.1 billion in lost productivity.1
DATA SOURCES
A MEDLINE search was conducted to identify existing information about CFS and depression using the headings chronic fatigue syndrome AND depression. The alternative terms major depressive disorder and mood disorder were also searched in conjunction with the term chronic fatigue syndrome. Additionally, MEDLINE was searched using the term chronic fatigue. All searches were limited to articles published within the last 10 years, in English. A total of 302 articles were identified by these searches. Also, the term chronic fatigue syndrome was searched by itself. This search was limited to articles published within the last 5 years, in English, and resulted in an additional 460 articles. Additional publications were identified by manually searching the reference lists of the articles from both searches.
FATIGUE ETIOLOGIES
CFS cannot be considered either physical or psychological but instead requires a biopsychosocial approach to the illness. Numerous studies have tried to pinpoint specific etiologies by considering the following fields.
Genetic Etiologies
CFS is sometimes seen in members of the same family,13,14 but there is no evidence that it is contagious; instead, there may be a familial predisposition or a genetic link. The concordance rate was higher in monozygotic than in dizygotic female twins for chronic fatigue.15 Hickie et al.16 evaluated genetic and environmental determinants of prolonged fatigue in a twin study and found 44% (95% CI=25% to 60%) of the genetic variance for fatigue was not shared by the other forms of psychological distress, and also found that environmental factors made negligible contributions to fatigue. On the other hand, Cho et al.17 found evidence of a partly genetic influence, but environmental effects continued to be predominant. Clearly, further research is needed to explore these possible relationships.
Immunologic Etiologies
Abnormal natural killer cell cytotoxicity,18 increase immune activation markers,19 greater numbers of CD16+/CD3- natural killer cells,20 and the presence of interferon in serum and cerebrospinal fluid in CFS patients21 have been identified. Staines22 suggested the loss of immunologic tolerance to vasoactive neuropeptides or their receptors following infection, other events, or de novo as a mechanism.
Infectious Etiologies
Possible infectious etiologies have generated the most interest among CFS researchers. It has been postulated that chronic fatigue is a continuum ranging from cases with chronic viremia on the one hand to instances of frank psychiatric illness on the other.23 Multiple infectious agents have been linked to CFS, including Borna disease virus,24,25 parvovirus B19,26,27 glandular fever,28 Enterovirus,29 human herpesviruses 4, 6, and 7,30-32 infectious mononucleosis,33 Nipah virus encephalitis,34 and Q fever.35
Infections have not only played important etiologic roles, but also have been considered predictors of better prognoses when compared to noninfectious CFS cases.36 Human herpesvirus 6 reactivation has been suggested as an objective biomarker for fatigue.30
Endocrinology/Metabolism Etiologies
Hypothalamic-pituitary-adrenal (HPA) axis abnormalities have been studied as potential biological tests to diagnose CFS. Studies have shown HPA hypoactivity and higher chronic adrenocorticotropic hormone (ACTH) autoantibody levels as significant pathologic factors in CFS.37-39 Also reduced area under the ACTH response curve in CFS patients undergoing insulin tolerance test was significantly associated with the duration of CFS symptoms (r=-0.592, p=.005) and the severity of fatigue symptomatology.40 Other studies have suggested upregulation of hypothalamic 5-hydroxytryptamine receptors in patients with postviral fatigue syndrome but not in those with primary depression.41 However, another study showed no etiologic role for deficiency in central opioids or the HPA axis in the symptoms of CFS.42 Other biological factors have been investigated and considered as biological markers in CFS, including low magnesium level,43 low arachidonic acid level, low L-carnitine level,25 serum dehydroepiandrosterone (DHEA) sulfate deficiency,44 and impairments of the 2',5'-oligoadenylate (2-5A) synthetase/RNase L pathway.45 Other studies showed no role of linoleic acid, eicosatrienoic acid (both p>.05),25 ferritin, vitamin B12, folate, or serum erythropoietin levels.46
Mental/Neurologic Etiologies
Psychosocial factors are frequently thought to contribute to fatigue. Rangel et al.13 found that CFSin childhood and adolescence is associated with higher levels of parental mental distress, emotional involvement, and family illness burden than those observed in association with juvenile rheumatoid arthritis, a chronic pediatric physical illness. Endicott14 described stressors including earlier mortality age and increased prevalence of cancer, autoimmune disorders, and CFS-like conditions in parents of psychiatric patients with CFS as compared to control groups. Thirty percent of the CFS patients and none of the controls reported dilemmas in the 3 months prior to the CFS onset in one study.47 History of abuse, particularly during childhood, may play a role in the development and perpetuation of chronic fatigue,48 and childhood trauma was associated with a 3- to 8-fold increased risk for CFS across different trauma types in one study.49 Sleep is also an interesting etiologic factor, as many patients with CFS have sleep disorders, and those with sleep disorders showed greater functional impairment independent of their psychiatric disorders.50-52
FATIGUE: DON'T ASSUME IT'S DEPRESSION
Fatigue is a part of a wide spectrum of diagnoses ranging from being a symptom in depression, anxiety, seasonal affective disorder,53 and multiple other diagnoses to being a full syndromal disorder in CFS, yet CFS goes undiagnosed in 80% of cases and is often misdiagnosed as depression. The Diagnostic and Statistical Manual of Mental Disorders doesn't list CFS as a diagnosis although the International Classification of Diseases, 10th Revision, does.12 In clinical practice, CFS presentations range from complicated cases associated with a psychotic state resulting in multiple murders in one case report54 to noncomplicated presentations with multiple psychiatric disorders, primarily depression.55 It is very important to understand the distinctive features between chronic fatigue and depressive disorder when evaluating a patient with a main complaint of fatigue. A full detailed history accompanied by questionnaire forms can be very helpful to differentiate CFS from major depressive disorder. There is still no specific test that can confidently differentiate between them. Multiple studies have tried to find distinctive factors and they are listed in Table 2.
EVALUATION OF FATIGUE
Diagnosing CFS can be challenging for health care professionals for many reasons; the most important one is finding fatiguein a large number of illnesses and disorders. We reviewed information available about evaluation of chronic fatigue and discuss it in 3 parts: history, exam, and diagnostic tests.
History and Differentials
Because CFS is a diagnosis of exclusion,1 a full detailed history is considered essential. The history should include a detailed account of the symptoms, the associated disability, the choice of coping strategies, and importantly, the patient's own understanding of his/her illness.65 Every patient should be carefully evaluated for certain medical, psychiatric, and neurologic diseases that can cause fatigue as the most prominent symptom (Table 3). Two of the important differential diagnoses are depression and fibromyalgia. Although it is difficult to differentiate CFS from fibromyalgia confidently depending on the history or other reported differences of cognitive dysfunction components or clinical pain measures,66,67 CFS and fibromyalgia commonly co-occur within the concept of central sensitivity syndromes or functional somatic syndromes.68 This co-occurring increases functional impairment when compared to CFS individuals alone.69,70 Some of the distinguishing features between CFS and fibromyalgia include evidence for triggering viral infection and lower level of serum acylcarnitine observed in CFS patients, which is lacking in the majority of patients with fibromyalgia;71 slower information-processing in CFS patients compared to impaired control of attention in fibromyalgia patients;66 and lacking of the characteristic diffuse soft tissue pain and pain on palpation in at least 11 of 18 paired tender points in CFS patients.
Exam
Every CFS evaluation should include a mental status examination to identify abnormalities in mood, intellectual function, memory, and personality. Particular attention should be directed toward current symptoms of depressive, anxious, self-destructive thoughts and observable signs such as psychomotor retardation.1 Although there is no definite physical finding, a full and thorough physical examination may be helpful in excluding other conditions. Multiple studies have suggested dysautonomia with greater increase in heart rate together with a more pronounced systolic blood pressure fall on standing in CFS patients compared to healthy individuals.46, 72 Other studies found no statistically significant differences in either heart rate or galvanic skin resistance both during a normal day and before, during, and after exercise testing.73
Tests
The CDC has recommended the following initial screening tests when evaluating patients with CFS: urinalysis, total protein, glucose, C-reactive protein, phosphorus, electrolyte, complete blood count with leukocyte differential, alkaline phosphatase, creatinine, blood urea nitrogen, albumin, antinuclear antibody and rheumatoid factor, globulin, calcium, alanine aminotransferase or aspartate transaminase serum level, and thyroid function tests (thyroid stimulating hormone and free T4).1 Further tests or referral to specialists may be indicated to confirm or exclude a diagnosis that better explains the fatigue state or to follow up on results of the initial screening tests.
Multiple other studies have tried to find biomarkers or radiological markers for CFS. Erythrocyte sedimentation rate was normal in all 23 CFS patients in one study.74 Another study found that concentrations of C-reactive protein, beta_2-microglobulin, and neopterin were higher in patients with CFS (p=<.01).75 On the other hand, a study by Swanink et al.76 found that complete blood cell count, serum chemistry panel, C-reactive protein, and serologic tests were not different in 88 patients with CFS when compared to a control group. A potential role for DHEA in CFS, both therapeutically and as a diagnostic tool, was suggested in one study.64
Magnetic resonance imaging studies have been inconsistent, with some of them suggesting larger ventricular volumes.77-84 Functional magnetic resonance was more promising, as it showed quantitative and qualitative differences in activation of the working memory network,85 attenuation of the responsiveness to stimuli not directly related to the fatigue-inducing tasks,86 utilization of more extensive regions of the network associated with the verbal working memory system,87 impaired functioning and reduced gray-matter volume in the bilateral prefrontal cortex,88 and inactive ventral anterior cingulate after making an error.89
Single-photon emission computed tomography (SPECT) and brain electrical activity mapping scans were promising in one study,90 and SPECT scans showed more abnormalities than did magnetic resonance scans in one study (p<.025).91 Siessmeier et al.92 detected abnormalities in 18-fluorodeoxyglucose positron emission tomography in approximately half the CFS patients examined, but found that no specific pattern for CFS could be identified. Positron emission tomography showed an alteration of the serotonergic system in the rostral anterior cingulate in one study, which was suggested as an etiology.93 Recently, Puri94 described the application of proton neurospectroscopy and 31-phosphorus neurospectroscopy in chronic fatigue syndrome. It is essential to mention that evidence to date does not support routine use of the imaging modalities discussed above in evaluating potential CFS patients.
Finally, it is important to remember that a good history is more important than any available test to diagnose CFS and differentiate it from depression.
The algorithm shown in Figure 1, which is based on the CDC recommendations and the results of the studies reviewed, is suggested for evaluating chronic fatigue.
20 comments:
Nov. 6, 2006 -- Childhood trauma raises a person's risk of chronic fatigue syndrome by three- to eightfold, CDC researchers find.
Another study, based on data from the Swedish twin registry, shows stress to be a triggering factor for chronic fatigue syndrome (CFS). It also shows that emotional instability is a significant CFS risk factor, although genetic and family factors determine whether this personality trait leads to fatigue.
"Our observations lend support for the hypothesis that CFS represents a disorder of adaptation that is promoted by early environmental insults, leading to failure to compensate in response to challenge," conclude CDC researcher Christine Heim, PhD, and colleagues.
"Stress is a significant risk factor for chronic fatigue-like illness, the effect of which may be buffered by genetic influences," conclude Karolinska Institute researcher Kenji Kato, PhD, and colleagues. "Emotional instability assessed 25 years earlier is associated with chronic fatigue through genetic mechanisms contributing to both personality style and expression of the disorder."
Both studies appear in the November issue of Archives of General Psychiatry.
Stress, Emotional Instability, and CFS
Kato and colleagues looked at data on more than 19,000 twins born in Sweden from 1935 to 1958.
They found that emotionally instability was linked to a 72% higher risk of CFS symptoms. Emotional instability is a personality trait. People with emotional instability tend to have low self-esteem and feelings of anxiety, depression, and guilt.
But emotional instability, Kato and colleagues find, is only part of the equation. High levels of stress -- reported up to 25 years before CFS symptoms appeared -- increased CFS risk by 64%.
When the researchers looked only at twins sharing the same genetic makeup, they found that emotional instability no longer predicted CFS. But stress upped a twin's odds of having CFS by nearly sixfold.
This, Kato and colleagues conclude, means that while emotional instability is an important risk for CFS, whether a person with this personality trait actually gets CFS depends on unknown genetic and family factors. Thus, emotional instability is an indirect risk factor for CFS, while stress is a direct risk factor.
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SOURCES: Heim, C. Archives of General Psychiatry, November 2006; vol 63: pp 1258-1266. Kato, K. Archives of General Psychiatry, November 2006; vol 63: pp 1267-1272.
Worse Trauma, Higher CFS Risk
Heim's CDC team is studying CFS in a community-based sample of more than 56,000 residents of Wichita, Kan. At the time of the study, they had identified 43 people with ongoing CFS. For the study, they compared these people to 60 matched people without fatigue.
A key finding was that more severe childhood trauma was linked to a higher risk of CFS. And the type of childhood trauma was important, too. They found:
Eightfold higher risk of CFS with childhood sexual abuse.
5.9-fold higher risk of CFS with childhood physical neglect.
4.6-fold higher risk of CFS with childhood emotional neglect.
4.3-fold higher risk of CFS with childhood physical abuse.
2.9-fold higher risk of CFS with childhood emotional abuse.
"It appears that CFS is part of a spectrum of disorders that are associated with childhood adversity," Heim and colleagues suggest. "In adulthood, these disorders frequently manifest or worsen in relation to acute stress or challenge. … These disorders might reflect the brain's inability to adapt or compensate in response to challenge, leading toward maladaptive responses and ultimately disease."
Define "CFS". If you're referring to the post-viral version that I have, then there's no correlation at all between CFS and trauma/stress/abuse.
If you're referring to the nebulous thing that CFS has been morphed into by the psychiatric lobby, then there may be a correlation because psychiatric fatigue syndrome (and the symptom of chronic fatigue) do have psychological causes.
The problem is that researchers are mixing apples and oranges under the label "CFS". Technically, what I have is post-infectious Myalgic Encephalomyelitis, caused by something similar to the polio virus, but it's been almost impossible to get that diagnosis in the US since 1988, when the CFS label was applied.
The current definition of CFS essentially excludes the original patients in Incline Village, yet, they have not reinstated the ME label that is more accurate, so we're like men without a country ... we no longer have CFS, but in the US we aren't allowed to have ME, either, because CDC abolished that disease by executive fiat when they invented CFS.
I'm confused. Are you saying that you do not agree with these researchers findings because they are psychiatrists, for it would appear that they are referencing CFS.
I'm saying that there's two types of CFS -- the original type, which is caused by a virus, and the type studied by psychiatrists, which does not require viral onset.
The psychiatric lobby glommed onto CFS, and exploited the similarity of the name to psychiatric Fatigue Syndrome in order to get the newly available research dollars. Thus, what Dr. Cheney talks about when he says CFS (True CFS, or Myalgic Encephalomyelitis) is not the same as what Wessely/Straus/Reeves et al. talk about when they say CFS (any condition which causes chronic fatigue).
You need to read Dr. Kerr's research, where he finds 88 genetic abnormalities, and all the research connecting CFS to a virus, done by people who are studying True CFS, and not only the psychiatrists who have decided to mix apples in with the oranges so they can get additional research grants to study patients who DON'T have the symptoms of True CFS (listed in an earlier post).
It's a very common practice, since the beginning, for those who want to prove CFS=depression to load up their studies with patients who actually have depression and would not pass muster with any of the True CFS experts as having post-infectious CFS..
The simplest way to tell whether a patient has CFS or a psychiatric disorder is to send them out to exercise. A depressive will come home energized, with all their endorphins running, and may even feel up to cleaning the house because they feel so good. A CFS patient will return exhausted and collapse into bed, unable to do anything the rest of the day.
I've had close relationships with several depressives, and can describe the differences in detail. In the depths of a relapse, I would get up, bring in the newspaper, and collapse on the couch, unable to walk any further. The depressive wouldn't even get out of bed. They lack motivation to get up and do things, we happily get up to do one thing, but lack the energy to stay up to do the second and third.
As one fellow patient described it, if the house were on fire, a depressive would sprint out the door; she, however, would have to wait for the firemen to come in and rescue her, because she was so debilitated that she could not walk more than ten feet without falling down, not even in a life-or-death emergency.
A good history that includes investigation of the onset is the key. If the patient says "sudden", or "virus", or "infection", it's True CFS. If the patient describes the onset as "gradual" or "after I was assaulted", there's a good chance it's a psychiatric problem and not post-viral CFS.
There are immune and neurological abnormalities in True CFS that are not present in psychiatric problems. I've been known to run a fever for months on end, which is not possible with a purely-psychiatric problem. Again, the problem is that people hungry for research grants mixed apples and oranges, to the detriment of patients. One Click and ME Free For All have more information on their websites on the way British psychiatrists have taken over the CFS name and the problems it's caused to those who have ME a/k/a CFS.
As Dr. Greensmith points out two posts hence,
"As far as I know, there are no statistics exclusively for people with M.E. (*Myalgic Encephalomyelitis*), which have not been distorted by adding in other patients, with a variety of illnesses, in which chronic fatigue is said to be a symptom and calling them all ME/CFS."
That's why you're finding research that says it's psychological in origin, because the researchers aren't limiting themselves to patients who have what we have -- the new/improved/revised definition of CFS used by those researchers calls for only the symptom of chronic fatigue, and not all the other symptoms which define True CFS.
Dr. Katrina Berne notes that in depression "most symptoms of CFS and FMS are absent", "incidence of mood disorder same as in general population", and further notes that on the MMPI, depression causes elevation in scales 2/4/7, while CFS/fibro shows elevations of 1/2/3 "typical of chronic illness" and 7/8, i.e., very different from the picture of depression.
Dr. Sheila Bastien has developed a "unique psychoneurologic signature" for CFS, which looks nothing like depression.
Greensmith, Berne and Bastien are talking about what I have, not about some nebulous "chronic fatigue" of unknown etiology. We know mine started with a severe virus, not with an emotional trauma.
As the author of this article points out "It is very important to understand the distinctive features between chronic fatigue and depressive disorder when evaluating a patient with a main complaint of fatigue. A full detailed history accompanied by questionnaire forms can be very helpful to differentiate CFS from major depressive disorder."
Anyone who thinks they're the same thing, doesn't know the first thing about CFS. I don't care if they're an MD or a psychiatrist/psychologist. Patient support groups can tell the difference with near 100% accuracy. Why can't professionals? Maybe because some professionals don't WANT to see the difference between them -- it's more lucrative for a psychiatrist to say the million Americans with CFS need talk-therapy, which he can provide, than to admit that we're physically ill and need a neurologist, an immunologist, and an endocrinologist.
There's evidence out of England of shrinks sending annual reports to NHS blaming the patient for being "uncooperative and not wanting to get well", and recommending yet another year of talk-therapy. And at the end of the next year, they again blame the patient so they can get paid for another year of useless therapy that doesn't do a thing for CFS, but does pad the shrink's bank account.
Despite the myth that "there are no blood tests that show CFS", there are, in fact, a lot of tests that show evidence of CFS. There's not a single blood test out there that says "this is CFS and not anything else", not like an HIV test, but there are tests that will be abnormal and the doctors who know about CFS can look at the pattern and say if A, B, C, and E are normal, and D, F, G and H are abnormal, there's only one thing it can possibly be".
Please understand that it is not my intent to be rude, this is after all your writing space, but your response to my inquiry gives the impression that one can pick and choose what and which information is accurate based on what they wish to believe. That simply is not how science works.All these researchers and their facilities are valid and respected by all except those it would seem in the cfs-me communities. It does have to make one wonder. Can you understand what I mean?And again please do not mistake my questions to be in any way belittling you. I am merely trying to understand how scientific data is interpeted and disposed of as heresay.
You're correct that proper science is not done by picking and choosing. That goes for the researchers as well. They cannot define an illness by picking and choosing which elements fit their desired result.
What CFS medical experts call CFS is not what psychiatrists call CFS. Their definition is entirely different from Original CFS, which has an infectious onset, and numerous neurological and immunological abnormalities, and is easily differentiated from psychiatric problems.
It's not that we're picking and choosing which science to believe, but that we are differentiating between apples and oranges, while they are not. Someone who loads up a "CFS" study with people who don't actually have CFS, they have depression, is not going to produce valid CFS research, because they are actually researching depression.
Some of our activists are very good at reading through the Selection Criteria of "CFS" research, and determining whether they're studying actual CFS patients or if they're studying patients who are "merely tired" or "psychosomatically fatigued" or "fatigued due to lifestyle" or "clinically depressed". It DOES make a difference in the validity of the study, whether they're studying "us" or "them". They can call it whatever they like, but it's not the same CFS that we have.
A trunk can be the back end of a car, or it can mean an old-fashioned steamer trunk. Same word, very different meanings. And that is what's going on here ... the psychiatrists found a new pool of research money and glommed onto it by using a different definition that suited their purposes. They know they can't prove that True CFS patients are depressed, so they prove that chronically-fatigued depressed people are depressed, and refer to their patients as CFS because that's what the research grant is available for.
Since you're apparently focusing your attention on this article only and not on the subsequent articles, let me point out recent research into the type of CFS I'm discussing:
"Dr. Huber found that both MS and CFS patients (whose illness had been triggered by infectious mononucleosis) were at a higher relative risk for containing HERV-K18 variants known to induce superantigen activity. ... Viral activity and/or immune activation has been shown to trigger HERV-K18 activity. ... HERV-K18 activation may be the endpoint of an HHV6/EBV interferon pathway operating in both MS and CFS. ... Other retroviruses, HERV-H and HERV-W, have been implicated in MS by other researchers. Over 75% of MS patients meet the criteria for CFS. Fatigue is often the most disabling symptom for MS patients. The two diseases also share characteristics such as grey matter atrophy, impaired cerebral glucose metabolism, autonomic nervous system activity and altered patterns of brain activity."
To suggest that CFS has a psychiatric cause is therefore no more logical than to suggest that MS has a psychiatric cause. They're caused by a virus, not by stress or emotional trauma.
As stated in this article, a PROPER medical history can differentiate True CFS from a psychiatric problem, because there are so many differences between the two.
The psych lobby can call anything they like "CFS", but that doesn't make it CFS in the minds of those who know what True CFS is. It's just something else masquerading for those who don't know enough about the subject to realize that it's not the real thing.
All that glitters is not gold, and all that fatigues is not CFS.
Again, quoting from Dr. John (doctor/patient/activist), which I quoted before and you have not responded to:
AS FAR AS I KNOW, THERE ARE NO STATISTICS EXCLUSIVELY FOR PEOPLE WITH M.E. (MYALGIC ENCEPHALOMYELITIS), WHICH HAVE NOT BEEN DISTORTED BY ADDING IN OTHER PATIENTS, WITH A VARIETY OF ILLNESSES, IN WHICH CHRONIC FATIGUE IS SAID TO BE A SYMPTOM AND CALLING THEM ALL ME/CFS.
This is the problem -- research is "distorted by adding in other patients, with a variety of illnesses ... and calling them all CFS".
We're not discounting valid CFS research, we're discounting research where we cannot agree that the patients studied actually have what we have. To those who read critically, those patients appear to have something quite different than what *we* refer to as CFS.
Some researchers have gone so far as to say that in their patient selection, they excluded patients who have certain symptoms which are common in True CFS but not seen in psychiatric illnesses. They can say they're studying CFS, but it's obvious to the knowledgeable reader that they turned away True CFS patients and studied only those patients they knew would give them the result they wanted. They want to say it's psychiatric, they stack the patient pool with psych patients and keep the True CFS patients out by picking and choosing which criteria they want to use.
True CFS patients have no improvement with psych drugs; they improve with anti-virals. A million patients can't be wrong.
The fact that this is CDC research you're citing automatically raises red flags among activists. From the first, CDC has pooh-poohed any evidence that Peterson/Cheney were seeing a physical illness, just as they did 10 years earlier when Dr. Ryll was investigating the Mercy San Juan Hospital epidemic, and now they have to adamantly maintain that it's psychiatric in order to avoid admitting "we were wrong". It's been concluded by post-viral CFS experts that "they don't WANT to find anything".
Read "Osler's Web" for the full scoop on why CDC's CFS research does not, and never will, use the same definition that Peterson/Cheney/Bell/etc. use, because they can't risk proving their initial stance was wrong. Having abolished the ME diagnosis in the US by executive fiat, they have now defined True CFS out of existence, too, by watering-down the original diagnostic criteria.
One of the early CDC researchers wanted to use "fatigue" as the only symptom for the diagnostic criteria, as a way of "proving" it was just hypochondria; True CFS researchers use many more criteria before making the diagnosis, things that can't be psychosomatic. Then CDC tried to relate it to menopause, which didn't sit well with the male patients (or those much too young for menopause -- I've been sick for 21 years and still have not gone through menopause).
There are just too many things in True CFS that cannot be explained away with psychiatry. My abnormal blood test is not a figment of my overactive imagination. My friend's abnormal brain scan is not a figment of his imagination. The viral damage noted in biopsy and autopsy, and the MS-like neurological abnormalities are not caused by having a screw loose. Autonomic dysfunction of the Central Nervous System is not something that can be faked.
Those are some of the symptoms that the psychiatric lobby don't accept in their research subjects, because then they'd lose the
Dr. Katrina Berne: “CFS and FMS share common factors with somatoform disorders – multiple symptoms, lack of consistent lab findings ... but are excluded from this category by symptom prevalence, age, suddenness of onset, lack of prevalent personality disorders, and exercise and alcohol intolerance.
“The term functional somatic syndromes refers to suffering in the absence of specific medical findings. This term is often inappropriately applied to poorly understood illnesses such as CFS, FMS ... FSS disorders are framed with circular reasoning: ‘You think you have a serious illness but you don’t because we have no specific test for it.’ The alleged secondary gains of illness are typically absent, yet patients are accused ...
“... a diagnosis of FSS more often provides a convenient way to dismiss patients’ symptomatic complaints whose cause is unknown. The absence of diagnostic tests for many known disorders creates fertile ground for physicians who view any difficult-to-diagnose disorder as imagined illness. However an illness that defies current scientific knowledge is still an illness.
“... Although multiple symptoms are seen in somatization disorder, symptom clusters typical of CFS and FMS are not found in this group, nor is sudden onset, which often characterizes CFS/FMS.
“... Many diseases are labeled psychiatric or “stress” disorders until causal agents or illness markers are identified, at which time they graduate to the status of legitimized, genuine illness.”
Dr. Katrina Berne: “...The history of psychiatric disorders in the CFS/FMS population is similar to that in the general population. ... Depression does not cause these syndromes and is not present in all cases; however, many patients are given a psychiatric diagnosis when a physiological diagnosis is not apparent. Overlapping symptoms ...and simple ignorance causes confusion between CFS/FMS and depression.
“The rate of depression is not necessarily higher in patients with the most severe symptoms. ... Nonantidepressant medications common in CFS/FMS treatment are not effective in treating [depression].
“Psychological tests are frequently used to ‘rule in’ depression and other psychiatric disorders; however, they cannot distinguish between a test-taker’s medical and psychological disorders. One who endorses numerous physical complaints is likely to be labeled depressed. ‘Results in ill populations may be falsely elevated for psychological disorders’ (Jason, Richman, et al. 1997).
“...When ‘neurological’ items were removed from the test and the tests were rescored, all scores dropped to within the normal range, that is, no elevations remained. This finding provides evidence that neurological dysfunction rather than psychopathology accounts for the typical CFS profile.”
Dr. Katrina Berne: “The medical profession often views depression or inability to cope productively with stress as the cause of any symptom for which a physiological cause is not evident. Psychiatry becomes a convenience dumping ground for those with unexplained illness. However, indiscriminate attribution of symptoms to psychological factors is inappropriate.
“... The notion that we cannot handle life, fabricate symptoms, or develop illnesses in order to receive special attention is ludicrous. Attribution of illness to such conscious or unconscious motivation is inaccurate, unfair and insulting. Phrases such as ‘can’t manage stress’ and ‘mind over matter’ add insult to illness. ... Some CFS/FMS patients experience little or no depression.
“Numerous chronic disorders share common features, including symptoms and abnormalities. The similarities are remarkable ... Skeptics who dismiss CFS, FMS ... imply that poorly understood conditions do not deserve the respect afforded ‘testable’ illnesses. This practice lifts a burden from disinterested physicians and blames – even traumatizes – sufferers.
“Double standards allow medical doctors to diagnose psychiatric illness ... in the absence of a known physiological cause, but do not typically allow the psychiatrist or psychologist who rules out emotional causes to rule in physiologic illness. That is, acceptable practice allows a physician to say ‘It is all in your head’ but how often does a psychiatrist or psychologist say ‘Nothing is wrong with your head, the illness is in your body’? ... Illnesses such as MS, rheumatoid arthritis, polio, HIV/AIDS, stomach ulcers and diabetes were once considered to be of psychiatric origin. When markers or diagnostic tests were developed, the diagnoses shifted to ‘real’ illnesses, those of the body. History repeats itself.”
Dr. Katrina Berne: “The medical profession often views depression or inability to cope productively with stress as the cause of any symptom for which a physiological cause is not evident. Psychiatry becomes a convenience dumping ground for those with unexplained illness. However, indiscriminate attribution of symptoms to psychological factors is inappropriate.
“... The notion that we cannot handle life, fabricate symptoms, or develop illnesses in order to receive special attention is ludicrous. Attribution of illness to such conscious or unconscious motivation is inaccurate, unfair and insulting. Phrases such as ‘can’t manage stress’ and ‘mind over matter’ add insult to illness. ... Some CFS/FMS patients experience little or no depression.
“Numerous chronic disorders share common features, including symptoms and abnormalities. The similarities are remarkable ... Skeptics who dismiss CFS, FMS ... imply that poorly understood conditions do not deserve the respect afforded ‘testable’ illnesses. This practice lifts a burden from disinterested physicians and blames – even traumatizes – sufferers.
“Double standards allow medical doctors to diagnose psychiatric illness ... in the absence of a known physiological cause, but do not typically allow the psychiatrist or psychologist who rules out emotional causes to rule in physiologic illness. That is, acceptable practice allows a physician to say ‘It is all in your head’ but how often does a psychiatrist or psychologist say ‘Nothing is wrong with your head, the illness is in your body’? ... Illnesses such as MS, rheumatoid arthritis, polio, HIV/AIDS, stomach ulcers and diabetes were once considered to be of psychiatric origin. When markers or diagnostic tests were developed, the diagnoses shifted to ‘real’ illnesses, those of the body. History repeats itself.”
My apologies for not responding sooner. After showing some of my colleagues your replies we took some time to read other writings on this site, and got a clearer idea of the mindset here. In short we wish you well and hope in time you will be able to resolve or come to terms with your present situation.
This has nothing to do with “mindset”. It’s a simple FACT that one group of researchers are looking into a post-infectious physical disease with proven immune/neurological/endocrine abnormalities, and that another group of researchers are using the same name for a psychiatric condition that has none of those telltale test results. They are obviously not the same condition despite researchers co-opting the same name and hoping most people are too stupid to tell the difference. Some of us intelligent/educated folk can.
You can tell which condition the researchers are investigating by reading their patient selection criteria. It becomes quite clear from a careful reading of that paragraph whether they’re using CFS a/k/a ME patients, or whether they’re using people with none of the physical symptoms of what I have. If they’re not studying the type of CFS that I have, then their research isn’t applicable to me.
The problem isn’t in the minds of the patients, who are quite clear – some of them with hospital records to prove it – that their condition has an infectious onset, but in the minds of the researchers who choose to blur the line between Chronic Fatigue SYNDROME and the SYMPTOM of chronic fatigue in order to get research grants that provide no useful information to those of us who have what used to be called ME because they’re researching something else entirely.
What I have is related to polio and MS, which are also viruses. Psychiatrists have continually given me a clean bill of psychiatric health, repeatedly saying “the most well-adjusted person I’ve ever met”. So, obviously, there’s no psychiatric component to what I have, and therefore, it’s not triggered by stress/trauma/abuse. Mine started with a 105 fever, not with any emotional attack, and I feel flu-ish, not depressed, because what I have is a virus. No one will convince me that I don’t have a virus, not when all the evidence
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