Number 1 |
1st March 2006 |
Baraniuk, JN., Casado, B., Maibach, H., Clauw, DJ., Pannell, LK and Hess, S. A chronic fatigue syndrome - related proteome in human cerebrospinal fluid. BMC Neurology, 2005, 5:22.
CFS, Persian Gulf War Illness (PGI), and fibromyalgia (FM) are overlapping symptom complexes without objective markers or known pathophysiology. Neurological dysfunction is common. We assessed cerebrospinal fluid to find proteins that were differentially expressed in this CFS-spectrum of illnesses compared to control subjects.
Cerebrospinal fluid specimens from 10 CFS (CDC ’94 criteria), 10 PGI, and 10 control subjects (50 μl/subject) were pooled into one sample per group (cohort 1). Cohort 2 of 12 control and 9 CFS subjects had their fluids (200 μl/subject) assessed individually. After trypsin digestion, peptides were analysed by capillary chromatography, quadruple-time-of-flight mass spectrometry, peptide sequencing, bioinformatic protein identification, and statistical analysis.
Pooled CFS and PGI samples shared 20 proteins that were not detectable in the pooled control sample (cohort 1 CFS-related proteome). Multilogistic regression analysis (GLM) of cohort 2 detected 10 proteins that were shared by CFS individuals and the cohort 1 CFS-related proteome, but were not detected in control samples. Detection of >1 of a select set of 5 CFS-related proteins predicted CFS status with 80% concordance (logistic model).
The proteins were α-1-macroglobulin, amyloid precursor-like protein 1, keratin 16, orosomucoid 2 and pigment epithelium-derived factor. Overall, 62 of 115 proteins were newly described.
This pilot study detected an identical set of central nervous system, innate immune and amyloidogenic proteins in cerebrospinal fluids from two independent cohorts of subjects with overlapping CFS, PGI and FM. Although syndrome names and definitions were different, the proteome and presumed pathological mechanism(s) may be shared.
For details, see:
Yoshiuchi, K, Farkas, J and Natelson, BH. Patients with chronic fatigue syndrome have reduced absolute cortical blood flow. Clinical Physiology and Functional Imaging, 2006, 26, 2, 83-86.
Prior studies on brain blood flow in CFS did not find consistent results. This may be because they used single-photon emission computed tomography to measure brain blood flow, which could not measure absolute blood flow. Therefore, the aim of this study was to test the hypothesis that patients with CFS have reduced absolute cerebral blood flow.
Xenon-computed tomography blood flow studies were done on 25 patients with CFS (CDC criteria ’94) and seven healthy controls. Analyses were done after stratifying the CFS patients based on the presence or absence of a current psychiatric disorder.
Flow was diminished in both groups as follows: patients with no current psychiatric disorders had reduced cortical blood flow in the distribution of both right and left middle cerebral arteries (p<0.05 for both) while those with current psychiatric disorders had reduced blood flow only in the left middle cerebral artery territory (p<0.05).
These data indicate that patients with CFS have reduced absolute cortical blood flow in rather broad areas when compared with data from healthy controls and that those devoid of psychopathology had the most reductions in cortical flow. These data support, in part, our earlier findings that patients devoid of psychopathology are the group most at risk of having some of the symptoms of CFS due to brain dysfunction.
Maher, KJ., Klimas, NG and Fletcher, MA. Chronic fatigue syndrome is associated with diminished intracellular perforin. Clinical and Experimental Immunology, 2005, 142, 3, 505-511.
Diminished natural killer cell cytotoxicity (NKCC) is a frequently reported finding in CFS. However, the molecular basis of this defect of in vitro cytotoxicy has not been described. Perforin is a protein found within intracellular granules of NK and cytotoxic T cells and is a key factor in the lytic processes mediated by these cells. Quantitative fluorescence flow cytometry was used to the intracellular perforin content in 30 subjects with CFS (CDC criteria ’94) and 19 healthy, sedentary controls.
A significant reduction in the NK cell associated perforin levels in samples from CFS patients, compared to healthy controls, was observed. There was also an indication of a reduced perforin level within the cytotoxic T cells of CFS subjects, providing the first evidence, to our knowledge, to suggest a T cell associated cytotoxic deficit in CFS. Because perforin is important in immune surveillance and homeostasis of the immune system, its deficiency may prove to be an important factor in the pathogenesis of CFS and its analysis may prove useful as a biomarker in research.
[Ed. Note: the researchers also found some evidence of immune activation. A control group to rule out the effects of stress might have been useful given the documented link between this and NKCC.]
Jones, JF., Nicholson, A., Nisenbaum, R., Papanicolaou, DA., Solomon, L., Boneva, R., Heim, C and Reeves, WC. Orthostatic instability in a population-based study of chronic fatigue syndrome. American Journal of Medicine, 2005, 118, 12, 1415, e19-28.
Autonomic nervous system dysfunction has been suggested as involved in the pathophysiology of CFS. This population-based case control study addressed the potential association between orthostatic instability (one sign of dysautonomia) and CFS.
Fifty-eight subjects with CFS (CDC criteria ’94) and 55 non-fatigued, healthy controls participated in a 2-day inpatient evaluation. Subjects had been identified during a 4-year population-based CFS surveillance study in Wichita, Kan. The present study evaluated subjects' current medical and psychiatric status, reviewed past medical/psychiatric history and medication use, used a stand-up test to screen for orthostatic instability, and conducted a head-up tilt table test to diagnose orthostatic instability (in eligible subjects e.g. <55 years old, not using antidepressants etc, n=17).
No one manifested orthostatic instability in the stand-up test. The head-up tilt test elicited orthostatic instability in 30% of eligible CFS subjects (all with postural orthostatic tachycardia) and 48% of controls (50% with neurally mediated hypotension); intolerance was present in only non-fatigued (n=7) subjects. Neither fatigue nor illness severity were associated with outcome.
Orthostatic instability was similar in persons with CFS and non-fatigued controls subjects recruited from the general Wichita population. Delayed responses to head-up tilt tests were common and may reflect hydration status. These findings suggest reappraisal of primary dysautonomia as a factor in the pathogenesis of CFS.
Maes, M., Mihaylova, I and De Ruyter, M. Lower serum zinc in chronic fatigue syndrome (CFS): Relationships to immune dysfunctions and relevance for the oxidative stress status in CFS. Journal of Affect Disorders, 2006, 90, 2-3, 141-147.
The present study examines serum zinc concentrations in patients with CFS (CDC criteria ’94, excluding lifetime diagnosis of psychiatric disorders) versus normal volunteers. Serum zinc levels were determined by means of an atomic absorption method.
We found that serum zinc was significantly lower in the CFS patients than in the normal controls. There was a trend toward a significant negative correlation between serum zinc and the severity of CFS and there was a significant and negative correlation between serum zinc and the subjective experience of infection. Serum zinc was significantly and negatively correlated to the increase in the alpha2 protein fraction and positively correlated to decreases in the expression of mitogen-induced CD69+ (a T cell activation marker) on CD3+ as well as CD3+CD8+ T cells.
These results show that CFS is accompanied by a low serum zinc status and that the latter is related to signs of inflammation and defects in early T cell activation pathways. Since zinc is a strong anti-oxidant, the present results further support the findings that CFS is accompanied by increased oxidative stress.
The results of these reports suggest that some patients with CFS should be treated with specific antioxidants, including zinc supplements.
McCully, KK., Malucelli, E and Iotti, S. Increase of free Mg2+ in the skeletal muscle of chronic fatigue syndrome patients. Dynamic Medicine, 2006, Jan 11, 5, 1.
In a previous study we evaluated muscle blood flow and muscle metabolism in patients diagnosed with CFS. To better understand muscle metabolism in CFS, we re-evaluated our data to calculate free Magnesium levels in skeletal muscle. Magnesium is an essential cofactor in a number of cell processes.
A total of 20 CFS patients (CDC criteria ’94) and 11 controls were evaluated. Phosphorus magnetic resonance spectroscopy from the medial gastrocnemius muscle was used to calculate free Mg2+ from the concentrations and chemical shifts of Pi, PCr, and beta ATP peaks.
CFS patients had higher magnesium levels in their muscles relative to controls (0.47 + 0.07 vs 0.36 + 0.06 mM, p<0.01), although there was no difference in the rate of phosphocreatine recovery in these subjects, as reported earlier. This finding was not associated with abnormal oxidative metabolism as measured by the rate of recovery of phosphocreatine after exercise.
In summary, calculation of free Mg2+ levels from previous data showed CFS patients had higher resting free Mg2+ levels compared to sedentary controls.
The full text:
Schmaling, KB., Fiedelak, JI., Bader, J and Buchwald D. A longitudinal study of physical activity and body mass index among persons with unexplained chronic fatigue. Journal of Psychosomatic Research, 2005, 58, 4, 375-381.
A cohort of 100 patients with unexplained chronic fatigue (CF, 93% of whom met the CDC criteria ’94 for CFS, the remainder had ICF) was assessed longitudinally for 1.5 years to determine if physical activity (kcal expended), exercise capacity (VO2max), perceived exertion, and body mass index (BMI) changed over time and were associated with changes in CF-related clinical status.
BMI increased significantly over time but did not predict changes in clinical status. Increasing energy expenditure was associated with increasing vitality and decreasing CF symptom severity over time, and decreasing perceived exertion was associated with increasing physical functioning. However, increasing perceived exertion was also associated with increasing CF symptoms.
These data do not support models that posit associations between CF and deconditioning.
[Ed. Note: Contrary to expectations, physical conditioning decreased (oxygen uptake decreased) as symptom severity and measures of physical functioning improved].
ENDOCRINOLOGY AND NEUROENDOCRINOLOGY
Jerjes, WK., Peters, TJ., Taylor, NF., Wood, PJ., Wessely, S and Cleare, AJ. Diurnal excretion of urinary cortisol, cortisone, and cortisol metabolites in chronic fatigue syndrome. Journal of Psychosomatic Research, 2006, 60, 2, 145-153.
The aim of this study was to obtain comprehensive information on basal
hypothalamic-pituitary-adrenal (HPA) axis activity in 15 CFS patients (CDC
criteria ’94) who were not affected by medication or co-morbid psychiatric
disorder likely to influence the HPA axis.
Data were obtained from steroid analysis of urine collections from 0600 to 2100 h at 3 hour intervals in CFS patients and in the 20 healthy controls. Urinary free cortisol and cortisone concentrations showed a significant normal diurnal rhythm, but levels were lower across the cycle in CFS. In contrast, while urinary cortisol metabolites also showed a normal diurnal rhythm, levels were not significantly different between the CFS and controls at any time. Derived metabolite ratios were similar in both groups.
This study provides further evidence for reduced basal HPA axis function in patients with CFS, based on lower free cortisol and cortisone levels, but this is not corroborated by cortisol metabolite data. The difference between these measures cannot be explained by an altered timing of the diurnal rhythm.
[Ed. Note: The HAD scores suggest that some patients had clinically significant anxiety and depression, which may have affected the results. The controls were not matched for levels of activity.]
Maes, M., Mihaylova, I and De Ruyter, M. Decreased dehydroepiandrosterone sulfate but normal insulin-like growth factor in chronic fatigue syndrome (CFS): relevance for the inflammatory response in CFS. Neuroendocrinology Letters, 2005, 26, 5, 487-492.
There are a few reports that CFS may be accompanied by changes in hormones, such as dehydroepiandrosterone (DHEA) and insulin-like growth factor (IGF1). This study examines the serum concentrations of DHEA-sulfate (DHEAS), IGF1 and IGF1 binding protein-3 (IGFBP3) in 20 patients with CFS and in 12 normal controls. The IGFBP3/IGF1 ratio was computed as an index for IGF1 availability.
We found significantly lower serum DHEAS concentrations in CFS, but no significant differences either in IGF1 or the IGFBP3/IGF1 ratio between CFS patients and normal controls. The decrease in serum DHEAS was highly sensitive and specific for CFS. There were significant and positive correlations between serum DHEAS and serum zinc and the mitogen-induced expression of the CD69 molecule on CD3+CD8+ T cells (an indicator of early T cell activation). There was a significant and negative correlation between serum DHEAS and the increase in the serum α-2 protein fraction (an inflammatory marker). Serum IGF1, but not DHEAS, was significantly and inversely correlated to age.
The results show that CFS is accompanied by lowered levels of DHEAS and that the latter may play a role in the immune (defect in the early activation of T cells) and the inflammatory pathophysiology of CFS.
GENETICS
Vernon, SD., Whistler, T., Cameron, B., Hickie, IB., Reeves, WC and Lloyd, A. Preliminary evidence of mitochondrial dysfunction associated with post-infective fatigue after acute infection with Epstein Barr Virus. BMC Infectious Diseases 2006, 6: 15.
Acute infectious diseases are typically accompanied by non-specific symptoms including fever, malaise, irritability and somnolence that usually resolve on recovery. However, in some individuals these symptoms persist in what is commonly termed post-infective fatigue. The objective of this pilot study was to determine the gene expression correlates of post-infective fatigue following acute Epstein Barr virus (EBV) infection.
We followed 5 people with acute mononucleosis who developed post-infective fatigue of more than 6 months duration (and met the CDC criteria ’94) and 5 HLA-matched control subjects who recovered within 3 months. Subjects had peripheral blood mononuclear cell (PBMC) samples collected at varying time points including at diagnosis, then every 2 weeks for 3 months, then every 3 months for a year. Total RNA was extracted from the PBMC samples and hybridized to microarrays spotted with 3,800 oligonucleotides.
Those who developed post-infective fatigue had gene expression profiles indicative of an altered host response during acute mononucleosis compared to those who recovered uneventfully. Several genes including ISG20 (interferon stimulated gene), DNAJB2 (DnaJ [Hsp40] homolog and CD99), CDK8 (cyclin-dependent kinase 8), E2F2 (E2F transcription factor 2), CDK8 (cyclin-dependent kinase 8), and ACTN2 (actinin, alpha 2), known to be regulated during EBV infection, were differentially expressed in post-infective fatigue cases. Several of the differentially expressed genes affect mitochondrial functions including fatty acid metabolism and the cell cycle.
These preliminary data provide insights into alterations in gene transcripts associated with the varied clinical outcomes from acute infectious mononucleosis.
Extracts from the paper:
To determine why the response to EBV varied between cases and controls, both early and late time points in the natural history were compared. Of the 24 differentially expressed genes, half are involved in mitochondrial functions including fatty acid metabolism (CRAT; carnitine acetyltransferase, APOA2; apolipoprotein A-II), apoptosis (BTG1; B-cell translocation gene 1, FOLR1; folate receptor 1, CTRL; chymotrypsin-like), and mitochondrial membrane function (COX8A; cytochrome c oxidase subunit VIII, COX11; cytochrome c oxidase assembly protein, KCNA10; potassium voltage-gated channel, MGP; matrix Gla protein; ATP5L; ATP synthase). Several EBV-associated proteins, such as BRLF1, BHRF1, EBNA and LMP1 have been shown to interfere with fatty acid metabolism, mitochondrial function and apoptosis pathways.
Since the majority of these genes are regulated during EBV replication, the fact that these were differentially expressed in cases potentially implicates a failure of the host to adequately control viral replication.
Because mitochondria serve several prominent and essential cellular functions such as energy homeostasis, signaling and apoptosis, it is reasonable to surmise that alterations in mitochondrial function could affect immune function. In fact, viral and immune factors have been evaluated in these same subjects and it was found that post-infective fatigue was associated with an altered pattern of humoral immune response against EBV antigens. An increase in the number of apoptotic peripheral blood cells has also been demonstrated in patients with CFS.
For details, see:
[Ed. Note: This study demonstrates the value of studying well-defined subgroups.]
EPIDEMIOLOGY
Saidi, G and Haines, L. The management of children with chronic fatigue syndrome-like illness in primary care: a cross-sectional study. British Journal of General Practice, 2006, 56, 522, 43-47.
Most studies on children with CFS/ME have been undertaken in tertiary care and little is known about their management in primary care. The aim was to describe the characteristics of patients aged 5-19 years with CFS-like illness in primary care and to examine how GPs investigate and manage patients. This is a descriptive retrospective questionnaire study. Setting was 62 UK GP practices in the MRC General Practice Research Framework (GPRF).
One hundred and twenty-two practices were approached; 62 identified 116 patients consulting a GP with severe fatigue lasting over 3 months. Practice nurses and GPs completed questionnaires from medical notes and patients completed postal questionnaires.
Ninety-four patients were considered by a clinical panel, blind to diagnosis, to meet the Oxford CFS criteria with a fatigue duration of 3 months. Seventy-three per cent were girls, 94% white, mean age was 12.9 years and median illness duration 3.3 years. GPs had principal responsibility for 62%. 82% reported good health in the 12 months prior to illness, 39% noted an Autumn onset and in 62% of cases, the onset was acute. A diagnosis of CFS/ME was made in 55%, 30% of these within 6 months. Fifty per cent had a moderate illness severity. Paediatric referrals were made in 82% and psychiatric referrals in 46% (median time of 2 and 13 months respectively). Advice given included setting activity goals, pacing (60%), rest (23%) and graded exercise (37%).
Patient characteristics are comparable to those reported in tertiary care, although fewer are severe cases. GPs have responsibility for the majority of patients, are diagnosing CFS/ME within a short time and applying a range of referral and advice strategies.
THERAPEUTICS
Blockmans, D., Persoons, P., Van Houdenhove, B and Bobbaers, H. Does methylphenidate reduce the symptoms of chronic fatigue syndrome? American Journal of Medicine, 2006, 119, 2, 167, e23-e30.
CFS is a clinical entity consisting of prolonged and debilitating fatigue in which concentration disturbances are very frequent. Until now, no medical treatment has shown any efficacy. The objectives of this study were to investigate the short-term effects of methylphenidate, an amphetamine derivative, on fatigue, concentration disturbances, and quality of life.
A double-blind randomized placebo-controlled crossover study was conducted in 60 patients with CFS (CDC criteria ’94), and concentration difficulties. Patients were enrolled between March 2003 and March 2004 at the outpatient department of a university hospital referral centre for CFS patients. Random assignment to 4 weeks treatment with methylphenidate 2 x 10 mg/day, followed by 4 weeks of placebo treatment, or 4 weeks of placebo treatment, followed by methylphenidate treatment. Fatigue and concentration were measured with a Checklist Individual Strength (CIS) and a Visual Analogue Scale (VAS), the latter also measured other CDC criteria.
Fatigue scores fell significantly during methylphenidate intake in comparison with baseline (mean difference: -0.7, p=.010 for VAS; mean difference: -11.8, p<.0001 for CIS) and in comparison with placebo (mean difference:-1.0, p=.001 for VAS; mean difference: -9.7, p<.0001 for CIS). Concentration disturbances, measured with a VAS improved significantly under methylphenidate treatment compared with baseline (mean difference: -1.3, p<.0001) and compared with placebo (mean difference: -1.1, p<.0001). A clinical significant effect (> or =33% improvement or CIS < or=76) on fatigue was achieved in 17% of patients, who were considered responders; on concentration in 22% of patients.
Methylphenidate at a dose of 2 x 10 mg/day is significantly better than placebo in relieving fatigue and concentration disturbances in a minority of CFS patients. Further studies are needed to investigate the long-term effects of this treatment.
[Ed. Note: There were no significant improvements on the MOS SF subscale for physical functioning (52.8 after treatment), and pain (40.4 after treatment), and other data also indicate continued disability. The VAS scores for physical symptoms (sore throat, adenopathy) showed no change. HAD scores were high, suggesting some emotional distress, and were not affected by treatment. It is difficult to assess the findings due to the lack of follow-up]
REVIEWS
Crawley, E and Chambers, T. It’s not all in the mind, doc. Archives of Disease in Childhood, Education and Practice, 2005, 90, 92-96.
Mihrshahi, R and Beirman R. Aetiology and pathogenesis of chronic fatigue syndrome: a review. New Zealand Medical Journal, 2005, 118, 1227: U1780
Nijs, J and De Meirleir, K. Impairments of the 2-5A synthetase/RNase L pathway in chronic fatigue syndrome. In Vivo, 2005, 19, 6, 1013-1021.
This paper provides an overview of the evidence addressing the impairments of the 2'-5' oligoadenylate (2-5A) synthetase/RNase L pathway in CFS patients. The 2-5A synthetase/RNase L pathway in CFS patients appears to be both up-regulated (i.e. increased levels of bioactive 2-5A synthetase and increased activity of the RNase L enzyme) and deregulated (elastase and calpain initiate 83 kDa RNase L proteolysis, generating two major fragments with molecular masses of 37 and 30 kDa, respectively). The deregulation of the 2-5A synthetase/RNase L pathway in CFS accompanies decreased NK-function and deregulation of apoptotic pathways. Since various components of the pathway appear to be related to performance during a graded exercise stress test, some evidence supportive of the clinical importance of the impaired pathway in CFS patients has been provided. Studies addressing the treatment of the deregulation of the 2-5A synthetase/RNase L pathway in CFS are warranted.
Prins, J., Van der Meer, JWM and Bleijenberg, G. Chronic fatigue syndrome. Lancet, 2006, 367, 346-355.
[Ed. Note: Highly selective review which promotes the CBT model of chronic fatigue.]
MISCELLANEOUS
Friedberg, F., Leung, DW and Quick, J. Do support groups help people with chronic fatigue syndrome and fibromyalgia? A comparison of active and inactive members. Journal of Rheumatology, 2005, 32, 12, 2416-2420.
The aim of this study was to examine the benefits and problems of a CFS and FM support organization as reported by its participants. Active members (n=32) and inactive members or dropouts (n=135) of a regional support organization for people with CFS and FM completed a 26 item questionnaire by telephone interview or by self-completion and postal return.
The most frequently endorsed benefits of membership were illness legitimization (67.8%), finding out helpful new information (66.4%), and feeling understood by others (62.2%). Lower frequency endorsements were given to: helped to find (35.0%) or deal with (38.5%) doctors, and helped to improve my illness (36.4%). The most frequently reported reasons for dropping out were inconvenient location (37.8%) or time (37.0%), too much negative talk or complaining (33.3%), too sick to attend (28.8%), and illness or coping improvement (29.6% each). The active-member group showed significantly higher (p<0.04) symptom severity scores and less illness improvement (p<0.01) in comparison to the inactive/dropout group.
This cross-sectional study suggests that support groups for CFS are viewed as helpful by participants on a number of illness related issues. On the other hand, active members reported greater symptom severity and less illness improvement than inactive members or dropouts.
Garralda, ME and Rangel, L. Chronic fatigue syndrome of childhood. Comparative study with emotional disorders. European Child & Adolescent Psychiatry, 2005, 14, 8, 424-430.
The aim of this study was to examine clinical specificity in CFS of childhood, by comparing clinical features in childhood CFS and in emotional disorders (ED). The sample comprised 28 children with CFS (Oxford/CDC ’94 criteria) and 27with ED. Measures included history of disorder; K-SADS psychiatric interviews; self-esteem and physical symptoms questionnaires; pre-morbid history, behavioural and personality assessments.
There were high levels of co-morbid emotional disorders in children with CFS, and the two groups were comparable on self-esteem, but CFS children endorsed more fatigue and other somatic symptoms. The two groups were comparable on age at illness onset, but parents of children with CFS reported more biological illness precipitants, more pre-morbid recurrent medical problems and infections. The CFS group had fewer pre-morbid psychological problems and less psychiatric co-morbidity than the ED group.
There is considerable clinical overlap between CFS and ED of childhood, but there are also differences in clinical presentation between these disorders.
Iwakami, E., Arashima, Y., Kato, K., Komiya, T., Matsukawa, Y., Ikeda, T., Arakawa, Y and Oshida S. Treatment of chronic fatigue syndrome with antibiotics: pilot study assessing the involvement of Coxiella burnetii infection. Internal Medicine, 2005, 44, 12, 1258-1263.
To examine whether Coxiella burnetii (C. burnetii) is involved in CFS, we administered tetracycline antibiotics to subjects with CFS, and followed changes in clinical symptoms, PCR findings, and C. burnetii antibody titers.
The subjects were 8 patients with CFS and 213 with non-specific complaints such as chronic fatigue and low-grade fever for several months or longer but not meeting the diagnostic criteria for CFS. All were examined for C. burnetii infection by nested PCR and the indirect immunofluorescence test (IF).
Four CFS patients (the CFS group) and 54 controls [the post-Q fever fatigue syndrome (QFS) group] positive for C. burnetii were treated mainly with minocycline or doxycycline (100 mg/day) for 3 months. After treatment, all 58 patients tested negative for C. burnetii infection. In the CFS group, no significant difference was noted between the mean pre- and post-treatment temperatures or headache scores. Similarly, there was no significant improvement in performance status (PS) scores. In the QFS group, however, mean temperatures and headache scores were significantly decreased after treatment (p<0.001). PS scores were also improved.
These results suggest the possibility of direct involvement of C. burnetii in the pathological state of CFS to be low, despite the C. burnetii infection rate being high in CFS patients. This is a pilot study and further larger investigations are necessary to confirm our preliminary results.
Maes, M., Mihaylova, I and Leunis, JC. In chronic fatigue syndrome, the decreased levels of omega-3 poly-unsaturated fatty acids are related to lowered serum zinc and defects in T cell activation. Neuroendocrinology Letters, 2005, 26, 6, 745-751
There is now evidence that major depression is accompanied by decreased levels of omega3 poly-unsaturated fatty acids (PUFA), such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). There is a strong co-morbidity between major depression and CFS. The present study has been carried out in order to examine PUFA levels in CFS.
In twenty-two CFS patients and 12 normal controls we measured serum PUFA levels using gas chromatography and mass spectrometry. We found that CFS was accompanied by increased levels of omega6 PUFAs, i.e. linoleic acid and arachidonic acid (AA), and mono-unsaturated fatty acids (MUFAs), i.e. oleic acid. The EPA/AA and total omega3/omega6 ratios were significantly lower in CFS patients than in normal controls. The omega3/omega6 ratio was significantly and negatively correlated to the severity of illness and some items of the FibroFatigue scale, i.e. aches and pain, fatigue and failing memory. The severity of illness was significantly and positively correlated to linoleic and arachidonic acid, oleic acid, omega9 fatty acids and one of the saturated fatty acids, i.e. palmitic acid. In CFS subjects, we found significant positive correlations between the omega3/omega6 ratio and lowered serum zinc levels and the lowered mitogen-stimulated CD69 expression on CD3+, CD3+CD4+, and CD3+CD8+ T cells, which indicate defects in early T cell activation.
The results of this study show that a decreased availability of omega3 PUFAs plays a role in the pathophysiology of CFS and is related to the immune pathophysiology of CFS. The results suggest that patients with CFS should respond favourably to treatment with - amongst other things - omega3 PUFAs, such as EPA and DHA.
Nijs, J., Van de Putte, K., Louckx, F and De Meirleir, K. Employment status in chronic fatigue syndrome. A cross-sectional study examining the value of exercise testing and self-reported measures for the assessment of employment status. Clinical Rehabilitation, 2005, 19, 895-899.
The aim of this cross-sectional study was to examine the value of exercise testing and self-reported disability for the assessment of employment status in patients with CFS. Subjects comprised 54 consecutive, Flemish, employed (not self-employed) CFS patients (CDC criteria, ’94, 49/54 female).
Participants were questioned about their current and pre-morbid employment status, filled in the Chronic Fatigue Syndrome Activities and Participation Questionnaire (CFS-APQ), the Medical Outcomes Short Form 36 Health Status Survey (SF-36), and performed a maximal exercise test on a bicycle ergometer with continuous monitoring of cardiorespiratory variables.
A significant association was observed between the current employment rate and two SF-36 subscales (i.e., role limitations due to physical functioning and social functioning; rho=0.39 and 0.35 respectively) (n=54). Analysing only the female CFS patients (n=49), the current employment rate correlated significantly with the peak workload (rho= 0.38).
The associations between either exercise testing or self-reported disability and employment status are too weak to predict employment status.
Theoharides, TC., Padaliodis, D., Tagen, M., Konstantinidou, A., Kempuraj, D and Clemons, A. Chronic fatigue syndrome, mast cells, and tricyclic antidepressants. Journal of Clinical Psychopharmacology, 2005, 25, 6, 515-520.
Editorial focusing on the relationship between acute stress and immune function. Activation of mast cells leads to the release of certain cytokines (e.g. IL-6) and peripheral vasodilation. The authors note that antidepressants such as amitriptyline and quercetin may help, as they are mast cell inhibitors. Acute stress increases blood–brain barrier permeability in rats and mice, but only in areas containing mast cells.
[Ed. Note: Some of the factual information, e.g. about ME and the co-morbid diseases found in CFS (e.g. PTSD), is not reliable.]
Thomas, MA and Smith, AP. Primary healthcare provision and chronic fatigue syndrome: a survey of patients' and General Practitioners' beliefs. BMC Family Practice, 2005, 6, 1, 49.
The current study was conducted as part of a research project into the evaluation and assessment of healthcare provision and education in CFS. One aim was the development of informative and educational literature for both General Practitioners (GP) and sufferers. Issues such as diagnosis, management and treatment of the syndrome should be included in information booklets written by healthcare professionals. It was important to begin the process by assessing the level of specialist knowledge that existed in typical GP surgeries. These data would then be compared to data from CFS patients.
In all, 197 survey booklets were sent to patients with CFS (CDC criteria ’94). The patients had been recruited following diagnosis at a specialised CFS outpatient clinic in South Wales. A further 120 booklets were sent to GP surgeries in the Gwent Health Authority region in Wales. In total, 92 patients replied, giving a 48% response rate while 45 of the GPs replied (39% response rate)
It was found that 78 of the patients were still suffering from CFS. Also noteworthy is that 55.8% of the GPs believed that CFS existed. Other results indicate that the level of specialist knowledge of CFS in primary care remains low. Steps are recommended to increase the knowledge base by compiling helpful and informative material for GPs and patient groups.
For details, see:
Reeves, WC., Wagner, D., Nisenbaum, R., Jones, JF., Gurbaxani, B., Solomon, L., Papanicolaou, DA., Unger, ER., Vernon, SD and Heim, C. Chronic fatigue syndrome - a clinically empirical approach to its definition and study. BMC Medicine, 2005, 3, 1, 19.
The lack of standardized criteria for defining CFS has constrained research. The objective of this study was to apply the 1994 CFS criteria by standardized reproducible criteria.
This population-based case control study enrolled 227 adults previously identified from the population of Wichita with: (1) CFS (n=58); (2) non-fatigued controls matched to CFS on sex, race, age and body mass index (n=55); (3) persons with medically unexplained fatigue not CFS, which we term ISF (n=59); (4) CFS accompanied by melancholic depression (n=27); and (5) ISF plus melancholic depression (n=28). Participants were admitted to a hospital for two days and underwent medical history and physical examination, the Diagnostic Interview Schedule (DIS), and laboratory testing to identify medical and psychiatric conditions exclusionary for CFS. Illness classification at the time of the clinical study utilized two algorithms: (1) the same criteria as in the surveillance study, i.e. according to Fukuda et al; (2) a standardized clinically empirical algorithm based on quantitative assessment of the major domains of CFS (impairment, fatigue, and accompanying symptoms).
More specifically, “we used information from the SF-36, MFI and Symptom Inventory to classify subjects according to the 3 main dimensions of CFS: functional impairment (SF-36), fatigue (MFI) and accompanying symptoms (Symptom Inventory). We defined substantial reduction in occupational, educational, social, or recreational activities as scores lower than the 25th percentile of published US population on the physical function (≤ 70), or role physical (≤ 50), or social function (≤ 75), or role emotional (≤ 66.7) subscales of the SF-36. We defined severe fatigue as ≥ medians of the MFI general fatigue (≥ 13) or reduced activity (≥ 10) scales. Finally, subjects reporting ≥ 4 symptoms and scoring ≥ 25 on the Symptom Inventory Case Definition Subscale were considered to have substantial accompanying symptoms. Subjects who met all 3 criteria (SF-36 and MFI and Symptom Inventory) when they entered the clinical study were classified as CFS according to standardized clinically empirical criteria.”
One hundred and sixty-four participants had no exclusionary conditions at the time of this study. The case definition identified 16 people with CFS and 76 with ISF. Thus 87% of those who met the case definition at recruitment did not meet the CDC criteria at the time of this study. Clinically empirical classification identified 43 subjects as CFS, 57 as ISF, and 64 as not ill. Thus 40% of those with CFS (CDC criteria ’94) at recruitment met the second set of criteria for CFS when assessed later.
Subjects empirically classified as CFS had significantly worse impairment (evaluated by the SF-36), more severe fatigue (documented by the multidimensional fatigue inventory), more frequent and severe accompanying symptoms than those with ISF, who in turn had significantly worse scores than the not ill; this was not true for classification by the surveillance algorithm.
There was minimal association between the empirical classification and classification by the surveillance criteria. The empirical definition includes all aspects of CFS specified in the 1994 case definition and identifies persons with CFS in a precise manner that can be readily reproduced by both investigators and clinicians.
For details, see:
Sankey, A., Hill, CM., Brown, J., Quinn, L and Fletcher, A. A follow-up study of chronic fatigue syndrome in children and adolescents: symptom persistence and school absenteeism Clinical Child Psychology and Psychiatry, 2006, 11, 1, 126-138.
This is a follow-up study of 28 young people aged between 7 and 17 meeting the Oxford criteria for the diagnosis of CFS (54% boys) treated in a specialist paediatric/psychiatric service. Retrospective case note analysis revealed a wide range and duration of symptoms together with high levels of school absenteeism prior to the diagnosis. The mean follow-up interval after discharge from the specialist service was 3 years and although most of the young people regarded themselves as fully recovered by this time, improvement was variable and about one third were still experiencing disabling symptoms. The illness had impacted on the education or career plans of all the young people to some extent with 15 experiencing difficulty returning to school. This article highlights the need for early recognition and diagnosis of chronic fatigue syndrome in young people and the importance of continuing paediatric support to reduce symptom persistence in the sensitive recovery period. Maintaining school attendance by close liaison between health and education services both before and after diagnosis and treatment is also vital if long-term morbidity is to be reduced.
[Ed. note: 32% were members of a support group. This was not correlated with “return to normality”.]
Wallman, KE., Morton, AR., Goodman, C and Grove, R. Reliability of physiological, psychological, and cognitive variables in chronic fatigue syndrome. Research in Sports Medicine 2005, 13, 3, 231-241.
The purpose of this study was to assess the reliability of specific physiological, psychological, and cognitive variables in 31 CFS subjects (CDC criteria ’94) and 31 matched control subjects. All variables were assessed weekly over a 4-week period and reliability was determined using an intraclass correlation coefficient (ICC). Measures included the Chalder Fatigue Scale, HAD and Stroop Colour Word test.
Results ranged from moderately to highly reliable for all variables assessed, except for mental and physical fatigue, which were of questionable reliability in both groups (ICC=0.61 and 0.65, respectively, for the CFS group; 0.62 and 0.52 for the control group). A Pearson product-moment correlation analysis that compared exercise performance with all psychological variables assessed, demonstrated a significant relationship between exercise performance and depression (r=.41, p=.02) in week 3 only, suggesting minimal association between objective performance and psychological responses. These correlation results support a central, as opposed to a peripheral, basis to the sensation of fatigue in CFS.
[Ed. Note: The lack of variability over the four weeks could be due to effective pacing by the patients, while the low ceiling of the Chalder Fatigue Scale may have limited the recording of fluctuations, particularly exacerbations in the more severely affected. Certain subgroups like ME may show more exercise-related variability in symptom scores than others, but this study did not stratify patients.]
Whitehead, LC. Quest, chaos and restitution: living with chronic fatigue syndrome/myalgic encephalomyelitis. Social Science and Medicine, 2005, Oct 19th. Online only.
Study on the experiences of 17 people with CFS/ME (undefined), showing differences from those of people with HIV and breast cancer.
Van Heukelom, RO., Prins, JB., Smits, MG and Bleijenberg, G. Influence of melatonin on fatigue severity in patients with chronic fatigue syndrome and late melatonin secretion. European Journal of Neurology, 2006, 13, 1, 55-60.
The effect of melatonin, a chronobiotic drug, was explored in 29 patients with CFS (own definition focusing on fatigue) plus insomnia, and Dim Light Melatonin onset (DLMO) later than 21.30 hours, reflective of delayed circadian rhythmicity.
The patients took 5 mg of melatonin orally, 5 hours before DLMO during 3 months. Their responses to the checklist individual strength (CIS), a reliable questionnaire measuring the severity of personally experienced fatigue, were assessed twice with a 6-week interval immediately before the treatment and once after 3 months treatment.
In the pre-treatment period the fatigue sub-score improved significantly. After treatment, the total CIS score and the sub-scores for fatigue, concentration, motivation and activity improved significantly. The sub-score fatigue normalized in two of the 29 patients in the pre-treatment period and in eight of 27 patients during treatment. This change was significant. In the patients with DLMO later than 22.00 hours (n=21) the total CIS score and the sub-scores for fatigue, concentration and activity improved significantly more than in the patients (n=8) with DLMO earlier than 22.00 hours.
Melatonin may be an effective treatment for patients with CFS and late DLMO, especially in those with DLMO later than 22.00 hours. It has a “hypnotic effect”.
Huibers, M and Wessely, S. The act of diagnosis: pros and cons of labelling chronic fatigue syndrome. Psychological Medicine, 2006, 36, 1, 1-6.
One of the many controversies surrounding CFS is the possible impact of the diagnostic label: is it disabling or enabling? In this paper, we discuss the pros and cons of labelling CFS.
Diagnosed CFS patients have a worse prognosis than fatigue syndrome patients without such a label. The ways in which CFS patients perceive themselves, label their symptoms and appraise stressors may perpetuate or exacerbate their symptoms, a process that involves psychological, psychosocial and cultural factors. Labels can also lead to conflicts with doctors who fear diagnosis might lead to worse outcomes. However, on the other hand, finding a label that fits one's condition can provide meaning, emotional relief and recognition, whilst the denial of the diagnosis of CFS in those who have already reached their own conclusion can be very counter productive. The act of diagnosis therefore seems to be a trade-off between empowerment, illness validation and group support, contrasted with the risk of diagnosis as self-fulfilling prophecy of non-recovery.
The answer to the question of 'to label or not to label' may turn out to depend not on the label, but on what that label implies. It is acceptable and often beneficial to make diagnoses such as CFS, provided that this is the beginning, and not the end, of the therapeutic encounter.
This ‘invited review’ is a highly selective discussion article which promotes the CBT model of CFS.
A diagnosis is always more helpful than continued uncertainty as the authors admit, but the real issue here is not whether to give the patient a ‘label’ but whether the label is accurate. The authors belong to the CBT school and in their view, any information which reinforces the belief that CFS is largely physical is likely to result in maladaptive behaviours. They recognise that infection may have triggered the original illness, but their model is limited and has no way of explaining the growing evidence of ongoing pathology in a significant proportion of these patients.
Initially, their response was to dismiss the findings as unreliable (as the same abnormality was not found in everyone) or a result of inactivity and stress. They also tended to ignore any research which supported the more traditional explanations implicating neurological disease and persisting infection. However, this review reveals a third strategy, namely, to question the diagnosis and to blur the boundaries between CFS and psychiatric conditions such as neurasthenia and somatisation. This not only distances the patients from the problematic literature but also allows the psychiatrists to regain some of the lost influence as far as CFS is concerned. Given the lack of evidence supporting a reclassification, I see this strategy first and foremost as a means of promoting psychological medicine. In addition to the central thesis that CFS is perpetuated and exacerbated by social and psychological factors, and that CBT is the most effective treatment, they are also trying to change the way in which doctors view this illness. This is old wine in new bottles. It’s a combination of psychosomatic illness, somatisation and the effects of Western culture. The problem is that patients refuse to accept this construct.
According to the authors, delaying the diagnosis will prevent people feeling more ill as a result of (mis)information from support groups and the internet. The assumption here is that this population is particularly suggestible and that they will accept advice from groups without question. In my view, the underlying aim is really to keep patients away from alternative explanations, so that they are more likely to accept interventions like CBT and graded exercise. But the new concept of CFS offers more than a simple theory and a relatively cheap form of treatment. If people are suffering as a result of unhealthy lifestyles, or misguided beliefs, they do not require benefits or adaptations to their homes and the government does not have to spend millions of pounds on researching the role of pathogens or neurological damage.
I will leave the political aspects of CFS for another time and focus here on the scientific aspects of the review. There are three main factors which undermine many of the authors’ arguments:
1. the poor quality of the evidence, specifically, their reliance on assumptions and generalisations, and on the systematic denial of evidence.
2. their tendency to misrepresent people’s views and events
3. the lack of logic.
For example, the authors claim that “many patients prefer the term ME” because they desire a biomedical label “which underlines the ‘realness of their complaints’. Note the assumption here that CFS is not biomedical, even though it is still coded by the WHO, with ME, under G93.3, as a neurological disease. They also claim that “the term indirectly implies that the condition is incurable, unless a medical solution is found”. Note the assumption that patients have obviously never heard of conditions like glandular fever, where infection can cause chronic symptoms but which usually resolve on their own. There’s the assumption that the patients do not read books or articles on ME which discuss the significant improvements which many make over time, and the implication that this population is particularly ignorant and prejudiced. There are no references, it’s basically opinion expressed as fact. In my view, it misrepresents what many patients think about CFS and ME. And why would so many prefer “ME” because a group of psychiatrists, whom they do not have contact with, regard CFS as something other than biomedical?
A more likely explanation is that people with ME do not recognise their illness in the descriptions of CFS and do not regard fatigue as their most disabling symptom. Is this argument therefore about the rejection of the label CFS or the fact that the CBT model cannot explain ME. It’s an illness which existed long before support groups, the internet and other factors which the authors have linked to somatisation and other factors which they believe have influenced CFS.
I’ve written before about the differences between ME and CFS. To summarise, the main characteristic of ME is not “fatigue” or even “post-exertional fatigue”, both of which are also found in other conditions. ME, as defined by Ramsay, features the diagnostic triad of muscle fatiguability after trivial exertion plus the delay in the return of muscle power after exertion ends, cerebral dysfunction and circulatory impairment. The CBT explanation and associated rehabilitation programme focus on tiredness and other ubiquitous symptoms (such as pain and headache), not the muscle weakness, vertigo, and neurological symptoms, experienced by people with ME. And CBT is not appropriate for the latter. This has led to the other common assumption of the CBT school, namely, that any differences between subgroups are of no clinical significance.
I accept that the lack of reliable information and a diagnostic test allows a small number of patients to claim that they have ME or CFS in order to avoid dealing with personal problems. However, the notion that most people with CFS prefer the term ME because they wish to avoid a psychosomatic label is, in my view, inaccurate, misleading and totally unhelpful.
Another suggestion which illustrates the modus operandi is that the term ME may have an adverse effect compared to the label CFS. They speculate about a ‘cause and effect’ in psychological terms but do not consider the possibility that the worse prognosis associated with ME and other post-viral syndromes may reflect the different criteria, more disabling nature or more complicated aetiology (e.g. Jason et al, Reeves et al*).
The sole reference relates to a study which defined prognosis purely in terms of duration, assessed on the basis of electronic records held by the GP. Thus, if a patient stayed with the GP for treatment and did not switch to a complementary practitioner, the records would show a greater duration and worse prognosis for the former compared to the latter, even if both had been ill for the same length of time. The median ‘duration’ of ME was found to be 106 days per year, that of CFS was 80 days. Both are short and atypical. The study did not assess differences in type and severity of symptoms.
Generalisations such as this “group of CFS patients tends to view their symptoms as part of an overwhelming, mysterious, unexplainable disease that struck them out of the blue and from which they most likely will never recover” is not referenced at all. This may be because there is no published evidence that this group exists, or if it does, that their characteristics are linked to a worse prognosis. In fact, studies have shown that many people with ME make significant improvements over time, that most have realistic thoughts about possible causes, and that few report the kind of hopelessness described (see review Goudsmit 1996). Admittedly, there will always be a proportion of patients with a more pessimistic outlook, but the majority do not conform to the stereotype portrayed by the authors. The problem is that the CBT model relies on the stereotype of the misinformed, misguided individual with psychological problems and poor coping strategies. And it seems that the proponents of this approach prefer to change the facts to fit the theory rather than adapt the theory to fit the facts.
To me, parts of the model make little sense. For instance, these patients are said to avoid even trivial activities and elsewhere, CBT school literature refers to ‘total rest’ and to universal feelings of helplessness and hopelessness. However, articles like these indicate that many patients continue to look for help, and that some are demanding and active lobbyists. So how inactive are these patients? And if these individuals cannot cope with modern life (see below) and develop symptoms which allows them a period of ‘rest’, why do they continue to search for a cure? If their unconscious offers them a way out, why does it not give them a sense of peace to go with it?
Another example concerns CBT. This treatment is available, free of charge, on the NHS and if done properly, does not appear to have serious or long-term side-effects. Why would a patient reject this in favour of untested, expensive approaches, some of which are known to cause highly unpleasant reactions (e.g. Marshall Protocol)? Unfortunately, the authors’ narrow focus means that they are reluctant to consider the possibility that CBT is often rejected because it just doesn’t work. It’s not faulty information from self-help groups but logic and experimentation which leads many to avoid graded exercise. And the model doesn’t make sense. It assumes that whatever triggered the symptoms has gone but doesn’t explain how beliefs or expectations can cause the exact same symptoms. It predicts that CFS should be a progressive illness, but in most cases it is not. It doesn’t deal with neurological symptoms or epidemics. Most of all, the essence of CFS is that the symptoms are triggered by minimal exertion. If graded exercise is effective, doesn’t it prove that the diagnosis was wrong? The lack of activity in the case of CFS (and ME) is not the cause of the symptoms, but the result, and there is no evidence to suggest otherwise.
I have already referred to what I see is the subtext of this review, namely, the rebranding of the CFS. This is reflected in statements like “CFS is a mirror of society” and a “cultural phenomenon”. It’s a way of linking the illness with modern society, information overload, speed and schedules. It suggests that CFS is a form of somatised distress, where patients develop symptoms, unconsciously, to avoid the demands, expectations and strain of every day life. It’s rebellion using body language, but wrongly labelled by groups, the media and the internet (p.3). In the same vein, CFS is supposedly a “metaphor of our times”. Perhaps it is, but not in the way the authors mean. In the olden days, I do not recall scientifically-trained professionals being given so much freedom in medical journals to promote a speculation-based and stigmatising view of a seriously disabling illness. Dispassionate objectivity wasn’t optional. I presume from what they have written that the authors do not like the speed of modern life. I don’t either but it doesn’t make me discard my scientific training and it certainly doesn’t make me feel fatigued. I switch off my mobile, say ‘no’ when I need to and pace myself through the day. If information overload was the cause of CFS, this illness would be a lot more common than it is. And if groups or the internet played such a significant role, how does one explain the literature on ME prior to the nineties, let alone the outbreaks in non-Western cultures like Sierra Leone?
The authors’ claim that CFS is restricted to “English-speaking countries and northern Europe” is a typical example of the way inconvenient facts are ignored. It isn’t true as the literature from Russia, China, Japan, and Southern Europe will confirm. However, linking the illness to the capitalist West with its health consumerism and demanding patients, allows one to argue that local culture, rather than pathogens, has “shaped” this disease. Which brings us back to the concept of CFS as a post-modernist form of somatisation.
For balance, there’s half a sentence alluding to the physical complexities of CFS, but it’s undone in the same paragraph by a comment about the lack of medically accepted disease verification and a pre-emptive response to critics; “our conclusions are primarily based on common sense”.
The former ignores the inclusion of both ME and CFS in ICD and a lot of the older literature. As for the conclusions, these may be based on common-sense but I’m not sure the rest of the text is. What this review reveals is a strong adherence to an exaggerated, negative stereotype and the deliberate avoidance of discussions about the role of infection and neurological abnormalities. It reveals individuals trained in science who ignore perfectly sound information in order to advance a specific argument and cling to beliefs despite growing evidence to the contrary. Attributing the chronicity and severity of CFS to factors such as unrealistic expectations, perception, culture and avoidance is overly simplistic, misleading and anything but common-sense.
The main message of the review is of course, that doctors should delay giving patients a diagnosis as the label is associated with a poor prognosis. As discussed above, this is supported by one, highly flawed study, which relied on electronic records and is hard to interpret. Aside from the lack of evidence, I do not see why CFS should be a special case. Doctors don’t delay giving people other diagnoses which have a poor outcome. If a patient meets the criteria and wishes to know what is wrong, isn’t the best policy to be honest? Moreover, the prognosis may be poorer than fatigue due to emotional distress but is it poorer than schizophrenia, lung cancer or most cases of MS? Is this a good enough reason to delay and deceive? Why not deal with CFS in the same way as one treats other conditions? Is it not better to do the best one can and leave the ultimate decisions to the patient? After all, they have to live with the consequences.
The authors also refer to the diagnosis as a self-fulfilling prophecy (p.4). This is based purely on speculation but reinforces the notion that CFS is largely psychological and avoidable. Their advice to doctors is therefore to rely on their common-sense, and to diagnose at a later stage, when the chances of recovery are reduced. But isn’t this also a self-fulfilling prophecy? Wouldn’t early diagnosis reduce the anxiety related to uncertainty, and prevent some of the complications, e.g. the effects of stress on the HPA axis, which can perpetuate the disease? And if the doctor gave accurate information concerning aetiology and management, in other words, that we don’t yet know what causes CFS but that it’s important to stay as active as possible, avoid overexertion, and to eat a good diet with lots of antioxidants, wouldn’t fewer people end up with the quacks and radical internet groups? If decisions are to be based on common-sense, surely it is essential to have some idea of what you are dealing with, and that goes for doctors as well as patients.
Finally, I wish to comment on the management strategy suggested by the authors, specifically, to “explore the meaning of suffering” and “discourage the sick role” (p. 5). I can imagine that many patients will interpret this as the kind of psychobabble which shows a lack of understanding as well as respect. To put it bluntly, when it comes to the sick role, people with CFS do not have a choice. The suggestion to the contrary is inappropriate, unhelpful and given what we know about this syndrome, insulting.
To summarise, there is too great a reliance on assumptions, speculation, and exaggeration. This review will undermine people’s trust in orthodox medicine in general, and psychological medicine in particular. It does not contribute to the knowledge base but offers an overly simplistic solution for a highly complex problem. The refusal to acknowledge reasonable alternative explanations suggests a degree of avoidance behaviour. Moreover, the claim that ideas are based on common-sense seems like a tactic to promote opinions for which there is little or no scientific evidence. The review is an eloquent essay, but it’s superficial and subjective. The contradictions and denial are inconsistent with the authors’ professional status and experience, and the end result is yet another example of the psychologisation of CFS and misrepresentation of ME.
E. Goudsmit. AFBPsS.
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