Tag: chronic fatigue

A twin study of chronic fatigue

Abstract:

OBJECTIVE: The etiology of chronic fatigue syndrome is unknown, but genetic influences may be important in its expression. Our objective was to assess the role of genetic and environmental factors in unexplained chronic fatigue.

METHODS: A classic twin study was conducted using 146 female-female twin pairs, of whom at least one member reported > or =6 months of fatigue. After completing questionnaires on symptoms, zygosity, physical health, and a psychiatric interview, twins were classified using three increasingly stringent definitions: 1) chronic fatigue for > or =6 months, 2) chronic fatigue not explained by exclusionary medical conditions, and 3) idiopathic chronic fatigue not explained by medical or psychiatric exclusionary criteria of the chronic fatigue syndrome case definition. Concordance rates in monozygotic and dizygotic twins were calculated for each fatigue definition along with estimates of the relative magnitude of genetic and environmental influences on chronic fatigue.

RESULTS: The concordance rate was higher in monozygotic than dizygotic twins for each definition of chronic fatigue. For idiopathic chronic fatigue, the concordance rates were 55% in monozygotic and 19% in dizygotic twins (p =.042). The estimated heritability in liability was 19% (95% confidence interval = 0-56) for chronic fatigue > or =6 months, 30% (95% confidence interval = 0-81) for chronic fatigue not explained by medical conditions, and 51% (95% confidence interval = 7-96) for idiopathic chronic fatigue.

CONCLUSIONS: These results provide evidence supporting the familial aggregation of fatigue and suggest that genes may play a role in the etiology of chronic fatigue syndrome.

 

Source: Buchwald D, Herrell R, Ashton S, Belcourt M, Schmaling K, Sullivan P, Neale M, Goldberg J. A twin study of chronic fatigue. Psychosom Med. 2001 Nov-Dec;63(6):936-43. http://www.ncbi.nlm.nih.gov/pubmed/11719632

 

Circulating tumour necrosis factor-alpha and interferon-gamma are detectable during acute and convalescent parvovirus B19 infection and are associated with prolonged and chronic fatigue

Abstract:

To investigate whether cytokine responses may have a bearing on the symptoms and outcome of parvovirus B19 infection, circulating cytokines were measured during acute infection (n=51), follow-up of acute infection (n=39) and in normal healthy controls (n=50).

At acute B19 virus infection (serum anti-B19 IgM-positive), patients ranged in age from 4 to 54 years, with a mean age of 28.2 years. The male:female ratio was 1:4.1 and symptoms were rash (n=15), arthralgia (n=31), fatigue (n=8), lymphadenopathy (n=4), foetal hydrops (n=3), transient aplastic crisis (n=2), neutropenia (n=2), myelodysplasia (n=1), thrombocytopenia (n=1) and pancytopenia (n=1). Of these patients, 39 were contacted after a follow-up period of 2-37 months (mean of 22.5 months).

In comparison with normal controls, detectable IL-6 was associated with acute B19 virus infection (26%; P=0.0003), but not with follow-up (6%; P=0.16). Detection of interferon (IFN)-gamma was associated with acute B19 virus infection (67%; P<0.0001) and follow-up (67%; P<0.0001). Detection of tumour necrosis factor (TNF)-alpha was associated with acute B19 virus infection (49%; P<0.0001) and follow-up (56%; P<0.0001). IL-1beta was detected in acute infection (20%), but not at follow-up. At acute B19 virus infection, detection of serum/plasma IL-6 was associated with rheumatoid factor (P=0.038) and IFN-gamma (> or =7 pg/ml) was associated with fatigue in those patients of > or =15 years of age (P=0.022). At follow-up, fatigue was associated with IFN-gamma (> or =7 pg/ml) and/or TNF-alpha (> or =40 pg/ml) (P=0.0275).

Prolonged upregulation of serum IFN-gamma and TNF-alpha appears to represent a consistent host response to symptomatic B19 virus infection.

 

Source: Kerr JR, Barah F, Mattey DL, Laing I, Hopkins SJ, Hutchinson IV, Tyrrell DA. Circulating tumour necrosis factor-alpha and interferon-gamma are detectable during acute and convalescent parvovirus B19 infection and are associated with prolonged and chronic fatigue. J Gen Virol. 2001 Dec;82(Pt 12):3011-9. http://www.ncbi.nlm.nih.gov/pubmed/11714978

 

Chronic fatigue

The possibility that fatigue may be an early manifestation of a serious medical illness not elicited through blood testing has been investigated by monitoring fatigued patients prospectively over time for the development of new diagnoses. At 1 year of follow-up, one study 3 showed no significant differences in new diagnoses, the incidences of diagnosed cancers, number of physician visits, or number of hospital admissions or hospital days.

This gives more weight to the conclusion that patients with chronic fatigue who otherwise have normal histories and no abnormalities on physical examination do not require extensive workups for occult medical illnesses.

You can read the full article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071607/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071607/

 

Source: Stevens DL. Chronic fatigue. West J Med. 2001 Nov;175(5):315-9. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071607/ (Full article)

 

A twin study of the etiology of prolonged fatigue and immune activation

Abstract:

Risk factors to prolonged fatigue syndromes (PFS) are controversial. Pre-morbid and/or current psychiatric disturbance, and/or disturbed cell-mediated immunity (CMI), have been proposed as etiologic factors.

Self-report measures of fatigue and psychologic distress and three in vitro measures of CMI were collected from 124 twin pairs. Crosstwin-crosstrait correlations were estimated for the complete monozygotic (MZ; 79 pairs) and dizygotic (DZ; 45 pairs) twin groups. Multivariate genetic and environmental models were fitted to explore the patterns of covariation between etiologic factors. For fatigue, the MZ correlation was more than double the DZ correlation (0.49 versus 0.16) indicating strong genetic control of familial aggregation.

By contrast, for in vitro immune activation measures MZ and DZ correlations were similar (0.49-0.69 versus 0.42-0.53) indicating the etiologic role of shared environments. As small univariate associations were noted between prolonged fatigue and the in vitro immune measures (r = -0.07 to -0.12), multivariate models were fitted. Relevant etiologic factors included: a common genetic factor accounting for 48% of the variance in fatigue which also accounted for 4%, 6% and 8% reductions in immune activation; specific genetic factors for each of the in vitro immune measures; a shared environment factor influencing the three immune activation measures; and, most interestingly, unique environmental influences which increased fatigue but also increased markers of immune activation.

PFS that are associated with in vitro measures of immune activation are most likely to be the consequence of current environmental rather than genetic factors. Such environmental factors could include physical agents such as infection and/or psychologic stress.

 

Source: Hickie IB, Bansal AS, Kirk KM, Lloyd AR, Martin NG. A twin study of the etiology of prolonged fatigue and immune activation. Twin Res. 2001 Apr;4(2):94-102. http://www.ncbi.nlm.nih.gov/pubmed/11665341

 

Chronic fatigue: symptom and syndrome

Abstract:

Chronic fatigue is common, is difficult to measure, can be associated with considerable morbidity, and is rarely a subject of controversy. The chronic fatigue syndrome also presents problems in definition and measurement, is associated with even more morbidity than chronic fatigue itself, and is often controversial. Particularly unclear is the way in which chronic fatigue and the chronic fatigue syndrome relate to each other: Is one the severe form of the other, or are they qualitatively and quantitatively different? We know that many things can cause chronic fatigue, and this is probably true for the chronic fatigue syndrome, too. We can anticipate that discrete causes of the chronic fatigue syndrome will be found in the future, even if these causes are unlikely to fall neatly along the physical-psychological divide that some expect. The causes of chronic fatigue are undoubtedly many, both in a population and in any individual person, even when a discrete cause, such as depression or cancer, is identified. Social, behavioral, and psychological variables are important in both chronic fatigue and the chronic fatigue syndrome. Interventions that address these general variables can be successful, and currently they are often more successful than interventions directed at specific causes.

 

Source: Wessely S. Chronic fatigue: symptom and syndrome. Ann Intern Med. 2001 May 1;134(9 Pt 2):838-43. http://www.ncbi.nlm.nih.gov/pubmed/11346319

 

Chemical sensitivity and chronic fatigue in Gulf War veterans: a brief report

Abstract:

The foci of this brief report are to (1) describe the prevalence of chemical sensitivity (CS) and chronic fatigue (CF) symptomatology and of presumptive multiple CS and CF syndrome diagnoses, and (2) explore the potential overlap between one purported case definition (i.e., chronic multi-symptom illness) and these unexplained symptom syndromes in a well-characterized group of Gulf War veterans. The number of subjects with CS and CF symptomatology and presumptive multiple CS and CF syndrome diagnoses was higher in the Gulf War-deployed group compared with a group deployed to Germany during the Gulf War. However, the percent differences were not significant when comparing the presumptive diagnoses of multiple CS and CF syndrome. The characteristic differences between the groups and the overlap with chronic multi-symptom illness are also discussed.

 

Source: Proctor SP, Heaton KJ, White RF, Wolfe J. Chemical sensitivity and chronic fatigue in Gulf War veterans: a brief report. J Occup Environ Med. 2001 Mar;43(3):259-64. http://www.ncbi.nlm.nih.gov/pubmed/11285874

 

Chronic fatigue in general practice: is counselling as good as cognitive behaviour therapy? A UK randomised trial

Abstract:

BACKGROUND: Fatigue is a common symptom for which patients consult their doctors in primary care. With usual medical management the majority of patients report that their symptoms persist and become chronic. There is little evidence for the effectiveness of any fatigue management in primary care.

AIM: To compare the effectiveness of cognitive behaviour therapy (CBT) with counselling for patients with chronic fatigue and to describe satisfaction with care.

DESIGN OF STUDY: Randomised trial with parallel group design.

SETTING: Ten general practices located in London and the South Thames region of the United Kingdom recruited patients to the trial between 1996 and 1998. Patients came from a wide range of socioeconomic backgrounds and lived in urban, suburban, and rural areas.

METHOD: Data were collected before randomisation, after treatment, and six months later. Patients were offered six sessions of up to one hour each of either CBT or counselling. Outcomes include: self-report of fatigue symptoms six months later, anxiety and depression, symptom attributions, social adjustment and patients’ satisfaction with care.

RESULTS: One hundred and sixty patients with chronic fatigue entered the trial, 45 (28%) met research criteria for chronic fatigue syndrome; 129 completed follow-up. All patients met Chalder et al’s standard criteria for fatigue. Mean fatigue scores were 23 on entry (at baseline) and 15 at six months’ follow-up. Sixty-one (47%) patients no longer met standard criteria for fatigue after six months. There was no significant difference in effect between the two therapies on fatigue (1.04 [95% CI = -1.7 to 3.7]), anxiety and depression or social adjustment outcomes for all patients and for the subgroup with chronic fatigue syndrome. Use of antidepressants and consultations with the doctor decreased after therapy but there were no differences between groups.

CONCLUSION: Counselling and CBT were equivalent in effect for patients with chronic fatigue in primary care. The choice between therapies can therefore depend on other considerations, such as cost and accessibility.

Comment in:

Chronic fatigue in general practice. [Br J Gen Pract. 2001]

Cognitive behaviour therapy and chronic fatigue syndrome. [Br J Gen Pract. 2001]

 

Source: Ridsdale L, Godfrey E, Chalder T, Seed P, King M, Wallace P, Wessely S; Fatigue Trialists’ Group. Chronic fatigue in general practice: is counselling as good as cognitive behaviour therapy? A UK randomised trial. Br J Gen Pract. 2001 Jan;51(462):19-24. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1313894/ (Full article)

 

Magnesium status and parameters of the oxidant-antioxidant balance in patients with chronic fatigue: effects of supplementation with magnesium

Abstract:

OBJECTIVE: Magnesium deficiency and oxidative stress have both been identified as pathogenic factors in aging and in several age-related diseases. The link between these two factors is unclear in humans although, in experimental animals, severe Mg deficiency has been shown to lead to increased oxidative stress.

METHODS: The relationship between Mg body stores, dietary intakes and supplements on the one hand and parameters of the oxidant-antioxidant balance on the other was investigated in human subjects.

RESULTS: The study population consisted of 93 patients with unexplained chronic fatigue (median age 38 years, 25% male, 16% smokers and 54% with Chronic Fatigue Syndrome (CFS). Mg deficient patients (47%) had lower total antioxidant capacity in plasma (p=0.007) which was related to serum albumin. Mg deficient patients whose Mg body stores did not improve after oral supplementation with Mg (10 mg/kg/day) had persistently lower blood glutathione levels (p=0.003). In vitro production of thiobarbituric acid reactive substances (TBARS) by non-HDL lipoproteins incubated with copper was related to serum cholesterol (p<0.001) but not to Mg or antioxidants and did not improve after Mg supplementation. In contrast, velocity of formation of fluorescent products of peroxidation (slope) correlated with serum vitamin E (p<0.001), which was, in turn, related to Mg dietary intakes. Both slope and serum vitamin E improved after Mg supplementation (p<0.001).

CONCLUSIONS: These results show that the lower antioxidant capacity found in moderate Mg deficiency was not due to a deficit in Mg dietary intakes and was not accompanied by increased lipid susceptibility to in vitro peroxidation. Nevertheless, Mg supplementation was followed by an improvement in Mg body stores, in serum vitamin E and its interrelated stage of lipid peroxidation.

 

Source: Manuel y Keenoy B, Moorkens G, Vertommen J, Noe M, Nève J, De Leeuw I. Magnesium status and parameters of the oxidant-antioxidant balance in patients with chronic fatigue: effects of supplementation with magnesium. J Am Coll Nutr. 2000 Jun;19(3):374-82. http://www.ncbi.nlm.nih.gov/pubmed/10872900

 

Prolonged fatigue, anxiety and depression: exploring relationships in a primary care sample

Abstract:

OBJECTIVE: While prolonged fatigue states are frequently comorbid with other forms of distress, they are now the subject of independent aetiological and treatment research. The objective of this study was to use principal component analysis to clarify the relationships between proposed measures of prolonged fatigue and anxiety and depression in data obtained from patients attending primary care.

METHOD: Self-report measures of prolonged fatigue and psychological distress (anxiety and depression) were administered to consecutive ambulatory care patients attending primary care.

RESULTS: Data from 1593 subjects were obtained. A two-factor principal component solution (varimax rotation) demonstrated a clear separation between fatigue-related items (Cronbach’s alpha = 0.81) as compared with those items describing anxiety and/or depression (Cronbach’s alpha = 0.95). A four-factor solution produced similar results with two factors describing general psychological distress (contrasting anxiety and depression), with two other factors describing the profiles of mental and physical fatigue.

CONCLUSIONS: The results lend weight to the argument that prolonged fatigue states can be measured independently of conventional notions of anxiety and depression in patients attending primary care. Epidemiological, aetiological and treatment research in psychiatry may need to focus greater attention on such prolonged fatigue states.

Comment in: Response to: ‘Prolonged fatigue, anxiety and depression: exploring relationships in a primary care sample‘. [Aust N Z J Psychiatry. 2000]

 

Source: Koschera A, Hickie I, Hadzi-Pavlovic D, Wilson A, Lloyd A. Prolonged fatigue, anxiety and depression: exploring relationships in a primary care sample. Aust N Z J Psychiatry. 1999 Aug;33(4):545-52. http://www.ncbi.nlm.nih.gov/pubmed/10483850

 

Fatigue and psychiatric disorder: different or the same?

Abstract:

BACKGROUND: Fatigue and psychiatric symptoms are common in the community, but their association and outcome are sparsely studied.

METHOD: A total of 1177 patients were recruited from UK primary care on attending their general practitioner. Fatigue and psychiatric disorder was measured at three time points with the 12-item General Health Questionnaire and the 11-item Fatigue Questionnaire.

RESULTS: Total scores for fatigue and psychiatric disorder did not differ between the three time points and were closely correlated (r around 0.6). The association between non-co-morbid (‘pure’) fatigue and developing psychiatric disorder 6 months later was the same as that for being well and subsequent psychiatric disorder. Similarly, having non-co-morbid psychiatric disorder did not predict having fatigue any more than being well 6 months previously. Between 13 and 15% suffered from non-co-morbid fatigue at each time point and 2.5% suffered from fatigue at two time points 6 months apart. Less than 1% of patients suffered from non-co-morbid fatigue at all three time points.

CONCLUSIONS: The data are consistent with the existence of ‘pure’ independent fatigue state. However, this state is unstable and the majority (about three-quarters) of patients become well or a case of psychiatric disorder over 6 months. A persistent, independent fatigue state lasting for 6 months can be identified in the primary-care setting, but it is uncommon of the order of 2.5%. Non-co-morbid (pure) fatigue did not predict subsequent psychiatric disorder.

 

Source: van der Linden G, Chalder T, Hickie I, Koschera A, Sham P, Wessely S. Fatigue and psychiatric disorder: different or the same? Psychol Med. 1999 Jul;29(4):863-8. http://www.ncbi.nlm.nih.gov/pubmed/10473313