We contrast Western medical views of chronic fatigue syndrome (CFS) etiology, diagnosis, and treatment with views maintained by a predominantly female CFS population. We argue that the failure of Western medicine to demonstrate a viral etiology for CFS led to a paradigmatic shift in research perspectives, which then embraced psychiatric and sociocultural explanations for CFS. As a result, CFS was delegitimized as a biomedical phenomenon within medical, academic, governmental, and public arenas. We compare alternative social constructions of CFS with issues pertaining to multiple sclerosis (MS), an illness that similarly predominates among women. Patient perspectives suggest that the history of medical attitudes toward CFS may eventually parallel the transformations that occurred in relation to MS. In particular, the discovery of biological markers for CFS may lay to rest the categorization of CFS as largely within the psychiatric realm.

Attitude to Health↗

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Chronic fatigue syndrome, fibromyalgia, and multiple chemical sensitivities in a community-based sample of persons with chronic fatigue syndrome-like symptoms.

OBJECTIVE: The aim of this study was to determine illness comorbidity rates for individuals with chronic fatigue syndrome (CFS), fibromyalgia (FM), and multiple chemical sensitivities (MCS). An additional objective was to identify characteristics related to the severity of fatigue, disability, and psychiatric comorbidity in each of these illness groups. METHODS: A random sample of 18,675 residents in Chicago, Illinois, was first interviewed by telephone. A control group and a group of individuals with chronic fatigue accompanied by at least four minor symptoms associated with CFS received medical and psychiatric examinations. RESULTS: Of the 32 individuals with CFS, 40.6% met criteria for MCS and 15.6% met criteria for FM. Individuals with MCS or more than one diagnosis reported more physical fatigue than those with no diagnosis. Individuals with more than one diagnosis also reported greater mental fatigue and were less likely to be working than those with no diagnosis. Individuals with CFS, MCS, FM, or more than one diagnosis reported greater disability than those with no diagnosis. CONCLUSIONS: Rates of coexisting disorders were lower than those reported in prior studies. Discrepancies may be in part attributable to differences in sampling procedures. People with CFS, MCS, or FM endure significant disability in terms of physical, occupational, and social functioning, and those with more than one of these diagnoses also report greater severity of physical and mental fatigue. The findings illustrate differences among the illness groups in the range of functional impairment experienced.

Adolescent↗

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The effect of chronic cardiac volume overload on regional myocardial blood flow in the dog.

1. Regional myocardial blood flow was studied in the anaesthetized, open-chest dog with a large chronic aorto-caval fistula, using carbonized microspheres of 7-10 mum diameter. The results from fourteen dogs with fistulae of 4-84 days duration were compared to those from nine normal animals. 2. Myocardial blood flow to all areas of both ventricles was increased to between 180 and 250% of the normal despite lower aortic diastolic (coronary diastolic) pressure. Myocardial blood flow in the right ventricle was lower than in the left in both groups of dogs although the increase above normal in dogs with fistulae was relatively greater in the right ventricle. Increased myocardial blood flow is attributed to coronary autoregulation resulting from increased myocardial oxygen consumption due to increase in myocardial tension development. 3. Although absolute blood flow to the inner left ventricular wall was markedly increased in all dogs with fistulae, in those with aortic diastolic pressure below 55 mmHg the ratio of flow in the inner to that in the outer free left ventricular wall was significantly less than in those with aortic diastolic pressure above 55 mmHg (P less than 0 with 02). Low aortic diastolic pressurere and diastolic coronary perfusion pressure probably resulted in relative ischaemia of the inner left ventricular wall.

Animals↗

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Increase in myocardial digoxin content associated with circulatory volume overload in the dog.

1. Tritiated (12alpha-3H) digoxin (0-05 mg/kg body weight) was administered intravenously to conscious dogs with circulatory volume overload induced by previous creation of aorto-caval fistulae. Dogs were killed after 5 min, 1, or 4 h, and the myocardium sampled. Digoxin was extracted and counted and results compared to those in normal dogs. 2. At each time, myocardial digoxin concentration of all cardiac chambers in test dogs was greater than normal. Plasma digoxin concentration measured 5 min after administration was greater in dogs with fistulae but the subsequent levels were not different. 3. Anaesthetized and open-chest dogs with fistulae studied 5 min after digoxin administration had greater myocardial concentrations than similarly studied normal dogs. Although myocardial concentrations of digoxin were higher in anaesthetized than in conscious dogs the group with fistulae had higher values than did the normal group, as was the case for unanaesthetized dogs. 4. The basis for the effect of fistula is probably multifactorial. Diminised peripheral blood flow and peripheral digoxin delivery and uptake, resulting initially in higher digoxin levels in plasma perfusing the myocardium, may play a role. Increased myocardial mechanical and metabolic activity almost certainly are important. Cardiac hypertrophy, cardiac failure per se and plasma electrolyte changes are probably not. 5. The results are consistent with previously demonstrated reduced digitalis tolerance in the dog with circulatory volume overload.

Animals↗

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The effect of heart rate on myocardial ouabain uptake and on the susceptibility to ouabain cardiotoxicity in the dog.

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Animals↗

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Cardiac beta-adrenoreceptors in the thyroxine-treated dog.

1. Myocardial beta-adrenoreceptors, assessed in membrane preparations of left ventricle by 3H-dihydroalprenolol binding, were compared in dogs following thyroxine administration (n = 6), aorto-caval fistula (n = 12), and in normal dogs (n = 7). 2. Left ventricular hypertrophy occurred in response to both aorto-caval fistula and thyroxine treatment. Yield of myocardial membrane between the different groups was not significantly different. 3. Binding site concentration (pmol/mg membrane protein) in dogs with aorto-caval fistulae was similar to that in normal dogs and was not significantly influenced by the presence or absence of cardiac failure, degree of hypertrophy or duration of fistula. 4. Thyroxine-treated dogs had an increased concentration of binding sites (c. 1.8-fold) compared with both fistula and normal groups, while binding affinities were similar in all groups. 5. The data suggest that beta-adrenoreceptor concentrations in myocardium increase as a direct result of thyroid hormone action rather than as a result of secondary haemodynamic changes or ventricular hypertrophy.

Animals↗

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The influence of heart rate on digoxin-induced inhibition of myocardial Na+-K+-ATPase activity in the dog.

1. Groups of sedated dogs were studied at spontaneous heart rates (HR), 55-100/min, or at paced HR 200/min, with or without intravenous digoxin administration. After 60 min, active rubidium uptake (86 Rb+) of ventricular samples was determined in vitro. 2. Untreated fast and slow HR groups had similar uptakes. Following digoxin, 0.08 mg/kg, uptake was less at fast than slow HR (63.8, s.e.m. = 4.5 v. 87.5, s.e.m. = 5.0 pmol/mg LV/15 min, P less than 0.01). After 0.125 mg/kg, values were again lower in the fast HR group in which five of seven developed ventricular tachycardia. 3. Heart rate does not alter in vitro activity of myocardial Na+-K+-ATPase but does influence inhibition of the enzyme resulting from digoxin administration.

Animals↗

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beta-Adrenoceptors in the hypertrophied right ventricle of the dog with pulmonary stenosis.

1. Right ventricular hypertrophy was produced in dogs by banding of the pulmonary artery for 28 days (n = 7) and results were compared with those in sham-operated dogs (n = 5). 2. Myocardial noradrenaline and adrenaline levels were depressed in both the hypertrophied right ventricle and the non-hypertrophied left ventricle and plasma levels were increased compared to the control dogs. 3. Myocardial beta-adrenoceptors were assessed in membrane preparations of both ventricles by 3H-dihydroalprenolol binding. No change in binding site concentration (pmol/mg membrane protein) or in binding affinity was found in either the hypertrophied right ventricle or in the left ventricle. 4. Divergent results of studies on beta-adrenoceptors in ventricular hypertrophy are difficult to reconcile.

Animals↗

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The measurement of plasma thromboxane B2 and the effect of smoking.

Plasma thromboxane B2 (TxB2) was measured by radioimmunoassay using an iodinated ligand following extraction and further purification by thin layer chromatography. Venous blood was sampled into a syringe containing the cyclooxygenase inhibitor meclofenamate. Normal levels, 15 pg/ml (s.d. = 8, n = 21), were lower than usually reported and measured values increased several fold over 20 min sampling from an indwelling needle. With appropriate sampling there was a statistically insignificant increase in plasma TxB2 after subjects smoked two cigarettes (n = 11). An average decrease occurred in a control group (n = 10) and the difference between groups was of borderline significance (P less than 0.05). Smoking did not change TxB2 production associated with platelet aggregation induced in vitro by collagen, whereas plasma adrenaline increased significantly. The results emphasize the importance of the technique of sampling and assay in the measurement of plasma TxB2.

Adult↗

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Increased protein synthesis during right ventricular hypertrophy following pulmonary stenosis in the dog.

The synthesis rates of mixed protein in the left and right ventricles were the same in normal dogs, averaging 7.8% per day. After five days, pulmonary stenosis protein synthesis rate in the right ventricle increased rapidly to 13.6% per day and subsequently decreased to near normal by 12 days, during which time the right ventricle protein mass increased by 48% after five days and by 73% after 12 days. Similarly the synthesis rate of the myofibrillar and sarcoplasmic proteins was almost doubled after five days of stenosis. The protein synthesis rate in the left ventricle did not change significantly during the 24 days of pulmonary stenosis.

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