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Chronic mild dehydration is a common condition in some population groups, including especially the elderly and those who participate in physical activity in warm environments. Hypohydration is recognised as a precipitating factor in a number of acute medical conditions in the elderly, and there may be an association, although not necessarily a causal one, between a low habitual fluid intake and some cancers, cardiovascular disease and diabetes. There is some evidence of impairments of cognitive function at moderate levels of hypohydration, but even short periods of fluid restriction, leading to a loss of body mass of 1-2%, lead to reductions in the subjective perception of alertness and ability to concentrate and to increases in self-reported tiredness and headache. In exercise lasting more than a few minutes, hypohydration clearly impairs performance capacity, but muscle strength appears to be relatively unaffected.
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PMID:Impact of mild dehydration on wellness and on exercise performance. 1468 9

The ability of insulin to stimulate glucose disposal varies more than six-fold in apparently healthy individuals. The one third of the population that is most insulin resistant is at greatly increased risk to develop cardiovascular disease (CVD), type 2 diabetes, hypertension, stroke, nonalcoholic fatty liver disease, polycystic ovary disease, and certain forms of cancer. Between 25-35% of the variability in insulin action is related to being overweight. The importance of the adverse effects of excess adiposity is apparent in light of the evidence that more than half of the adult population in the United States is classified as being overweight/obese, as defined by a body mass index greater than 25.0 kg/m(2). The current epidemic of overweight/obesity is most-likely related to a combination of increased caloric intake and decreased energy expenditure. In either instance, the fact that CVD risk is increased as individuals gain weight emphasizes the gravity of the health care dilemma posed by the explosive increase in the prevalence of overweight/obesity in the population at large. Given the enormity of the problem, it is necessary to differentiate between the CVD risk related to obesity per se, as distinct from the fact that the prevalence of insulin resistance and compensatory hyperinsulinemia are increased in overweight/obese individuals. Although the majority of individuals in the general population that can be considered insulin resistant are also overweight/obese, not all overweight/obese persons are insulin resistant. Furthermore, the cluster of abnormalities associated with insulin resistance - namely, glucose intolerance, hyperinsulinemia, dyslipidemia, and elevated plasma C-reactive protein concentrations -- is limited to the subset of overweight/obese individuals that are also insulin resistant. Of greater clinical relevance is the fact that significant improvement in these metabolic abnormalities following weight loss is seen only in the subset of overweight/obese individuals that are also insulin resistant. In view of the large number of overweight/obese subjects at potential risk to be insulin resistant/hyperinsulinemic (and at increased CVD risk), and the difficulty in achieving weight loss, it seems essential to identify those overweight/obese individuals who are also insulin resistant and will benefit the most from weight loss, then target this population for the most-intensive efforts to bring about weight loss.
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PMID:Obesity, insulin resistance, and cardiovascular disease. 1474 3

Androgens are important determinants of body composition in men. Androgen-deprivation therapy, the mainstay of treatment for advanced prostate cancer, increases fat mass and decreases lean body mass. These adverse changes in body composition may contribute to treatment-related fatigue, fracture risk, insulin resistance, and increased cardiovascular disease risk. Potential strategies to treat or prevent these adverse body composition changes include exercise training, alternative forms of hormonal therapy, and insulin-sensitizing agents.
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PMID:Changes in body composition during hormonal therapy for prostate cancer. 1504 79

Physical activity has many and varied effects on the human body. The physiologic effects of physical activity and exercise in persons with cancer have been largely unstudied. Cancer patients as a group are at risk for diseases and conditions related to lack of physical activity. In persons with cancer, exercise has been shown to improve fitness and physical functioning, reduce fatigue, and modestly decrease weight and body fat. The effects of physical activity on prognosis, however, are unknown. In persons without cancer, exercise has beneficial effects on the cardiovascular and endocrine systems, reducing risk of cardiovascular disease, cerebrovascular disease, and diabetes. Increased physical activity reduces risk for several common cancers, which is relevant to cancer survivors who are at increased risk for new primary cancers. Additional benefits of physical activity include improvements in fitness, muscular-skeletal problems including arthritis symptoms, immune system function, cognition and sleep. Risks of increased physical activity in cancer patients and survivors have not been defined, but could be expected to include musculo-skeletal injuries, and a small increased risk in sudden death with vigorous exercise and serious accidents with some sports. The effect of physical activity on survival from cancer is unknown, but physical activity might improve prognosis through beneficial effect on cancer biomarkers and energy balance, as well as decreasing risk for cardiovascular disease, an important cause of death for many cancer survivors. The long-term benefits and risks of physical activity in cancer patients and survivors are unknown. Nevertheless, increasing physical activity is probably beneficial and safe in the majority of cancer survivors.
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PMID:Physical activity after cancer: physiologic outcomes. 1506 64

Obesity is associated with high blood cholesterol and high risk for developing diabetes and cardiovascular disease. Therefore, management of body weight and obesity are increasingly considered as an important approach to maintaining healthy cholesterol profiles and reducing cardiovascular risk. The present review addresses the effects of conjugated linoleic acid (CLA) on fat deposition, body weight and composition, safety, as well as mechanisms involved in animals and humans. Animal studies have shown promising effects of CLA on body weight and fat deposition. The majority of the animal studies have been conducted using CLA mixtures that contained approximately equal amounts of trans-10, cis-12 (t10c12) and cis-9, trans-11 (c9t11) isomers. Results of a few studies in mice fed CLA mixtures with different ratios of c9t11 and t10c12 isomers have indicated that the t10c12 isomer CLA may be the active form of CLA affecting weight gain and fat deposition. Inductions of leptin reduction and insulin resistance are the adverse effects of CLA observed in only mice. In pigs, the effects of CLA on weight gain and fat deposition are inconsistent, and no adverse effects of CLA have been reported. A number of human studies suggest that CLA supplementation has no effect on body weight and insulin sensitivity. Although it is suggested that the t10c12 CLA is the antiadipogenic isomer of CLA in humans, the effects of CLA on fat deposition are marginal and more equivocal as compared to results observed in animal studies. Mechanisms through which CLA reduces body weight and fat deposition remain to be fully understood. Proposed antiobesity mechanisms of CLA include decreased energy/food intake and increased energy expenditure, decreased preadipocyte differentiation and proliferation, decreased lipogenesis, and increased lipolysis and fat oxidation. In summary, CLA reduces weight gain and fat deposition in rodents, while produces less significant and inconsistent effects on body weight and composition in pigs and humans. New studies are required to examine isomer-specific effects and mechanisms of CLA in animals and humans using purified individual CLA isomers.
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PMID:Conjugated linoleic acid and obesity control: efficacy and mechanisms. 1525 84

Obstructive sleep apnea (OSA) is a common medical condition that occurs in approximately 5% to 15% of the population. The pathophysiology of OSA is characterized by repetitive occlusions of the posterior pharynx during sleep that obstruct the airway, followed by oxyhemoglobin desaturation, persistent inspiratory efforts against the occluded airway, and termination by arousal from sleep. Obstructive sleep apnea is associated with daytime sleepiness and fatigue, likely due to fragmented sleep from recurrent arousals. Substantial evidence shows that patients with OSA have an increased incidence of hypertension compared with individuals without OSA and that OSA is a risk factor for the development of hypertension. Recent studies show that OSA may be implicated in stroke and transient ischemic attacks. Obstructive sleep apnea appears to be associated with coronary heart disease, heart failure, and cardiac arrhythmias. Pulmonary hypertension may be associated with OSA, especially in patients with preexisting pulmonary disease. Although the exact cause that links OSA with cardiovascular disease is unknown, there is evidence that OSA is associated with a group of proinflammatory and prothrombotic factors that have been identified to be important in the development of atherosclerosis. Obstructive sleep apnea is associated with increased daytime and nocturnal sympathetic activity. Autonomic abnormalities seen in patients with OSA include increased resting heart rate, decreased R-R interval variability, and increased blood pressure variability. Both atherosclerosis and OSA are associated with endothelial dysfunction, increased C-reactive protein, interleukin 6, fibrinogen, and plasminogen activator inhibitor, and reduced fibrinolytic activity. Obstructive sleep apnea has been associated with enhanced platelet activity and aggregation. Leukocyte adhesion and accumulation on endothelial cells are common in both OSA and atherosclerosis. Clinicians should be aware that OSA may be a risk factor for the development of cardiovascular disease.
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PMID:Obstructive sleep apnea and cardiovascular disease. 1530 32

Atrial fibrillation is the most common supraventricular tachyarrhythmia encountered in clinical practice, affecting over 5% of persons over the age of 65 years. A common pathophysiological mechanism for arrhythmia development is atrial distention and fibrosis induced by hypertension, coronary artery disease or ventricular dysfunction. Less frequently, atrial fibrillation is caused by mitral stenosis or other provocative factors such as thyrotoxicosis, pericarditis or alcohol intoxication. Depending on the extent of associated cardiovascular disease, atrial fibrillation may produce haemodynamic compromise, or symptoms such as palpitations, fatigue, chest pain or dyspnoea. Arrhythmia-induced atrial stasis can precipitate clot formation and the potential for subsequent thromboembolism. Comprehensive management of atrial fibrillation requires a multifaceted approach directed at controlling symptoms, protecting the patient from ischaemic stroke or peripheral embolism and possible conversion to or maintenance of sinus rhythm. Numerous randomised trials have demonstrated the efficacy of warfarin--and less so aspirin (acetylsalicylic acid)--in reducing the risk of embolic events. Furthermore, therapeutic strategies exist that can favourably modify symptoms by restoring and maintaining sinus rhythm with cardioversion and antiarrhythmic prophylaxis. However, the risks and benefits of various treatments is highly dependent on patient-specific features, emphasising the need for an individualised approach. This article reviews the findings of cost-effectiveness studies published over the past decade that have evaluated different components of treatment strategies for atrial fibrillation. These studies demonstrate the economic attractiveness of acute management options, long term warfarin prophylaxis, telemetry-guided initiation of antiarrhythmic therapy, approaches to restore and maintain sinus rhythm, and the potential role of transoesophageal echocardiographic screening for atrial thrombus prior to pharmacological or electrical cardioversion. Further, we discuss the merits and limitations of the cost-effectiveness analyses in the context of overall treatment strategies. Finally, we identify areas that will require additional research to achieve the goal of effective and economically efficient management of atrial fibrillation.
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PMID:Cost effectiveness of therapies for atrial fibrillation. A review. 1534 2

Vital exhaustion, a state characterized by unusual fatigue, loss of energy, increased irritability, and feelings of demoralization, is one of the cardiovascular risk factors. The authors investigated whether vital exhaustion contributes to the identification of subjects at increased risk of myocardial infarction in general practice. In this prospective cohort study, vital exhaustion was assessed with the Maastricht Interview on Vital Exhaustion. Other cardiovascular risk factors established were age, gender, systolic and diastolic blood pressure, total cholesterol, body mass index, smoking habits, cardiovascular disease, and diabetes mellitus. A Cox regression analysis was used. The subjects were adults (41-66 years) in an average Dutch village population. Outcome measures were fatal and nonfatal myocardial infarction. At the univariate level, vital exhaustion doubled the risk of myocardial infarction. The effect of exhaustion was confounded by gender; women had higher exhaustion scores and a lower incidence of myocardial infarction. With control for gender, age, systolic blood pressure, total cholesterol, smoking habits, self-reported cardiovascular disease, and diabetes mellitus, vital exhaustion almost tripled the risk of myocardial infarction. Assessment of vital exhaustion contributes to the identification of subjects at increased risk of myocardial infarction in general practice.
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PMID:Assessment of vital exhaustion and identification of subjects at increased risk of myocardial infarction in general practice. 1534 86

An inverse relation exists between omega-3 fatty acid intake and risk of cardiovascular disease development/mortality and sudden cardiac death in humans. Mechanisms underlying this cardioprotective effect are unknown, but could involve the autonomic nervous system. We tested the hypothesis that omega-3 fatty acid supplementation ("fish oil") would reduce muscle sympathetic nerve activity (MSNA) at rest and attenuate increases during physiological stressors. MSNA (peroneal microneurography) was measured during rest, ischemic handgrip to fatigue (IHG), and a cold pressor test (CPT). Measurements were obtained before (PRE) and after (POST) 1 month of daily ingestion of either fish oil (experimental group, n=9) or olive oil capsules (control group, n=9). MSNA at rest was comparable PRE and POST in control (3+/-1 versus 3+/-1 bursts/30 seconds) and experimental (4+/-1 versus 5+/-1 bursts/30 seconds) subjects. IHG and CPT increased MSNA in both groups PRE and POST. MSNA, arterial blood pressure, and heart rate responses to the stressors were similar PRE and POST in the control group. In contrast, MSNA responses to IHG (Delta4+/-2 and Delta9+/-2 bursts/30 seconds; P<0.05 for PRE and POST, respectively) and CPT (Delta4+/-1 versus Delta10+/-2 bursts/30 seconds; P<0.05) were augmented after omega-3 fatty acid supplementation whereas arterial blood pressure and heart rate responses were unchanged. These data indicate that 1 month of omega-3 fatty acid supplementation does not change MSNA at rest but augments sympathetic outflow to physiological stressors. The mechanism underlying augmented MSNA responses to physiological stressors after omega-3 fatty acid supplementation is unknown, but may involve impaired peripheral vasoconstriction.
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PMID:Omega-3 fatty acid supplementation augments sympathetic nerve activity responses to physiological stressors in humans. 1545 23

Rheumatoid arthritis (RA) is the most common inflammatory synovitis in older adults. The primary care physician may see its presentatiion as the late stage of a long-term disorder, or alternatively as an elderly-onset disease. These two presentations of RA may differ significantly with respect to mode of onset, prevalence of associated systemic symptoms (eg, fatigue, weight loss, depression), criteria for diagnosis (eg, rheumatoid factor or rheumatoid nodules), progression of diseases and functional outcomes. Because RA is responsive to treatmentt, and new treatments are available, diagnosis of this disorder is imperative. Differential diagnostic possibilities and therapies are reviewed, with particular emphasis on the cause and effect of comorbid disease such as infection, osteoporosis, and cardiovascular disease.
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PMID:Inflammatory arthropathy: a review of rheumatoid arthritis in older patients. 1550 53


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