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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study examined central adiposity, as measured by waist circumference (WC), in relation to mental-stress induced systolic (SBP) and diastolic blood pressure (DBP) and heart rate (HR) responses, body composition, the metabolic syndrome, and health practices in 22 older, African American men and women (ages 52-79 years). The high WC (> 100 cm) group showed significantly greater SBP, DBP, and HR reactivity, greater fasting insulin levels, lower high density lipoprotein cholesterol levels, greater fat mass in both truncal and peripheral regions, and greater body mass index as compared to the low WC (< 100 cm) group. Groups were comparable with respect to fat-free mass, peak oxygen consumption (VO2), leisure time activity, dietary intake, resting blood pressure, and other metabolic variables. The findings support a clustering of metabolic and mental stress risk factors that may predispose older African Americans to increased cardiovascular and metabolic disease.
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PMID:Cardiovascular reactivity and central adiposity in older African Americans. 1035 3

The cardiovascular metabolic syndrome is characterized by the presence of several cardiovascular risk factors, including blood pressure (BP) elevation. We aimed to study the relation between mental stress, plasma catecholamines, BP and BP responses to mental stress in healthy young Caucasian men selected from different levels of screening BP. We included 98 men with high and 22 men with normal screening BP. They were examined at baseline in the laboratory, during a hyperinsulinemic, isoglycemic glucose clamp and during mental stress. At baseline in the laboratory, the men with high screening BP were characterized by elevated BP (p < 0.005) and plasma catecholamines (p < 0.05), but unaltered serum lipid levels compared to men with normal screening BP. After 2 h rest the differences almost disappeared, but could be reproduced during a mental arithmetic stress test. The men with elevated screening BP had significantly higher fasting glucose (p = 0.01) and lower insulin sensitivity (p < 0.005). In a multiple regression model, norepinephrine during mental stress (R2 = 0.10, p < 0.05) was the main variable to retrospectively explain allocation to the normal or high screening BP group. In conclusion, young healthy men with elevated screening BP are characterized by increased sympathetic activity and insulin resistance. Norepinephrine during mental stress is the main variable to explain allocation to the normal or elevated screening BP group. We have shown that one single screening BP measurement predicts insulin resistance and elevated fasting glucose in this cohort.
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PMID:High screening blood pressure is related to sympathetic nervous system activity and insulin resistance in healthy young men. 1518 11

The various mechanisms that may explain the association between brain dysfunction and the pathogenesis of metabolic syndrome (MS) leading to cardiovascular disease and type 2 diabetes have been reviewed. A Medline search was conducted until September 2003, and articles published in various national and international journals were reviewed. Experts working in the field were also consulted. Compelling evidence was found that saturated and total fat and low dietary n-3 fatty acids and other long-chain polyunsaturated fatty acids (PUFAs) in conjunction with sedentary behavior and mental stress combined with various personality traits can enhance sympathetic activity and increase the secretion of catecholamine, cortisol and serotonin, all of which appear to be underlying mechanisms involved in MS. Excess secretion of these neurotransmitters in conjunction with underlying long-chain PUFA deficiency may damage the neurons in the ventromedial hypothalamus and insulin receptors in the brain, in particular during fetal life, infancy and childhood, and lead to their dysfunction. Since 30-50% of the fatty acids in the brain are long-chain PUFAs, especially omega-3 fatty acids which are incorporated in the cell membrane phospholipids, it is possible that their supplementation may have a protective effect. Omega-3 fatty acids are also known to enhance parasympathetic activity and to increase the secretion of anti-inflammatory cytokines as well as acetylecholine in the hippocampus. It is possible that a marginal deficiency of long-chain PUFAs, especially n-3 fatty acids, due to poor dietary intake during the critical period of brain growth and development in the fetus, and later in the infant and also possibly in the child, adolescent and adult may enhance the release of tumor necrosis factor-alpha (TNF-alpha) interleukin (IL)-1, 2 and 6 and cause neuronal dysfunction. Experimental studies indicate that ventromedial hypothalamic lesions in rats induce hyperphagia, resulting in glucose intolerance and insulin resistance. Treatment with neuropeptide Y abolished hyperphagia and ob mRNA (leptin mRNA) in this animal model. Long-term infusion of norepinephrine and serotonin into the ventromedial hypothalamus impaired pancreatic islet function inasmuch as ventromedial hypothalamic norepinephrine and serotonin levels were elevated in hyperinsulinemic and insulin-resistant animals. Treatment with insulin was associated with restoration of hypothalamic neurotransmitter abnormalities, indicating that ventromedial hypothalamus dysfunction can impair pancreatic beta cells resulting in metabolic abnormalities consistent with MS. Treatment with omega-3 fatty acids, beta blockers, ACE inhibitors, estrogen, and meditation may have a beneficial effect on insulin receptors and ventromedial hypothalamic dysfunction. However, no definite or precise insight into the pathophysiological link between MS, brain function and nutrition is available. Despite this, epidemiological studies and intervention trials indicate that treatment with n-3 fatty acids may be adopted in clinical practice and used to direct therapy for prevention of type 2 diabetes, hypertension, coronary artery disease (CAD), and atherosclerosis, thereby indicating that MS may also respond to this treatment.
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PMID:Can brain dysfunction be a predisposing factor for metabolic syndrome? 1575 41

Repeated mental stress may lead to chronic alterations in cortisol and catecholamine concentrations and to insulin resistance. Furthermore, chronically elevated cortisol concentrations may favour the development of abdominal obesity and of the metabolic syndrome. Oxidative stress impairs glucose uptake in muscle and fat and correlates with BMI. Obese subjects with type 2 diabetes, especially soon after the onset of diabetes, usually exhibit postprandial hyperglycemia with delayed hyperinsulinemia. It is recognized that insulin resistance causes postprandial hyperglycemia; however, it is also possible that impairment of early insulin secretion in response to an oral glucose load is the reason why postprandial hyperglycemia occurs. Since even modest increases in postprandial glucose values can be a risk factor for cardiovascular disease. Therefore, the effects of palatinose based functional food which reduces postprandial hyperglycemia and hyperinsulinemia were investigated in rats. This novel food definitely reduced visceral fat accumulation and improved insulin sensitivity. Therefore, it is suggested that functional food which suppresses postprandial glucose level is beneficial for both stress and metabolic controls.
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PMID:Control of oxidative stress and metabolic homeostasis by the suppression of postprandial hyperglycemia. 1636 12

Coronary heart disease is still highly prevalent worldwide, and stable angina pectoris is one of its more common presentations. Three major controversies are risk factor management, drug therapy, and intervention. As well as the major risk factors stated by the Framingham study and European guidelines, other factors include abdominal obesity, metabolic syndrome, and psychological stress. How should these additional factors be rated? With respect to drug therapy, apart from aspirin, all patients with stable angina should be assessed for statin treatment. Although statins will reduce coronary events by about one third in patients with vascular disease, the absolute benefit depends on the absolute risk. Non-controversially, all patients should be considered for angiotensin-converting-enzyme inhibitors. The concept that beta blockers are protective from future coronary events can be disputed. Percutaneous coronary intervention can relieve symptoms without extending lifespan beyond medical therapy. However, strong mortality data favour coronary-artery bypass grafting in individuals with triple-vessel or even double-vessel disease. Thus, effort angina needs comprehensive assessment, lifestyle changes, and treatment tailored to the individual patient.
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PMID:Controversies in stable coronary artery disease. 1663 2

A hypothetical role of glucocorticoids in human obesity has been suggested since the abdominal obesity phenotype and syndromes of endogenous or exogenous hypercortisolism share several clinical, metabolic, and cardiovascular similarities. An emerging body of evidence indicates that both neuroendocrine dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis as well as peripheral alterations of cortisol metabolism may play a role in the pathophysiology of abdominal obesity. Major alterations of the HPA axis in vivo may be identified in different ways. They include evaluation of hormone concentrations: (a) in basal conditions, in blood, urine, or saliva samples; (b) during dynamic studies following stimulation with different neuropeptides or psychological stress challenges, or suppression with inhibiting agents of the HPA axis at different levels; and (c) after mixed meals or meals containing different nutrient compositions. In addition, alteration of peripheral cortisol metabolism can be detected by direct measurement of cortisol metabolites in urine, although this is a matter of more complex investigation. Alterations of the HPA axis in abdominal obesity are associated with insulin resistance, which suggests a direct responsibility of these hormonal alterations in the susceptibility of affected patients to develop both metabolic and cardiovascular diseases. According to available data, no single marker probably has the power to detect subtle alterations of the HPA axis in conditions, such as the abdominal obesity and the metabolic syndrome. On the contrary, they indicate the need for multiple parameters. At present, evaluation of urinary free cortisol, particularly during the night-time, and salivary-free cortisol appear to be promising for these purposes, whereas dynamic tests should be reserved for specific clinical settings, involving well-characterized patients.
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PMID:The hypothalamic-pituitary-adrenal axis activity in obesity and the metabolic syndrome. 1714 36

The human body, when under threat, elicits a set of neuroendocrine responses, including an increased secretion of glucocorticoids (GCs) and catecholamines from the adrenal gland and the activation of the sympathetic nervous system. These hormonal secretions allow a "fight or flight" response by mobilizing endogenous substrate and inducing a state of insulin resistance in the liver and skeletal muscles. Although the stress response was essential in ancient times to survive physical aggression, this threat has disappeared in our industrialized societies. However, in today's environment, the same stress responses can be elicited by emotional stimuli or professional and social stress. Such psychological stress may be protracted and unrelated to an increased metabolic demand. Thus, the energy mobilized is not used but is stored in visceral fat depots by the combined action of hypercortisolism and hyperinsulinemia. In addition, chronic activation of the stress system causes suppression of the gonadal, growth hormone (GH), and thyroid axes. These metabolic disturbances, in concert, lead to the clinical expression of a number of comorbidities including central obesity, hypertension, dyslipidemia, and endothelial dysfunction, all components of the metabolic syndrome and cardiometabolic risk factors. Moreover, chronic stress has deleterious effects on the brain and, in particular, affects hippocampal structure and function leading to cognitive and mood disturbances. Importantly, this stress-induced clinical phenotype is likely to be exaggerated in the presence of physical inactivity, resulting in a "stress-induced/exercise deficient" phenotype. Assuming that the stress response is a neuroendocrine mechanism that occurs in anticipation of physical action, then physical activity should be the natural means to prevent the consequences of stress. Indeed, accumulating evidence documents the beneficial effects of regular exercise in preventing or ameliorating the metabolic and psychological comorbidities induced by chronic stress. These benefits are thought to derive from a central effect of exercise to reduce the sensitivity to stress and also peripheral actions influencing metabolic functions and, in particular, insulin sensitivity and the partitioning of fuels toward oxidation rather than storage. It is concluded that chronic psychosocial stress, in the presence of physical inactivity, is likely to contribute to the epidemic of cardiometabolic and emotional disease of our current society. The way to prevent and combat this burden is by regular exercise.
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PMID:The protective role of exercise on stress system dysregulation and comorbidities. 1714 41

In 2003 were promulgated the texts regulating rest and safety, in the USA (approved by the ACGME) and in France (January 9th, 2001 and September 14th, 2001). The institution of the "rest for safety", an eleven hours duration interruption of activity, immediately after a night-call, can be viewed as a progress in the search for safety. Several studies showed a link between excessive work hours and occurrence of medical incidents related to tiredness. However published data do not show a link between tiredness and patients endangering. The tiredness resulting from sleep deprivation and disturbances in circadian rhythms is a cumulative phenomenon erased by a period of rest. In spite of a large individual variability, tiredness increases anxiety scores, irritability, depression and it deteriorates cognitive performances. The concept of "prophylactic" rest considers that a subject cannot start, rested, a work if he did not sleep at least 5 hours the previous night, or 12 hours during the previous 48 hours. The second important aspect of the rest for safety is the long-term prevention of potential pathologies in medical staff, in particular burnout syndrome. In our profession, night calls are considered most stressful; the psychological stress related to anticipation and night context causes measurable cardiovascular disturbances in anesthesiologists. Shift-work sleep disorders may induce gastric ulcers, heart attacks, metabolic syndrome, depression and accidents related to somnolence. Long duration work-hours, accompanied by sleep deprivation, may double the risk of car accidents in junior physicians, in whom vigilance levels can compare with those of patients concerned by narcolepsy or with the cognitive disturbances induced by alcohol intoxication. Reduced work-hours improve vigilance and divide by three the rate of serious medical errors. True opportunities of sleep and control of sleep duration at the individual level could be suggested. The idea that taking the necessary rest would be synonymous with a decrease of efficiency in patient care is not demonstrated, but the danger of a poorer information transmission should be handed with an optimization of our manpower and organization. Aging is accompanied by a progressive disorganization of sleep. The foreseeable shortage of manpower, synonymous with aging of the medical actors and increased vulnerability to tiredness, is a posteriori the justification of the institution of the rest for safety.
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PMID:[Rest for safety: which stakes?]. 1748 45

Diabetes mellitus as well as psychiatric disorders are common. These may occur with one another and/or one may worsen the other. Psychological stress may follow screening for diabetes, as well as when diabetes is first identified. Acting through the hypothalamo-pituitary-adrenal axis, stress may initiate or worsen hyperglycaemia. Depression may be a risk factor for the development of diabetes; it also commonly occurs in subjects with diabetes. Identification and management are both important in preventing the disability. A variety of antipsychotic medications, especially the newer agents can induce weight gain, dyslipidaemia, insulin resistance and diabetes. Therefore in choosing a drug, one must consider the risk factors and screen for metabolic syndrome. Subjects with type 1 diabetes can have cognitive dysfunction, eating disorders and developmental disturbances. Physicians caring for people with diabetes must be trained to recognize and manage co-morbid psychiatric conditions that commonly occur. A biopsychosocial disease model for both conditions can leverage the social strengths and medical knowledge in developing countries.
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PMID:Psychiatric co-morbidity & diabetes. 1749 58

Insulin Resistance along with endothelial dysfunction give rise to a constellation of syndromes designated as IRS/MBS metabolic syndrome. Endothelial dysfunction starts early in life much before the development of structural atherosclerosis. Recent insights into vascular biology enable us to understand the molecular mechanisms underlying endothelial dysfunction, and the scope and need for prevention of "pre-clinical" coronary atherosclerosis through lifestyle modification; diet, exercise and stress management. Diminished production of nitric oxide (NO) and/or increased inactivation of NO through oxidative stress (reactive oxygen species ROS and reactive nitrogen species (RNS) are the basis of endothelial dysfunction hence increasing the bioavailability of NO and decreasing its inactivation is the aim of prevention and reversal of endothelial dysfunction. Insulin regulates constitutive NOS gene expression in endothelial cells in vivo; vasodilation is an important component of Insulin-stimulated whole body glucose uptake. Successful strategies are: PPAR alpha and gamma agonists which increase NO production in endothelium; anti-oxidants such as vit. E and C; supplementation with L-arginine, tetrahydrobiopterin-BH4 or sepiapterin (precursor of BH4), SOD mimetic tempol, statins which apart from lowering cholesterol improve NO production, selective beta1 adrenoreceptor antagonists such as nebivolol; suppression of angiotensin-mediated endothelin production by ACE inhibitors and ATR blockers; CB1 receptor blockers, PKCb inhibitors, nitric oxide donors (glyceryl trinitrate and isosorbide dinitrate), dietary supplements of EPA/DHA and regular physical exercise and control of mental stress.
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PMID:Causation, prevention and reversal of vascular endothelial dysfunction. 1805 38


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