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

A large proportion of the adult population complains over difficulties in falling asleep, difficulties in maintaining sleep, or early awakening. Despite the fact that sleep disorders may be secondary symptoms to established or subclinical disease processes, more and more evidence has now accumulated to support the notion that sleep disorders may also play a primary role in the pathophysiology of cardiovascular disease. This has recently been documented in association with metabolic disturbances and impaired insulin action following experimental sleep deprivation. Sleep disorders may finally prove to be part of the pathophysiological chain linking adverse psychosocial stress with the metabolic syndrome, and ultimately premature ageing and early mortality.
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PMID:[Sleep disorders--a public health problem. Potential risk factor in the development of type 2 diabetes, hypertension, dyslipidemia and premature aging]. 1183 69

Sleep is an important modulator of cardiovascular function, both in physiological conditions and in disease states. In individuals without a primary sleep disorder, sleep may exert significant effects on the autonomic nervous system, systemic hemodynamics, cardiac function, endothelial function, and coagulation. Some of these influences can be directly linked to specific modulatory effects of sleep stages per se; others result from the natural circadian rhythm of various physiological processes. There is a temporal association between physiological sleep and occurrence of vascular events, cardiac arrhythmias, and sudden death. Epidemiological and pathophysiological studies also indicate that there may be a causal link between primary sleep abnormalities (sleep curtailment, shift work, and sleep-disordered breathing) and cardiovascular and metabolic disease, such as hypertension, atherosclerosis, stroke, heart failure, cardiac arrhythmias, sudden death, obesity, and the metabolic syndrome. Finally, sleep disturbances may occur as a result of several medical conditions (including obesity, chronic heart failure, and menopause) and may therefore contribute to cardiovascular morbidity associated with these conditions. Further understanding of specific pathophysiological pathways linking sleep disorders to cardiovascular disease is important for developing therapeutic strategies and may have important implications for cardiovascular chronotherapeutics.
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PMID:Sleep and cardiovascular disease. 1630 Oct 95

In spite of a progressive fall in the incidence of traditional risk factors of cardiovascular morbidity (cigarette smoking, high blood pressure, and hyperlipidemia), there is an upward trend in the prevalence of obesity and chronic kidney disease (CKD). Furthermore, there is a strong correlation between body mass indices and the relative risk of progression of CKD. The close biophysiological interaction between obesity and CKD is evident by a similar occurrence of comorbidities including insulin resistance, hyperlipidermia, endothelial dysfunction, and sleep disorders. Truncal obesity is a primary component of metabolic syndrome; unlike peripheral fat, the visceral adipocytes are more resistant to insulin. In addition, lipolysis results in a release of free fatty acid and TG, whereas hypertriglycedemia is potentiated by uremic activation of fatty acid synthase. Hypertriglycedemia and low HDL cholesterol increase the relative risk of progression of CKD. Furthermore, endothelial inflammation and premature atherosclerosis are promoted by hyperhomocysteinemia and oxidation of LDL, both of which are commonly observed in CKD and obesity. Predominance of oxidative stress in both obesity and azotemia stimulate synthesis of angiotensin II, which in turn increases TGF-B and plasminogen activator inhibitor-1, thereby propagating glomerular fibrosis. Furthermore, local synthesis of angiotensinogen by adipocytes, leptin activation of sympathetic nervous system, and hyperinsulinemia contribute to the development of hypertension in obesity and CKD. In addition, increased renal tubular expression of Na-K-ATPase and a blunted response to natiuretic hormones in obesity promote salt and water retention. Glomerular hyperfiltration from systemic volume load and hypertension results in mesangial cellular proliferation and progressive renal fibrosis. In addition, maternal nutritional deprivation increases the incidence of obesity, hypertension, and diabetes in adulthood. Reduced fetal protein synthesis contributes to oxidative glomerular injury and impairment of renal morphogenesis. Thus, kidneys are poorly equipped to handle physiologic stress that may result from the rapid body growth and programmed metabolic dysfunction later in life. Finally, in order to minimize morbidity of obesity-related kidney disease, preventive strategy must include optimal maternal health care, promotion of healthy nutrition and routine physical exercise, and early detection of CKD.
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PMID:The role of obesity and its bioclinical correlates in the progression of chronic kidney disease. 1704 21

The metabolic syndrome represents a clustering of several interrelated risk factors of metabolic origin that are thought to increase cardiovascular risk. It is still uncertain whether this clustering results from multiple underlying risk factors or whether it has a single cause. One metabolic abnormality that may underlie several clinical characteristics of the metabolic syndrome is insulin resistance. This review discusses the evidence that sleep disturbances (obstructive sleep apnoea, sleep deprivation and shift work) may independently lead to the development of both insulin resistance and individual clinical components of the metabolic syndrome. The converse may also be true, in that metabolic abnormalities associated with the metabolic syndrome and insulin resistance may potentially exacerbate sleep disorders. The notion that sleep disturbances exert detrimental metabolic effects may help explain the increasing prevalence of the metabolic syndrome and insulin resistance in the general population and may have important implications for population-based approaches to combat the increasing epidemic of metabolic and cardiovascular disease.
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PMID:Sleep and the metabolic syndrome. 1708 78

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

Nontraditional risk factors for cerebrovascular disease are rapidly emerging. The categories are expanding, and include those related to infection, inflammation, sleep disorders, hemostasis, nutrition, endocrine, and one's individual genotype. Many of the promising factors lack large randomized prospective population studies confirming direct cause and effect. However there have been strong evidence supporting increased stroke risk factor for infection, obstructive sleep disorders, the metabolic syndrome and impaired glucose tolerance in particular. Unique drug targets have already been identified in some of these emerging risk factors. The complexity of the pathophysiology of this disease remains a challenge. For example despite repeated evidence of estrogen-related neuroprotection, large population-based studies in postmenopausal women receiving estrogen replacement did not demonstrate the expected neuroprotection. This suggests that aggressive research both at the basic science and transitional level needs to evolve, to ensure targeted successful stroke therapy. The advent of nanotechnology including the development of targeted therapeutic nanospheres, and of revolutionary molecular technology resulting in the synthesis of specific peptide mimetics, bodes well for the future development of cerebrovascular drug treatment.
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PMID:Emerging risk factors for cerebrovascular disease. 1763 Sep 33

Type 2 diabetes mellitus is a systemic disease characterized by intolerance to glucose and peripheral resistance to insulin. This endocrine disease affects fundamental mechanisms of the central nervous system and jeopardizes the balance of vital functions such as the cardiovascular and circadian rhythm. The increased prevalence of metabolic disorders in our society is aggravated by endemic voluntary postponement of bedtime and by the current sedentary lifestyle, leading to epidemic proportions of obese people. Diabetes and chronic loss of sleep share the fact that both affect millions and one is detrimental to the other. Indeed, sleep deficits have marked modulatory effects on glucose metabolism and insulin sensitivity and foster metabolic syndrome that culminates in sleep disorders like restless syndrome and sleep apnea, which in turn lead to poor sleep quality. We examine the hypothesis that these two worldwide emerging disorders are due to two interlinked cycles. In our paradigm, we establish an intimate relationship between diabetes and sleep disturbances and postulate possible mechanisms that provide support for this conjecture. In addition, we propose some perspectives about the development of the reciprocal interaction between predictor components of metabolic syndrome and sleep disturbances that lead to poor sleep quality. The ability to predict the development and identify or associate a given mode of sleep disturbance to diabetes would be a valuable asset in the assessment of both. Furthermore, major advances in care coupled with healthy lifestyles can ensure a higher quality of life for people with diabetes.
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PMID:The reciprocal interaction between sleep and type 2 diabetes mellitus: facts and perspectives. 1806 Mar 21

Obstructive sleep apnea-hypopnea syndrome involves recurring episodes of total obstruction (apnea) or partial obstruction (hypopnea) of airways during sleep. Obstructive sleep apnea-hypopnea syndrome affects mainly obese individuals and it is defined by an apnea-hypopnea index of five or more episodes per hour associated with daytime somnolence. In addition to anatomical factors and neuromuscular and genetic factors, sleep disorders are also involved in the pathogenesis of sleep apnea. Obesity affects upper airway anatomy because of fat deposition and metabolic activity of adipose tissue. Obstructive sleep apnea-hypopnea syndrome and metabolic syndrome have several characteristics such as visceral obesity, hypertension and insulin resistance. Inflammatory cytokines might be related to the pathogenesis of sleep apnea and metabolic syndrome. Sleep apnea treatment includes obesity treatment, use of equipment such as continuous positive airway pressure, drug therapy and surgical procedures in selected patients. Currently, there is no specific drug therapy available with proven efficacy for the treatment of obstructive sleep apnea-hypopnea syndrome. Body-weight reduction results in improvement of sleep apnea, and obesity treatment must be emphasized, including lifestyle changes, anti-obesity drugs and bariatric surgery.
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PMID:Obesity and obstructive sleep apnea-hypopnea syndrome. 1836 35

Obstructive sleep apnea syndrome (OSAS) is a highly prevalent sleep disorder, characterized by repeated disruptions of breathing during sleep. This disease has many potential consequences including excessive daytime sleepiness, neurocognitive deterioration, endocrinologic and metabolic effects, and decreased quality of life. Metabolic syndrome is another highly prevalence emerging public health problem that represents a constellation of cardiovascular risk factors. Each single component of the cluster increases the cardiovascular risk, but the combination of factors is much more significant. It has been suggested that the presence of OSAS may increase the risk of developing some metabolic syndrome features. Moreover, OSAS patients are at an increased risk for vascular events, which represent the greatest morbidity and mortality of all associated complications. Although the etiology of OSAS is uncertain, intense local and systemic inflammation is present. A variety of phenomena are implicated in this disease such as modifications in the autonomic nervous system, hypoxemia-reoxygenation cycles, inflammation, and coagulation-fibrinolysis imbalance. OSAS patients also present increased levels of certain biomarkers linked to endocrine-metabolic and cardiovascular alterations among other systemic consequences. All of this indicates that, more than a local abnormality, OSAS should be considered a systemic disease.
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PMID:Obstructive sleep apnea syndrome is a systemic disease. Current evidence. 1884 71

Obstructive sleep apnea is a common disorder in childhood, particularly in the last decade when an increased prevalence of obesity has been documented. The neurocognitive and behavioral problems associated with this disorder have been known for a long time. However, the increased knowledge of cardiovascular and metabolic complications in adults with sleep apnea has been followed by a better understanding of the systemic effects of upper airway obstruction in children. Obstructive sleep apnea (OSA) has been shown to induce autonomic imbalance in children and to affect blood pressure, cerebral blood flow and cardiac function in an early phase. OSA may also induce chronic systemic inflammation and may contribute to the development of metabolic syndrome in obese children. Very recent research indicates that in children primary snoring, the mildest form of the sleep-disordered breathing spectrum, may also be associated with morbidity. It is, therefore, likely that these respiratory sleep disorders do not simply influence children's' performance in private and social life, but may more seriously affect children's' health. The aim of this review is to outline early systemic complications of obstructive sleep apnea and primary snoring in infants and children.
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PMID:Pediatric sleep apnea: early onset of the 'syndrome'? 1905 83


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