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The aim of this study was to analyze whether snoring and excessive daytime sleepiness (EDS), the main symptoms of obstructive sleep apnea syndrome (OSAS), are associated with hypertension and diabetes in women. A random sample of 6779 women aged 20-99 years answered questionnaires on sleep disturbances, daytime symptoms and somatic diseases. The women were categorized into four groups: "no EDS or snoring" (reference group), "snoring but no EDS", "EDS but no snoring" and "snoring and EDS". Prevalences of hypertension and diabetes were lowest in the reference group (8.7% and 1.6%, respectively) and highest among women with both snoring and EDS (hypertension: 26.3%, diabetes: 5.8%). In a multivariate model adjusting for age, body mass index, smoking, physical activity and alcohol dependency, "snoring and EDS" was a risk factor for hypertension (adjusted OR 1.82 (95% CI 1.30-2.55)) while isolated snoring or EDS was not. "Snoring and EDS" was more closely related to hypertension among women aged <50 years (adj. OR 3.41 (1.78-6.54) vs. 1.50 (1.02-2.19), P=0.01). For diabetes, both "EDS but no snoring" and "snoring and EDS" were risk factors and the associations were most pronounced in women aged >50 years (adj. OR 2.33 (1.28-4.26) for "EDS but no snoring" and 2.00 (1.05-3.84) for "snoring and EDS"). We conclude that the combination of snoring and EDS is a risk factor for hypertension and diabetes in women. For hypertension, the risk is partly age dependent and, for diabetes, EDS without snoring is a risk factor of similar magnitude. These differences might indicate differences in pathophysiologic mechanisms underlying the association between sleep-disordered breathing and hypertension and diabetes respectively.
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PMID:Snoring and daytime sleepiness as risk factors for hypertension and diabetes in women--a population-based study. 1712 49

Restorative sleep is as essential for well-being as proper diet or exercise in persons with type 2 diabetes. However, sleep disorders such as insomnia, restless leg syndrome/periodic leg movements, and obstructive sleep apnea increase in prevalence with age and are very common in persons with type 2 diabetes. Disrupted sleep may result in weight gain, increased insulin resistance, and decreased daytime functioning. Although sleep disturbances have a major influence on health and quality of life, diagnosis and treatment can reduce their negative effects. Diabetes educators are pivotal in patient assessment, management, teaching, and collaborating with the primary health care provider to deliver holistic management of the patient with diabetes. This article will provide diabetes educators with various strategies for assessing sleep, including an easy 8-item questionnaire that can be used in the clinical setting. In addition, interventions to improve sleep hygiene that can be easily implemented by diabetes educators will be described.
Diabetes Educ
PMID:Understanding sleep in persons with diabetes. 1757 Aug 74

Angina pectoris is usually the first clinical sign of underlying myocardial ischemia, which results from an imbalance between oxygen supply and oxygen demand in the heart. This report describes the pharmacology of beta-adrenoceptor antagonists as it relates to the treatment of angina. The beta-adrenoceptor antagonists are widely used in long-term maintenance therapy to prevent acute ischemic episodes in patients with chronic stable angina. Beta-adrenoceptor antagonists competitively inhibit the binding of endogenous catecholamines to beta1-adrenoceptors in the heart. Their anti-ischemic effects are due primarily to a reduction in myocardial oxygen demand. By decreasing heart rate, myocardial contractility and afterload, beta-adrenoceptor antagonists reduce myocardial workload and oxygen consumption at rest as well as during periods of exertion or stress. Predictable adverse effects include bradycardia and cardiac depression, both of which are a direct result of the blockade of cardiac beta1-adrenoceptors, but adverse effects related to the central nervous system (eg, lethargy, sleep disturbances, and depression) may also be bothersome to some patients. Beta-adrenoceptor antagonists must be used cautiously in patients with diabetes mellitus, peripheral vascular disease, heart failure, and asthma or other obstructive airway diseases. Beta-adrenoceptor antagonists may be used in combination with nitrates or calcium channel blockers, which takes advantage of the diverse mechanisms of action of drugs from each pharmacologic category. Moreover, concurrent use of beta-adrenoceptor antagonists may alleviate the reflex tachycardia that sometimes occurs with other antianginal agents.
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PMID:Antianginal actions of beta-adrenoceptor antagonists. 1799 92

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

Making a definite diagnosis of Cushing's syndrome is a challenging problem. Unsuspected Cushing's syndrome occurs in 2-3% of patients with poorly controlled diabetes, 0.5-1% with hypertension, 6-9% with incidental adrenal masses, and 11% with unexplained osteoporosis and vertebral fractures. The increasing recognition of this syndrome highlights the need for a simple, sensitive, and specific diagnostic test. Patients with Cushing's syndrome consistently do not reach a normal nadir of cortisol secretion at night. The measurement of late-night salivary cortisol levels might, therefore, provide a new diagnostic approach for this disorder. Salivary cortisol concentrations reflect those of active free cortisol in plasma and saliva samples can easily be obtained in a nonstressful environment (e.g. at home). Late-night salivary cortisol measurement yields excellent overall diagnostic accuracy for Cushing's syndrome, with a sensitivity of 92-100% and a specificity of 93-100%. Several factors can, however, make interpretation of results difficult; these factors include disturbed sleep-wake cycles, contamination of samples (particularly by topical corticosteroids), and illnesses known to cause physiologic activation of the pituitary-adrenal axis. In this Review, we discuss the methods and value of measuring salivary cortisol for the diagnosis of Cushing's syndrome, and put forward some recommendations to maximize accuracy of results.
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PMID:Late-night salivary cortisol measurement in the diagnosis of Cushing's syndrome. 1844 40

Sleep disturbances may be associated with impaired glucose metabolism. The aim of this study was to evaluate sleep duration and quality in relation to glycemic control in patients with type 2 diabetes. In a cross-sectional study, sleep duration and quality were assessed in 47 middle-aged patients with type 2 diabetes treated with oral agents and without sleep disturbing complications and 23 healthy control subjects similar by age, sex, body mass index, occupation and schooling. Sleep was recorded by wrist-actigraphy for three consecutive days under free-living conditions. Univariate analysis showed lower sleep maintenance (P = 0.002) and sleep efficiency (P = 0.005), and higher fragmentation index (P < 0.0001), total activity score (P = 0.05) and moving time (P < 0.0001) in patients with type 2 diabetes. After adjusting for age, gender and schooling, fragmentation index and moving time remained significantly higher in the patients with diabetes (P < 0.05, both). HbA1c correlated inversely with sleep efficiency (r = -0.29; P = 0.047) and positively with moving time (r = 0.31; P = 0.031). These findings suggest that type 2 diabetes is associated with sleep disruptions even in the absence of complications or obesity. The relevance of sleep abnormalities to metabolic control and possible strategies to improve sleep quality in type 2 diabetes deserve further investigation.
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PMID:Sleep abnormalities in type 2 diabetes may be associated with glycemic control. 1868 6

Nominal group technique was used with persons with type 2 diabetes to identify and rank the severity of problems associated with being sleepy. Participants were adults who were subjectively sleepy according to the Epworth Sleepiness Scale. Daytime sleepiness was associated with a general decrease in motivation to engage in activities that are important to the management of diabetes. Because decreased motivation may have a negative influence on psychological well-being, it is important that health care providers assess not only for how well their patients' diabetes is being controlled, but also for sleep disturbances and the patients' general state of psychological well-being.
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PMID:Daytime sleepiness, diabetes, and psychological well-being. 1885 51

Association between sleep disturbances and hormonal imbalances can result in metabolic disorders, including obesity and diabetes. The hypothalamus is likely to play a part in these pathophysiological conditions because it contains sleep-wake circuits that are sensitive to metabolic hormones, including leptin and ghrelin. Thus, shared hypothalamic circuits such as the hypocretin and melanin-concentrating hormone systems are strong candidates for mediating both sleep and metabolic imbalances. This review reveals new roles for these systems as sensors and effectors of sleep and wakefulness, and discusses their plasticity in regulating sleep and energy balance. New optical tools that remotely control neuronal circuit activity provide an effective means to understand the cooperativity of shared circuits in regulating hypothalamic functions such as sleep and metabolism.
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PMID:Sleep and metabolism: shared circuits, new connections. 1893 86

Obesity, excessive daytime sleepiness (EDS), and self-reported short sleep duration appear to be on the rise, while there is evidence that obesity and these sleep disorders are strongly connected. In this paper, we review data that challenge the common belief that the sleep apnoea and sleep loss, frequently associated with obesity, are the primary determinants of obesity-related objective daytime sleepiness and subjective fatigue (tiredness without increased sleep propensity). Specifically, obesity is associated with objective and subjective EDS regardless of the presence of sleep apnoea. The association between obesity and EDS was confirmed in recent studies of large random samples of the general population or clinical samples, which showed that the primary determinants of subjective EDS were depression, metabolic disturbances, i.e. obesity/diabetes and insulin resistance, and lack of physical activity, and, secondarily, sleep apnoea or sleep loss. Paradoxically, within the obese, with or without sleep apnoea, those who slept objectively better at night are sleepier (objectively) during the day than those who slept worse. The distinguishing factor between those that slept better vs. those that slept worse appears to be level of emotional stress. Furthermore, many studies reported that obesity is associated with self-reported short sleep duration; however, it appears that short sleep duration is a marker of emotional stress rather than a reflection of true sleep loss. Based on these data, we propose that obesity-related deeper sleep and objective EDS are primarily related to metabolic disturbances, whereas obesity-related poorer sleep and subjective fatigue appear to be the result of psychological distress. Furthermore, based on data from studies in normal controls and patients with sleep disorders, it appears that the interaction of the hypothalamic-pituitary-adrenal (HPA) axis and pro-inflammatory cytokines determines the level of sleep/arousal within the 24-hour cycle, i.e. "eucortisolemia" or "hypocortisolemia" plus hypercytokinemia is associated with high sleep efficiency and objective sleepiness, whereas "hypercortisolemia" plus hypercytokinemia is associated with low sleep efficiency and fatigue. In conclusion, we propose that the above-reviewed data provide the basis for a meaningful phenotypic and pathophysiologic sub-typing of obesity. One subtype is associated with emotional distress, poor sleep, fatigue, HPA axis "hyperactivity," and hypercytokinemia while the other is associated with non-distress, better sleep but more sleepiness, HPA axis "normo or hypoactivity," and hypercytokinemia. This proposed sub-typing may lead to novel, preventive and therapeutic strategies for obesity and its associated sleep disturbances.
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PMID:Obesity and sleep disturbances: meaningful sub-typing of obesity. 1894 83

Sleep disturbances are associated with hormonal imbalances and may result in metabolic disorders including obesity and diabetes. Therefore, circuits controlling both sleep and metabolism are likely to play a role in these physiopathological conditions. The hypocretin (Hcrt) system is a strong candidate for mediating both sleep and metabolic imbalances because Hcrt neurons are sensitive to metabolic hormones, including leptin and ghrelin, and modulate arousal and goal-orientated behaviours. This review discusses the role of Hcrt neurons as a sensors of energy balance and arousal and proposes new ways of probing local hypothalamic circuits regulating sleep and metabolism with unprecedented cellular specificity and temporal resolution.
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PMID:The hypocretins as sensors for metabolism and arousal. 1904 1


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