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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Disordered nocturnal breathing with significant arterial oxygen desaturation and sleep apnoea is a feature of extreme obesity which is often difficult to manage in the short term. We have evaluated the effect of fluoxetine, a centrally acting 5-HT re-uptake inhibitor, on sleep-breathing patterns in asymptomatic extremely obese subjects. A double-blind cross-over study was used to compare fluoxetine (60 mg for three days) to placebo. Eleven obese subjects (ten males, one female, mean weight +/- s.d. 131 +/- 2 kg) slept overnight in a sleep laboratory with the polysomnographic study recorded after an initial acclimatization night. The obese subjects had normal respiratory function and normal fully awake arterial oxygen saturation (%SaO2 97 +/- 1). Marked O2 desaturation was seen in all the subjects during sleep but the average asleep %SaO2 did not differ between the two treatment phases (placebo 90 +/- 5; fluoxetine 92 + 2%). However, fluoxetine significantly increased the minimum %SaO2 recorded during the study night either by abolishing or reducing REM sleep (placebo 73 +/- 2%; fluoxetine 81 +/- 8%; P < 0.05, 95% CI -12.3 to -2.03). Frequent hypopnoea was observed in all subjects in both REM and non-REM sleep whereas apnoea was uncommon. The total apnoea/hypopnoea index fell in six subjects during the fluoxetine night, the largest reduction being seen in the most severely affected. In five of the six the improvement was associated with the abolition of REM sleep. Total sleep time did not differ between the placebo and fluoxetine nights nor did a qualitative assessment of sleep using a visual analogue score.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Short-term use of fluoxetine in asymptomatic obese subjects with sleep-related hypoventilation. 133 Sep 62

The cyclical changes in heart rate and systemic blood pressure that accompany apneic events are predominantly mediated by fluctuations in the activity of the autonomic nervous system. Increased vagal efferent parasympathetic activity is responsible for the cyclical reductions in heart rate during apnea. In contrast, the cyclical elevations in systemic blood pressure are believed to result from recurrent peripheral vasoconstriction mediated by repetitive activation of the sympathetic nervous system. Maximal activation and pressures coincide with apnea termination and brief arousal from sleep. These cyclical elevations in systemic pressure during sleep increase ventricular workload and, thereby, may contribute to the development of ventricular hypertrophy. Systemic hypertension is present during wakefulness in approximately 50% of patients with OSA. Although age and obesity are the predominant risk factors for diurnal hypertension, OSA probably makes an independent contribution in younger obese men. Sinus bradycardia, Mobitz type 1 second-degree heart block, and prolonged sinus arrest have all been documented in association with the apneic events. Increased ventricular ectopy has been observed with oxyhemoglobin desaturations below 60%. Myocardial ischemia, infarction, sudden death, and stroke all demonstrate similar circadian variations in time of onset. Peak frequencies occur between 6 AM and noon, generally within several hours of awakening. Although sleep is associated with decreased frequencies of these adverse cardiovascular events in the general population, evidence exists linking REM sleep to an increased risk of myocardial ischemia. In men who habitually snore, epidemiologic data have detected an increased risk for ischemic heart disease and stroke. Habitual snoring has also been associated with an increased risk of sudden death during sleep. In patients with clinically significant OSA, there is reasonable information indicating excessive mortality in the absence of treatment. This mortality is predominantly cardiovascular and tends to occur during sleep.
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PMID:Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. 152 12

In order to assess the complications of sleep apnea, we have reviewed a data base of 619 consecutive admissions to a university sleep disorders center. Although patients with obstructive sleep apnea (OSA) described more subjective sleepiness than patients with central sleep apnea (CSA) or primary snoring (PS), the multiple sleep latency test (MSLT) indicated similar levels of physiologic sleepiness in the two apneic groups, which was greater than among those with PS. There was no significant relationship between individual subjective estimates of habitual sleepiness and the MSLT values. Among the OSA patients the mean minimum arterial oxygen desaturation during REM sleep accounted for 65 percent of the variance of the mean sleep latency on the MSLT, with an additional, smaller, contribution of the disordered breathing rate per hour. Subjective reports of sleepiness were associated with sleep efficiency and the number of disordered breathing events in NREM sleep. Patients with OSA or CSA had similar diastolic blood pressures and frequencies of history of treatment for hypertension, which were significantly higher in OSA than in the PS group. In the OSA group the absolute minimum arterial oxygen desaturation during NREM sleep was the most significant contributor to waking diastolic blood pressure, with an additional small contribution by weight. A history of treatment for hypertension was most strongly associated with weight, without significant additional contributions by measures of disordered breathing events or oxygen desaturation; however, weight was highly intercorrelated with measures of the apnea/hypopnea index and minimum arterial oxygen desaturation. In summary, these data support recent findings which show a close relation of obesity to a history of hypertension in OSA, and extend to this group a previous observation that in regular heavy snorers, there may be a disparity between levels of physiologic and subjective sleepiness.
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PMID:Sleepiness and hypertension in obstructive sleep apnea. 155 54

Respiratory function undergoes sleep-associated changes which in normal subjects leave it unaffected. However in some cases they may be more marked than usual or may be superimposed on a pre-existing disease, thus giving rise to sleep-related ventilation disorders. These include obstructive sleep apnea syndrome (OSAS), nocturnal desaturation events of chronic obstructive pulmonary disease (COPD) and restrictive syndromes, as well as nocturnal asthmatic attacks. OSAS is a condition characterized by the frequent recurrence of interruptions of oronasal flow (greater than 10 s.) due to upper airway occlusion induced by a reduction in pharyngeal muscle tone. This phenomenon, particularly prominent in REM sleep, results in oxyhemoglobin desaturation and marked cardiovascular consequences (arrhythmias, increases in pulmonary and systemic arterial pressure), as well as symptoms (loud intermittent snoring, daytime sleepiness, intellectual deterioration etc.). Obesity is often associated with OSAS or may lead to a sleep-related hypoventilation syndrome. Treatment is based on weight loss, surgery of upper airway abnormalities, if present, and on splinting of the upper airway by the application of nasal continuous positive airway pressure. In COPD and restrictive disorders, nocturnal hypoxemia is mainly due to REM-associated loss of respiratory muscle tone, as well as in the sleep-related exaggeration of functional defects due to COPD (low chemoreceptor sensitivity, high closing volume etc.). Treatment is based on oxygen administration, provided that possible side-effects are carefully monitored. Nocturnal asthma is due to circadian changes in hormonal secretion (catecholamines, cortisol), as well as supine posture, reduced muco-ciliary clearance, gastro-esophageal reflux etc. Sleep itself plays some role through a depressed arousal reaction in slow wave sleep, resulting in more marked and prolonged attacks in this stage. Slow-release theophylline or beta-mimetic medications, as well as new chromones and antimuscarinic drugs are therapeutic alternatives.
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PMID:Cardio-respiratory function during sleep. 174 49

Eight obese patients (4 male, 4 female; mean age = 35.9 years) before [mean body mass index (BMI) = 37.1] and after (mean BMI = 31.4) weight loss by means of a mixed hypocaloric diet were compared with 8 lean subjects (4 male, 4 female; mean age = 37.1 years, mean BMI = 22.3) in a study of their nocturnal sleep patterns and sleep-related growth hormone (GH) secretions. Although no sleep disorders (in particular, sleep apnea and hypersomnia) were observed, GH secretion was markedly altered in obese patients that showed no sleep-related GH peaks. After weight loss, the sleep architecture in obese subjects was unchanged. On the contrary, GH peak appeared to be only partially restored and delayed until after stage III-IV of non-REM sleep. Our study on obese subjects suggests that the altered nocturnal GH secretion, probably related to a hypothalamic dysfunction, may be the result of the obesity per se.
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PMID:Sleep-related growth hormone secretion in human obesity: effect of dietary treatment. 175 83

The acute effects of dexfenfluramine on nocturnal sleep were studied in ten healthy male subjects by means of sleep EEG recordings and ratings of subjective sleep quality. Four different dosages (3 mg, 7 mg, 15 mg, and 30 mg) were tested, administered over a period of 3 days each. Under 15 mg and 30 mg dexfenfluramine, only slight effects on sleep were observed: 15 mg led to decreased sleep efficiency in the first night of medication, and to reduced percentage of slow wave sleep in the first and third night. A significant lengthening of REM latency was present in the third night under 30 mg dexfenfluramine, without changes in other REM sleep parameters. Daily doses of 3 mg and 7 mg dexfenfluramine did not influence sleep, except for a significant REM latency reduction observed in the first night under 3 mg. Apart from a transient slight impairment under 30 mg, ratings of subjective sleep quality did not mirror any impact of dexfenfluramine. The data suggest that therapeutic dosages of dexfenfluramine only slightly influence nocturnal sleep, which contrasts with the known impact of other anti-obesity agents like the amphetamines. Unlike classical antidepressants, dexfenfluramine does not reduce REM sleep; in light of a hypothetical link between REM sleep reduction and antidepressant action of a drug, dexfenfluramine is not expected to have a pronounced antidepressant effect.
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PMID:Effect of dexfenfluramine on sleep in healthy subjects. 179 29

Fifty-seven patients with obstructive sleep apnoea (OSA) were treated for at least six months with nasal continuous positive airway pressure (CPAP). At follow-up, sleep studies were performed in which CPAP was not used for the first half of the night. We compared the severity of OSA at follow-up without CPAP to the severity of OSA during the patient's initial diagnostic study. Apnoea and hypopnoea index (AHI) fell from 41.4 +/- 7.5 (mean +/- 95% CI) to 34.8 +/- 7.9 (p = 0.06 by Wilcoxon test) and minimum oxygen saturation rose from 71.6 +/- 3.2 to 78.5 +/- 2.6 (p less than 0.001). Some of this change may have been due to reduced REM sleep in the follow-up study (10.5 +/- 2.1% Total Sleep Time vs 7.4 +/- 2.4% TST, p less than 0.05). Long-term nasal CPAP was not associated with any reduction of obesity (BMI before CPAP 31.9 +/- 1.0, after CPAP 31.7 +/- 1.0 (p = 0.39). Systolic arterial pressure fell (before CPAP 143.0 +/- 4.5 mmHg, after CPAP 136.3 +/- 4.6, p less than 0.05) but diastolic pressure did not (before CPAP 88.5 +/- 3.0 mmHg, after CPAP 85.6 +/- 2.9 mmHg, p = 0.11). We concluded that the effect of CPAP treatment for six or more months was a small fall in AHI and a small rise in minimum SaO2, but that this would be of marginal clinical significance, and may be artefactual.
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PMID:Long-term nasal CPAP does not ameliorate obstructive sleep apnoea. 187 51

Interactions between sleep and respiration have been noticed in several lung diseases. In COPD (chronic obstructive pulmonary disease) patients, the night sleep is delayed or shortened and deep sleep is often reduced or even absent. These disturbances are associated with hypoxaemic episodes occurring either in light slow wave sleep or in REM sleep, the former being short in duration and mild but repetitive and related to ventilatory changes, the latter prolonged, often severe, and resulting from both decrease in ventilation and alterations of ventilation-perfusion ratios. Restrictive syndrome due to interstitial pneumonia, kyphoscoliosis, neuromuscular diseases or, more commonly, to obesity or even pregnancy also alter sleep in a non-specific manner. Most of them result in hypoxia during paradoxical sleep. Unquestionably, there exists a relationship between sleep and asthma (aggravation of dyspnoea at night, reduction of peak expiratory flow when awaking, stage 2 asthmatic attacks). This relationship is probably caused by multifactorial interactions.
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PMID:[Changes in sleep and night respiration in asthma and obstructive or restrictive lung diseases]. 214 79

The night shiftwork on the one hand, the obesity on the other hand, are at the origin of sleep modifications. Is the overweight an aggravating factor which damages the recovering sleep? A study on sleep conducted in the laboratory on 7 reference subjects and 7 obese subjects, randomly allocated with regard to age, seniority and Body Mass Index, has shown only a small influence of the overweight on the slow wave sleep during the night shortened by shift work. Obesity does not seem to alter the REM sleep.
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PMID:[Sleep alterations of obese night shiftworkers]. 253 44

We studied the influence of hypoxia due to sleep apnea on testosterone (T) secretion. It was conducted on the basis of an idea that sustained hypoxia may depress T secretion. The subjects consisted of 15 male patients with no drug administration whose complaints were snoring and/or obesity. The subjects participated in a sleep study on two consecutive nights. During the first night we collected blood samples starting every 4 hours from 10 PM via a catheter and measured T. From the data of the second night, we calculated total desaturation time with more than 4% from the baseline SaO2. According to the amount of this desaturation time, the subjects were divided into 2 groups; desaturation time less than 80 min in group 1 and longer in group 2, respectively. The peak value was seen at 6 AM in group 1 and at 10 AM in group 2. We investigated the correlation between the ratio of T10/T6, which is the ratio of T level at 10 AM to that at 6 AM, and parameters of sleep disorders related to oxygen desaturation. Total 4% desaturation time in total sleep period and non REM period significantly correlated with this ratio. From the diagram illustrating the correlation between the ratio and total 4% desaturation time in total sleep period, we could assume that if the ratio is beyond 1, the subject may have had more than about 80 min of total 4% desaturation time.
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PMID:[Prediction of the degree of nocturnal oxygen desaturation in sleep apnea syndrome by estimating the testosterone level]. 261 9


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