مشخصات مقاله | |
انتشار | مقاله سال 2018 |
تعداد صفحات مقاله انگلیسی | 33 صفحه |
هزینه | دانلود مقاله انگلیسی رایگان میباشد. |
منتشر شده در | نشریه الزویر |
نوع مقاله | ISI |
عنوان انگلیسی مقاله | Effects of obesity therapies on sleep disorders |
ترجمه عنوان مقاله | اثرات درمان چاقی بر اختلالات خواب |
فرمت مقاله انگلیسی | |
رشته های مرتبط | روانشناسی |
گرایش های مرتبط | روانشناسی بالینی |
مجله | متابولیسم – بالینی و تجربی – Metabolism – Clinical and Experimental |
دانشگاه | Perelman School of Medicine at the University of Pennsylvania Philadelphia – PA – USA |
کلمات کلیدی | مداخلات چاقی، کاهش وزن، خواب، سندرم آپنه خواب بازدارنده |
کلمات کلیدی انگلیسی | obesity interventions, weight loss, sleep, obstructive sleep apnea syndrome |
کد محصول | E6633 |
وضعیت ترجمه مقاله | ترجمه آماده این مقاله موجود نمیباشد. میتوانید از طریق دکمه پایین سفارش دهید. |
دانلود رایگان مقاله | دانلود رایگان مقاله انگلیسی |
سفارش ترجمه این مقاله | سفارش ترجمه این مقاله |
بخشی از متن مقاله: |
1.1 Introduction
Over the past decade, the relationship between obesity and sleep has become more salient. Obesity has been identified as an important risk factor for the obstructive sleep apnea syndrome (OSAS) [1-6]; therefore, this syndrome will be the main focus of this review. OSAS is a common disorder with prevalence estimates of 15-25% in adult men and 5-10% in adult women [6-11], and between 2-15% in children [2, 12, 13]. It is associated with intermittent hypoxemia, hypercapnia, arousals and sleep fragmentation. Symptoms include snoring, snorting, pauses in breathing, mouth breathing and daytime sleepiness. Children may also exhibit hyperactivity or daytime behavioral problems [14-16]. In adults, there is an association with increased morbidity and mortality, stroke, hypertension, atrial fibrillation, injuries, and cognitive impairment and Alzheimer’s disease [17-21]. Short- and long-term effects of untreated OSAS in pediatric patients include significant morbidity such growth failure [22], systemic [23-25] and pulmonary hypertension [26, 27], endothelial dysfunction [28, 29], and cognitive and behavioral deficits [16, 30-34]. Children who have both obesity and OSAS have increased cardiometabolic risk compared to children who are obese without OSAS. They also present with sleepiness, attention and executive dysfunction, mood concerns, and decreased quality of life [35-41]. There are little data regarding the long-term consequences of having both pediatric obesity and OSAS. One common risk factor for OSAS in adults is excess adiposity [4-6, 10, 11, 42]. An estimated 1% increase in BMI is associated with a 3% increase in the apnea hypopnea index (AHI) [4]. In children 2-5 years of age, the most common cause of OSAS is adenotonsillar hypertrophy. However, as the prevalence of obesity in youth has dramatically increased, it is now recognized as a significant contributor to OSAS, particularly in adolescence [1-3]. Further, there is a bidirectional relationship such that OSAS may promote further weight gain or may hinder weight loss efforts [42-48]. There are currently three interventions for weight loss: lifestyle modification altering diet and/or physical activity along with behavior change procedures, pharmacologic and surgical modalities. Often pharmacologic and surgical therapies are paired with lifestyle modification strategies. However, these are more limited in the pediatric population, reserved for the most severely obese and most often delayed until adolescence. We will discuss the three main modalities of weight loss as they relate to sleep with a primary focus on OSAS. Their impact on sleep duration, sleep architecture, and insomnia will also be discussed. |