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Obstructive Sleep Apnea and obesity

  1. 1. Obstructive Sleep Apnea A Serious Epidemic
  2. 2. • Obstructive sleep apnea (OSA)—also referred to as obstructive sleep apnea-hypopnea (OSAH)—is a sleep disorder that involves cessation or significant decrease in airflow in the presence of breathing effort. • There are cases where breathing stops for more than 60 seconds during sleep WHAT IS OSA?
  3. 3. • OSA is the most common type of sleep-disordered breathing (SDB) and is characterized by recurrent episodes of upper airway collapse during sleep. • These episodes are associated with recurrent oxyhemoglobin desaturations and arousals from sleep.
  4. 4. Alae nasi Tensor palatini Genioglossis Geniohyoid Thyrohyoid Sternohyoid Adv Physiol Educ 32: 196–202, 2008Levitsky – LSU Normal State
  5. 5. Adv Physiol Educ 32: 196–202, 2008Levitsky – LSU Sleep Apnea Event
  6. 6. WHAT IS OSA? • Episodes of complete or partial collapse of airway are translated to # of apnea and hypopnea events (AHI). – Apnea = Cessation of airflow > 10 seconds – Hypopnea = Decreased airflow > 10 seconds associated with: • Arousal • Oxyhemoglobin desaturation
  7. 7. Measures of Sleep Apnea Frequency • Apnea Index – # apneas per hour of sleep • Apnea / Hypopnea Index (AHI) – # apneas + hypopneas per hour of sleep
  8. 8. Diagnosis • Clinical Manifestations • AHI (Apnea Hypopnea Index) – Normal: 0-5 events/hr – Mild: 6-15 events/hr*** – Moderate: 16-30 events/hr – Severe: > 30 ***Must have clinical symptoms of OSA
  9. 9. OSA • Obstructive Sleep Apnea – Cessation of airflow for 10 seconds – Usually associated with 4% oxygen desaturation • Obstructive Sleep hypopnea – Decrease of 30–50% in airflow for 10 seconds – May be associated with 4% oxygen desaturation OSA syndrome AHI ≥ 5 + Symptom
  10. 10. Suggestion of sleep apnea Snoring Witnessed apnea, gasping Obesity (esp. neck circumference) Hypertension Excessive daytime sleepness Family history Previous tonsillectomy Non-restorative sleep AHI ≥ 5+ OSA syndrome
  11. 11. Sleep Apnea-hypopnoea syndrome Abnormal Breathing Event Oxygen Desaturation Daytime Sleepiness Apneas + Hypopneas (AHI)  5 per hour Arousal/ Sleep Fragmentation Vascular Consequences
  12. 12. • OSA associated with excessive daytime sleepiness (EDS) is commonly called obstructive sleep apnea syndrome (OSAS)—also referred to as obstructive sleep apnea-hypopnea syndrome (OSAHS). • Despite being a common disease, OSAS is under recognized by most primary care physicians in the United States; an estimated 80% of Americans with OSAS are not diagnosed.
  13. 13. Why does OSA occur? • Upper airway tone is decreased during sleep, especially in REM • Collapse/obstruction of the upper airway during sleep causes obstruction & apnea - - - - - Nares /hard palate Pharynx Larynx / trachea
  14. 14. Most of apneic episodes occur within the pharynx, due to the deformation of soft tissue (tongue, soft-palate).
  15. 15. Upper Airways
  16. 16. Pathophysiology of Sleep Apnea Awake: Small airway + neuromuscular compensation Loss of neuromuscular compensation + Decreased pharyngeal muscle activity Sleep Onset Hyperventilate: correct hypoxia & hypercapnia Airway opens Airway collapses Pharyngeal muscle activity restored Apnea Arousal from sleep Hypoxia & Hypercapnia Increased ventilatory effort
  17. 17. http:// im.knuh.or.kr Sequences
  18. 18. Clinical Consequences Cardiovascular Complications Morbidity Mortality Sleep Fragmentation Hypoxia/ Hypercapnia Excessive Daytime Sleepiness Sleep Apnea
  19. 19. http:// im.knuh.or.kr Cardiovascular Complications Neuro-cognitive Complications Significant Co-morbidities HTN CAD Stroke CHF
  20. 20. OSA Increases Co-Morbid Health Risks • OSA is an independent risk factor for HTN & Type II DM Obesity Depression 40% Diabetes 50% CHF 50% 50% Stroke 50% Hypertension 35% Wolk et al 2003 Javaheri et al 1999, Somers et al 2007 Einhorn ADA 2005 Sjostrom et al 2004Sandberg et al 2008Smith et al 2002, Schroder et al 2005 • Left undiagnosed, OSA increases risk of stroke by 2X, risk of fatal cardiovascular events by 5X, and risk of serious vehicular accidents %DiseaseCo-morbiditywithOSA = With OSA Sources: Yaggi et al, NEJM 2005; Young et al, Sleep 2008; Teran-Santos, NEJM 1999
  21. 21. Sleep Apnea is: • Common • Dangerous • Easily recognized • Treatable
  22. 22. • Identification of at-risk individuals for this potentially serious condition continues to pose a challenge. • Underrecognition of presenting symptoms by physcians, and by patients, may be one contributing factor for improper identification and management of OSA.
  23. 23. Prevalence in Middle Aged Adults % Men % Women AHI ≥ 5 AHI ≥ 5 + daytime somnolence 24 9 4 2 AHI = Apnea Hypopnea Index Symptomatic OSA (OSA with EDS)present in 4% of middle aged men and 2% of women
  24. 24. Prevalence of Sleep Apnea Sleep apnea is a common disorder. 0 5 10 15 20 25 AHI > 5 SAS Asthma Male Female U.S. Pop 30-60 year olds Percent of Population Adapted from Young T et al. N Engl J Med 1993;328.
  25. 25. OSA is a Largely Undiagnosed Epidemic • 18 million suffer (prevalence similar to Diabetes) • 85% have not been diagnosed Diabetes and OSA Prevalence is Similar Diabetes OSA Undiagnosed Diagnosed Millions of Americans (Adults) 10 20 Young 2002, 1997
  26. 26. Sleep apnea can effect anyone at anytime. From children to star athletes, no one is immune to the condition which is why it is all too important to be tested for sleep disorders if you display any of the common symptoms, such as snoring and daytime sleepiness that never goes away. While anyone can suffer from sleep apnea, certain groups of people are more prone to suffering from the condition
  27. 27. Risk Factors for OSA • Obesity • Obesity • Obesity
  28. 28. Sleep Apnea Risk Factors Obesity Increasing age Male gender Post-menopausal state Family history Alcohol or sedative use / sleeping pills Smoking Associated conditions e.g. Endocrinal abnormalities Craniofacial/Upper Airway Soft Tissue Anatomic Abnormalities
  29. 29. • Although obesity is the most common cause of OSA, sleep apnea also occurs in non-obese patients with craniofacial features e.g 1. Narrowing of the hard palate, 2. Small jaw (or Micrognathia) 3. Long or large tongue (or macroglossia) 4. Mandible displaced backward (or retrognathism) 5. Large tonsils and adenoids (especially in children), 6. people with Down Syndrome 7. Nasal abnormalities, including septal deviation and allergic rhinitis.
  30. 30. Obesity
  31. 31. Obesity Epidemic • World epidemic encompasses 1.7 billion people • Highest in the U.S. • Approximately 2/3 of Americans are overweight, and almost half are obese • BMI subgroups of >35 and >40 are experiencing most rapid growth
  32. 32. What is Body Mass Index ( BMI ) ?
  33. 33. BMI = W(kg)/H (m²)
  34. 34. Equipment needed to calculate BMI
  35. 35. Measuring weight • Calibrated weighing scales. • Empty pockets. • Remove shoes • Keeping patient’s dignity – remove heavy items of clothing. • Ensure scales are calibrated regularly.
  36. 36. STADIOMETER – measures height • Remove shoes • Stand upright • Ears level with eye line • Feet back against wall
  37. 37. Body mass index (BMI) • Body mass index (BMI) is a measure of body fat based on height and weight that applies to both adult men and women. BMI Categories  Underweight = <18.5  Normal weight = 18.5-24.9  Overweight = 25-29.9  Obesity = 30 or greater  Severe Obesity = 30.0 – 34.9  Morbid Obesity = >40
  38. 38. • Being 100 pounds over “ideal weight” (your ideal body weight will be calculated during your first visit with your surgeon) • Using the Body Mass Index (BMI) Morbid Obesity is defined as a person: -BMI of 40 or higher OR -BMI of 35 or higher with co-morbidities related to morbid obesity What is Morbid Obesity?
  39. 39. Obesity Trends* Among U.S. Adults BRFSS, 1985 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10. These maps show obesity as a percentage of the total adult population. This data comes from CDC.
  40. 40. Obesity Trends* Among U.S. Adults BRFSS, 1986 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10.
  41. 41. Obesity Trends* Among U.S. Adults BRFSS, 1987 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10.
  42. 42. Obesity Trends* Among U.S. Adults BRFSS, 1988 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10.
  43. 43. Obesity Trends* Among U.S. Adults BRFSS, 1989 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10.
  44. 44. Obesity Trends* Among U.S. Adults BRFSS, 1990 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10.
  45. 45. Obesity Trends* Among U.S. Adults BRFSS, 1991 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10.
  46. 46. Obesity Trends* Among U.S. Adults BRFSS, 1992 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10.
  47. 47. Obesity Trends* Among U.S. Adults BRFSS, 1993 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10.
  48. 48. Obesity Trends* Among U.S. Adults BRFSS, 1994 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10.
  49. 49. Obesity Trends* Among U.S. Adults BRFSS, 1995 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10.
  50. 50. Obesity Trends* Among U.S. Adults BRFSS, 1996 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10.
  51. 51. Obesity Trends* Among U.S. Adults BRFSS, 1997 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10. No Data <10% 10%-14% 15%-19% 20%-24%  25%
  52. 52. Obesity Trends* Among U.S. Adults BRFSS, 1998 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10. No Data <10% 10%-14% 15%-19% 20%-24%  25%
  53. 53. Obesity Trends* Among U.S. Adults BRFSS, 1999 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10. No Data <10% 10%-14% 15%-19% 20%-24%  25%
  54. 54. Obesity Trends* Among U.S. Adults BRFSS, 2000 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10. No Data <10% 10%-14% 15%-19% 20%-24%  25%
  55. 55. Obesity Trends* Among U.S. Adults BRFSS, 2001 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10. No Data <10% 10%-14% 15%-19% 20%-24%  25%
  56. 56. Source: Behavioral Risk Factor Surveillance System, CDC Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10. Obesity Trends* Among U.S. Adults BRFSS, 2002 No Data <10% 10%-14% 15%-19% 20%-24%  25%
  57. 57. Obesity* Trends Among U.S. Adults BRFSS, 2003 Source: Mokdad A H, et al. J Am Med Assoc 1999;282:16, 2001;286:10. No Data <10% 10%-14% 15%-19% 20%-24%  25%
  58. 58. Source: Behavioral Risk Factor Surveillance System, CDC. 19961991 2003 Obesity Trends* Among U.S. Adults BRFSS, 1991, 1996, 2003 No Data <10% 10%-14% 15%-19% 20%-24%  25% (*BMI 30, or about 30 lbs overweight for 5’4” person)
  59. 59. 1999 Obesity Trends Among U.S. Adults BRFSS, 1990, 1999, 2009 2009 1990 No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%
  60. 60. The Obesity Epidemic  Obesity rate has doubled in adults in the past two decades.  Obesity rate has tripled in adolescents in the past two decades. The Epidemic within the Epidemic  Morbid obesity rate has quadrupled in the past two decades.  Sturn R. Arch Intern Med. 2003;163:2146-2148.  1999 National Health and Nutrition Examination Survey, CDC National Center for Health Statistics
  61. 61. WHY WORRY ABOUT OBESITY?
  62. 62. The Problem Prevalence of obesity in U.S. increased from 12% to 21% between 1991 and 2001 = 15 million people Obesity is the 2nd most common cause of death from a modifiable behavioral risk factor 111,909 excess deaths annually Mokdad AH et al. JAMA. 2003;289:76-79 Flegal KM et al. JAMA 2005;293:1861-1919
  63. 63. Pulmonary disease abnormal function obstructive sleep apnea hypoventilation syndrome Nonalcoholic fatty liver disease steatosis steatohepatitis cirrhosis Coronary heart disease Diabetes Dyslipidemia Hypertension Gynecologic abnormalities abnormal menses infertility polycystic ovarian syndrome Osteoarthritis Skin Gall bladder disease Cancer breast, uterus, cervix colon, esophagus, pancreas kidney, prostate Phlebitis venous stasis Gout Medical Complications of Obesity Idiopathic intracranial hypertension Stroke Cataracts Severe pancreatitis
  64. 64. Obesity Growing Global Health Problems
  65. 65. Diabetes Gall bladder disease Hypertension Dyslipidemia Insulin resistance Breathlessness Sleep apnea Greatly increased (relative risk >>3) Coronary heart disease Osteoarthritis (knees) Hyperuricemia and gout Cancer (breast cancer in postmenopausal women, endometrial cancer, colon cancer) Reproductive hormone abnormalities Polycystic ovary syndrome Impaired fertility Low back pain Increased anesthetic risk Fetal defects arising from maternal obesity Moderately increased (relative risk 2-3) Slightly increased (relative risk 1-2) Relative risk of health problems associated with obesity
  66. 66. 2/3 of overweight patients have comorbid conditions such as diabetes, hpyerlipidemia, hypertensive, CAD, sleep apnea, etc. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. National Institutes of Health, National Heart, Lung, and Blood Institute. September 1998.
  67. 67. The more overweight one is , the more likely it is that you will have one or more chronic health conditions Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. National Institutes of Health, National Heart, Lung, and Blood Institute. September 1998.
  68. 68. Obesity is more costly than chronic smoking and drinking Sturn R., The Effects of Obesity, Smoking and Problem Drinking On Chronic Medical Problems and Health Care Cost, Health Affairs, 21 (2), 2002, 245-253
  69. 69. Obesity • Lowers life-expectancy • Associated with various diseases – Type 2 diabetes – Cardiovascular disease (CVD) – Sleep apnoea – Some cancers – Osteoarthritis
  70. 70. Obesity as a Risk Factor For OSA Structural Factors • Airway obstruction occurs when the nasopharynx and oropharynx are occluded by posterior movement of the tongue and palate against the posterior pharyngeal wall • Narrower airways are more easily collapsible and prone to airway occlusion
  71. 71. Obesity as a Risk Factor For OSA Structural Factors • Obese people have extrinsic narrowing of the area surrounding collapsible region of the pharynx and regional soft tissue enlargement • Increased fat deposits posteriolateral to oropharyngeal airspace at level of soft palate,, and in submental area
  72. 72. OBESITY • Strongest risk factor for OSA – Present in > 60% of patients referred for a diagnostic sleep evaluation – Wisconsin Sleep Cohort Study • A one standard deviation difference in BMI was associated with a 4-fold increase in disease prevalence
  73. 73. Obesity • Alters upper airway mechanics during sleep 1. Increased parapharyngeal fat deposition: neck circumference: > 17” males > 16” females With subsequent: Excessive fat deposition in the neck would tend to narrow the pharyngeal cross-sectional area smaller upper airway  increase the collapsibility of the pharyngeal airway
  74. 74. Risk Factor: Obesity Davies RJ et al. Eur Respir J 1990;3. 0 10 20 30 40 50 60 70 80 70 80 90 100 110 120 130 140 >4%Arterialsaturationdipah-1 % Predicted normal neck circumference After passing a threshold neck circumference, the severity of apnea increases linearly with increasing neck size.
  75. 75. Obesity 2. Changes in neural compensatory mechanisms that maintain airway patency:  diminished protective reflexes which otherwise would increase upper airway dilator muscle activity to maintain airway patency
  76. 76. Obesity 3. Waist circumference Fat deposition around the abdomen produces  reduced lung volumes (functional residual capacity) which can lead to loss of caudal traction on the upper airway  low lung volumes are associated with diminished oxygen stores
  77. 77. Body Fat Distribution • An excess deposition of adipose tissue focused on the trunk is Upper Body Obesity or Andriod Obesity. Upper body obesity, more specifically, visceral body fat distribution is related to disease etiologies. • An excess of deposition on the limbs or buttox is Lower Body Obesity or Gynoid Obesity.
  78. 78. Obesity as a Risk Factor For OSA Apple shape is riskier than Pear shape
  79. 79. Hip to Waist Ratio • Central Obesity defined by an increased waist-to- hip ratio • Excess fat in the abdominal region poses a greater health risk than excess fat in the hips and thighs and is associated with a higher risk of high blood pressure, diabetes, early onset of heart disease, and certain types of cancers
  80. 80. • A high waist hip ratio (> 0.85 for women; > 1.0 for men) indicates an apple-shaped or barrel-shaped figure, with a non-existing waistline and a higher risk for heart disease. • (Waist circumference for a woman should not exceed 88 cm and for a man not 102 cm.) Hip to Waist Ratio
  81. 81. • A healthy waist hip ratio for men is considered to be below 0.9 Borderline cases are between 0.9 and 1 but above 1 is considered to be unhealthy. • A healthy waist hip ratio for women is considered to be below 0.8. Borderline cases are between 0.8 and 0.85 but above 0.85 is considered to be unhealthy. Hip to Waist Ratio
  82. 82. • WHO STEPS states that abdominal obesity is defined as a waist–hip ratio above 0.90 for males and above 0.85 for females, or a body mass index (BMI) above 30 • The National Institute of Diabetes, Digestive and Kidney Diseases (NIDDK) states that women with waist–hip ratios of more than 0.8, and men with more than 1.0, are at increased health risk because of their fat distribution
  83. 83. Adipose deposits can be sex specific.
  84. 84. ● In general, men deposit adipose on the trunk where as women on the limbs. ● Male Gender androgenic patterns of body fat distribution favor fat deposition in the neck area ● Premenopausal women distribute more on the limbs, but redistribute to abdominal fat after menopause. Adipose deposits can be sex specific.
  85. 85. Obesity as a Risk Factor For OSA • Fat accumulation in the central, android (apple shape), and upper body correlate with metabolic syndrome, atherosclerosis, and OSA • Waist circumference more important than BMI, weight, or total fat content • Increased waist circumference predicts OSA even in non-obese (Grunstein 1993)
  86. 86. • Obesity is the most powerful risk factor for obstructive sleep apnea (OSA) - especially central type • Scientists discovered that people who are overweight (BMI of 25 to 29) and obese (BMI of 30 and above) have the higher risk for OSA.
  87. 87. • Excessive upper body fat distribution (truncal obesity) is one of the major contributing factors in the development of OSA; 70% of OSA patients are obese • The studies have demonstrated that obesity increases the rate of progression of sleep apnea, and weight gain further accelerates disease progression.
  88. 88. • With every 10% weight gain, the apnea hyponea index (AHI) increases with almost 32%. • However, losing 10% of weight will decrease the AHI with 26%. • Obesity is essentially the only reversible risk factor for obstructive sleep apnea (OSA)
  89. 89. Obesity and OSA • About 70% of those with OSA are obese (Malhotra et al 2002) • Prevalence of OSA in obese men and women is about 40% (Young et al 2002) • Higher BMI associated with higher prevalence – BMI>30: 26% with AHI>15 , 60% with AHI>5 – BMI>40: 33% with AHI>15 , 98% with AHI>5 (Valencia-flores 2000)
  90. 90. Obesity and OSA • Total body weight, BMI, and fat distribution all correlate with odds of having OSA – Every 10 kg increase in weight increases risk by 2X – Every increase in BMI by 6 increases risk by 4X – Every increase in waist or hip circumference by 13 to 15 cm increases risk by 4X (Young et al 1993)
  91. 91. • Obesity - More than 60% of sleep apnea patients are overweight, so it should ring a bell to anyone who has body fat. However, it is not the excess of the weight that triggers sleep apnea, but the neck size that counts. Here are the facts: – Men with a neck circumference of 17 inches or larger, – Women with a neck circumference of 16 inches or larger, – People with double chins – People with a lot of fat at the waist are more likely to have their airway collapse while they sleep.
  92. 92. The concept of Leptin and Ghrelin ↓Ghrelin↑Ghrelin
  93. 93. Leptin • Leptin is an appetite suppressant • Obese and pts with OSA (independently) have high leptin due to leptin resistance rather than as a result of leptin deficiency • Sleep deprivation/disordered sleep causes decreased leptin making you feel more hungry (Patel et al 2004) • Treatment of OSA with CPAP decreases leptin (after 2 months) and ghrelin levels (after 2 days) (Harsch et al 2003) • ?? Treating OSA could lead to decreased appetite
  94. 94. Ghrelin • Ghrelin is an appetite stimulant • Ghrelin levels increase after weight loss • Ghrelin levels higher in OSA pts • Treatment of OSA may reduce ghrelin levels leading to decreased appetite
  95. 95. Gale SM et al. J Nutr 2004; 134:295-8 LACK OF SLEEP less more
  96. 96. Can Obesity be a consequence of OSA? • OSA reduces physical activity and exercise performance • OSA reduces energy metabolism • OSA reduces motivation (from underlying comorbidities like depression: several studies have found correlation between OSA and depression)
  97. 97. OSA Decreased physical activity, exercise performance, energy metabolism, motivation Obesity
  98. 98. Potential mechanisms formatting a vicious cycle where obesity may result in OSA and OSA may lead to weight gain
  99. 99. Ministry of Health & population, Egypt Community based survey study On Non-communicable diseases and their Risk Factors, Egypt, 2005- 2006
  100. 100. The prevalence of diabetes mellitus in Egypt as a results of STEP wise survey is 15.8 % with higher elevation in females 18 % than in males 13.6 %
  101. 101. The percentage of mild hypertension (SBP ≥ 140 and/or DBP ≥ 90 mmHg ) in Egypt is 26.7% with irrelevant differences between males and females
  102. 102. The percentage of severe hypertension in Egypt (SBP ≥ 170 and/or DBP ≥ 100 mmHg) is 6.9 %
  103. 103. Dietary weight loss can improve OSA • Reduces upper airway collapse by modifying anatomy and function – 13% weight loss decreased nasopharyngeal airway collapsibility in obese patients with OSA after diet. All had decrease in AHI. – Improved pharyngeal and glottic fxn and significant decrease in AHI after 26 kg weight loss in obese patients with OSA
  104. 104. Dietary weight loss can improve OSA • Impact of weight loss is greater in those with severe OSA (AHI>30) and those higher in BMI – In obese patients, even minimal weight loss can be beneficial – Thought to be related to preferential loss of visceral fat first as oppose to subcutaneous fat which has metabolic advantages
  105. 105. Treatment of OSA and its effect on weight • Weight loss may be helped by CPAP in obese with OSA in compliant vs. noncompliant (use >4 hrs) (Loube 1997) • 6 mo. of CPAP could reduce intra-abdominal visceral fat and serum leptin even in absence of weight loss (Chin, 1999) • 2 mo. of CPAP assoc. with reduced serum leptin in absence of weight change (Harsch 2003)
  106. 106. Non-operative Treatment of Obesity How does it add up? • Diet • Exercise • Behavioral therapy • + Drug therapy . • ??????
  107. 107. How to manage your weight • Reducing caloric intake is the most common form, but difficult long term • Reducing calorie intake is most important: portion of fat vs. protein vs. carbs doesn’t matter in regards to weight loss, satiety, hunger, and satisfaction (Sacks et al. 2009) • Diet + exercise is most effective method of weight loss recommended by most doctors
  108. 108. How to manage your weight • Diet alone may be just as good as diet and exercise – Metanalysis of 25 yrs of weight loss research on diet alone, exercise alone, vs. diet + exercise – Concluded: 15-week diet or diet plus exercise program, produces a weight loss of about 24 lbs, with a 15 and 19 lb maintained loss after one year, respectively. (Miller 1997) • Many studies suggest diet + exercise provides about a 20% greater weight loss initially than diet alone • Exercise alone probably doesn’t work that well (Caudwell 2009)
  109. 109. The Weight Loss Rule > >+
  110. 110. Weight Loss Should be prescribed for all obese patients Can be curative but has low success rate Other treatment is required until optimal weight loss is achieved
  111. 111. Because of the high correlation between sleep apnea and obesity, particularly increased upper body mass, all patients who are obese should be encouraged to lose weight. Exercise and fitness should be recommended to all patients, both to improve sleep apnea and reduce cardiovascular disease risk. Weight loss can be very effective and, in some cases, even curative.
  112. 112. The problem that frequently occurs is that weight loss, while effective, is difficult to achieve and to maintain. In patients with significant sleep apnea, other forms of treatment should not be delayed until proper weight loss is achieved since they may continue to experience the complications of sleep apnea during the period of attempted weight loss.
  113. 113. Big patient Big risk
  114. 114. Weight Loss and Sleep Apnea -4 -20 to <- 10% -10 to <- 5% -5% to <+5 +5 to +10% +10% to +20 -3 -2 -1 0 1 2 3 4 5 6 Change in Body WeightAdapted from Peppard PE et al. JAMA 2000;284. Mean Change in AHI, Events/hr
  115. 115. Even a modest degree of weight loss can have a significant impact on apnea severity The frequency of apneas drops significantly with weight loss, often into the normal range, and the drops in oxyhemoglobin saturation accompanying the apneas are less severe Weight control can be an effective method for managing sleep apnea.
  116. 116. • Obesity : BMI, neck circumference, waist-to- hip ratio • The most common risk factor is the presence of obesity, specifically measures of central obesity. • Upper body fat distribution is one of the major contributing factors to the development of sleep apnea.. Conclusions
  117. 117. Conclusions • OSA may lead to weight gain and weight gain leads to OSA • Losing weight can improve OSA/lessens symptoms. • Unclear if treating OSA leads to weight loss although some studies show this is the case/weight loss is easier in patients who are treated by nasal CPAP • Diet and exercise as well as diet alone are good weight loss techniques
  118. 118. Surgical Treatment of Obesity Indications and Surgical Options
  119. 119. Patient Selection • Age 18 - 55 AND • BMI ≥ 40 kg/m2 OR • BMI 35 - 40 kg/m2 with – High risk health problems OR – Obesity-induced physical problems NIH Consensus Development Conference
  120. 120. Weight-loss surgery There are many types of weight-loss surgery, known collectively as bariatric surgery. Bariatric surgery is currently the only modality that provides a significant, sustained weight loss for the patient who is morbidly obese, with resultant improvement in obesity-related comorbidities Gastric bypass is one of the most common types of bariatric surgery in the United States. Many surgeons prefer gastric bypass surgery because it generally has fewer complications than do other weight-loss surgeries.
  121. 121. • The U.S. National Institutes of Health recommends bariatric surgery for obese people with a body mass index (BMI) of at least 40, and for people with BMI 35 and serious coexisting medical conditions
  122. 122. • A medical guideline by the American College of Physicians concluded: " Bariatric Surgery should be considered as a treatment option for patients with a BMI of 40 kg/m2 or greater who instituted but failed an adequate exercise and diet program (with or without adjunctive drug therapy) and For patients who present with obesity-related comorbid conditions, such as hypertension, diabetes mellitus, hyperlipidemia, and obstructive sleep apnea
  123. 123. Who Qualifies for Weight-Loss Surgery? Normal Weight (BMI 18.5 to 24.9) Overweight (BMI 25 to 29.9) Obese (BMI 30 to 34.9) Severely Obese (BMI 35 to 39.9 ) Morbidly Obese (BMI 40 or more) BMI 18.5-24.9 BMI 25-29.9 BMI 30-34.9 BMI 35-39.9 BMI>40
  124. 124. Gastric bypass and other weight-loss surgeries are typically done only after you've tried to lose weight by improving your diet and exercise habits. Still, all forms of weight-loss surgery, including gastric bypass, are major procedures that can pose serious risks and side effects keep in mind that bariatric surgery is expensive
  125. 125. Regarding bariatric surgery for weight loss, OSA is prevalent in at least 45% of these patients Surgically induced weight loss significantly improves obesity-related OSA and sleep quality parameters. Although many such morbidly obese patients who undergo bariatric surgery can expect reduction of AHI and CPAP pressure needed to maintain patent airway, most surgical patients with preoperative OSA will continue to need CPAP after surgery
  126. 126. Weight loss is an important long-range goal. Patients who are obese should be informed that obesity strongly correlates with OSA, particularly with heavy upper body mass. Weight loss can be very effective and, in some cases, even curative, but its rate of success is low. Nonetheless, a 10% weight loss is associated with a 26% decrease in AHI. In patients with significant OSA, other treatments should not be delayed until proper weight loss is achieved, since OSA complications may continue during the weight loss period.
  127. 127. Weight loss is strongly encouraged for all patients Increasing body weight will worsen OSAS. The patient needs to be aware that weight loss is not the sole treatment for moderate-to-severe OSAS, but is an adjunctive treatment that needs to occur in conjunction with other forms of treatment
  128. 128. • OSAS is strongly associated with obesity but is also increasingly identified in the less obese, in whom a particular craniofacial structure is an important contributory factor. • The prevalence of OSAS is likely to be increasing in parallel with the epidemic of obesity currently occurring in many countries
  129. 129. • Great eaters and great sleepers are incapable of doing anything that is great. William Shakespeare “Henry IV”
  130. 130. To sleep, or not to sleep, that is the question!

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