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SLEEPING SWEETLY:

SLEEPING SWEETLY:. How Sleep Deprivation & Obstructive Sleep Apnea Effect Type 2 Diabetes Mellitus.

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SLEEPING SWEETLY:

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  1. SLEEPING SWEETLY: How Sleep Deprivation & Obstructive Sleep Apnea Effect Type 2 Diabetes Mellitus

  2. Ronald J. Green, MD, FCCP, FAASMDiplomate, American Board of Sleep MedicineSleep Medicine, Pulmonary Disease & Smoking Cessation, The Everett Clinic Associate Medical DirectorNorth Puget Sound Center for Sleep DisordersEverett, WA425-339-5410; www.ilikesleep.com

  3. Pre-test QUESTION 1 • Sleep deprivation in healthy, non-diabetics leads to impaired glucose metabolism • True • False

  4. Pre-test QUESTION 1 • Sleep deprivation in healthy, non-diabetics leads to impaired glucose metabolism • True • False

  5. Pre-test QUESTION 2 • Proposed factors linking obstructive sleep apnea with impairments in glucose metabolism include: • Interleukin 6 • Catecholamines • Cortisol • 2 & 3 • All of the above

  6. Pre-test QUESTION 2 • Proposed factors linking obstructive sleep apnea with impairments in glucose metabolism include: • Interleukin 6 • Catecholamines • Cortisol • 2 & 3 • All of the above

  7. Chronic sleep deprivation is • Common • Dangerous • Easily recognized • Treatable

  8. Obstructive Sleep Apnea Syndrome (OSAS) is • Common • Dangerous • Easily recognized • Treatable

  9. Type 2 Diabetes Mellitus (DM) is • Common • Dangerous • Easily recognized • Treatable

  10. I hope to convince you today that OSAS is independently associated with impairments in glucose metabolism & type 2 DM (independent of obesity)

  11. OUTLINE • Overview of obstructive sleep apnea syndrome (OSAS) • Case presentation • Effects of sleep restriction & sleep deprivation on glucose metabolism • OSAS’s effects on glucose metabolism and type 2 diabetes mellitus (DM) • Proposed mechanisms linking OSAS with impairments in glucose metabolism • Effects of treatment of OSAS on type 2 DM

  12. Overview of The obstructive sleep apnea syndrome

  13. What is the “apnea” in sleep apnea? • Apnea • Cessation of airflow > 10 seconds • Hypopnea • Decreased airflow > 10 seconds associated with: • Arousal from sleep • Oxyhemoglobin desaturation

  14. Measures of Sleep Apnea Frequency • Apnea Index • # apneas per hour of sleep • Apnea / Hypopnea Index (AHI) • # apneas + hypopneas per hour of sleep • > 5 considered abnormal in adults

  15. Pathophysiology of an obstructive apnea

  16. Awake: Small airway + neuromuscular compensation Loss of neuromuscular compensation SleepOnset Hyperventilate: connect hypoxia & hypercapnia + Decreased pharyngeal muscle activity Airway opens Airway collapses Pharyngeal muscle activity restored Apnea Arousal from sleep Hypoxia & Hypercapnia Increased ventilatory effort Pathophysiology of Obstructive Sleep Apnea

  17. Clinical Consequences Obstructive Sleep Apnea Sleep fragmentation, Hypoxia / Hypercapnia excessive daytime sleepiness cardiovascular & metabolic complications Morbidity Mortality

  18. Obstructive Sleep Apnea: Most common risk factors • Obesity • Increasing age • Male gender • Anatomic abnormalities of upper airway • Family history of OSAS • Alcohol or sedative use

  19. Diagnosis: History • Loud snoring (not all snore) • Nocturnal gasping and choking • Ask bed partner (witnessed apneas) • Automobile or work related accidents • Personality changes or cognitive problems • Risk factors • Excessive daytime sleepiness (often not recognized by patient) • Frequent nocturia Sleep Apnea: Is Your Patient at Risk? NIH Publication, No 95-3803.

  20. Diagnosis: Physical Examination • Upper body obesity / thick neck > 17” males > 16” females • Hypertension • Obvious airway abnormality

  21. Exam: Oropharynx

  22. Physical Examination Guilleminault C et al. Sleep Apnea Syndromes. New York: Alan R. Liss, 1978.

  23. Why Get a Sleep Study? • Signs and symptoms poorly predict disease severity • Appropriate therapy dependent on severity • Failure to treat leads to: • Increased morbidity • Motor vehicle crashes • Mortality • Help diagnose other causes of daytime sleepiness

  24. Polysomnography

  25. Treatment of Obstructive Sleep Apnea Syndrome

  26. Treatment Objectives Reduce mortality and morbidity Decrease cardiovascular complications Reduce sleepiness Improve metabolic derangements, including type 2 diabetes mellitus Improve quality of life

  27. Therapeutic Approach Risk counseling Motor vehicle crashes Job-related hazards Judgment impairment Apnea treatment Weight loss; avoidance of alcohol & sedatives CPAP Oral appliance Surgery (UPPP)

  28. Positive Airway Pressure

  29. Positive Airway Pressure

  30. Oral Appliance: Mechanics

  31. Uvulopalatopharyngoplasty (UPPP)

  32. Primary Care Management Risk counseling Behavior modification (weight loss, etc) Monitor symptoms and compliance Monitor weight and blood pressure Ask about recurrence of symptoms Evaluate CPAP use and side effects Sleep Apnea: Is Your Patient at Risk? NIH Publication No.95-3803.

  33. CASE PRESENTATION

  34. Case Presentation • 34 year old woman with history of morbid obesity, type 2 DM & polycystic ovarian syndrome • Per husband, loud snoring & witnessed apneas at night for yrs • Awakens herself choking/gasping at night and during naps

  35. Case Presentation, cont’d • Hypersomnolence for years • Near misses driving due to falling asleep briefly at the wheel • Steady weight gain for years • Drinks one pot coffee daily plus caffeinated soda all day long

  36. Case Presentation, cont’d • Medications: metformin • No tobacco or alcohol use • Physical exam: BMI = 48.71 (311 pounds, 5’7” tall); very crowded posterior pharyngeal airway; obese neck

  37. Case Presentation, cont’d • Epworth sleepiness scale = 15 (>10 is abnormal) • Fasting glucose (lab draw) 155 • Hg A1C 7.6 • TSH 2.77

  38. Case Presentation, cont’d • IMPRESSION: severe, long standing obstructive sleep apnea syndrome • RECOMMENDATIONS: • Overnight sleep study and titration of CPAP, and initiate CPAP therapy • Risk counseling: driving safety, weight loss

  39. Case Presentation:diagnostic sleep study • Apnea/hypopnea index = 136 per hr • 33% of the events caused arousals (45 arousals per hour) • Low oxygen saturation = 63% • 40% of the night spent with oxygen saturations below 90%

  40. Case Presentation:diagnostic sleep study

  41. Case Presentation, cont’d • Treatment: CPAP • CPAP titration done with resolution of respiratory events and stabilization of oxygen desaturations • Optimal pressure: 15 cm H20

  42. Case Presentation:CPAP titration

  43. Case Presentation:Treatment with CPAP On CPAP at pressure of 15 cm H2O “It’s just like a whole new world.” Able to exercise again and has great energy Excessive Daytime Sleepiness gone (ESS = 5 vs 15 pre-Tx) 13 pound weight loss in 6 weeks (unable to lose any weight prior to CPAP) Fasting, morning glucose dropped 15-20 points (from mid-150s to low 130s, as low as 127) with no change in medication

  44. Effects of sleep restriction & sleep deprivationon glucose metabolism

  45. Definition of terms Insulin resistance: normal amounts of insulin are inadequate to produce a normal drop in blood glucose Insulin sensitivity: systemic responsiveness to glucose Glucose intolerance: blood glucose levels are higher than normal, but not high enough to classify as diabetes mellitus Glucose effectiveness: ability of glucose to mobilize itself independent of an insulin response

  46. Sleep restriction & sleep deprivation adversely effectglucose metabolism

  47. Effects of sleep restriction on glucose metabolism (no OSAS) • Results of sleep restriction (5.5h vs 8.5h for 14 nights) on healthy, non-diabetic, non-obese subjects (Nedelcheva, et al) • Sleep restriction resulted in: • Reduced oral glucose tolerance • Reduced insulin sensitivity • Modest increase in epinephrine & norepinephrine levels Nedeltcheva, J Clin Endocrinol Metab 2009 Sep; 94(9): 3242-50

  48. Effects of sleep fragmentation on glucose metabolism (no OSAS) • Normal, healthy non-diabetics were subjected to sleep fragmentation with auditory & mechanical stimuli for just two nights (Stamatakis & Punjabi) • Results: • Insulin sensitivity decreased • Glucose effectiveness decreased • Morning cortisol levels increased Stamatakis, Chest 2010 Jan; 137(1):95-101

  49. Short sleep duration is associated with development of type 2 Diabetes Mellitus

  50. Short sleep duration is associated with development of type 2 DM • Yaggi, et al (Cohort of Mass. Male Aging Study) • Short sleepers (< 6h per night) twice as likely to develop DM vs those sleeping 7-8h per night • Adjusted for age, HTN, waist circum, health status • Gangwisch, et al (Cohort of 1st National Health & Nutrition Examination Survey) • Short sleepers (< 5h per night) were 1.5 times more likely to develop DM vs 7-8h per night Yaggi, Diabetes Care, 2006. Mar; 29(3): 657-61. Gangwisch, Sleep, 2007. Dec 1; 30(12): 1667-73.

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