Metabolic Study of Sleep Apnea in Men and Women

Obstructive Sleep Apnea (OSA) Clinical Trial

Official title:

Sleep and Metabolism in Obesity: Impact of Gender

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT00706511
• Other study ID #: 15870
• Secondary ID: P50HD057796
• Status: Completed
• Phase: N/A
• Start date: December 2007
• Est. completion date: August 22, 2012

Study information

• Verified date: September 2016
• Source: University of Chicago
• Contact: n/a
• Is FDA regulated: No
• Study type: Interventional

Clinical Trial Summary

The purpose of this study is to look at the metabolic (use of energy) and hormonal features of sleep problems in men and women.

Description:

Obesity is a major risk factor for obstructive sleep apnea (OSA), a condition characterized by repetitive respiratory disturbances, intermittent hypoxia, sleep fragmentation by frequent microarousals and low amounts of deep slow wave sleep (SWS). Today, more than 10 million American women suffer from OSA. OSA has been identified as an independent risk factor for the metabolic syndrome. Because OSA is more prevalent in men than in women, a disproportionate number of studies of OSA and its consequences have been conducted in men. Thus, OSA has been characterized as a disorder associated with gender-based health care inequity. Recent evidence, including data from our group, suggests that reduced amounts and intensity of SWS (i.e. slow-wave activity [SWA]) may play a pivotal role in the development of metabolic and cardiovascular disturbances in obese men and women, particularly those with OSA. This project will focus on sex differences in SWA and their relationship with daytime sleepiness and metabolic vulnerability in obese men and women with and without OSA. We propose to simultaneously characterize: 1. sleep-wake regulation; 2. measures of diabetes risk; 3. measures of cardiovascular risk; and 4. profiles of sex steroids, cortisol and adipokines in a. obese men without OSA, b. obese men with OSA before and after treatment with continuous positive airway pressure (CPAP), c. obese pre-menopausal women without OSA, and d. obese pre-menopausal women with OSA before and after CPAP treatment. The completion of these interdisciplinary studies will provide a unique data set contrasting in obese women versus obese men the relationships between sleep and the metabolic syndrome, OSA and the metabolic syndrome and the impact of CPAP treatment on the metabolic syndrome. This work will provide important insights regarding the pathophysiology of OSA and its adverse consequences in obese men and women, and the basis for the development of effective sex-specific prevention and treatment strategies.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 27
• Est. completion date: August 22, 2012
• Est. primary completion date: August 16, 2012
• Accepts healthy volunteers: No
• Gender: All
• Age group: 18 Years to 40 Years

Eligibility

Inclusion Criteria:

• Obese (BMI of at least 30 kg/m2)

Exclusion Criteria:

• Clinically significant depression

• Positive pregnancy test

• Diagnosis of diabetes mellitus

• Hypertension (systolic > 140 mmHg and/or diastolic > 90 mmHg) not well-controlled on stable medication with either ACE inhibitors or diuretics

• Habitual alcohol use

• Excessive caffeine intake of more than 300 mg/day

• Hemoglobin < 11g/dL and/or hematocrit < 33%

• Systemic illnesses, including heart, renal, liver, or malignant disease

• Taking steroid preparations (including oral contraceptives), medications known to alter insulin secretion and/or action, or medications known to influence sleep during the 2 months prior to starting the study

• Travel across time zones during the 4 weeks prior to starting the study

• Irregular sleeping habits (including shift work)

Related Conditions & MeSH terms

• Obstructive Sleep Apnea (OSA)
• Sleep Apnea Syndromes
• Sleep Apnea, Obstructive

Intervention

Device:
• CPAP
CPAP (continuous positive airway pressure) treatment at home for 6 weeks

Locations

Country	Name	City	State
United States	University of Chicago Department of Medicine, Section of Endocrinology, Diabetes & Metabolism	Chicago	Illinois

Sponsors (3)

Lead Sponsor	Collaborator
University of Chicago	Duke University, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD)

Country where clinical trial is conducted

United States, 

References & Publications (7)

Knutson KL, Ryden AM, Mander BA, Van Cauter E. Role of sleep duration and quality in the risk and severity of type 2 diabetes mellitus. Arch Intern Med. 2006 Sep 18;166(16):1768-74. — View Citation

Knutson KL, Spiegel K, Penev P, Van Cauter E. The metabolic consequences of sleep deprivation. Sleep Med Rev. 2007 Jun;11(3):163-78. Epub 2007 Apr 17. Review. — View Citation

Latta F, Leproult R, Tasali E, Hofmann E, L'Hermite-Balériaux M, Copinschi G, Van Cauter E. Sex differences in nocturnal growth hormone and prolactin secretion in healthy older adults: relationships with sleep EEG variables. Sleep. 2005 Dec;28(12):1519-24. — View Citation

Tasali E, Leproult R, Ehrmann DA, Van Cauter E. Slow-wave sleep and the risk of type 2 diabetes in humans. Proc Natl Acad Sci U S A. 2008 Jan 22;105(3):1044-9. doi: 10.1073/pnas.0706446105. Epub 2008 Jan 2. — View Citation

Tasali E, Mokhlesi B, Van Cauter E. Obstructive sleep apnea and type 2 diabetes: interacting epidemics. Chest. 2008 Feb;133(2):496-506. doi: 10.1378/chest.07-0828. Review. — View Citation

Tasali E, Van Cauter E, Ehrmann DA. Relationships between sleep disordered breathing and glucose metabolism in polycystic ovary syndrome. J Clin Endocrinol Metab. 2006 Jan;91(1):36-42. Epub 2005 Oct 11. — View Citation

Van Cauter E, Holmback U, Knutson K, Leproult R, Miller A, Nedeltcheva A, Pannain S, Penev P, Tasali E, Spiegel K. Impact of sleep and sleep loss on neuroendocrine and metabolic function. Horm Res. 2007;67 Suppl 1:2-9. Epub 2007 Feb 15. Review. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Polysomnography - Apnea-hypopnea Index (AHI)	apnea-hypopnea index: number of apneas and hypopneas per hour of recording; a measure of the severity of obstructive sleep apnea; varies from min=0 to max=120; AHI between 0 and <5: no significant sleep apnea; AHI between 5 and <15: mild sleep apnea; AHI between 15 and <30: moderate sleep apnea; AHI of 30 and above: severe sleep apnea.	After 6 weeks of CPAP (Treatment)
Primary	Polysomnography - Minutes of N3 Stage	Stage N3, sometimes referred to as "delta sleep" or "slow wave sleep", is characterized by slow waves in the electro-encephalogram (EEG) that reflect synchronization of firing of cortical neurons. N3 sleep is considered the most restorative stage of sleep for both the brain and the rest of the body.	After 6 weeks of CPAP (Treatment)
Primary	Polysomnography - Minutes of REM Stage		After 6 weeks of CPAP (Treatment)
Primary	Polysomnography - Sleep Efficiency	Sleep efficiency: a measure of objective sleep quality; calculated from the polygraphic sleep recording as the ratio of time spent asleep during the scheduled sleep period to total scheduled sleep period. Expressed in %. Varies from 0% (the subject did not sleep at all) to 100% (the subject spent the entire scheduled sleep period asleep).	After 6 weeks of CPAP (Treatment)
Secondary	IVGTT (Intravenous Tolerance Test) - Sensitivity Index (SI)	Sensitivity Index (SI): a measure of how much insulin the body needs to metabolize a given amount of glucose. SI is calculated using a mathematical model describing the profiles of blood glucose and serum insulin after intravenous glucose injection. SI varies from 0 to an undefined upper limit but generally under 20. Higher values of SI represent a better outcome.	After treatment (6 weeks)
Secondary	IVGTT (Intravenous Tolerance Test) - Acute Insulin Response	Acute Insulin Response is calculated as the area under the insulin curve for the first 19 minutes after intravenous glucose injection. "Area under the insulin curve" is expressed in pmol x min/L.	After treatment (6 weeks)
Secondary	IVGTT (Intravenous Tolerance Test) - Disposition Index (DI)	Disposition Index (DI) is the product of sensitivity index (SI) by the amount of insulin secreted in response to blood glucose levels. It is a marker of the risk of type 2 diabetes. Low DI reflects a high risk of diabetes. DI can vary from 0 to an undefined upper limit. The physiological range for the Disposition Index is 500 to 5,000. Higher values represent a better outcome.	After treatment (6 weeks)

External Links

•   University of Chicago Sleep Disorders Center