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Original Studies |
Sleep Research and Treatment Center, Department of Psychiatry (A.N.V., E.O.B., A.K.), Department of Radiology (K.H.), and Department of Health Evaluation Sciences (H.-M.L.), Pennsylvania State University, Hershey, Pennsylvania 17033; and Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health (D.A.P., A.L., G.P.C.), Bethesda, Maryland 20892
Address all correspondence and requests for reprints to: Alexandros N. Vgontzas, M.D., Sleep Research and Treatment Center, Department of Psychiatry, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, Pennsylvania 17033. E-mail: axv3{at}psu.edu
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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and interleukin-6) and
leptin levels independently of obesity? 2) Among obese patients, is it
generalized or visceral obesity that predisposes to sleep apnea? 3) Is
apnea a factor independent from obesity in the development of insulin
resistance? Obese middle-aged men with sleep apnea were first compared
with nonapneic age- and body mass index (BMI)-matched obese and
age-matched lean men. All subjects were monitored in the sleep
laboratory for 4 consecutive nights. We obtained simultaneous indexes
of sleep, sleep stages, and sleep apnea, including apnea/hypopnea index
and percent minimum oxygen saturation. The sleep apneic men had higher
plasma concentrations of the adipose tissue-derived hormone, leptin,
and of the inflammatory, fatigue-causing, and insulin
resistance-producing cytokines tumor necrosis factor- and
interleukin-6 than nonapneic obese men, who had intermediate values, or
lean men, who had the lowest values. Because these findings suggested
that sleep apneics might have a higher degree of insulin resistance
than the BMI-matched controls, we studied groups of sleep-apneic obese
and age- and BMI-matched nonapneic controls in whom we obtained
computed tomographic scan measures of total, sc, and visceral abdominal
fat, and additional biochemical indexes of insulin resistance,
including fasting plasma glucose and insulin. The sleep apnea patients
had a significantly greater amount of visceral fat compared to obese
controls (<0.05) and indexes of sleep disordered breathing were
positively correlated with visceral fat, but not with BMI or total or
sc fat. Furthermore, the biochemical data confirmed a higher degree of
insulin resistance in the group of apneics than in BMI-matched
nonapneic controls. We conclude that there is a strong independent
association among sleep apnea, visceral obesity, insulin resistance and
hypercytokinemia, which may contribute to the pathological
manifestations and somatic sequelae of this condition. |
Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The pathophysiology of sleep apnea remains obscure, and most currently
available treatments for this disorder are mechanical and associated
with either variable response and/or poor compliance. Recently, we
reported that the inflammatory cytokines tumor necrosis factor-
(TNF) and interleukin-6 (IL-6), both of which produce sleepiness and
fatigue, are elevated in sleep apnea and obesity and might play a role
in the pathogenesis and pathological sequelae of both disorders (6).
Like the adipostatic hormone leptin, these cytokines are released into
the interstitial fluid of adipose tissue, and their circulating levels
correlate positively with the body mass index (BMI) (7, 8, 9). TNF
correlates strongly with lipolysis, and this cytokine causes marked
insulin resistance (7, 9, 10) and stimulates leptin secretion (11, 12, 13).
Circulating concentrations of leptin are proportional not only to total
body fat but also to the degree of insulin resistance (14). Chronic
leptin administration has been associated with sympathetic system
activation and elevation of blood pressure (15), suggesting that it
might play a role in the pathogenesis of manifestations that frequently
accompany sleep apnea, namely hypertension and its sequelae.
The purpose of this study was to evaluate whether the biochemical
indexes of chronic inflammation, including the proinflammatory
cytokines TNF and IL-6, and the adipose-derived tissue hormone,
leptin, are elevated in sleep apnea independently of obesity; whether
sleep apnea is an independent variable in the development of insulin
resistance; and whether among obese individuals it is visceral, rather
than generalized, obesity that predisposes to the development of sleep
apnea.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Subjects
Fourteen male patients with obstructive sleep apnea and 11 obese and 12 normal weight male controls participated in the study. The subjects were recruited from the Sleep Disorders Clinic or through advertisement from the community. The mean ± SE ages of the apneics, obese controls, and normal weight controls were 46.6 ± 3.0, 40.2 ± 2.2, and 45.4 ± 2.8 yr, respectively (P = NS), whereas their BMIs were 38.4 ± 1.6, 36.2 ± 2.4, and 26.0 ± 0.8, respectively (P = NS between sleep apneics and obese controls; P < 0.01 between sleep apneics or obese controls and normal weight controls).
To qualify for the study, apneic patients had to have apnea of sufficient severity to warrant recommendation for treatment (16). These criteria included an apnea/hypopnea index (A/HI) of more that 20 events/h of sleep and clinical symptoms such as excessive daytime sleepiness and/or the presence of cardiovascular abnormalities, i.e. hypertension or cardiac arrhythmias. Control subjects who demonstrated an A/HI of more than 5 events/h of sleep were excluded from the study. Also apneics and control subjects with a diagnosis of diabetes mellitus or who were receiving treatment with psychotropics, steroids, sympathomimetics, or sympatholytics, including ß-blockers, were excluded from the study. All patients and controls were asked to abstain from nonsteroidal antiinflammatory medication for 1 week before the study. Five of the sleep apneics and none of the obese or the normal weight controls were treated for hypertension. Three of the apneics were treated with angiotensin-converting enzyme inhibitors, and two were treated with calcium channel blockers.
Procedures
Sleep laboratory. A thorough medical assessment, including physical examination, routine laboratory tests (including complete blood cell count, urinalysis, thyroid function tests, and electrocardiography), and sleep history, was completed for each patient and control subject. All potential participants in the study were screened in the sleep laboratory for 1 night for 8 h employing standard polysomnographic procedures (17). Throughout the night, respiration was monitored by thermocouples at the nose and mouth (model TCT1R, Grass Instrument Co., Quincey, MA) and thoracic strain gauges. All-night recordings of hemoglobin oxygen saturation (SaO2) were obtained using a cardiorespiratory oximeter (model 8800, Nonin Medical, Inc., Plymouth, MN) attached to the finger. The subjects who met the inclusion criteria were monitored in the Sleep Laboratory for 4 consecutive nights (1 adaptation and 3 baseline nights). The sleep records were scored independently of any knowledge of the experimental conditions according to standardized criteria (17). Also, the respiratory data were quantified as previously described (16).
Blood pressure was measured in the evening during the physical examination using a pneumoelectric microprocessor-controlled instrument. The recorded blood pressure was the average of three consecutive readings during a 5-min period following 10 min of rest in the supine position.
Assays. Single blood samples for measurement of plasma
IL-6, TNF, and leptin were drawn from the three groups in the
morning between 0600–0700 h after completion of the nocturnal sleep
laboratory recording and in the evening between 1900–2000 h for 3
consecutive days. In addition, in the group of sleep apneics and obese
controls, single blood samples for measurement of fasting blood glucose
and insulin were drawn in the morning for the same 3 consecutive days.
Plasma was stored at -70 C until assay. All samples were processed in
the same manner. Plasma TNF and IL-6 were measured by enzyme-linked
immunosorbent assay (R & D Systems, Minneapolis, MN). The intra- and
interassay coefficients of variation ranged from 5.6–6.1% and
7.5–10.4%, respectively, for TNF and from 3.2–8.5% and
3.5–8.7% for IL-6. The lower detection limits for TNF and IL-6
were 0.18, and 0.094 pg/mL, respectively. Leptin was measured by a
commercially available RIA (Linco Research, Inc., St.
Charles, MO). Samples were run in duplicate, and standards were run in
triplicate. The intra- and interassay coefficients of variation were
both below 5%. Plasma insulin was measured by specific RIA. The intra-
and interassay coefficients of variation for insulin ranged from
3.5–4.6% and 4.5–7.0%, respectively.
Computed tomographic (CT) scanning. The objective of these measurements was to assess and compare the distribution of abdominal fat (intraabdominal vs. sc fat) in sleep apneics and their obese controls. One of the obese controls did not complete this part of the study. Axial 8-mm CT sections were taken through the midvertebral bodies of L1, L3, L4, and L5 plus a fifth slice at the top of the femoral heads. No iv or oral contrast was used. The specific levels to be scanned were localized from an initial sagittal topogram. All scans were performed on a PQ5000 (130 kV; 200 mA, Picker International, Highland Heights, OH).
Each image was segmented twice, once for intra-abdominal fat and once for sc fat. A CT range of -120 to -40 hounsfield units was used to encompass all fat. The total cross-sectional area was also calculated at each level so that the percentages of intraabdominal, sc, and total fat could be calculated. Subcutaneous fat was defined as fat between the skin surface and the outer margin of the back and abdominal wall musculature, and intraabdominal fat was defined as fat within the cavity formed by the back and abdominal wall musculature.
Statistical analyses
The results of parametric values are expressed as the mean ± SE. For comparison of parametric values among the three groups we used MANOVA, which controlled for repeated measures. For comparisons between the two groups we employed the Student’s two-tailed t test. Relations among sleep variables, respiratory data, BMI, CT measures, and hormonal values were calculated using the Pearson product-moment correlation analysis and multiple regression analysis. The sleep variables were calculated based on the mean values from the 3 consecutive baseline nights (2, 3, 4). The critical statistical confidence level selected for all analyses was P < 0.05.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The group of sleep apneics, compared to both obese and
normal weight controls, demonstrated a significantly longer wake time
after sleep onset, total wake time, and percentage of stage 1 sleep
(P < 0.01; Table 1
). The
same patients demonstrated a significantly lower percentage of sleep
time and stage 2 sleep (P < 0.05) than either control
group. The A/HI in sleep apneics was 48.7 ± 5.6, whereas in the
obese and normal weight controls it was 1.3 ± 0.5 and 0.5 ±
0.3, respectively (P < 0.01). In addition, the apneics
had a significantly lower minimum hemoglobin oxygen saturation
(SaO2) than the two control groups (74.6 ±
3.3 vs. 91.1 ± 1.6 vs. 94.4 ± 0.9;
P < 0.01, respectively, for the comparisons
between sleep apneics and either control group). Finally, systolic,
diastolic, and mean arterial pressures were highest in the sleep apneic
group (144.3 ± 7.0, 89.4 ± 3.6, and 107.7 ± 4.6,
respectively), lowest in the normal weight controls (123.0 ± 1.6,
76.3 ± 1.4, and 91.9 ± 1.0), and intermediate in the obese
controls (133.6 ± 2.8, 86.2 ± 3.4, and 102.0 ± 2.9),
with differences between sleep apneics and normal weight controls being
significant (P < 0.01) for all three blood pressure
variables.
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,
IL-6, and leptin
Plasma TNF values were highest in the sleep apneic group and
lowest in the normal weight controls for the average value
(P = 0.04) as well as for the evening concentration
(P = 0.005, Table 2 and
Fig. 1). Plasma TNF values were
intermediate between the other two groups for the average as well as
the evening values. Plasma IL-6 values were also highest in the sleep
apneic group and lowest in the normal weight controls for the average
(P = 0.005) as well as for the morning
(P = 0.04) and evening concentrations
(P = 0.002). Again, the values for the obese controls
were midway between those for the other two groups. Mean plasma levels
for leptin were highest in the sleep apneics and lowest in the normal
weight controls (P = 0.0001). In addition, the obese
controls had significantly higher values than the normal weight
controls (P = 0.05) and lower values than the sleep
apneics (P = 0.02). This general relationship among the
three groups was present within both morning and evening
measurements.
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, 3.0 ± 0.2 vs. 3.6 ± 0.2 and 2.6 ±
0.2 vs. 3.2 ± 0.2 for morning and evening,
respectively; IL-6, 1.8 ± 0.4 vs. 2.6 ± 0.9 and
2.7 ± 0.3 vs. 4.3 ± 0.8 for morning and evening,
respectively; leptin, 24.3 ± 5.5 vs. 26.3 ± 3.9
and 22.7 ± 4.2 vs. 31.3 ± 4.6 for morning and
evening, respectively; all comparisons were nonsignificant).
The ratio of morning/evening secretion of TNF, IL-6, and leptin was
significantly lower in sleep apneics and obese controls than in normal
weight controls, indicating that not only the amount but also the daily
pattern of secretion of cytokines is altered in obese subjects (Table 2
).
Mean (the average of morning and evening concentrations) IL-6 and
leptin values and evening TNF values were positively correlated with
BMI (rxy = 0.74, P < 0.01;
rxy = 0.82, P < 0.01; and
rxy = 0.40, P < 0.05,
respectively; Fig. 2). Mean TNF, IL-6,
and leptin values were significantly correlated with indexes of sleep
apnea (rxy = 0.32, P < 0.05;
rxy = 0.38, P < 0.05; and
rxy = 0.55, P < 0.01,
respectively, for A/HI and rxy = -0.45,
rxy = -0.52, and rxy =
-0.44, all P < 0.01, respectively, for minimum
SaO2). Mean IL-6 values were positively
correlated with mean leptin (rxy = 0.64;
P < 0.001) and TNF values
(rxy = 0.39; P < 0.05). Evening
plasma TNF values were positively correlated with the corresponding
leptin levels (rxy = 0.28; P <
0.1).
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There were no differences between the two groups in terms of total
body fat or sc fat at all five levels. In contrast, sleep apneics
compared to obese controls had a significantly greater amount of
visceral fat at L1, L3, L4, and L5 levels (all P <
0.05; numerical data at the L3 level are shown in Table 3). BMI correlated significantly with
total body fat (measured at L3: rxy = 0.83;
P < 0.01) and sc fat (rxy =
0.88; P < 0.01), but not with visceral fat. Visceral,
but not sc, fat was significantly correlated with indexes of sleep
apnea (rxy = 0.70; P < 0.01 for
A/HI and rxy = -0.60; P < 0.01
for minimum SaO2; Fig. 3).
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). Mean
plasma insulin levels were also higher in sleep apneics than in obese
controls (25.7 ± 4.2 vs. 14.6 ± 2.5;
P < 0.05; Fig. 4). The
sleep apneics who were taking medication for hypertension compared to
those who were not taking medication demonstrated lower insulin levels,
which, however, were not different from control values (16.9 ±
4.2 vs. 29.8 ± 5.0; P = NS).
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Multivariate analysis among plasma cytokine concentrations, types of fat, and sleep apnea indexes
The multiple regression analysis for IL-6 indicated that in terms
of the fat types, sc fat was making the strongest contribution for both
groups (P = 0.0003). Yet, IL-6 correlated with visceral
fat within the obese control group, but not within the sleep apnea
group. After adjustment for fat type, A/HI continued to make an
independent contribution to the IL-6 levels (P = 0.01).
For TNF, there was a significant association with sc fat within the
obese control group, but not within the sleep apnea group. As with
IL-6, when fat types were adjusted for, A/HI made a significant
contribution to TNF concentrations (P = 0.05). As
expected, multiple regression analysis for leptin indicated that both
sc and visceral fat made significant contributions (P
< 0.0001), with visceral fat being the stronger of the two. Unlike its
effect on plasma cytokine concentrations, A/HI did not make an
additional contribution to leptin levels.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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and IL-6 elevations
independently from obesity; among obese patients, it was the visceral
rather than the sc or total body fat that predisposed to the
development of sleep apnea, and sleep apnea contributed to the
development of fasting hyperinsulinemia independently from obesity.
Indeed, both TNF and IL-6 were highest in the sleep apneics,
whereras in the BMI-matched obese controls, the cytokine values were
intermediate between those of normal weight controls and apneics. In a
previous study we demonstrated that plasma levels of TNF and IL-6
were elevated in sleep apnea, with a positive correlation to BMI (6).
This study confirms our earlier findings and suggests that the
elevation of both cytokines in sleep apnea has an additional component
that is independent of obesity. Although the mean plasma IL-6 levels of
obese controls were not significantly different from the sleep apnea or
the normal weight control groups, they were approximately equidistant
from those of the other two groups, both in absolute terms and as
estimated differences generated by the MANOVA. In addition, the TNF
values for the obese controls were actually closer to the normal weight
control values than to values in the sleep apnea group. These data
support a typical dose-response pattern. The fact that the sleep apneic
and nonsleep apneic obese patients had similar BMIs and body weights
further supports the conclusion that sleep apnea represents an
additional independent factor leading to elevations of the inflammatory
cytokines. One possible reason why the plasma cytokine concentrations
of obese controls were not significantly different from those of the
two extreme groups could have been the sample size.
We previously proposed that cytokines, particularly TNF and IL-6,
may mediate daytime sleepiness associated with disorders of excessive
daytime sleepiness (EDS), such as sleep apnea or obesity (6). An
important question is whether the observed peripheral elevation of
cytokines in the patients with EDS is of any relevance to phenomena
generated in the brain, e.g. sleep and sleepiness. It is
possible that the observed increases in inflammatory cytokines in the
plasma of patients with EDS may, in fact, reflect much higher
elevations in the production and/or target sites of these cytokines, in
this case the central nervous system. Furthermore, there are several
ways that peripheral cytokines can communicate and signal the brain to
elicit central nervous system manifestations, e.g.
sleepiness, including acting in areas outside the blood-brain barrier
(periventricular organs), crossing the blood-brain barrier (18, 19),
and through peripheral autonomic afferent nerves (20). Indeed, even
small doses of IL-1 administered peripherally in rats can produce sleep
(20).
In this study we also demonstrated that leptin was significantly
increased in sleep apneics compared to levels in both BMI-matched obese
and normal weight subjects. Leptin is elevated in obese subjects in
proportion to their BMI or percent body fat (12), and its secretion is
further modulated by the stress system and cytokines (9, 21). Our study
suggests that the increase in leptin levels in sleep apnea is possibly
related to the higher amount of visceral fat and/or cytokines in this
group. We also demonstrated that not only the amount but also the daily
patterns of TNF, IL-6, and leptin secretion were disturbed in sleep
apneics and obese controls. The relative increase in the evening levels
of these hormones in apneics and obese subjects may contribute to
pathological manifestations in the cardiovascular system, including
nighttime elevation of blood pressure (22, 23).
Our sleep apneics had significantly higher fasting plasma insulin levels than BMI-matched obese controls. Previous studies reported inconsistent results in terms of an association between sleep apnea and insulin resistance. A large study showed a modest relation (r2 = 0.10) between the A/HI and fasting insulin levels, but not fasting blood glucose levels (24). Two other studies showed an association between severity of sleep apnea and indexes of insulin resistance (25) and that sleep apnea occurred commonly in obese patients with diabetes type II who had excessive daytime sleepiness or heavy snoring (26). In contrast, two other controlled studies suggested that the relation between sleep apnea and plasma insulin levels (4) or insulin resistance (5) reflected the known effects of obesity. However, in one of these studies the apneics were otherwise healthy normotensive individuals (5), whereas in the second one they were lean and less symptomatic than our patients (4).
Our study demonstrated that in obese patients with significant sleep apnea (diagnosed on the basis of both clinical and laboratory criteria), nocturnal sleep and respiratory disturbances were strong independent risk factors for hyperinsulinemia. The independent effects of these disturbances could be explained by microawakening- and/or hypoxia-related nocturnal increases in sympathetic system and hypothalamic-pituitary-adrenal axis activities. The fact that two previous studies showed no effect of treatment of apnea on insulin levels may be due either to the short term assessment of these effects (27, 28) or to the fact that the currently available treatments for sleep apnea are not effective in reversing the metabolic manifestations of this disorder, particularly when the disorder has existed for several years and has led to an adverse and probably irreversible redistribution of fat.
Previous studies have shown that obesity is a significant risk factor for sleep apnea (1, 2, 16, 29). Our study suggests that among obese individuals, it is visceral fat, rather than generalized obesity, that predisposes to the development of sleep apnea. Our sleep apneics had a significantly higher amount of visceral fat compared to our obese control subjects, whereas there were no differences between the two groups in terms of BMI or amount of sc or total body fat. Central obesity with increased visceral fat is closely associated with insulin resistance, dyslipidemia, hypertension, diabetes mellitus type II, and their cardiovascular sequelae (3). Our study suggests that visceral fat may also play a significant role in the development of sleep apnea.
Our overall findings indicate that sleep apnea in obese middle-aged men is associated with visceral obesity, inflammatory cytokine elevations, hyperleptinemia, and hyperinsulinemia. It appears that visceral obesity/insulin resistance determined by both genetic/constitutional and environmental factors may be the principal culprits, progressively leading to worsening metabolic syndrome manifestations and sleep apnea. Progressive deterioration of sleep apnea may then accelerate the worsening of visceral obesity and the metabolic syndrome by providing a stress stimulus and causing nocturnal elevations of hormones, such as cortisol and insulin, that promote visceral adiposity, metabolic abnormalities, and cardiovascular complications (30, 31).
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Acknowledgments |
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Received June 16, 1999.
Revised November 19, 1999.
Accepted December 3, 1999.
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G. K. Sakkas, K. I. Gourgoulianis, C. Karatzaferi, V. Liakopoulos, M. D. Maridaki, C. Pastaka, E. Lavdas, B. J. Soher, S. Dovas, I. Fezoulidis, et al. Haemodialysis patients with sleep apnoea syndrome experience increased central adiposity and altered muscular composition and functionality Nephrol. Dial. Transplant., January 1, 2008; 23(1): 336 - 344. [Abstract] [Full Text] [PDF]
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 D E J Jones Pathogenesis of primary biliary cirrhosis Postgrad. Med. J., January 1, 2008; 84(987): 23 - 33. [Full Text] [PDF]
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B. Buyse and the participants of working group 2 Treatment effects of sleep apnoea: where are we now? Eur. Respir. Rev., December 1, 2007; 16(106): 146 - 168. [Abstract] [Full Text] [PDF]
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I. A. Harsch Metabolic disturbances in patients with obstructive sleep apnoea syndrome Eur. Respir. Rev., December 1, 2007; 16(106): 196 - 202. [Abstract] [Full Text] [PDF]
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 A. N. Vgontzas, S. Pejovic, E. Zoumakis, H.-M. Lin, C. M. Bentley, E. O. Bixler, A. Sarrigiannidis, M. Basta, and G. P. Chrousos Hypothalamic-Pituitary-Adrenal Axis Activity in Obese Men with and without Sleep Apnea: Effects of Continuous Positive Airway Pressure Therapy J. Clin. Endocrinol. Metab., November 1, 2007; 92(11): 4199 - 4207. [Abstract] [Full Text] [PDF]
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 D. E J Jones Pathogenesis of Primary Biliary Cirrhosis Gut, November 1, 2007; 56(11): 1615 - 1624. [Full Text] [PDF]
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J. Ye, Z. Gao, J. Yin, and Q. He Hypoxia is a potential risk factor for chronic inflammation and adiponectin reduction in adipose tissue of ob/ob and dietary obese mice Am J Physiol Endocrinol Metab, October 1, 2007; 293(4): E1118 - E1128. [Abstract] [Full Text] [PDF]
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 M. L. Okun, M. Hall, and M. E. Coussons-Read Sleep Disturbances Increase Interleukin-6 Production During Pregnancy: Implications for Pregnancy Complications Reproductive Sciences, September 1, 2007; 14(6): 560 - 567. [Abstract] [PDF]
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A. Campo, G. Fruhbeck, J. J. Zulueta, J. Iriarte, L. M. Seijo, A. B. Alcaide, J. B. Galdiz, and J. Salvador Hyperleptinaemia, respiratory drive and hypercapnic response in obese patients Eur. Respir. J., August 1, 2007; 30(2): 223 - 231. [Abstract] [Full Text] [PDF]
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V. Savransky, A. Nanayakkara, J. Li, S. Bevans, P. L. Smith, A. Rodriguez, and V. Y. Polotsky Chronic Intermittent Hypoxia Induces Atherosclerosis Am. J. Respir. Crit. Care Med., June 15, 2007; 175(12): 1290 - 1297. [Abstract] [Full Text] [PDF]
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 E. R. Chasens Obstructive Sleep Apnea, Daytime Sleepiness, and Type 2 Diabetes The Diabetes Educator, May 1, 2007; 33(3): 475 - 482. [Abstract] [Full Text] [PDF]
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 E. Cereda and A. E. Malavazos A Possible Role of Visceral Fat-Related Inflammation in Linking Obstructive Sleep Apnea to Left Ventricular Hypertrophy Hypertension, April 1, 2007; 49(4): e23 - e23. [Full Text] [PDF]
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 S. L Verhulst, N. Schrauwen, D. Haentjens, B. Suys, R. P Rooman, L. Van Gaal, W. A De Backer, and K. N Desager Sleep-disordered breathing in overweight and obese children and adolescents: prevalence, characteristics and the role of fat distribution Arch. Dis. Child., March 1, 2007; 92(3): 205 - 208. [Abstract] [Full Text] [PDF]
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 A. S. Gami, D. O. Hodge, R. M. Herges, E. J. Olson, J. Nykodym, T. Kara, and V. K. Somers Obstructive Sleep Apnea, Obesity, and the Risk of Incident Atrial Fibrillation J. Am. Coll. Cardiol., February 6, 2007; 49(5): 565 - 571. [Abstract] [Full Text] [PDF]
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N. McArdle, D. Hillman, L. Beilin, and G. Watts Metabolic Risk Factors for Vascular Disease in Obstructive Sleep Apnea: A Matched Controlled Study Am. J. Respir. Crit. Care Med., January 15, 2007; 175(2): 190 - 195. [Abstract] [Full Text] [PDF]
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W. T. McNicholas, M. R. Bonsignore, and the Management Committee of EU COST ACTION B26 Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities Eur. Respir. J., January 1, 2007; 29(1): 156 - 178. [Abstract] [Full Text] [PDF]
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A. N. Vgontzas, S. Pejovic, E. Zoumakis, H. M. Lin, E. O. Bixler, M. Basta, J. Fang, A. Sarrigiannidis, and G. P. Chrousos Daytime napping after a night of sleep loss decreases sleepiness, improves performance, and causes beneficial changes in cortisol and interleukin-6 secretion Am J Physiol Endocrinol Metab, January 1, 2007; 292(1): E253 - E261. [Abstract] [Full Text] [PDF]
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 R. Wolk and V. K. Somers Sleep Apnoea & Hypertension: Physiological bases for a causal relation: Sleep and the metabolic syndrome Exp Physiol, January 1, 2007; 92(1): 67 - 78. [Abstract] [Full Text] [PDF]
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 A. G. Hoppin, E. S. Katz, L. M. Kaplan, and G. Y. Lauwers Case 31-2006 -- A 15-Year-Old Girl with Severe Obesity. N. Engl. J. Med., October 12, 2006; 355(15): 1593 - 1602. [Full Text] [PDF]
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S. Ryan, C. T. Taylor, and W. T. McNicholas Predictors of Elevated Nuclear Factor-{kappa}B-dependent Genes in Obstructive Sleep Apnea Syndrome Am. J. Respir. Crit. Care Med., October 1, 2006; 174(7): 824 - 830. [Abstract] [Full Text] [PDF]
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 R. Mehra, A. Storfer-Isser, H. L. Kirchner, N. Johnson, N. Jenny, R. P. Tracy, and S. Redline Soluble interleukin 6 receptor: a novel marker of moderate to severe sleep-related breathing disorder. Arch Intern Med, September 18, 2006; 166(16): 1725 - 1731. [Abstract] [Full Text] [PDF]
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K. L. Knutson, A. M. Ryden, B. A. Mander, and E. Van Cauter Role of sleep duration and quality in the risk and severity of type 2 diabetes mellitus. Arch Intern Med, September 18, 2006; 166(16): 1768 - 1774. [Abstract] [Full Text] [PDF]
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Z. T. Bloomgarden Third Annual World Congress on the Insulin Resistance Syndrome: Associated conditions. Diabetes Care, September 1, 2006; 29(9): 2165 - 2174. [Full Text] [PDF]
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K. A. Waters, S. Sitha, L. M. O'Brien, S. Bibby, C. de Torres, S. Vella, and R. de la Eva Follow-up on Metabolic Markers in Children Treated for Obstructive Sleep Apnea Am. J. Respir. Crit. Care Med., August 15, 2006; 174(4): 455 - 460. [Abstract] [Full Text] [PDF]
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 D. Chida, T. Osaka, O. Hashimoto, and Y. Iwakura Combined interleukin-6 and interleukin-1 deficiency causes obesity in young mice. Diabetes, April 1, 2006; 55(4): 971 - 977. [Abstract] [Full Text] [PDF]
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 C Heesen, L Nawrath, C Reich, N Bauer, K-H Schulz, and S M Gold Fatigue in multiple sclerosis: an example of cytokine mediated sickness behaviour? J. Neurol. Neurosurg. Psychiatry, January 1, 2006; 77(1): 34 - 39. [Abstract] [Full Text] [PDF]
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D. P. White Sleep apnea. Proceedings of the ATS, January 1, 2006; 3(1): 124 - 128. [Abstract] [Full Text] [PDF]
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E. Tasali, E. Van Cauter, and D. A. Ehrmann Relationships between Sleep Disordered Breathing and Glucose Metabolism in Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., January 1, 2006; 91(1): 36 - 42. [Abstract] [Full Text] [PDF]
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N. M. Punjabi and V. Y. Polotsky Disorders of glucose metabolism in sleep apnea J Appl Physiol, November 1, 2005; 99(5): 1998 - 2007. [Abstract] [Full Text] [PDF]
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K. Spiegel, K. Knutson, R. Leproult, E. Tasali, and E. V. Cauter Sleep loss: a novel risk factor for insulin resistance and Type 2 diabetes J Appl Physiol, November 1, 2005; 99(5): 2008 - 2019. [Abstract] [Full Text] [PDF]
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J. Li, D. N. Grigoryev, S. Q. Ye, L. Thorne, A. R. Schwartz, P. L. Smith, C. P. O'Donnell, and V. Y. Polotsky Chronic intermittent hypoxia upregulates genes of lipid biosynthesis in obese mice J Appl Physiol, November 1, 2005; 99(5): 1643 - 1648. [Abstract] [Full Text] [PDF]
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C. Bjorkelund, D. Bondyr-Carlsson, L. Lapidus, L. Lissner, J. Mansson, I. Skoog, and C. Bengtsson Sleep Disturbances in Midlife Unrelated to 32-Year Diabetes Incidence: The prospective Population Study of Women in Gothenburg Diabetes Care, November 1, 2005; 28(11): 2739 - 2744. [Abstract] [Full Text] [PDF]
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R. L. Riha, P. Brander, M. Vennelle, N. McArdle, S. M. Kerr, N. H. Anderson, and N. J. Douglas Tumour necrosis factor-{alpha} (-308) gene polymorphism in obstructive sleep apnoea-hypopnoea syndrome Eur. Respir. J., October 1, 2005; 26(4): 673 - 678. [Abstract] [Full Text] [PDF]
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 J. F. Wilson Is Sleep the New Vital Sign? Ann Intern Med, May 17, 2005; 142(10): 877 - 880. [Full Text] [PDF]
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T. M. Buckley and A. F. Schatzberg On the Interactions of the Hypothalamic-Pituitary-Adrenal (HPA) Axis and Sleep: Normal HPA Axis Activity and Circadian Rhythm, Exemplary Sleep Disorders J. Clin. Endocrinol. Metab., May 1, 2005; 90(5): 3106 - 3114. [Abstract] [Full Text] [PDF]
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W. Lim, S. Hong, R. Nelesen, and J. E. Dimsdale The Association of Obesity, Cytokine Levels, and Depressive Symptoms With Diverse Measures of Fatigue in Healthy Subjects Arch Intern Med, April 25, 2005; 165(8): 910 - 915. [Abstract] [Full Text] [PDF]
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A. M. W. Petersen and B. K. Pedersen The anti-inflammatory effect of exercise J Appl Physiol, April 1, 2005; 98(4): 1154 - 1162. [Abstract] [Full Text] [PDF]
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 E. R. Chasens, A. I. Pack, G. Maislin, D. F. Dinges, and T. E. Weaver Claustrophobia and Adherence to CPAP Treatment West J Nurs Res, April 1, 2005; 27(3): 307 - 321. [Abstract] [PDF]
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S. Teramoto, H. Yamamoto, Y. Yamaguchi, R. Namba, and Y. Ouchi Obstructive Sleep Apnea Causes Systemic Inflammation and Metabolic Syndrome Chest, March 1, 2005; 127(3): 1074 - 1075. [Full Text] [PDF]
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A. R. Babu, J. Herdegen, L. Fogelfeld, S. Shott, and T. Mazzone Type 2 Diabetes, Glycemic Control, and Continuous Positive Airway Pressure in Obstructive Sleep Apnea Arch Intern Med, February 28, 2005; 165(4): 447 - 452. [Abstract] [Full Text] [PDF]
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C. Shin, J. Kim, J. Kim, S. Lee, J. Shim, K. In, K. Kang, S. Yoo, N. Cho, K. Kimm, et al. Association of Habitual Snoring with Glucose and Insulin Metabolism in Nonobese Korean Adult Men Am. J. Respir. Crit. Care Med., February 1, 2005; 171(3): 287 - 291. [Abstract] [Full Text] [PDF]
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A. Barcelo, F. Barbe, E. Llompart, M. de la Pena, J. Duran-Cantolla, A. Ladaria, M. Bosch, L. Guerra, and A. G. N. Agusti Neuropeptide Y and Leptin in Patients with Obstructive Sleep Apnea Syndrome: Role of Obesity Am. J. Respir. Crit. Care Med., January 15, 2005; 171(2): 183 - 187. [Abstract] [Full Text] [PDF]
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T. Vassilakopoulos, C. Roussos, and S. Zakynthinos The immune response to resistive breathing Eur. Respir. J., December 1, 2004; 24(6): 1033 - 1043. [Abstract] [Full Text] [PDF]
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F. Series, J. Chakir, and D. Boivin Influence of Weight and Sleep Apnea Status on Immunologic and Structural Features of the Uvula Am. J. Respir. Crit. Care Med., November 15, 2004; 170(10): 1114 - 1119. [Abstract] [Full Text] [PDF]
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 M. Ekstedt, T. Akerstedt, and M. Soderstrom Microarousals During Sleep Are Associated With Increased Levels of Lipids, Cortisol, and Blood Pressure Psychosom Med, November 1, 2004; 66(6): 925 - 931. [Abstract] [Full Text] [PDF]
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P. M. Nilsson, M. Roost, G. Engstrom, B. Hedblad, and G. Berglund Incidence of Diabetes in Middle-Aged Men Is Related to Sleep Disturbances Diabetes Care, October 1, 2004; 27(10): 2464 - 2469. [Abstract] [Full Text] [PDF]
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N. M. Punjabi, E. Shahar, S. Redline, D. J. Gottlieb, R. Givelber, and H. E. Resnick Sleep-Disordered Breathing, Glucose Intolerance, and Insulin Resistance: The Sleep Heart Health Study Am. J. Epidemiol., September 15, 2004; 160(6): 521 - 530. [Abstract] [Full Text] [PDF]
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A. N. Vgontzas, E. Zoumakis, H.-M. Lin, E. O. Bixler, G. Trakada, and G. P. Chrousos Marked Decrease in Sleepiness in Patients with Sleep Apnea by Etanercept, a Tumor Necrosis Factor-{alpha} Antagonist J. Clin. Endocrinol. Metab., September 1, 2004; 89(9): 4409 - 4413. [Abstract] [Full Text] [PDF]
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T. Vassilakopoulos, M. Divangahi, G. Rallis, O. Kishta, B. Petrof, A. Comtois, and S. N. A. Hussain Differential Cytokine Gene Expression in the Diaphragm in Response to Strenuous Resistive Breathing Am. J. Respir. Crit. Care Med., July 15, 2004; 170(2): 154 - 161. [Abstract] [Full Text] [PDF]
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U. Hatipoglu and I. Rubinstein Inflammation and Obstructive Sleep Apnea Syndrome: How Many Ways Do I Look at Thee? Chest, July 1, 2004; 126(1): 1 - 2. [Full Text] [PDF]
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L. J. Palmer, S. G. Buxbaum, E. K. Larkin, S. R. Patel, R. C. Elston, P. V. Tishler, and S. Redline Whole Genome Scan for Obstructive Sleep Apnea and Obesity in African-American Families Am. J. Respir. Crit. Care Med., June 15, 2004; 169(12): 1314 - 1321. [Abstract] [Full Text] [PDF]
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C. E. Juge-Aubry, E. Somm, R. Chicheportiche, D. Burger, A. Pernin, B. Cuenod-Pittet, P. Quinodoz, V. Giusti, J.-M. Dayer, and C. A. Meier Regulatory Effects of Interleukin (IL)-1, Interferon-{beta}, and IL-4 on the Production of IL-1 Receptor Antagonist by Human Adipose Tissue J. Clin. Endocrinol. Metab., June 1, 2004; 89(6): 2652 - 2658. [Abstract] [Full Text] [PDF]
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K. M. Oltmanns, H. Gehring, S. Rudolf, B. Schultes, S. Rook, U. Schweiger, J. Born, H. L. Fehm, and A. Peters Hypoxia Causes Glucose Intolerance in Humans Am. J. Respir. Crit. Care Med., June 1, 2004; 169(11): 1231 - 1237. [Abstract] [Full Text] [PDF]
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 S. R Coughlin, L. Mawdsley, J. A Mugarza, P. M.A Calverley, and J. P.H Wilding Obstructive sleep apnoea is independently associated with an increased prevalence of metabolic syndrome Eur. Heart J., May 1, 2004; 25(9): 735 - 741. [Abstract] [Full Text] [PDF]
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A. N. Vgontzas, E. Zoumakis, E. O. Bixler, H.-M. Lin, H. Follett, A. Kales, and G. P. Chrousos Adverse Effects of Modest Sleep Restriction on Sleepiness, Performance, and Inflammatory Cytokines J. Clin. Endocrinol. Metab., May 1, 2004; 89(5): 2119 - 2126. [Abstract] [Full Text] [PDF]
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S. Teramoto, H. Yamamoto, Y. Ouchi, K.-i. Inoue, H. Takano, and T. Yoshika Increased Plasma Interleukin-6 Is Associated With the Pathogenesis of Obstructive Sleep Apnea Syndrome Chest, May 1, 2004; 125(5): 1964 - 1965. [Full Text] [PDF]
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B.M. Sanner, P. Kollhosser, N. Buechner, W. Zidek, and M. Tepel Influence of treatment on leptin levels in patients with obstructive sleep apnoea Eur. Respir. J., April 1, 2004; 23(4): 601 - 604. [Abstract] [Full Text] [PDF]
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T. You, D. M. Berman, A. S. Ryan, and B. J. Nicklas Effects of Hypocaloric Diet and Exercise Training on Inflammation and Adipocyte Lipolysis in Obese Postmenopausal Women J. Clin. Endocrinol. Metab., April 1, 2004; 89(4): 1739 - 1746. [Abstract] [Full Text] [PDF]
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 P. Flachenecker, I. Bihler, F Weber, M Gottschalk, K. V Toyka, and P. Rieckmann Cytokine mRNA expression in patients with multiple sclerosis and fatigue Multiple Sclerosis, April 1, 2004; 10(2): 165 - 169. [Abstract] [PDF]
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J. C. Pickup Inflammation and Activated Innate Immunity in the Pathogenesis of Type 2 Diabetes Diabetes Care, March 1, 2004; 27(3): 813 - 823. [Abstract] [Full Text] [PDF]
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H. K. Meier-Ewert, P. M. Ridker, N. Rifai, M. M. Regan, N. J. Price, D. F. Dinges, and J. M. Mullington Effect of sleep loss on C-Reactive protein, an inflammatory marker of cardiovascular risk J. Am. Coll. Cardiol., February 18, 2004; 43(4): 678 - 683. [Abstract] [Full Text] [PDF]
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I. A. Harsch, S. P. Schahin, M. Radespiel-Troger, O. Weintz, H. Jahreiss, F. S. Fuchs, G. H. Wiest, E. G. Hahn, T. Lohmann, P. C. Konturek, et al. Continuous Positive Airway Pressure Treatment Rapidly Improves Insulin Sensitivity in Patients with Obstructive Sleep Apnea Syndrome Am. J. Respir. Crit. Care Med., January 15, 2004; 169(2): 156 - 162. [Abstract] [Full Text] [PDF]
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 K. Ahlberg, T. Ekman, and F. Gaston-Johansson Levels of Fatigue Compared to Levels of Cytokines and Hemoglobin during Pelvic Radiotherapy: a Pilot Study Biol Res Nurs, January 1, 2004; 5(3): 203 - 210. [Abstract] [PDF]
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A. Bradford Festschrift for R. G. O'Regan - Sensing and adaptation to alterations in respiratory gases: oxygen and carbon dioxide: Effects of chronic intermittent asphyxia on haematocrit, pulmonary arterial pressure and skeletal muscle structure in rats Exp Physiol, January 1, 2004; 89(1): 44 - 52. [Abstract] [Full Text] [PDF]
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A. V. Chobanian, G. L. Bakris, H. R. Black, W. C. Cushman, L. A. Green, J. L. Izzo Jr, D. W. Jones, B. J. Materson, S. Oparil, J. T. Wright Jr, et al. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure Hypertension, December 1, 2003; 42(6): 1206 - 1252. [Abstract] [Full Text] [PDF]
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 A. S. M. Shamsuzzaman, B. J. Gersh, and V. K. Somers Obstructive Sleep Apnea: Implications for Cardiac and Vascular Disease JAMA, October 8, 2003; 290(14): 1906 - 1914. [Abstract] [Full Text] [PDF]
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E. R. Chasens, T. E. Weaver, and M. G. Umlauf Insulin Resistance and Obstructive Sleep Apnea: Is Increased Sympathetic Stimulation the Link? Biol Res Nurs, October 1, 2003; 5(2): 87 - 96. [Abstract] [PDF]
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 V. Y Polotsky, J. Li, N. M Punjabi, A. E Rubin, P. L Smith, A. R Schwartz, and C. P O'Donnell Intermittent Hypoxia Increases Insulin Resistance in Genetically Obese Mice J. Physiol., October 1, 2003; 552(1): 253 - 264. [Abstract] [Full Text] [PDF]
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K. Stenlof, I. Wernstedt, T. Fjallman, V. Wallenius, K. Wallenius, and J.-O. Jansson Interleukin-6 Levels in the Central Nervous System Are Negatively Correlated with Fat Mass in Overweight/Obese Subjects J. Clin. Endocrinol. Metab., September 1, 2003; 88(9): 4379 - 4383. [Abstract] [Full Text] [PDF]
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P. Y. Liu, B. Yee, S. M. Wishart, M. Jimenez, D. G. Jung, R. R. Grunstein, and D. J. Handelsman The Short-Term Effects of High-Dose Testosterone on Sleep, Breathing, and Function in Older Men J. Clin. Endocrinol. Metab., August 1, 2003; 88(8): 3605 - 3613. [Abstract] [Full Text] [PDF]
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G. D. Foster Principles and Practices in the Management of Obesity Am. J. Respir. Crit. Care Med., August 1, 2003; 168(3): 274 - 280. [Full Text] [PDF]
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L. Dyugovskaya, P. Lavie, and L. Lavie Phenotypic and Functional Characterization of Blood {gamma}{delta} T Cells in Sleep Apnea Am. J. Respir. Crit. Care Med., July 15, 2003; 168(2): 242 - 249. [Abstract] [Full Text] [PDF]
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N. Meslier, F. Gagnadoux, P. Giraud, C. Person, H. Ouksel, T. Urban, and J-L. Racineux Impaired glucose-insulin metabolism in males with obstructive sleep apnoea syndrome Eur. Respir. J., July 1, 2003; 22(1): 156 - 160. [Abstract] [Full Text] [PDF]
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