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Sleep-related breathing disorders, loud snoring and excessive daytime sleepiness in obese subjects


OBJECTIVE: To investigate the prevalence of sleep breathing disorders, loud snoring and excessive daytime sleepiness in a group of obese subjects, and to identify the predictors of obstructive sleep apnea (OSA) severity in these patients.

SUBJECTS: A total of 161 consecutive obese patients (body mass index (BMI)≥30.0 kg/m2), ranging between 30.0 and 67.3, represented by 57 men and 104 women, aged 16–75 y. Forty (15 men and 25 women) age-matched (20–70 y) nonobese (BMI<27 kg/m2) volunteers were also recruited for the study.

MEASUREMENTS: Respiratory function parameters, nocturnal sleep quality (evaluated by a specific questionnaire), nocturnal hypoventilation and OSA (evaluated by night polysomnography) were examined in all subjects. Anthropometric parameters (neck circumference, waist circumference, waist-to-hip ratio) were also investigated.

RESULTS: Eighty-three obese patients (51.5% of the obese group) had a respiratory disturbance index (RDI)≥10, corresponding to a moderate or severe sleep apnea. In particular, 24.8% (40/161), ie a quarter of all obese patients, were affected by severe OSA and this alteration was present in 42.1% of obese men (24/57) and in 15.4% (16/104) of obese women. When a stepwise multiple regression analysis was performed, neck circumference in men and BMI in women were shown to be the strongest predictors of sleep apnea. Twenty-nine percent of all obese subjects (40.3% of men and 23.1% of women) showed nocturnal hypoventilation; however, it was present as a unique breathing alteration in only 5% of the obese population. The percentage of patients having excessive daytime sleepiness was significantly higher than in nonobese subjects, even when only nonapneic obese patients were considered (P<0.001).

CONCLUSION: This study shows that OSA is present in more than 50% of a population of obese patients with a mean BMI higher than 40.0, this percentage being much higher than that commonly reported in previous studies, particularly in women. Neck circumference in men and BMI in women seem to be the strongest predictors of the severity of OSA in obese patients. Nocturnal hypoventilation seems to be present in more than 29% of a severe obese population. Moreover, this study indicates that morbid obesity can be associated with excessive daytime sleepiness even in the absence of sleep apnea.


Obesity is an independent risk factor for the development of cardiovascular diseases,1 and several studies have demonstrated that visceral obesity, in particular, is strongly associated with the prevalence of coronary heart disease.23,4,5 Obstructive sleep apnea (OSA) is a well-known cardiovascular risk factor5,6,7 and, even though obesity is not essential for the development of OSA, a significant percentage of patients with OSA are obese and the onset of sleep apnea frequently follows a marked increase in body weight.8,9,10 Moreover, weight loss in obese patients with OSA can eliminate this condition and ameliorate pulmonary function and gas exchange abnormalities.11,12,13 However, information on the prevalence of sleep breathing disorders, snoring and daytime sleepiness in obese patients are conflicting. Vgontzas et al showed that 40% of obese men and only 3% of obese women are affected by OSA with such severity to require therapeutic intervention.14 In another study, sleep apnea was diagnosed in 77% of obese men and in 7% of obese women.11 By contrast, Richman et al found that about 40% of obese women had OSA.15 Daytime sleepiness and fatigue are also a frequent complaint of obese people. In this regard, Vgontzas et al recently reported that obese patients can be sleepier than normal-weight controls during the daytime even if they do not demonstrate any degree of sleep disorder breathing.16

This study, performed by full-night polysomnography, aimed to investigate the prevalence and severity of sleep breathing disorder and loud snoring in obese patients, and the possible independent influence of body mass index (BMI) and body fat distribution on these alterations. The possibility of a difference in daytime sleepiness between nonapnoeic obese and normal-weight subjects was also examined.

Patients and methods


A total of 187 obese patients (BMI≥30.0 kg/m2), 67 men and 120 women, aged 16–75 y, were consecutively recruited at the Outpatient Clinic for the Study of Obesity, Institute of Internal Medicine, Endocrinology and Metabolic Diseases, University of Bari, School of Medicine, over a 5 y period. Sixteen of these patients refused to participate in the study because of poor compliance, personal reasons or lack of time. In all, 171 obese patients accepted to undergo the overnight sleep study protocol, performed at the Sleep Laboratory of Respiratory Diseases, University of Bari, School of Medicine. A further 10 patients were excluded because they could not sleep in a supine position, did not reach the rapid eyes movement sleep stage (REM) during polysomnography or had a total sleep time (TST) lower than 3 h per night. Finally, 161 obese subjects underwent the complete study; they were 57 men and 104 women, aged 16–75 y, with BMI ranging between 30.0 and 67.3. It is noteworthy that more than 50% were morbidly obese patients (BMI>40.0; Table 1).

Table 1 Characteristics of 161 obese subjects

Control subjects consisted of 40 nonobese subjects (BMI<27 kg/m2, ranging between 19.0 and 26.7), 25 women and 15 men, aged 20–70 y (mean age 43.3±13.0). These were healthy volunteers, consecutively recruited from physicians and medical students and had no sleep complaints and were in good general health. The study was approved by the local Ethical Committee and all subjects gave informed consent to the study.

A complete physical examination was performed, including neurological, cardiopulmonary, and ear nose and throat evaluations. For the clinical laboratory examination, pulmonary function tests, ECG and thyroid echography were performed. None of the subjects participating in the study had a previous diagnosis of sleep apnea or was spontaneously complaining of sleep apnea signs or symptoms. Moreover, none of them showed any clinical endocrinological disease, narcolepsy or idiopathic hypersomnia, neuromuscular disease, psychiatric disorders, overt cardiopulmonary disease, airway obstruction (FEV1/FVC<70%), anatomic maxillo-mandibular skeletal abnormalities, heavy ear, nose and throat pathology, abuse of alcohol or of any kind of drug. None of women were pregnant.

None of participants had diabetes mellitus in accordance with the Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus17 or positive clinical history of stroke, transient ischemic attack, angina pectoris, heart infarction, claudicatio intermittens, congenital heart disease or ECG abnormalities.

Biochemical markers of thyroid, liver and kidney function were within the normal range in all subjects. During the testing period, all subjects were asked to keep their normal mixed diet and not to perform any sport activity.

Anthropometric parameters

Central fat accumulation was evaluated by the waist circumference, measured as the midway between the lower rib margin and the superior anterior iliac spine. Hip circumference was evaluated at the widest circumference overt the great trochanter. The waist-to-hip circumference ratio (WHR) was also calculated. Neck circumference was determined at the level of the cricothyroid membrane, and the percentage of predicted normal neck circumference (PPNC) was calculated according to the method of Davies and Stradling.18 Blood pressure was recorded on at least three different occasions, using a mercury manometer with an appropriate cuff size.

Respiratory function data

A flow volume spirometry was performed with the patient in the sitting position and by using a pneumotachograph spyrometer connected to a microcomputer system (PK Morgan Ltd, Gillingham, Kent, England). The values reported by Vilijanen were used as references.19

Forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) were measured, and the FEV1/FVC ratio was calculated. Functional residual capacity (FRC), residual volume (RV) and total lung capacity (TLC) were measured by the helium equilibration method, by using a ‘pulmonary function laboratory 2400’ (Sensor Medics, Bilthooven, The Netherlands). The mean of three different determinations was recorded for all the above parameters.

Arterial blood samples were drawn from the brachial or the radial artery for blood gas analysis, after the patient had been in the supine position for at least 3 min. Arterial blood paCO2, paO2, pH and base excess were analyzed by an automatic acid–base analyser (ABL 30 Radiometer, Copenhagen, Denmark). The alveolar–arterial pO2 difference ((A-a) O2 gradient) was calculated, paO2 being obtained from the ideal alveolar air equation.20 These measurements were performed in the evening, just before the sleep study.

Measurement of sleep-related symptoms

All obese and control subjects were interviewed in the presence of their partners, and they were also required to fill out a comprehensive questionnaire, which was a modified version of the Sleep and the Health Questionnaire.21 Information concerning sleep habits, snoring and daytime sleepiness were obtained. Loud snoring was assessed by the question ‘Has your snoring ever been so loud that it has disturbed others?’ Daytime sleepiness was assessed by the question ‘Over the last month, have you experienced excessive sleepiness during the day or during your normal working hours?’ Moreover, the subjects were requested to quantitate the frequency of symptoms with the use of a four-point scale (patient score) that included the responses: never=0; sometimes (1–2 times per week)=1; frequently (3–4 times per week)=2; almost always or always (5–7 times per week)=3. Finally, the Epwort Sleepiness Scale (ESS) was used to measure the sleep propensity.22 The ESS has been tested previously in both healthy subjects and patients with different kinds of sleep disorders.23,24

Measurement of sleep disorders of breathing

All subjects were evaluated in the sleep laboratory (Sleep Laboratory of Respiratory Diseases, University of Bari, School of Medicine) for one night, and they were monitored continuously for 8 h using a 12 channel polysomnograph (Vitalog HMS 5000, Vitalog Monitoring Inc., Redwood City, California, USA). Polysomnography was performed after a night of adaptation in the hospital. Electroencephalographic, electrooculographic and chin electromyographic recordings were obtained with surface electrodes according to standard methods.25 Airflow was monitored by thermocouples placed at the nose and at the mouth. Abdominal and ribcage movements were assessed by respiratory inductive plethysmography with recording of paradoxical breathing. All night recordings of hemoglobin oxygen saturation were obtained by finger pulse oxymetry. Snoring sound (by a microphone attached to the neck), electrocardiography and sleeping position were also recorded. Transcutaneous CO2 was measured by a Radiometer apparatus (Radiometer TC 100, Copenhagen, Denmark).

Respiratory events (apnea or hypopnea) were defined as cessation or discrete reduction (two-thirds) of airflow and/or abdominal ribcage movements lasting ≥10 s, and associated with a decrease greater than 2.5% in oxygen saturation.

Since more than 85% of respiratory events were obstructive (characterised by an increasing ventilatory effort and paradoxical breathing), the specific pattern of apnea episodes was not taken into account in the statistical analysis. The number of events per hour was obtained by dividing the total number of events per the TST and was defined as the respiratory disturbances index (RDI). On this basis, according to a paper by Grunstein et al,26 subjects were divided into three groups: non-apneic (RDI<10); with moderate sleep apnea (RDI between 10 and 29); and with severe sleep apnea (RDI≥30), Oxyhemoglobin desaturation was evaluated in terms of the percentage of total sleep time with oxyhemoglobin saturation<90% (TSTSaO2<90%). Hypoventilation was defined as a period of persistent (≥2 min) discrete reduction (two-thirds) of abdominal ribcage excursion, associated with persistent sustained oxygen desaturation of 10% and a mean increase of transcutaneous CO2>7 mmHg.27,28,29 Subjects having 15% of total sleep time as hypoventilation were diagnosed as patients with nocturnal hypoventilation (nHyp). To simplify analysis, sleep was divided into that with nonrapid eyes movements (NREM) and in that with REM; then, the percentage of NREM and REM of the TST was calculated. Sleep efficiency (SE) was defined as the percentage of TST of the time spent in the bed. Sleep record was scored according to standardised criteria.25

Statistical analysis

Statistical analysis was performed using the STATISTICA® 6.0 for Windows, StatSoft Inc. (1995) software (Tulsa, OK, USA). Results are presented as mean±standard deviation (s.d.). Comparisons between two groups were performed by using Student's t-test for unpaired data, whereas comparisons among three groups were carried out by analysis of variance or χ2 test, when appropriate. Pearson's correlation coefficients were used to quantify the univariate associations among variables, and a forward stepwise multiple regression analysis was carried out to test the joint effect of different variables (independent variables) on RDI (dependent variable), in obese males and in obese women. P-values less than or equal to 0.05 were considered significant.


Our results show that the RDI of the whole population was 20.7±22.82 (range: 0–90). Eighty-three (43 men and 40 women) of 161 obese patients had RDI≥10, meaning that 51.5% of the whole obese population had moderate or severe OSA. In particular, 24.8% (40/161), ie a quarter of all obese patients, were affected by severe sleep apnea; this alteration was present in 42.1% of obese men (24/57) and in 15.4% (16/104) of obese women.

Tables 2 and 3 show anthropometric, pulmonary function data and sleep parameters in obese patients, according to the level of sleep apnea severity. Increasing severity of RDI was associated with a significant increase of body weight, BMI, neck and waist circumferences, PPNC, paCO2, TST with oxyhemoglobin saturation lower than 90%, and a significant decrease of paO2, FCV (percentage of predicted), FRC (percentage of predicted), and percentage of REM sleep.

Table 2 Anthropomorphic and pulmonary function parameters in 161 obese patients, according to sleep apnea severity (mean±s.d.)
Table 3 Sleep parameters in 161 obese patients, according to sleep apnea severity (mean±s.d.)

nHyp was present in 29.1% of the obese population (n=47); in particular, 40.3% of obese men (n=23) and 23.1% of obese women (n=24) had nHyp. In all, 48.9% (n=23) of nHyp patients had severe sleep apnea (RDI≥30), whereas nHyp was the only breathing disturbance in eight patients. Forty-seven patients with nocturnal hypoventilation had a worse arterial blood gas profile (paO2—nHyp, 75.88±12.62 mmHg; wHyp, 85.13±10.84 mmHg; P<0.001; PaCO2—nHyp, 40.61±4.92 mmHg; wHyp, 37.67±3.35mmHg; P<0.001) and a more severe restrictive defects (FVC% of predicted—nHyp, 76.33±17.43 mmHg; wHyp, 92.67±15.12 mmHg; P<0.001; FEV1% of predicted—nHyp, 80.15±10.04 mmHg; wHyp, 94.57±15.99 mmHg; P<0.001) than patients without hypoventilation (wHyp); on the other hand, since patients with airway obstruction were excluded from the study, FEV1/FVC% was not different between the two groups (nHyp, 88.85±8.93; wHyp, 90.08±8.41, NS). Moreover, nHyp patients had a higher (A-a) O2 gradient (nHyp, 31.44±13.61 mmHg; wHyp, 25.48±8.41 mmHg; P<0.05) and a higher BMI (nHyp, 46.15±9.71 mmHg; wHyp, 40.30±6.96 mmHg; P<0.001) as compared to wHyp patients. Concerning the significant associations of anthropometric parameters with the different pulmonary function and sleep parameters in the whole population, BMI was directly correlated with TSTSaO2<90% (r=0.32, P<0.001), and negatively correlated with FCV (percentage of predicted; r=−0.38, P<0.001); waist circumference was inversely associated with FCV (percentage of predicted; r=−0.36, P<0.001) and neck circumference was directly correlated with TSTSaO2<90% (r=0.30, P<0.001).

Table 4 shows the loud snoring (LS) (percentage of patients and patient score), the excessive daytime sleepiness (EDS) (percentage of patients and patient score) and the Epworth sleepiness scale (ESS) levels in obese patients, subdivided by the level of RDI, and in control subjects.

Table 4 Distribution of loud snoring (percentage of patients and patient score), excessive daytime sleepiness (percentage of patients and patient score) and Epworth sleepiness scale in subgroups of obese patients according to the RDI and in controls

More than 46% of non-apneic obese patients had loud snoring, and this percentage was significantly higher than in the non-obese group; the percentage of this alteration was progressively higher with the increase of RDI, with almost 100% of the patients affected by severe sleep apnea having this symptom. Seemingly, non-apneic obese patients had a higher loud snoring score than nonobese subjects. Similar results were obtained when the percentage of patients with EDS, the EDS patient score and the sleep propensity, as evaluated by the ESS, were examined. The mean values of EDS (both percentage of patients and patient score) and ESS were not significantly different between patients with RDI<10 and those with RDI between 10 and 29. For instance, no significant correlation was found between the ESS value and age (r=0.21), BMI (r=0.23) and RDI (r=0.19) in the nonapneic subgroup.

As far as the difference of sleep disorders breathing between men and women is concerned, 75% (n=43) of obese men and 38% (n=40) of obese women showed a RDI≥10; four men and four women showed only nHyp. When apneic obese women and apneic obese men were compared, men were older (46.0±12 y vs 40±12 y) and heavier (BMI 42.3±8 vs 42.2±7), but these differences were not significant. Moreover, men had higher neck circumference (men, 47.1±3.5 cm; women, 42.9±4.0 cm; P<0.001); waist circumference (men, 137±20 cm; women, 121±22 cm; P<0.001) and WHR (men, 1.04±0.08; women, 0.96±0.11; P<0.001). Among women, 61% (25/40) of postmenopausal and only 21% (14/64) of premenopausal had sleep apnea (χ2, P<0.001). When only women affected by sleep apnea were considered, postmenopausal women had higher neck circumference (post- 43.5±3.7 cm; pre- 40.2±4.0 cm; P<0.01) and waist circumference (post- 138.8±15.0 cm; pre- 128.1±19 cm; P<0.05) circumferences as compared to premenopausal women, even though postmenopausal (BMI 43.8±7.0) were not significantly heavier than premenopausal (BMI 41.5±8.0) women.

Table 5 shows the correlation between RDI and anthropometric and pulmonary function parameters in obese men and women. RDI was positively correlated with BMI, neck circumference, PPNC, waist circumference, WHR, paCO2 and TSTSaO2<90% either in men or in women. RDI was directly correlated with age in women, but not in men. RDI was negatively correlated with FEV1 (percentage of predicted), FVC (percentage of predicted) and paO2 only in women.

Table 5 Correlation between RDI and anthropometric and pulmonary function parameters in obese men and women

When a forward stepwise multiple regression analysis was carried out to identify the variables independently associated with RDI (dependent variable), and age, BMI, neck circumference, waist circumference, WHR and PPNC were considered as independent variables, neck circumference in obese men and BMI and age in obese women were the strongest predictors of the severity of sleep apnea.

Table 6 shows the best model for predicting RDI in obese men and women. The r2 value of the prediction equation of RDI was 0.35 (P<0.001) in women and 0.15 (P<0.001) in men. BMI was the strongest predictor of RDI in women; in particular, BMI, age and neck circumference contributed to 17%, 4% and 2%, respectively, of the variance of RDI. Neck circumference was the strongest predictor of RDI in men; in particular, neck circumference, BMI and age contributed to 11%, 1.7% and 1.5% of the variance of RDI.

Table 6 Stepwise multiple regression analysis of RDI in obese men and women


The most relevant result of this study, performed by a polysomnographic evaluation, is that more than half of a population mainly represented by subjects with severe obesity are affected by moderate or severe sleep apnea. In particular, 24.8% of obese patients were affected by severe OSA, and this alteration was present in 42.1% of men and in 15.4% of women. These results are particularly important if it is taken into account that OSA is a risk factor for hypertension,30 cardiovascular diseases,5,6,7 pulmonary hypertension,31 asthma,32 and impairment of carbohydrate metabolism and endocrine function.33 It is also possible that the effect of weight loss in reducing the cardiovascular risk associated with severe obesity might be due, at least in part, to a simultaneous reduction of sleep breathing disorders in these patients.

Concerning the influence of body fatness and body fat distribution on RDI, neck circumference was the best predictor of RDI in obese men, suggesting that upper body fat accumulation is more important than the total amount of body fat for the risk of sleep apnea. Accumulation of adipose tissue in the neck and enlarged neck have been proposed as possible causes of OSA in obese patients.34 Neck circumference was a better predictor of RDI than waist circumference, and this result is apparently opposite to that reported by Grunstein et al in obese men.26 However, it is notable that these authors investigated overweight and moderately obese patients, whereas we investigated severely obese patients; therefore, it is possible that waist circumference looses and neck circumference maintains its predictive power on sleep apnea in very fat men.

In contrast with men, BMI (and to a lesser extent, age and neck circumference) was the best predictor of RDI in our women, suggesting that body fatness has the leading role in the development of sleep apnea in women. This result is in line with previous studies, showing that massive obesity rather than structural abnormalities of the upper airway is the main factor for the appearance of OSA in women,35 and that women having more fat in the lower part of the body have more severe signs of OSA.36

The percentage of OSA in our sample is much higher than that reported in most of the previous studies, particularly in women, and the significance of these findings is raised by the fact that none of our patients was complaining about the quality of his sleep. Charuzl et al found severe sleep apnea in 12% of men and only in 0.3% of women.37 This finding may possibly be due to the fact that most of our patients had BMI higher than 40, thus being affected by severe obesity. Moreover, it is noteworthy that only a small proportion of patients underwent a polysomnographic evaluation in the study of Charuzl et al; therefore, it is possible that these authors have underestimated the real frequency of severe sleep apnea in their sample. Vgontzas et al also found a lower prevalence (40% in men and 3% in women) of severe sleep apnea in their study,14 but they did not measure parameters of body fat distribution; moreover, their subjects were younger, and the percentage of their postmenopausal women (9%) was lower than in our study (39%). This seems to be a very important point, since we found that the percentage of women with RDI≥10 was higher in postmenopausal (61%) than in premenopausal (21%) women, even though postmenopausal were not heavier than premenopausal women. Interestingly, very few studies have used polysomnography to investigate whether the changes from fertile to postmenopausal status is responsible for important changes in the sleep respiratory function. However, body fat distribution (higher neck and waist circumferences in postmenopausal women) may possibly explain the differences between the studies; in fact, menopause is well known to be responsible for increased body fatness, central fat accumulation and development of sleep apnea.38

To the best of our knowledge, this is the first study reporting the prevalence of nocturnal hypoventilation in obesity, possibly because the diagnosis criteria of this alteration are still controversial.39 According to our definition described in the methods section, it was present in 29% of obese subjects, and in particular in 40.3% of men and in 23.1% of women; however, since this alteration was the exclusive breathing disturbance in only 5% of the whole population and was simultaneously present in almost half of the patients having severe sleep apnea, the influence of nocturnal hypoventilation itself on the sleep disturbances and on the healthy status is very difficult to understand. On the other hand, it is interesting that nocturnal hypoventilation, as considered as an isolated phenomenon, is not frequent in obese patients.

Another interesting finding of our study is that 35% of nonapneic obese patients, ie subjects without any kind of sleep breathing disorder, showed an excessive daytime sleepiness. It is noteworthy that the mean value of propensity to sleep, as evaluated by the ESS, was significantly higher in nonapneic obese patients than in nonobese subjects and similar to that in obese patients with moderate sleep apnea. To the best of our knowledge, the only previous study reporting data on daytime sleepiness in obese patients is the one performed by Vgontzas et al;14 these authors, who used the multiple sleep latency test, reported that 57% of obese patients without sleep apnea complained of daytime sleepiness and showed that these patients were significantly sleepier as compared to normal-weight subjects. These findings suggest that daytime sleepiness is a underevaluated disturbance in obese patients, who rarely complain about this symptom. The pathophysiological mechanism and the clinical consequences of excessive daytime sleepiness are not known. However, this parameter was not significantly correlated with BMI, age, and RDI in nonapneic obese patients.

In conclusion, this study shows that OSA is present in more than 50% of patients with a mean BMI higher than 40.0, and that neck circumference in men and BMI and age in women are the strongest predictors of sleep apnea severity. It also suggests that morbid obesity may well be responsible for daytime sleepiness, even in the absence of sleep apnea.


  1. 1

    Tuomilehto J, Salonen JT, Martti B, Jalkanen L, Puska P, Nissinen A, Wolf E . Body weight and risk of myocardial infarction and death in the adult population of eastern Finland Br Med J 1987 295: 623–627.

    CAS  Article  Google Scholar 

  2. 2

    Donahue RP, Abbott RD, Bloom E, Reed DM, Yano K . Central obesity and coronary heart disease in men Lancet 1987 i: 821–824.

    Article  Google Scholar 

  3. 3

    Bjorntorp P . Portal adipose tissue as a generator of risk factors for cardiovascular disease and diabetes Arteriosclerosis 1990 10: 493–496.

    CAS  Article  Google Scholar 

  4. 4

    Zamboni M, Armellini F, Sheriban I, De Marchi M, Todesco T, Bergamo-Andreis IA, Cominacini L, Bosello O . Relation of body fat distribution in men and degree of coronary narrowings in coronary artery disease Am J Cardiol 1992 70: 1135–1138.

    CAS  Article  Google Scholar 

  5. 5

    Pi-Sunyer FX . Medical hazards of obesity Ann Intern Med 1993 119: 655–660.

    CAS  Article  Google Scholar 

  6. 6

    Koskenvuo M, Kaprio J, Telakivi T, Partinen M, Heikkila K, Sarna S . Snoring as a risk factor for ischemic heart disease and stroke Br Med J 1987 294: 16–19.

    CAS  Article  Google Scholar 

  7. 7

    Hung J, Whitford EG, Parson RW, Hillman DR . Association of sleep apnea and myocardial infarction in men Lancet 1987 294: 16–19.

    Google Scholar 

  8. 8

    Guilleminault C, Van Den Hoed J, Mifler MM . Clinical overview of the sleep apnea syndromes. In: Guilleminault C, Dement WC (eds). Sleep apnea syndromes Liss: New York 1978 1–12.

    Google Scholar 

  9. 9

    Kales A, Caldwell AB, Cadleux RJ, Vela-Bueno A, Ruch LG, Mayes SD . Severe obstructive sleep apnea. Associated psychopathology and psychosocial consequences J Chron Dis 1985 38: 427–434.

    CAS  Article  Google Scholar 

  10. 10

    Peiser J, Lavie P, Ovnat A, Charuzl I . Sleep apnea syndrome in the morbidly obese as an indication for weight reduction surgery Sleep 1984 199: 112–115.

    CAS  Google Scholar 

  11. 11

    Rajala R, Partinen M, Sane T, Palkonen R, Huikuri K, Seppalainen AM . Obstructive sleep apnoea syndrome in morbidly obese patients J Intern Med 1991 230: 125–129.

    CAS  Article  Google Scholar 

  12. 12

    Pasquali R, Colella P, Cirignotta F, Mondini S, Gerardi R, Buratti P, Rinaldi Ceroni A, Tartari F, Schiavina M, Melchionda N, Lugaresi E, Barbara L . Treatment of obese patients with obstructive sleep apnea syndrome (OSAS): effect of weight loss and interference of otorhinolaryngoiatric pathology Int J Obes 1990 14: 207–217.

    CAS  PubMed  Google Scholar 

  13. 13

    Hakala K, Mustajoki P, Aittomaki J, Sovijarvi ARA . Effect of weight loss and body position on pulmonary function and gas exchange abnormalities in morbid obesity Int J Obes Relat Metab Disord 1995 19: 343–346.

    CAS  PubMed  Google Scholar 

  14. 14

    Vgontzas AN, Tan TL, Bixler EO, Martin LF, Shubert D, Kales A . Sleep apnea and sleep disruption in obese patients Arch Intern Med 1994 154: 1705–1711.

    CAS  Article  Google Scholar 

  15. 15

    Richman RM, Elliot LM, Burns CM, Bearpark HM, Steinbeck KS, Caterson ID . The prevalence of obstructive sleep apnea in a obese female population Int J Obes Relat Metab Disord 1994 18: 173–177.

    CAS  PubMed  Google Scholar 

  16. 16

    Vgontzas AN, Bixler EO, Tan TL, Kantner D, Martin LF, Kales A . Obesity without sleep apnea is associated with daytime sleepiness Arch Intern Med 1998 158: 1333–1337.

    CAS  Article  Google Scholar 

  17. 17

    Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus Diabetes Care 1997 20: 1183–1197.

  18. 18

    Davies RJO, Stradling JR . The relationship between neck circumference, radiographic pharyngeal anatomy, and obstructive sleep apnea Eur Respir 1990 3: 509–514.

    CAS  Google Scholar 

  19. 19

    Vilijanen AA, Halttunen PK, Kreus KE, Vilijanen BC . Spirometric studies in non-smoking, healthy adults Scand J Clin Lab Invest 1982 42 (Suppl 1159): 5–20.

    Article  Google Scholar 

  20. 20

    Fenn O, Rahn H, Otis AB . A theoretical study of the composition of alveolar air Am J Physiol 1946 146: 637–641.

    Article  Google Scholar 

  21. 21

    Kump K, Whalen C, Tishler PV, Browner I, Ferrette V, Strohl KP, Rosenberg C, Redline S . Assessment of the validity and the utility of a sleep-symptom questionnaire Am J Respir Crit Care Med 1994 150: 735–741.

    CAS  Article  Google Scholar 

  22. 22

    Johns M . Rethinking the assessment of sleepiness Sleep Med Rev 1998 2: 3–15.

    CAS  Article  Google Scholar 

  23. 23

    Johns MW . Reliability and factor analysis of the Epworth Sleepiness Scale Sleep 1992 15: 376–381.

    CAS  Article  Google Scholar 

  24. 24

    Johns MW . Sleepiness in different situations measured by the Epworth Sleepiness Scale Sleep 1994 17: 703–710.

    CAS  Article  Google Scholar 

  25. 25

    Rechtschaffen A, Kales A . A manual of standardized terminology, techniques and scoring system for sleep stages of human subjects NIH publication no: 204. US Government Printing Office: Washington, DC 1968.

  26. 26

    Grunstein R, Wilcox I, Yang TS, Gould Y, Hedner J . Snoring and sleep apnoea in men: association with central obesity and hypertension Int J Obes Relat Metab Disord 1993 17: 533–540.

    CAS  PubMed  Google Scholar 

  27. 27

    Kopelman PG . Sleep apnoea and hypoventilation in obesity Int J Obes Relat Metab Disord 1992 16 (Suppl 2): S37–S42.

    PubMed  Google Scholar 

  28. 28

    Kryger MH . Restrictive lung diseases. In: Kryger MH, Roth T, Dement WC (eds) Principles and practice of sleep medicine W.B. Saunders: Philadelphia, PA 1994 769–775.

    Google Scholar 

  29. 29

    Piper AJ, Sullivan CE . Pressure support ventilation. (Letter to the Editor). Chest 1995 107: 591.

    Article  Google Scholar 

  30. 30

    Young T, Peppard P, Palta M, Hla KM, Finn L, Morgan B, Skatrud J . Population-based study of sleep-disordered breathing as a risk factor for hypertension Arch Intern Med 1997 157: 1746–1752.

    CAS  Article  Google Scholar 

  31. 31

    Sanner BM, Doberauer C, Konermann M, Sturn A, Zidek W . Pulmonary hypertension in patients with obstructive sleep apnea syndrome Arch Intern Med 1997 157: 2483–2487.

    CAS  Article  Google Scholar 

  32. 32

    Camargo CA Jr, Weiss ST, Zhang S, Willett WC, Speizer FE . Prospective study of body mass index, weight change, and risk of adult-onset asthma in women Arch Intern Med 1999 159: 2582–2588.

    Article  Google Scholar 

  33. 33

    Spiegel K, Leproult R, Van Cauter E . Impact of sleep debt on metabolic and endocrine function Lancet 1999 354: 1435–1439.

    CAS  Article  Google Scholar 

  34. 34

    Katz I, Stradling J, Slutsky AS, Zamel N, Hoffstein V . Do patients with obstructive sleep apnea have thick necks? Am Rev Respir Dis 1990 141: 1228–1231.

    CAS  Article  Google Scholar 

  35. 35

    Guilleminault C, Quera Salva MA, Partinen M, Jamieson A . Women and the obstructive sleep apnoea syndrome Chest 1998 93: 104–109.

    Article  Google Scholar 

  36. 36

    Sloan EP, Shapiro CM . Obstructive sleep apnea in a consecutive series of obese women Int J Eating Disord 1995 17: 167–173.

    CAS  Article  Google Scholar 

  37. 37

    Charuzl I, Pelser OA, Saltz H, Weltzman S, Lavie P . The effect of surgical weight reduction on sleep quality in obesity-related sleep apnea syndrome Surgery 1984 97: 535–538.

    Google Scholar 

  38. 38

    Wilhoit SC, Suratt PM . Obstructive sleep apnea in premenopausal women. A comparison with men and with postmenopausal women Chest 1987 91: 654–658.

    CAS  Article  Google Scholar 

  39. 39

    Piper AJ, Sullivan CE . Pressure support ventilation (Letter to the Editor.) Chest 1995 107: 591.

    Article  Google Scholar 

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Correspondence to G De Pergola.

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Resta, O., Foschino-Barbaro, M., Legari, G. et al. Sleep-related breathing disorders, loud snoring and excessive daytime sleepiness in obese subjects. Int J Obes 25, 669–675 (2001).

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  • obesity
  • obstructive sleep apnea
  • body fat distribution
  • sleepiness

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