Sleep & the metabolic syndrome.
Sleep is an essential part of our daily living, and sleep
disturbances may intervene with the biological and physiological
processes in human body leading to the development of metabolic
dysfunction. Short sleep duration and poor sleep quality have adverse
effects on metabolism and hormonal processes, contributing to increased
cardiovascular risk. Obstructive sleep apnoea is a chronic condition
characterized by repetitive upper airway collapse during sleep, causing
intermittent hypoxaemia, recurrent arousals and sleep fragmentation.
Sleep disturbances can increase sympathetic activity, provoke systemic
inflammation and oxidative stress, and impair vascular endothelial
function. Obstructive sleep apnoea is increasingly recognized to be an
independent cardiovascular risk factor. There is intense research
interest in the association between obstructive sleep apnoea and the
metabolic syndrome--the constellation of inter-related metabolic
derangements including central obesity, hypertension, insulin resistance
and dyslipidaemia, which appears to directly promote the development of
atherosclerosis. The underlying pathophysiologic pathways or mechanistic
links between obstructive sleep apnoea and metabolic syndrome have not
been well delineated. This article reviews the current knowledge of the
relationship between sleep disturbances, sleep-disordered breathing and
the metabolic syndrome in adults.
Key words Diabetes mellitus--hypertension--metabolic syndrome--obesity--obstructive sleep apnoea--sleep-disordered breathing--sleep disturbances
Sleep apnea syndromes
(Complications and side effects)
Sleep deprivation (Complications and side effects)
Metabolic syndrome X (Risk factors)
Metabolic syndrome X (Development and progression)
Metabolic syndrome X (Research)
Lam, Jamie C.M.
Ip, Mary S.M.
|Publication:||Name: Indian Journal of Medical Research Publisher: Indian Council of Medical Research Audience: Academic Format: Magazine/Journal Subject: Biological sciences; Health Copyright: COPYRIGHT 2010 Indian Council of Medical Research ISSN: 0971-5916|
|Issue:||Date: Feb, 2010 Source Volume: 131 Source Issue: 2|
|Topic:||Event Code: 310 Science & research|
|Geographic:||Geographic Scope: China Geographic Code: 9CHIN China|
Short sleep duration and poor quality of sleep, increasingly common in our modern society, have many effects on our endocrine and metabolic function. Sleep is a major buffer for hormonal release, glucose regulation and cardiovascular function (1). The quality of sleep declines with age, with predominant light and fragmented sleep in the elderly (2). Deep or slow wave sleep occurs during stages 3 and 4 of non rapid eye movement (NREM) sleep and is considered to be the most restorative of all sleep stages. Chronic sleep insufficiency or deprivation not only leads to frequent mental and physical distress, physical incapability and anxiety (3) but also contributes to the ageing process, and may increase the risk for diabetes and obesity (4).
Sleep-disordered breathing (SDB) disrupts sleep pattern and quality. Obstructive sleep apnoea (OSA) is the most common sleep disorder being diagnosed. It is a chronic condition characterized by repetitive episodes of the upper airway collapse during sleep. The effects of intermittent hypoxia and re-oxygenation may provoke a number of pathological cascades which involve sympathetic overactivity, systemic inflammation, oxidative stress and endothelial dysfunction. These are believed to be the underlying mechanisms of OSA contributing independently to increased cardiometabolic risk (5). Untreated OSA subjects have been shown to suffer a significantly increased risk of both fatal and non fatal cardiovascular events by 3-fold, when compared to healthy subjects (6).
The metabolic syndrome is a constellation of inter-related risk factors of metabolic origin and its prevalence is increasing due to the obesity epidemic. Metabolic syndrome is associated with cardiovascular mortality because it comprises established risk factors for cardiometabolic diseases (7). Recent data show a strong association between OSA and the metabolic syndrome, which is indicative of adverse cardiovascular outcomes (8). This article reviews the current knowledge of the relationship between sleep disturbances, sleep-disordered breathing and the metabolic syndrome in adults.
The metabolic syndrome
Metabolic syndrome was first described as a cluster of metabolic abnormalities, with insulin resistance as the central pathophysiological feature, and it was labelled as "Syndrome X" (9). There are different accepted criteria for its definitions, and the most widely used criteria have been proposed by the World Health Organization (WHO), the European Group for the Study of Insulin Resistance (EGIR), the National Cholesterol Education Program--Third Adult Treatment Panel (NCEP ATP III) and International Diabetes Federation (Table). All these organizations have suggested that the core features of metabolic syndrome are central/visceral obesity, hypertension, insulin resistance and dyslipidaemia but they have applied the criteria differently in identifying the cluster of syndrome components (10). Therefore, there have been cases that could be classified as metabolic syndrome by one definition but not by the others. Today, insulin resistance and central obesity have been acknowledged as key driving forces for metabolic syndrome, and these are, independently, also well known cardiovascular risk factors. Patients with metabolic syndrome are at increased risk for the development of type II diabetes mellitus and cardiovascular disease (11).
Different definitions for the metabolic syndrome inevitably led to limited comparability between studies. Besides, there are problems of applicability of these definitions to different ethnic groups, especially in relation to obesity cut-offs. With the current metabolic syndrome definitions, particularly NCEP ATP III, low prevalence figures in Asian population resulted. In a study of over 2800 Chinese subjects, the prevalence of the metabolic syndrome was at 16.7 per cent, however, if using WHO recommendations for waist circumference for Asians (12), the age and gender-adjusted prevalence significantly increased to 21.2 per cent (13). Knowing the recent evidence and with the spreading obesity epidemic, the prevalence of metabolic syndrome and its associated complications is definitely on the rising trend regardless of the exact criteria used for the syndrome.
Obstructive sleep apnoea and metabolic syndrome
A number of neural, humoral, metabolic, vascular and inflammatory abnormalities are evident in subjects with OSA, and it is increasingly recognized to be an independent cardiovascular risk factor (14). Current data suggest that OSA increases cardiovascular morbidity and mortality, and continuous positive airway pressure (CPAP) treatment has the potential to diminish such risk (15). Different mechanisms have been proposed for these derangements to better understand the pathophysiologic core features and hence to formulate treatment strategies (16).
Many studies have investigated the relationship of OSA and different cardiometabolic parameters (17-21), and CPAP treatment has produced some beneficial effects on individual metabolic components (22,23). There is also recent focus on the relationship between sleep apnoea and the metabolic syndrome as a single entity (24). OSA or snoring is shown to be independently associated with an increased prevalence of metabolic syndrome, and this is consistent across different ethnic origins (25-30).
In a cross-sectional clinic-based study (31) of 184 patients with co-morbidities, those who suffered from OSA and the metabolic syndrome had higher brachial-ankle pulse wave velocity (a measure of endothelial dysfunction) and plasma levels of C-reactive protein (an inflammatory marker) compared to those without metabolic syndrome. Therefore, the concurrent presence of metabolic syndrome in OSA patients may have an additive effect on cardiovascular risk (31). In another observational study of 195 patients with cardiovascular diseases, the metabolic syndrome was a better predictor of nocturnal desaturation than apnoea-hypoapnoea index (AHI) in those patients with sleep apnoea, with the odds ratio of 2.63 (32). However, in an interventional study of 89 OSA patients, the presence of metabolic syndrome did not increase the risk of cardiovascular events in OSA patients who had good CPAP compliance after 22 [+ or -] 10 months of follow up (33).
The co-existence of OSA and metabolic syndrome may increase the risk for the development of cardiovascular diseases either additively or synergistically. The underlying mechanisms are as yet poorly defined, but intermittent hypoxia and sleep fragmentation in OSA are thought to be the main triggers of various pathogenetic mediating pathways leading to metabolic dysfunction with multi-directional interactions and feedback (Fig. 1).
Sleep and metabolic dysfunction
Sleep is closely related to the regulation of physical and emotional well being (34). Hormonal events during sleep are dependent upon sleep duration and sleep quality, and the multiple peripheral effects of sleep suggest that sleep loss might be associated with deleterious health consequences (35). Sleep duration plays a role in the regulation of leptin and ghrelin levels in humans. Both of these hormones integrate control of feeding, wakefulness and energy expenditure in the body although the mechanisms are unclear, and may act in parallel as metabolic counterparts for body weight control (36).
[FIGURE 1 OMITTED]
The Wisconsin sleep cohort study has provided important data on sleep duration, showing that a loss of 3 h of sleep from a baseline of approximately 8 h was associated with an average 4-5 per cent higher body weight (37). A recent systemic review of both cross-sectional and longitudinal studies revealed that short sleep duration is independently associated with weight gain, particularly in young age groups (38). In a retrospective study of 1000 patients from four different primary care practices, women were found to sleep more than men, and overweight [body mass index (BMI) 25 - 29.9 kg/[m.sup.2]] and obese (BMI 30-39.9 kg/ [m.sup.2]) patients slept less than patients with a normal BMI (<25 kg/[m.sup.2]) (39). Interestingly, in a cross-sectional study of 500 Chinese adolescent twins who were relatively lean, short sleep duration was significantly associated with higher adiposity measures in terms of total and central adiposity rather than lean body mass (40).
Short sleep duration is associated with an upregulation of appetite and has an adverse impact on glucose homeostasis (41). A limited number of prospective studies have examined the association between sleep duration and the development of diabetes mellitus. The Sleep Heart Health Study of 1500 subjects shows that a sleep duration of 6 h or less or 9 h or more is associated with increased prevalence of diabetes and glucose intolerance, compared to those sleeping 7 to 8 h per night, after adjustment for age, sex, BMI and AHI (42). In the Massachusetts Male Aging Study, 1139 men participated, those who had sleep duration < 5 h or > 8 h were found to be two to three times more likely to develop incident diabetes respectively (43). For over 70,000 middle-aged women in the United States Nurses Health Study, who were not diabetic at baseline, an increased risk of incident symptomatic diabetes was found among those reporting sleep durations of < 5 h and > 9 h over 10 yr, but the risk became insignificant after adjustment for BMI and other confounders (44). Similarly, in another Finnish study of 1336 men and 1434 women, sleep duration of < 6 h or > 8 h was independently associated with type II diabetes in women only after adjustment for confounders (45). For the First National Health and Nutrition Examination Survey (NHANES) in the United States, with a large population size of 8992 subjects, also concluded that subjects with sleep durations of < 5 h or [greater than or equal to] 9 h were significantly more likely to have incident diabetes over 10 yr after controlling for covariates, with odds ratios of 1.47 and 1.52 respectively (46). Therefore, both short and long sleep durations may play a role in the aetiology of diabetes in some individuals.
The influence of sleep quality on glucose metabolism has also been investigated in some longitudinal studies (47-50). Some reported that sleep disturbances, such as difficulty initiating sleep, difficulty maintaining sleep and regular use of hypnotics, were associated with an increased risk for incident diabetes (47-49). However, in a prospective population study of female participants, there was no association between sleep problems at baseline and diabetic risk in a 32 yr follow-up (50). In addition, poor sleep quality was also reported by those who had diabetes compared to those did not (51), and sleep duration and quality were shown to be significant predictors of glycaemic control in a cross-sectional study of volunteers with type II diabetes (52). It is possible that both the quantity and quality of sleep are equally important in glucose regulation that involves P-cell responsiveness and insulin sensitivity, and the underlying mechanisms are likely to be multifactorial (53) (Fig. 2).
Hypertension is another component of the metabolic syndrome. It was reported that short sleep duration of < 5 h was associated with increased risk of hypertension in the NHANES (54). Further, the combination of short sleep duration and higher nighttime, relative to daytime and systolic blood pressure are strongly predictive of future cardiovascular disease (55).
There have been studies evaluating the relationship between sleep duration and the metabolic syndrome. In a community--based cross-sectional study of 1214 subjects, the odds for having metabolic syndrome was increased by 45 per cent in both short and long sleepers after adjustment of co-variates, compared to those sleeping 7 to 8 h per night, and sleep duration was also associated with visceral obesity, elevated fasting glucose and hypertriglyceridaemia (56). In the Korean National Health and Nutrition Survey, of the 4222 participants, those who slept < 5 h and > 9 h had increased risk of developing metabolic syndrome with odds ratios of 1.74 (95% CI 1.33-2.26) and 1.69 (95% CI 1.17-2.45) respectively (57).
[FIGURE 2 OMITTED]
Obstructive sleep apnoea and hypertension
There is strong evidence that OSA is an independent risk factor for hypertension independent of obesity (58). The putative mediating pathways involved are sympathetic activation, arterial chemoreceptor response, baroreceptor sensitivity and vasoactive mediators affecting endothelial function (59). The Wisconsin study with longitudinal follow-up of over 700 subjects is considered as a landmark study in the independent association of OSA and hypertension (60). For an AHI > 15 versus AHI=0 at baseline, the odds of developing hypertension over 4-8 yr was 2.89, independent of confounding factors. This association was present throughout the whole spectrum of OSA, from mild to severe degree, but those with moderate to severe OSA had almost three times greater risk for developing hypertension than controls without OSA (60).
Several randomized trials have assessed the effect of CPAP on ambulatory blood pressure in patients with OSA, and both positive (61-64) and negative findings have been reported (65-67). In a study of 118 normotensive and sleepy patients, 1-month of CPAP treatment reduced 24 h mean blood pressure by 2.5mmHg. Further subgroup analyses showed that mean blood pressure reduced by 5mm Hg in those with severe OSA, and by 8 mmHg in those with hypertension on treatment (62). In another randomized controlled study of 60 sleepy subjects, mostly hypertensive on medications, both systolic and diastolic blood pressures were reduced by 10 mm Hg after 2 months of CPAP treatment (63). However, in a 6 wk randomized controlled trial of CPAP treatment group (n=29) versus sham CPAP group (n=25), there was no improvement of arterial blood pressure in subjects with severe OSA but no daytime sleepiness after treatment (65). Further, in a study of 35 OSA patients without sleepiness, most of whom had elevated blood pressure at the entry point, 1- month therapeutic CPAP treatment did not reduce blood pressure (66). In another trial of 68 hypertensive patients, 1 month of CPAP treatment had no effect on blood pressure (67), but the lack of effect may be related to the good baseline control of blood pressure by medications in these subjects.
All of these trials were of short treatment periods, and ambulatory blood pressure was measured with different ambulatory devices. Besides, blood pressure was on the rising trend in the sham CPAP groups in two of these trials (62,64), indicating that sham CPAP might not be the best placebo and tended to give more stress to subjects with OSA during sleep. In two recent meta-analyses of 12 and 16 placebo-controlled randomized trials respectively, comprising both normotensive and hypertensive subjects, an average reduction of 2 mm Hg in mean arterial blood pressure was reported (68,69), while a third meta-analysis did not show any therapeutic effect of CPAP on blood pressure (70). Taken together, these findings suggest that CPAP treatment of OSA can lower blood pressure, but the effect is not uniform in all, and a bigger blood pressure lowering effect is more likely seen in those with severe OSA, greater degree of sleepiness and higher baseline blood pressure.
The association of OSA and hypertension has additive effects on the development of atherosclerosis. In a recent study of 94 middle-aged patients, the intima-media thickness of carotid artery was positively related to systolic blood pressure and AHI (71). So, the rate of progression of carotid atherosclerosis not only predicts future cardiovascular events but also contributes to the increased risk of cerebrovascular accidents.
Obstructive sleep apnoea and obesity
Obesity is becoming a global epidemic in both children and adults, and it is associated with a number of co-morbidities such as cardiovascular diseases, type II diabetes, hypertension and obstructive sleep apnoea (72). The most important risk factor for OSA is obesity. The prevalence of OSA among obese patients has been reported to exceed 30 per cent, and 60-90 per cent of adults with OSA are overweight, and the relative risk of sleep apnoea from obesity with a BMI >30 kg/ [m.sup.2] may be as great as 10 (73). Previous studies revealed that a 10 per cent increase in body weight in 4 yr was associated with a six-fold higher risk of developing OSA (74), and a 6 kg/[m.sup.2] increase in BMI was associated with a four-fold increased risk for the development of OSA (75).
Obesity affects upper airway anatomy because of increased fat deposition in the neck region which in turn predisposes to upper airway collapsibility during sleep. In addition to anatomical factors, collapsibility can be increased by upper airway structural / functional control, disturbances in neuromuscular balance and genetic predisposition (76). Hormonal status and metabolic activity of adipose tissue may impact on sleep apnoea susceptibility, particularly in women. In postmenopausal women fat redistribution to a more central pattern may be responsible for the increased risk of developing OSA (77).
Adipose tissue is metabolically active, it secretes humoral factors and adipokines that regulate the distribution of body fat (78). Leptin plays a key role in body weight regulation through the stimulation of satiety hypothalamic pathways. Human obesity is typically associated with increased leptin levels, thus suggesting a condition of leptin resistance which may contribute to the pathogenesis of sleep apnoea. On the other hand, adiponectin is closely related to visceral adiposity and insulin resistance (79). Recent data suggest that hypoadiponectinaemia is related to sympathetic activity and severity of OSA (80). Obesity and sleep apnoea are often associated with dysregulation of glucose and lipid metabolism, although the precise mechanisms are not clear. Visceral fat produces large amounts of proinflammatory cytokines which are thought to provoke inflammation, oxidative stress, cell adhesion and endothelial dysfunction, and hence, contributing to the development of atherosclersis as well as the sleep-disordered breathing in association with the metabolic syndrome (81).
Obstructive sleep apnoea and insulin resistance/ glucose intolerance/diabetes mellitus
There are accumulating data that obstructive sleep apnoea is independently associated with adverse glucose homeostasis. Previous studies have found increased insulin resistance/glucose intolerance/ diabetes in OSA patients, independent of obesity (82-85), particularly amongst those with excessive daytime sleepiness (86). Very recently, a study on in vivo kinetics of glucose and insulin confirmed that sleep-disordered breathing is associated not only with insulin sensitivity but also with the ability of glucose to mediate its own disposal and pancreatic beta-cell function (87). However, in the Winconsin Sleep Cohort, a four-year follow up of 1387 participants failed to find increased incidence of diabetes mellitus in those with OSA defined by AHI >15 (88).
Previous studies on the treatment effects of CPAP on insulin resistance or glycaemic control in OSA subjects showed conflicting results (89,90). Most did not show any improvement in glucose metabolism (91,92). It was reported that two nights of CPAP treatment improved insulin sensitivity as assessed by the hyperinsulinaemic euglycaemic clamp in a group of non-diabetic men with moderate OSA, and the effect was more prominent in non obese patients with a BMI <30 kg/[m.sup.2] compared to those who were obese with a BMI > 30 kg/[m.sup.2] (93). Recently, it was reported that the improvement in insulin sensitivity was well maintained at 3 yr in the same group of subjects (94). However, in a randomized controlled study with a cross-over design, otherwise healthy men with severe OSA showed no difference in insulin resistance, estimated by Homeostasis Model Assessment Method, after 6 wk of CPAP treatment versus 6 wk of sham CPAP (95).
Interventional studies on glucose metabolism in diabetic subjects with OSA are scanty. Three observational studies of small sample sizes showed improvement in glycaemic control with CPAP treatment (96-98). A randomized controlled study of diabetic patients treated with CPAP for 3 months demonstrated that there was no effect on insulin resistance or glycaemic control compared to sham CPAP (99).
Obesity is a risk factor for both OSA and insulin resistance. The strong association between OSA and obesity has long been recognized, and the severity of OSA is significantly correlated with visceral fat volume rather than subcutaneous fat in the body or in the neck (100). However, in the recent Sleep Heart Health Study of nondiabetic subjects in the community, those who suffered from sleep disordered breathing had higher prevalence of impaired glucose metabolism, in both non-overweight and overweight subjects (101). So, adiposity may play a role in some but not all individuals to account for the adverse glucose metabolism. The underlying pathophysiological pathways between sleep disordered breathing and altered glucose metabolism may involve adipose tissue as a source of sympathetic activation or inflammatory mediators (102). Indeed, sympathetic activation can affect glucose homeostatic state by increasing muscle glycogen breakdown, hepatic glucose output, and the release of free fatty acids via lipolysis.
OSA results in intermittent hypoxaemia with repetitive oxygen desaturation and re-oxygenation during sleep. In experimental animal models, leptin-deficient obese mice exposed to intermittent hypoxia for 12 wk had increased insulin levels and glucose intolerance (103). Another study showed that lean mice exposed to intermittent hypoxia had decreased glucose disposal as assessed with hyperinsulinaemic euglycaemic clamp, and the impairment of insulin sensitivity was independent of sympathetic activation as well as obesity (104).
Obstructive sleep apnoea and dyslipidaemia
Dyslipidaemia is a major cardiovascular risk factor and also part of the metabolic syndrome, characterized by elevated levels of triglycerides, decreased high -density lipoprotein cholesterol and normal or slightly elevated low-density lipoprotein cholesterol. There are a number of reports of abnormal lipid profiles in subjects with sleep-disordered breathing (17,19,20,21,25). In the Sleep Heart health study, there was an independent association between the severity of OSA and high-density lipoprotein cholesterol levels in females only; and in males, a minor but significant association with total cholesterol levels. These findings were evident in the age group < 65 yr after adjustment for co-variates (17). In contrast, in a recent case-control study of apnoeic obese, non apnoeic obese and non obese subjects, there was no significant difference in the lipid profile between obese apnoeic subjects and obese controls (18).
The effects of CPAP treatment of OSA on lipid parameters are inconsistent. In an analysis of 2 randomized placebo-controlled trials of one-month CPAP treatment, a significant fall of total cholesterol in OSA patients was observed but the difference between changes in the therapeutic CPAP and subtherapeutic CPAP groups failed to achieve statistical significance (105). In another randomized study with a cross-over design for 6 wk of CPAP treatment, there were no changes in the lipid profiles compared to sham CPAP (22). Nevertheless, there are positive studies with increase in high-density lipoprotein cholesterol by 5.8 per cent after CPAP treatment (106), and with good CPAP compliance, total cholesterol, triglycerides, low-density lipoprotein cholesterol and apolipoprotein B levels were all reduced (23).
Lipid metabolism involves a series of enzymatic interactions. Lipoprotein lipase may play a major role in lipid metabolism by hydrolyzing triglyceride-rich lipoproteins. Decreased lipoprotein lipase activity can trigger early inflammatory responses central to atheroslcerosis. In an interventional study, lipoprotein lipase was found to be decreased with the severity of OSA, and 3-month CPAP treatment significantly increased its concentrations (107). This may imply that CPAP treatment could be effective in reducing inflammatory responses and ameliorating lipid metabolism in OSA subjects. Interestingly, sleep apnoea may affect the function of lipids. In a Chinese study, high-density lipoprotein cholesterol was found to be less effective in preventing low-density lipoprotein oxidation in vivo (108). In addition to clinical data, animal experiments also support a role of intermittent hypoxia in the pathogenesis of dyslipidaemia in sleep-disordered breathing (109-111).
There is evidence that insulin resistance is the major underlying abnormality that drives the dyslipidaemia (112). There are convincing data showing that the effect on the assembly and secretion of very-low-density lipoprotein apolipoprotein B and triglycerides is central abnormality, especially in diabetic patients, and therefore, it appears that OSA, insulin resistance and dyslipidaemia are inter-related in a complex cascade of cardiovascular co-morbidities (14).
Both sleep disturbances and the metabolic syndrome are escalating throughout the world, in spite of, or perhaps due to modernization. Understanding the relationships between sleep disturbances, sleep-disordered breathing and metabolic syndrome will enable medical practitioners to approach the common problems, such as hypertension, diabetes, obesity and dyslipidaemia, in a rational and holistic manner.
Received March 13, 2009
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Reprint requests: Dr M.S.M. Ip, University Department of Medicine, Queen Mary Hospital, 102 Pokfulam Road Hong Kong, SAR, China e-mail: email@example.com
Jamie C.M. Lam & Mary S.M. Ip
Division of Respiratory Medicine, University Department of Medicine, Queen Mary Hospital The University of Hong Kong, SAR, China
Table. Different definitions of the metabolic syndrome WHO (1999) (10) EGIR (1999) (10) Diabetes or impaired Insulin resistance or glucose tolerance or hyperinsulinaemia (only non- insulin resistance, plus diabetic subjects), 2 or more of the following, plus 2 or more of the following, BMI > 30 kg/[m.sup.2] Waist circumference: or waist to hip ratio > 0.9 > 94 cm in men , [greater in men, > 0.85 in women than or equal to] 80 cm in women Triglycerides: Triglycerides: [greater than or equal to] > 2 mmol/l 1.7 mmol/l HDL-C: HDL-C: < 0.9 mmol/l in men < 1.0 mmol/l < 1.0 mmol/l in women Blood pressure: Blood pressure: >140/90 mmHg or medication > 140/90 mm Hg or medication Urine albumin excretion Fasting plasma glucose: [greater than or equal to] 20 > 6.1 mmol/l [micro]g/min or albumin- creatinine ratio > 30mg/g WHO (1999) (10) NCEP ATP III (2001) (13) Diabetes or impaired Three or more of the glucose tolerance or following, insulin resistance, plus 2 or more of the following, BMI > 30 kg/[m.sup.2] Waist circumference: or waist to hip ratio > 0.9 >102 cm in men, >88 cm in in men, > 0.85 in women women Triglycerides: Triglycerides: [greater than or equal to] > 1.7 mmol/l 1.7 mmol/l HDL-C: HDL-C: < 0.9 mmol/l in men < 1.03 mmol /l in men < 1.0 mmol/l in women <1.29 mmol/l in women Blood pressure: Blood pressure: >140/90 mmHg or medication > 130/85 mmHg or medication Urine albumin excretion Fasting plasma glucose: [greater than or equal to] 20 > 6.1 mmol/l [micro]g/min or albumin- creatinine ratio > 30mg/g WHO (1999) (10) IDF (2005) (10) Diabetes or impaired Waist circumference-- glucose tolerance or ethnicity specific, insulin resistance, plus plus two or more of 2 or more of the following, the following, BMI > 30 kg/[m.sup.2] or waist to hip ratio > 0.9 in men, > 0.85 in women Triglycerides: Triglycerides: [greater than or equal to] > 1.7 mmol/l or 1.7 mmol/l medicaition HDL-C: HDL-C: < 0.9 mmol/l in men <1.03 mmol/l in men < 1.0 mmol/l in women <1.29 mmol/l in women or medication Blood pressure: Blood pressure: >140/90 mmHg or medication > 130/85 mmHg or medication Urine albumin excretion Fasting plasma glucose: [greater than or equal to] 20 > 5.6 mmol/l or type II [micro]g/min or albumin- diabetes creatinine ratio > 30mg/g WHO, World Health Organization; EGIR, European Group for the Study of Insulin Resistance; NCEP ATP III, National Cholesterol Education Program--Third Adult Treatment Panel; IDF, International Diabetes Federation; BMI, body mass index; HDL-C, high density lipoprotein cholesterol
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