Indian J Med Sci About us | Subscription  |  Top cited articles | Contact Us | Feedback | Login   
Print this page Email this page   Small font size Default font size Increase font size 
 Users Online : 14
Home Current Issue Ahead of print Back Issues  Instructions Search e-Alerts
  Navigate here 
  Search
 
 ¤  Next article
 ¤  Previous article 
 ¤  Table of Contents
  
 Resource links
 ¤   Similar in PUBMED
 ¤  Search Pubmed for
 ¤  Search in Google Scholar for
 ¤Related articles
 ¤   Article in PDF (130 KB)
 ¤   Citation Manager
 ¤   Access Statistics
 ¤   Reader Comments
 ¤   Email Alert *
 ¤   Add to My List *
* Registration required (free)  


  In this article
 ¤  Abstract
 ¤  Introduction
 ¤  Summary
 ¤  References
 ¤  Article Tables

 Article Access Statistics
    Viewed24284    
    Printed728    
    Emailed43    
    PDF Downloaded2034    
    Comments [Add]    
    Cited by others 33    

Recommend this journal

 


 
PRACTITIONERS SECTION
Year : 2006  |  Volume : 60  |  Issue : 2  |  Page : 72-81
 

Metabolic syndrome


Department of Medicine, Sir Ganga Ram, Hospital, Rajinder Nagar, New Delhi-110 060, India

Correspondence Address:
Atul Gogia
Department of Medicine, J-6/27 Rajouri Garden, New Delhi-110 027
India
Login to access the Email id


DOI: 10.4103/0019-5359.19918

PMID: 16505579

Get Permissions

 ¤ Abstract 

The Metabolic syndrome is a widely prevalent and multi-factorial disorder. The syndrome has been given several names, including- the metabolic syndrome, the insulin resistance syndrome, the plurimetabolic syndrome, and the deadly quartet. With the formulation of NCEP/ATP III guidelines, some uniformity and standardization has occurred in the definition of metabolic syndrome and has been very useful for epidemiological purposes. The mechanisms underlying the metabolic syndrome are not fully known; however resistance to insulin stimulated glucose uptake seems to modify biochemical responses in a way that predisposes to metabolic risk factors. The clinical relevance of the metabolic syndrome is related to its role in the development of cardiovascular disease. Management of the metabolic syndrome involves patient-education and intervention at various levels. Weight reduction is one of the main stays of treatment. In this article we comprehensively discuss this syndrome- the epidemiology, pathogenesis, clinical relevance and management. The need to do a comprehensive review of this particular syndrome has arisen in view of the ever increasing incidence of this entitiy. Soon, metabolic syndrome will overtake cigarette smoking as the number one risk factor for heart disease among the US population. Hardly any issue of any primary care medical journal can be opened without encountering an article on type 2 diabetes, dyslipidemia or hypertension. It is rare to see type 2 diabetes, dyslipidemia, obesity or hypertension in isolation. Insulin resistance and resulting hyperinsulinemia have been implicated in the development of glucose intolerance (and progression to type 2 diabetes), hypertriglyceridemia, hypertension, polycystic ovary yndrome, hypercoagulability and vascular inflammation, as well as the eventual development of atherosclerotic cardiovascular disease manifested as myocardial infarction, stroke and myriad end organ diseases. Conversely, treatment and consequent improvement of insulin resistance have been shown to result in better outcomes in virtually all of these conditions.


Keywords: Metabolic Syndrome, Insulin resistance, Obesity


How to cite this article:
Gogia A, Agarwal P K. Metabolic syndrome. Indian J Med Sci 2006;60:72-81

How to cite this URL:
Gogia A, Agarwal P K. Metabolic syndrome. Indian J Med Sci [serial online] 2006 [cited 2014 Oct 23];60:72-81. Available from: http://www.indianjmedsci.org/text.asp?2006/60/2/72/19918



 ¤ Introduction Top


The 'Metabolic Syndrome' is a widely prevalent and multi-factorial disorder that presents in a distinct, albeit heterogenous phenotype[1] Although obesity and insulin resistance are not synonymous with the metabolic syndrome, they are integral features in this derangement of adipocyte physiology and carbohydrate metabolism. It is now established that this syndrome predicts the development of type 2 diabetes mellitus and cardiovascular disease.[1]

Metabolic syndrome was initially observed in 1923 by Kyln, who described the clustering of hypertension, hyperglycemia and gout as the syndrome. Subsequently, several other metabolic abnormalities have been associated with this syndrome, including obesity, microalbuminuria, and abnormalities in fibrinolysis and coagulation.[2] In 1988, Gerald Reaven reintroduced the concept of Syndrome X for the clustering of cardiovascular risk factors like hypertension, glucose intolerance, high triglycerides and low HDL concentration.[3] The syndrome has been given several names, including the 'metabolic syndrome', the 'insulin resistance syndrome', the 'plurimetabolic syndrome', and the 'deadly quartet'.[2]

In 1998, WHO proposed a unifying definition for the syndrome and chose to call it the 'metabolic syndrome' rather than the 'insulin resistance syndrome'.[4] This name was chosen primarily because it was the cause of all the components of the syndrome.

The Third Report of the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP III) included clinical diagnosis guidelines for the Metabolic Syndrome. Compared with findings from earlier studies and WHO guidelines the new ATP III defines criteria measured in clinical practice[1] [Table - 1].

Individuals who met the criteria for high blood pressure or high fasting glucose concentration if they are currently using blood pressure medications or oral hypoglycemic agents were also included in the definition.[7]

European Group for study of Insulin resistance (EGIR 1999) definition for Metabolic Syndrome[5]

Insulin resistance (defined as hyperinsulinemia, top 25% of fasting insulin values among the non diabetics population)

Plus two or more of the following:

1. Central obesity: Waist circumference >102 cm (male) > 88 cm (female)

2. Dyslipidemia: Triglycerides >2.0 mmol/L or HDL cholesterol <1.0

3. Hypertension: Blood pressure >= 140/90 mmHg

4. Fasting plasma glucose >= 6.1 mmol/L

Prevalence of Metabolic Syndrome in India and the World

With the formulation of NCEP/ATP III guidelines some uniformity and standardization has occurred in the definition of metabolic syndrome and has been very useful for epidemiological purposes. At present, metabolic syndrome is an all or none diagnosis. The study results based on third National Health and Nutrition Examination Survey (NHANES III), indicate that approximately one fourth of the US adults 20 years or older meet the diagnostic criteria for metabolic syndrome.[6] The prevalence of the metabolic syndrome depends on age, ethnic background, and gender. It rises linearly from 20 to 50 years and plateaus thereafter. Looking at various studies around the world, which included population samples, aged from 20 to 25 and upwards, the prevalence varies from 8% (India) to 24% (United States) in men and from 7% (France) to 46% (India) in women.[8] Two Indian studies, which differed in their definition of obesity: first[9] used the obesity criteria suitable for Indians, while the second[10] used the standard ATP III definition of obesity. Both studies used population based samples within the age range but reported prevalence of 13% in Jaipur[10] and 41% in Chennai.[9] The prevalence of obesity in two study groups was quite similar (31% versus 33%), despite the different definitions used. Far larger differences were observed between the two studies for the prevalence of elevated triglycerides (46% vs. 30%), hypertension (55% vs. 39%) and elevated fasting plasma glucose (27% vs. 5%), each of which reported having used the same cut off points. Interestingly, a third Indian study,[11] also from Chennai, reported a metabolic syndrome prevalence of 11.2% (Using EGIR criteria), which was much closer to the prevalence rate reported for Jaipur than the other Chennai study. Therefore, even within the same ethnic population group it appears that there can be significant differences in the prevalence of both the individual factors that constitute the metabolic syndrome and the metabolic syndrome itself.

Metabolic syndrome prevalence rates as described earlier vary among ethnic groups as defined by the ATP III criteria among Finnish and Native American men. Both studies involved subjects with comparable age ranges (42-60 and 44-49 years, respectively), with the Finnish study showing prevalence of only 14% compared with the prevalence in the Native American study of 43.6%. The prevalence varies from a low of 13.9% in black men to a high of 27.2% in Mexican American women.[12]

Various Factors contributing to increasing prevalence of metabolic syndrome:

1. Atherogenic dyslipidemia, Elevated Triglycerides, apolipoprotein B and small low-density lipoprotein, low HDL.

2. Elevated plasma glucose

3. Elevated blood pressure

4. Pro-thrombotic state

5. Pro-inflammatory state

Many studies[15],[16],[17] have reported that low socio-economic status is associated with a higher mortality rate due to cardiovascular disease. A low education level links cardiovascular disease with risk factors such as smoking, hypertension, impaired glucose tolerance, diabetes mellitus, physical inactivity and overweight associated with other metabolic abnormalities. The prevalence of metabolic syndrome was found to be elevated in women who abstained from alcohol.[7] Slight and moderate alcohol consumption has been found to be associated with low CHD risk, possibly through beneficial alterations in HDL cholesterol and blood pressure.

Aetiopathogenesis

The mechanisms underlying the metabolic syndrome are not fully known; however resistance to insulin stimulated glucose uptake seems to modify biochemical responses in a way that predisposes to metabolic risk factors.[3],[18],[19] A central role has been attributed to the pro-inflammatory cytokines, tumor necrosis factor a (TNF- a) and interleukin (IL)-6, supported by the fact that both are produced in substantial amounts by human adipose tissue. TNF- a impairs insulin-stimulated glucose uptake in a variety of cells and decreases lipoprotein lipase activity. Both cytokines increase hepatic lipogensis and elicit a systemic acute- phase response.[20] Furthermore, various aspects of the acute-phase response, such as fibrinogen and plasminogen activator inhibitor-1 levels, whole-blood viscosity, and white blood cell count, have recently been found to correlate positively with the metabolic syndrome.[21] This is of particular interest because inflammation plays an important role in the pathogenesis of atherothrombosis.[2],[23]

Macrophage and T-cell infiltration is a major feature of atherosclerotic plaques, especially at sites of plaque rupture, and epidemiological studies show strong positive associations of systemic markers of inflammation with atherothrombotic disease.[21],[22],[24],[25],[26] Moreover, C-reactive protein (CRP), the classic and exquisitively sensitive acute phase reactant, shows a strong independent association with the risk of Coronary Heart Disease and other atherothrombotic events. CRP levels have also been found to correlate with BMI and some features of the metabolic syndrome.

The AHA/NHLBI/ADA conference identified three potential etiologic categories:

1. Obesity and disorders of adipose tissue

2. Insulin resistance

3. A constellation of independent risk factors (e.g. molecules of hepatic, vascular and immunologic origin) that mediate specific component of syndrome like hypertension, prothrombotic state, lipoprotein metabolic ageing and physical inactivity. Metabolically, several risk factors tend to cluster in middle-aged adults, including HDL-C, BMI, systolic pressure, TGs, glucose and cholesterol.[23] Risk factors occur in isolation only 30% of the time, and clustering of three or more factors occurs 17% of the time in both genders. Clustering of the factors was related to baseline obesity and weight gain during adulthood.[13] Loss of weight over a 16-year period was highly related to a reduced tendency toward clustering of risk factors. In addition, clusters of risk factors were related to greater risk of CHD over the follow up period, and the presence of 3 or more metabolic risk factors led to a doubling of risk for CHD in men and a five-fold increase in risk for women.[13] In Framingham and in other observational studies, the central core of metabolic risk factors were found to be highly related, including triglycerides, HDL-C, BMI, waist circumference, or fasting insulin levels, to insulin levels after an oral glucose challenge test. In addition to a central metabolic syndrome core, there has been a hypertension cluster with shared variance components that included BMI, systolic pressure and diastolic pressure.[13]

Clinical Relevance

The clinical relevance of the metabolic syndrome is related to its role in the development of cardiovascular disease. Two recent prospective population-based studies confirmed that the metabolic syndrome identified a high-risk group of persons who would have been missed by only consideration of the conventional risk factors. The incidence of coronary disease along with carotid atherosclerosis is higher in patients with metabolic syndrome along with higher mortality from all such causes.[14] Although for many obese patients the risk of developing metabolic syndrome is quiet evident, but studies[4] also show that the risk of having the metabolic syndrome increases steeply even within the overweight or the "preobese" range. Detecting these overweight individuals and the 6% of normal weight individuals with the metabolic syndrome and implementing preventive lifestyle interventions-diet education, physical activity, weight control, smoking cessation, and related behavior modification- is a high clinical priority.

Management of metabolic syndrome

Treatment strategies

Currently, no Randomized control trials specifically examining the treatment of metabolic syndrome have been published. Based on clinical trials, aggressive management of the individual components of the syndrome should make it possible to prevent or delay the onset of diabetes mellitus, hypertension and cardiovascular disease. All patents diagnosed with metabolic syndrome should be encouraged to change their diet and exercise habits as primary therapy. Management of the metabolic syndrome involves education and intervention at various levels. Weight reduction is one of the main stay of treatment.

Weight gained after the age of 18 years carries a heavy metabolic tag. In the Nurse's Health Study, a weight gain of 10 kg or more since the age of 18 was associated with increased mortality in middle adulthood.[28] The diet advocated by the ATP III panel and the AHA is a modified fat diet. This diet includes 27% total fat content with 8% saturated fats and high pectin containing fruits. The American Heart Association (AHA)[28] espoused an overall healthy eating pattern that would include a variety of fruits, vegetables, grains, low fat or non fat dairy products, fish, legumes and poultry or lean meats and specific guidelines for attaining appropriate body weight, a desirable cholesterol profile, or a desirable blood pressure.

Life style Changes

Try to prevent weight gain in patients who have metabolic syndrome.

• Look for ways to incorporate more activity into the day.

• Aim for at least 30 minutes of activity at least 5 days per week.

• Keep an activity log and bring it to the next visit.

• Involve family and friends in a healthy life style.

Pharmacological Treatment

The metabolic syndrome features to be taken care of include atherogenic dyslipidemia, hypertension and insulin resistance.

Role of Statins

There is accumulating evidence that statins effectively modify the atherogenic lipoprotein particle distribution, resulting in a decrease of oxidized and small, dense LDL subfractions and a reduction of remnant lipoprotein cholesterol levels. The magnitude of this effect depends upon the particular statin used and the dose that is used.[29] Atorvastatin, simvastatin, pravastatin and rosuvastatin all have beneficial effects on LDL subpopulations. Statins also have non-lipid pleotropic effects like anti-inflammatory effects, improve endothelial function.[30] and enhance insulin sensitivity directly.

Most high-risk patients who have atherogenic dyslipidemia require statin therapy. Co-administration of drugs targeted for the reduction of LDL precursors (VLDL and IDL) are likely to improve the profile of atherogenic lipoproteins. In addition, co-administration produces a significant rise in HDL cholesterol.[31]

Although fibrates reduce plasma triglycerides by 30%-50% and increase HDL by 10% to 15% when used in patients with type 2 diabetes, but there have been no studies specifically examining the effect of fibrate treatment in patients with metabolic syndrome.[31]

Role of Aspirin in treatment of metabolic syndrome

Primary prevention

Virtually all patients with metabolic syndrome who have not yet suffered from a clinical cardiovascular event have a 10-year risk of a first event that are far in excess of 10%. For aspirin in primary prevention, the current totality of evidence provides strong support for the initial finding from the US PHS that aspirin conclusively reduces the risk of a first Myocardial Infarction in apparently healthy individuals. A recently published meta-analysis[32] shows that aspirin significantly reduces the risk of a first Myocardial Infarction by approximately by a third, stroke by approximately one fourth and Cardiovascular Diseaseby approximately one sixth. The usual recommended dose is 75 to 325 mg daily.[33]

Role of Glitazones

All available evidence on surrogate markers suggest that glitazones have effects to decrease the negative manifestations and risk factors associated with insulin resistance, in individuals with or without diabetes. In the absence of outcome data, it is not possible to make a recommendation for the use of glitazones in clinical practice except for the treatment of type- 2 diabetes mellitus.

Hypertension management

NHANES III data shows that upto the age of 60 years, higher the BMI, the greater the prevalence of hypertension. The Normative Aging study demonstrated that diastolic blood pressure is a function of increasing abdominal girth.[34] Increases in abdominal circumference are particularly concerning in individuals with a BMI range of 25 to 30; in these individuals, the opportunity to improve blood pressure with small amounts of weight loss should not be missed. When weight loss occurs in obese adolescents and adults with hypertension, a significant relation between improvement in insulin sensitivity and a decreased blood pressure can be seen. It has been estimated that 50% of hypertensive patients are insulin resistant and hyperinsulinemic.[35] The Dietary approaches to Stop Hypertension (DASH) trial has shown convincingly that a healthful dietary patterns can favorably influence elevated blood pressure even without sodium restriction.[36] The DASH trial diet is high in fruits, vegetables, low-fat dairy products, whole grains, poultry, fish and nuts, which are good sources of potassium, calcium, and magnesium and low in fats, red meat and sweets.[37]

Treatment of Hypercoagulability / Inflammation

Ridker et al[38] found that among 14,719 healthy women followed up prospectively, as the number of risk factors for the metabolic syndrome increased, the levels of C- reactive protein (CRP) increased.

Exercise plays an important role in combating this unwanted aspect of metabolic syndrome. A survey of 3800 British men showed that whether they had CHD or not, physical activity showed a significant and inverse dose-response relationship with fibrinogen, plasma and blood viscosity, platelet count, coagulation factors VIII and IX, von Willebrand factor, fibrin-D-dimer, tissue plasma activator antigen, CRP and white cell count, even after adjustment for possible confounders.[39]

In addition, a study of obesity-related inflammatory markers and leisure time activity indicated a beneficial effect of frequent physical activity.[40]

Prevention

The USPSTF recommends intensive behavioral dietary counselling for adult patients with known risk factors for cardiovascular disease.[44]

The diabetes prevention programme[45] demonstrated that vigorous lifestyle intervention in patients who are pre-diabetic could reduce the rate of developing diabetes by >50% (from 11% to 4.8%)


 ¤ Summary Top


1. Metabolic Syndrome is one of the commonest risk factors for Cardiovascular mortality.

2. The major characteristics of metabolic syndrome include insulin resistance, abdominal obesity, elevated blood pressure and lipid abnormalities.

3. Currently, no randomized controlled studies are aimed specifically at treating metabolic syndrome.

4. The primary goals of dietary management for persons with metabolic syndrome are to reduce the risk of cardiovascular disease and diabetes mellitus.

5. The long term effects of low-carbohydrate diets have not been studied adequately in patients with metabolic syndrome, although short-term effects show benefit[Tabel 2].

 
 ¤ References Top

1.Vega GL. Obesity, the metabolic syndrome, and Cardiovascular disease. Am Heart J 2001;142:1108-16.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Isomaa B, Almgren P, Tuomi T, Torsen B, Lahti K, Nissen M, et al. Cardiovascular Morbidity and Mortality Associated with the Metabolic Syndrome. Diabetes Care 2001;24:683-9.  Back to cited text no. 2    
3.Reaven GM. Role of insulin resistance in human disease. Diabetes 1988;37:1595-607.  Back to cited text no. 3    
4.Alberti KG, Zimmet PZ. For the WHO Consultation: Definition, diagnosis and classification of diabetes mellitus and its complications. Part I: Diagnosis and classification of diabetes mellitus, provisional report of a WHO Consultation. Diabet Med 1998;15:539-53.  Back to cited text no. 4    
5.Balkau B, Charles MA. Comment on the provisional report from THE who Consultation. European Group for the study of Insulin Resistance (EGIR). Diabet Med 1999;16:442-3.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Ford GS, Giles WH, Dietz WH. Prevalence of the Metabolic syndrome among US adults: findings from the Third National Health and Nutrition Examination Survey. JAMA 2002;287:356-9.   Back to cited text no. 6    
7.Park YW, Zhn S, Palaniappan L, Heshka S, Carnethon MR, Heymsfield SB. The Metabolic Syndrome: Prevalence and associated risk factor findings in the US population From the Third National Health and Nutrition Examination Survey, 1993-1994. Arch Intern Med 2003;163:427-36.  Back to cited text no. 7    
8.Cameron AJ, Shaw JE, Zimmet PZ . . The metabolic syndrome: prevalence in worldwide populations. Endocrinol Metab Clin N Am 2004;33:351-35.  Back to cited text no. 8    
9.Ramachandran A, Snehalatha C, Satyavani K, Sivasankari S, Vijay V. Metabolic syndrome in urban Asian Indian adults-a population study using modified ATP III criteria. Diabetes Res Clin Pract 2003;60:199-204.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Gupta A, Gupta R, Sarna M, Rastogi S, Gupta VP, Kothari K. Prevalence of diabetes, impaired fasting glucose and insulin resistance syndrome in an urban Indian population. Diab Res Clin Pract 2003;61:69-76.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Deepa R, Shantiram CS, Premlalitha G, Shanti NG, Mohan V. Prevalence of insulin resistance syndrome in a selected south Indian population-the Chennai urban population study-7 [CUPS-7]. Indian J Med Res 2002;115:118-27.  Back to cited text no. 11    
12.Okosun IS, Liao Y, Rotimi CN, Prewitt TE, Cooper RS. Abdominal Obesity and clustering of multiple factors in metabolic syndrome in White, Black and Hispanic Americans. Ann Epidemiol 2000;10:263-70.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]
13.Wilson PW. Estimating cardiovascular disease risk and the metabolic syndrome: a Framingham view. Endocrinol Metab Clin N Am 2004;33:467-81.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Haffner SM, Stern MP, Hazuda HP, Pugh JA, Patterson JK, Malina RM. Upper body and centralized adiposity inn Mexican Americans and non-Hispanic Whites: relationship to body mass index and other behavioral and demographic variables. Int J Obes. 1986;10:493-502.  Back to cited text no. 14    
15.Pekkanen J, Tuomilehto J, Uutela A, Vartiainen E, Nissinen A. Social class, health behaviours and mortality among men and women in eastern Finland. BMJ 1995;311:589-93.  Back to cited text no. 15  [PUBMED]  [FULLTEXT]
16.Davey SG, Neaton JD, Wentworth D, Stamler J. Mortality differences between black and white men in USA: Contribution of income and other risk factors among men screened for the MRFIT. Lancet 1998;351:934-9.  Back to cited text no. 16    
17.Kaplan GA, Keil JE. Socioeconomic factors and cardiovascular disease: a review of the literature. Circulation 1993;88:1973-98.  Back to cited text no. 17  [PUBMED]  [FULLTEXT]
18.Defronzo RA, Ferrannini E. Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. Diabetes Care 1991;14:173-94.  Back to cited text no. 18    
19.Ferrannini E, Haffner SM, Mitchell BD, Stern MP. Hyperinsulinemia: the key feature of a cardiovascular and metabolic syndrome. Diabetologica 1991;34:416-27.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]
20.Manson JE, Willet WC, Stampfer MJ, Colditz GA, Hunter DJ, Hankinson SE, et al. Body weight and mortality among women. N Eng J Med 1995;333:677-85.  Back to cited text no. 20    
21.Juahan-Vague I, Alessi MC. PAI-1, obesity, insulin resistance and risk of cardiovascular events. Thromb Haemost 1997;78:656-60.  Back to cited text no. 21    
22.Thompson SG, Kienast J, Pyke SD, Haverkate F, Van de Loo JC. Hemostatic factors and the risk of Myocardial infarction or sudden death in patients with angina pectoris. N Eng J Med 1995;332:635-41.   Back to cited text no. 22  [PUBMED]  [FULLTEXT]
23.Ross R. Atherosclerosis: an inflammatory disease. N Eng J Med 1999;340:115-26.  Back to cited text no. 23    
24.Kannel WB, Anderson K, Wilson PW. White blood cell count and cardiovascular disease: insights from the Framingham Study. JAMA 1992;257:1253-6.   Back to cited text no. 24    
25.Munro JM, Cotran RS. Biology of disease: atherogenesis and inflammation. Lab Invest 1988;58:249-61.  Back to cited text no. 25  [PUBMED]  [FULLTEXT]
26.Yarnell JW, Baker IA, Sweetnam PM, Bainton D, O'Brien JR, Whitehead PJ, et al. Fibrinogen, viscosity and white blood cell count are major risk factors for ischemic heart disease: the Caerphilly Speedwell Collaborative Heart Disease studies. Circulation 1991;83:836-44.  Back to cited text no. 26  [PUBMED]  [FULLTEXT]
27.Wilson BW, Kannel WB, Silbershatz I, D'Agostino RB. Clustering of metabolic factors and coronary heart disease. Arch Intern Med. 1999;159:1104-9.  Back to cited text no. 27    
28.Krause RM, Eckel RH, Howard B, Appel LJ, Daniels SR, Deckelbaum RJ, et al. AHA dietary guidelines: revision 2000:a statement for health care professionals from the Committee of the American Heart Association. Circulation 2000;102:2284-99.  Back to cited text no. 28    
29.Stein DT, Devaraj S, Balis D, Adams -Huet B, Jialal I. Effect of statin therapy on remnant lipoprotein cholesterol levels in patients with combined hyperlipidemia. Arterioscler Thromb Vasc Biol 2001;21:2026-31.  Back to cited text no. 29    
30.Tan KC, Chow WS, Tam SC, Ai VH, Lam CH, Lam KS. Atorvastatin lowers C-reactive protein and improves endothelial-dependent vasodilatation in type 2 diabetes mellitus. J Clin Endocrinol Metab 2002;87:563-8.  Back to cited text no. 30  [PUBMED]  [FULLTEXT]
31.Steiner G. Fibrates in the metabolic syndrome and in diabetes. Endocrinol Metab Clin N Am 2004;33:545-6.  Back to cited text no. 31  [PUBMED]  [FULLTEXT]
32.Eidelman R, Herbert P, Weisman S, Henneken S. An update on aspirin in the primary prevention of cardiovascular disease. Arch Intern Med 2003;163:2006-10.  Back to cited text no. 32    
33.Antithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomized trials of anti-platelet therapy for prevention of death, myocardial infarction and stroke in high-risk patients. BMJ 2002;324:71-86.  Back to cited text no. 33    
34.Casson PA, Segal MR, Vokonas PS, Weiss ST. Body fat distribution, blood pressure and hypertension. A prospective cohort study of men in the normative aging study. Ann Epidemiol 1990;1:33-48.  Back to cited text no. 34    
35.Zavaroni I, Mazza S, Dall' AE, Gasparini P, Passeri M, Reavan GM. Prevalence of hyperinsulinaemia in patients with blood pressure. J Intern Med 1992;231:235-40.  Back to cited text no. 35    
36.Appel LJ, Moore FJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM, et al. A clinical trial of the effects of dietary patterns on blood pressure. N Eng J Med 1997;336:1117-24.  Back to cited text no. 36    
37.Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, et al. Effects on blood pressure of reduced dietary sodium and the Dietary approaches to Stop Hypertension (DASH) diet. N Eng J Med 2001;344:3-10.  Back to cited text no. 37    
38.Ridker PM, Buring JE, Cook NR, Rifai N. C-reactive protein, the metabolic syndrome and risk of incident cardiovascular events an eight year follow up of 14,719 initially healthy American women. Circulation 2003;107:391-7.  Back to cited text no. 38    
39.Wannamethee SG, Lowe GD, Whincup PH, Whincup PH, Rumley A, Walker M, et al. Physical activity and hemostatic and inflammatory variables in elderly men. Circulation 2002;105:1785-90.  Back to cited text no. 39    
40.Pischon T, Hankinson SE, Hotamisligil GS, Rifai N, Rimm EB. Leisure- time physical activity and reduced plasma levels of obesity-related inflammatory markers. Obes Res 2003;11:1055-64.  Back to cited text no. 40    
41.Pearson TA, Mensah GA, Alexander RW, Anderson JL, Cammon RO 3rd, Criqui M, et al. Markers of Inflammation and cardiovascular disease: application to clinical and public health practice. A statement for healthcare professionals from the Center for Disease Control and Prevention and the American Heart Association. Circulation 2003;107:499-511.  Back to cited text no. 41    
42.Hooper L, Barlett C, Davey SG, Ebrahim S. Advice to reduce dietary salt for prevetion of cardiovascular disease. Cochrane Database Syst Rev 2004;2:CD003656.  Back to cited text no. 42    
43.Hooper L, Summerbell CD, Higgins JP, Thompson RL, Clements G, Capps N, et al. Reduced or modified dietary fat for preventing cardiovascular disease. Cochrane Database Syst Rev 2004;2:CD002137.  Back to cited text no. 43    
44.US Preventive Services Task Force. Behavioral counselling in primary care to promote a healthy diet: recommendations and rationale. Am J Prev Med 2003;24:93-100.  Back to cited text no. 44    
45.Duncan GE, Perri MG, Theriaque DW, Hutson AD, Eckel RH, Stacpoole PW. Exercise training, without weight loss, increases insulin sensitivity and postheparin plasma lipase activity in previously sedentary adults. Diabetes Care 2003;26:557-62.  Back to cited text no. 45    


    Tables

[Table - 1], [Table - 2]

This article has been cited by
1 Efficacy and safety of rosuvastatin in late-onset hypogonadism patients with dyslipidaemia
S. Kangwanvanich,S. Permpongkosol
Andrologia. 2013; : n/a
[Pubmed]
2 Neuroprotective and neurotrophic curcuminoids to treat stroke: A translational perspective
Lapchak, P.A.
Expert Opinion on Investigational Drugs. 2011; 20(1): 13-22
[Pubmed]
3 Association of benign prostatic hyperplasia (BPH) with the metabolic syndrome (MS) and its components - æa growing dilemmaæ
Tewari, R., Prabhat, P., Natu, S.M., Dalela, D., Goel, A., Goel, M.M., Tandon, P.
Journal of Menæs Health. 2011; 8(1): 66-71
[Pubmed]
4 Vascular insulin resistance in prehypertensive rats: Role of PI3-kinase/Akt/eNOS signaling
Li, R., Zhang, H., Wang, W., Wang, X., Huang, Y., Huang, C., Gao, F.
European Journal of Pharmacology. 2010; 628(1-3): 140-147
[Pubmed]
5 Effects of an Extract Obtained From Fruits of Euterpe oleracea Mart. in the Components of Metabolic Syndrome Induced in C57BL/6J Mice Fed a High-fat Diet :
Paola Raquel Braz de Oliveira, Cristiane Aguiar da Costa, Graziele Freitas de Bem, Lenize Costa Reis Marins de Cavalho, Marcelo Augusto Vieira de Souza, Miguel de Lemos Neto, Pergentino José da Cunha Sousa, Roberto Soares de Moura, Angela Castro Resende
Journal of Cardiovascular Pharmacology. 2010; 56(6): 619
[VIEW]
6 Fatty acid- and cholesterol transporter protein expression along the human intestinal tract
Masson, C.J., Plat, J., Mensink, R.P., Namiot, A., Kisielewski, W., Namiot, Z., Füllekrug, J., (...), Pelsers, M.M.A.L.
PLoS ONE. 2010; 5(4): art -e10380
[Pubmed]
7 Dietary restriction and brain health
Guang Qiu, Shan Liu, Kwok-Fai So
Neuroscience Bulletin. 2010; 26(1): 55-65
[Pubmed]
8 Vascular insulin resistance in prehypertensive rats: Role of PI3-kinase/Akt/eNOS signaling
Rong Li,Haifeng Zhang,Wenqing Wang,Xiaoming Wang,Yuxiao Huang,Chen Huang,Feng Gao
European Journal of Pharmacology. 2010; 628(1-3): 140
[Pubmed]
9 Improvement of high-fat-diet-induced metabolic syndrome by a compound from Balanophora polyandra Griff in mice
Rongya Tao,Fei Ye,Yibo He,Jinying Tian,Gengtao Liu,Tengfei Ji,Yalun Su
European Journal of Pharmacology. 2009; 616(1-3): 328
[Pubmed]
10 A mixture of Salacia reticulata (Kotala himbutu) aqueous extract and cyclodextrin reduces body weight gain, visceral fat accumulation, and total cholesterol and insulin increases in male Wistar fatty rats
Eriko Kishino, Tetsuya Ito, Koki Fujita, Yoshihiro Kiuchi
Nutrition Research. 2009; 29(1): 55
[VIEW]
11 Psychological distress within cardiovascular risks behaviors, conditions and diseases conceptual framework
Brborović, O., Rukavina, T.V., Pavleković, G., Džakula, A., Šogorić, S., Vuletić, S.
Collegium Antropologicum. 2009; 33(1 Suppl 1): 93-98
[Pubmed]
12 result5. A mixture of Salacia reticulata (Kotala himbutu) aqueous extract and cyclodextrin reduces body weight gain, visceral fat accumulation, and total cholesterol and insulin increases in male Wistar fatty rats
Kishino, E., Ito, T., Fujita, K., Kiuchi, Y.
Nutrition Research. 2009; 29(1): 55-63
[Pubmed]
13 Improvement of high-fat-diet-induced metabolic syndrome by a compound from Balanophora polyandra Griff in mice
Tao, R., Ye, F., He, Y., Tian, J., Liu, G., Ji, T., Su, Y.
European Journal of Pharmacology. 2009; 616(1-3): 328-333
[Pubmed]
14 Impact of metabolic syndromeæs components on the development of cardiovascular disease in a Jordanian cohort with metabolic syndrome
Haddad, F.H., Mahafza, S.M.
Saudi Medical Journal. 2008; 29(9): 1299-1305
[Pubmed]
15 The Association of the Metabolic Syndrome with T-wave Axis Deviation in NHANES III
Faramawi, M.F., Sall, M., Abdul Kareem, M.Y.
Annals of Epidemiology. 2008; 18(9): 702-707
[Pubmed]
16 The association of the metabolic syndrome with QTc interval in NHANES III
Faramawi, M.F., Wildman, R.P., Gustat, J., Rice, J., Abdul Kareem, M.Y.
European Journal of Epidemiology. 2008; 23(7): 459-465
[Pubmed]
17 The islet autoantibody titres: their clinical relevance in latent autoimmune diabetes in adults (LADA) and the classification of diabetes mellitus
Van Deutekom, AW and Heine, RJ and Simsek, S.
Diabetic Medicine. 2008; 25(2): 117-125
[Pubmed]
18 Traditional chinese medicine in treatment of metabolic syndrome.
Yin, J. and Zhang, H. and Ye, J.
Endocrine, metabolic & immune disorders drug targets. 2008; 8(2): 99-111
[Pubmed]
19 The Metabolic Syndrome Among Patients Undergoing Cardiac Catheterization in Jordan
Khader, Y. and Khatatbeh, M. and EL-Salem, K. and Amarin, Z. and Bateiha, A.
Journal of the CardioMetabolic Syndrome. 2008; 3(4): 224-228
[Pubmed]
20 Frecuencia y caracteristicas clinicas, hormonales y ultrasonograficas sugestivas de sindrome de ovarios poliquisticos en un grupo de mujeres con sindrome metabolico
Carballo, G.O. and Alonso, E.D. and Varela, O.L.V. and Recinos, H.Z.
Rev. cuba. endocrinol. 2008; 19(1)
[Pubmed]
21 Metabolic comorbidity in schizophrenia
Rajesh, J. and ArabindaNarayan, C.
Indian Journal of Medical Sciences. 2008; 62(1): 23-31
[Pubmed]
22 The islet autoantibody titres: their clinical relevance in latent autoimmune diabetes in adults (LADA) and the classification of diabetes mellitus
A. W. van Deutekom,R. J. Heine,S. Simsek
Diabetic Medicine. 2008; 25(2): 117
[Pubmed]
23 The Metabolic Syndrome Among Patients Undergoing Cardiac Catheterization in Jordan
Yousef Khader,Moawiah Khatatbeh,Khalid EL-Salem,Zouhair Amarin,Anwar Bateiha
Journal of the CardioMetabolic Syndrome. 2008; 3(4): 224
[Pubmed]
24 The Association of the Metabolic Syndrome with T-wave Axis Deviation in NHANES III
Mohammed F. Faramawi,Macodu Sall,Mohammed Y. Abdul Kareem
Annals of Epidemiology. 2008; 18(9): 702
[Pubmed]
25 The association of the metabolic syndrome with QTc interval in NHANES III
Mohammed F. Faramawi,Rachel P. Wildman,Jeanette Gustat,Janet Rice,Mohammed Y. Abdul Kareem
European Journal of Epidemiology. 2008; 23(7): 459
[Pubmed]
26 Differential Effects of Oral Hypoglycemic Agents on Glucose Control and Cardiovascular Risk
Gabriel I. Uwaifo,Robert E. Ratner
The American Journal of Cardiology. 2007; 99(4): 51
[Pubmed]
27 Impact of Obesity in Pediatric Anesthesia
Carole Lin
Advances in Anesthesia. 2007; 25: 79
[Pubmed]
28 Metabolic syndrome in the Croatian population - The multiple cardiovascular risks | [Metabolički sindrom u populaciji Hrvatske - Kardiovaskularna multirizičnost]
Vuletić, S., Kern, J., Ivanković, D., Polašek, O., Brborović, O.
Acta Medica Croatica. 2007; 61(3): 239-243
[Pubmed]
29 Differential Effects of Oral Hypoglycemic Agents on Glucose Control and Cardiovascular Risk
Uwaifo, G.I., Ratner, R.E.
American Journal of Cardiology. 2007; 99(4 Suppl): 51-67
[Pubmed]
30 Prevalence of the metabolic syndrome in women with polycystic ovary syndrome | [Prevalência da síndrome metabólica em portadoras da síndrome dos ovários policísticos]
Costa, L.O.B.F., Viana, A.D.O.R., De Oliveira, M.
Revista Brasileira de Ginecologia e Obstetricia. 2007; 29(1): 10-17
[Pubmed]
31 Metabolic Syndrome in Drug Abuse
Virmani, A. and Binienda, Z.K. and Ali, S.F. and Gaetani, F.
Annals of the New York Academy of Sciences. 2007; 1122: 50-68
[Pubmed]
32 Impact of Obesity in Pediatric Anesthesia
Lin, C.
Advances in Anesthesia. 2007; 25: 79-101
[Pubmed]
33 Prevalence and characteristics of metabolic syndrome in 111 Royal Jordanian Air Force pilots.
Khazale, NS and Haddad, F.
Aviation, space, and environmental medicine. 2007; 78(10): 968
[Pubmed]



 

Top
Print this article  Email this article
Previous article Next article

    

© 2004 - Indian Journal of Medical Sciences
Published by Medknow
Online since 15th December '04