Home | About us | Editorial board | Search | Ahead of print | Current issue | Archives | Submit article | Instructions | Subscribe | Contacts | Advertise | Login 
 
Search Article 
  
Advanced search 
  Users Online: 652 Home Print this page Email this page Small font sizeDefault font sizeIncrease font size  

 
Table of Contents
REVIEW ARTICLE
Year : 2012  |  Volume : 16  |  Issue : 1  |  Page : 81-87

Tobacco and metabolic syndrome


Department of Psychiatry, Lady Harding Medical College and Associated Hospitals, New Delhi, India

Date of Web Publication26-Dec-2011

Correspondence Address:
Yatan Pal Singh Balhara
Department of Psychiatry, Lady Harding Medical College and Associated Hospitals, New Delhi
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2230-8210.91197

Rights and Permissions
   Abstract 

Tobacco is a leading contributor to morbidity and mortality globally. Metabolic syndrome is a constellation of abdominal obesity, atherogenic dyslipidemia, raised blood pressure, insulin resistance (with and without glucose intolerance), pro-inflammatory state, and pro-thrombotic state. Tobacco use is associated with various core components of metabolic syndrome. It has been found to play a causal role in various pathways leading on to development this condition, the current article discusses various facets of this association.

Keywords: Metabolic syndrome, second-hand smoke, tobacco


How to cite this article:
Balhara Y. Tobacco and metabolic syndrome. Indian J Endocr Metab 2012;16:81-7

How to cite this URL:
Balhara Y. Tobacco and metabolic syndrome. Indian J Endocr Metab [serial online] 2012 [cited 2018 Dec 9];16:81-7. Available from: http://www.ijem.in/text.asp?2012/16/1/81/91197


   Introduction Top


Adverse impact of tobacco products on health has been well established for more than 50 years. [1] Consumption of tobacco is a risk factor for six of the world's eight leading causes of death. [2] Projected to kill around 1 billion people in this century, it remains the commonest preventable and modifiable contributor to morbidity and mortality globally. Apart from the direct tobacco smoke, exposure to second-hand tobacco smoke (SHS) causes illness, disability, and death from a wide range of diseases. [3] In fact, it contributes to about 1% of the total global disease burden. [4]

Contrary to popular belief the problem of tobacco use hits developing countries the hardest. By 2030, tobacco is projected to take a toll of 8 million lives per year, with 80% of these deaths occurring in low and middle income countries like India. [5]

In India, the National Family Health Survey (NFHS-3) conducted in the years 2005-2006 puts the prevalence rate of current tobacco use at 57% and 10.8% among males and females aged 15-49 years. [6] A more recent Global Adult Tobacco Survey (GATS) reported that more than one-third (35%) of adults in India use tobacco in some form or the other. Among them, 21% adults use only smokeless tobacco, 9% only smoke and 5% smoke as well as use smokeless tobacco. The prevalence of overall tobacco use among males and females was found to be 48% and 20%, respectively. [7]

Metabolic syndrome remains an evolving concept with different work groups presenting varied criteria for this condition. The state of controversy is reflected in the fact that the American Diabetes Association and the European Association for the Study of Diabetes made a joint statement in 2005 that no existing definition of this condition meets the criteria of a syndrome. [8] However, abdominal obesity, atherogenic dyslipidemia, raised blood pressure, insulin resistance (with and without glucose intolerance), pro-inflammatory state, and prothrombotic state continue to remain core features of different definitions of metabolic syndrome. [9] [Table 1] presents the 2009 consensus criteria proposed by International Diabetes Federation Task Force on Epidemiology and Prevention, National Heart, Lung, and Blood Institute, American Heart Association, World Heart Federation International Atherosclerosis Society, and International Association for the Study of Obesity. [10]
Table 1: 2009 consensus criteria for metabolic syndrome and it is diagnosed if three or more of the following criteria are present

Click here to view


Metabolic syndrome predicts the development of type 2 diabetes mellitus and cardiovascular disease. [11] It has also been identified as a pre-disease state of fatty liver disease, [12] chronic kidney disease (CKD), [13] and chronic lung disease [Box 1]. [14]

Studies exploring the prevalence of metabolic syndrome have come up with varied findings, primarily due to differences in cut-off points for various components of the syndrome. It is estimated that around 20-25% of the world's adult population has metabolic syndrome. [15] General population based studies from India have reported variable prevalence rates of 11.2%, [16] 13%, [17] 24.6%, [18] and 41% [19] for metabolic syndrome. This wide variation in prevalence is partially explained by the different diagnostic criteria used across these studies. Additionally, the differences in population characteristics, specially the place of residence, have also contributed to this variation. The prevalence rate of metabolic syndrome has been consistently found to be higher in urban setting.




   Tobacco and Metabolic Syndrome Top


Association between tobacco and metabolic syndrome has been well established. Exposure to tobacco, direst as well as indirect, has been found to play a causal role in emergence of various core components of this condition.


   Epidemiological Findings Top


Tobacco use has been associated with an increased risk of developing metabolic syndrome. [20],[21] It acts at multiple levels in the etiopathogenesis of metabolic syndrome. There is a positive dose-response relationship between the daily number of cigarettes smoked and the risk of metabolic syndrome. [22] Both the former and current smoking are associated with an increased incidence of metabolic syndrome. [23] In fact the risk has been shown to persist for up to 20 years after quitting tobacco use. [24] A national nutrition examination survey in USA reported an increase in risk of development of metabolic syndrome among women (OR, 1.8; 95% CI: 1.2-2.6) and men (OR, 1.5; 95% CI: 1.1-2.2) who were current smokers compared with those who never smoked. [25] Exposure to tobacco smoke is associated with a 4-fold increased risk of development of metabolic syndrome among adolescents who are either overweight or at risk for overweight. [26]

The prevalence rate of smoking among patients diagnosed with metabolic syndrome tends to vary across studies. One of the major limitations of most of these studies is the reliance on self-report on tobacco use as it might underestimate the prevalence rates. Takeuchi et al., reported the smoking rate of 40% among individuals diagnosed with metabolic syndrome. The rate of smoking was found to be 71% among individuals with metabolic syndrome in a Columbian study. [27] A recent study from urban India found the rate of smoking to be 26% and 3% among males and females diagnosed with metabolic syndrome. [28]


   Type of Tobacco Exposure and Metabolic Syndrome Top


Exposure to tobacco smoke in all forms has been associated with metabolic syndrome. The strongest evidence base linking tobacco and metabolic syndrome is for smoking. Smoking has been found to play a causal role in emergence of core components of metabolic syndrome. Although the evidence base is much wider and stronger for the smoking, even the smokeless forms have been associated with increased prevalence of metabolic syndrome. Additionally exposure to SHS (also called environmental tobacco smoke, ETS) has been found to contribute to increased prevalence of this syndrome. [29]


   Association of Tobacco use and Core Components of Metabolic Syndrome Top


The various pathways of etiopathogenesis of metabolic syndrome include increased adiposity, insulin resistance, leptin resistance, low-grade systemic inflammation, endothelial dysfunction, and autonomic dysfunction. [30] Tobacco use is associated with all these cascades and hence could contribute to development of metabolic syndrome through multiple mechanisms.

Smoking has been associated with an increased waist circumference (and increased waist-hip ratio, WHR), increased triglycerides, and reduced HDL cholesterol. [31],[32] WHR is positively associated with the number of pack-years of smoking, [33] and there is a dose-response relation between WHR and the number of cigarettes smoked. [34] The association among smoking amount and high triglyceride level and low HDL level has also been reported to be dose-dependent. [35] It has been associated with endothelial dysfunction and a hypercoagulable state. [36] Interestingly, smoking is associated with a reduced prevalence of hypertension as compared to non-smokers. [37],[38] However, the methodological issues have been carted as reasons behind this observation. Although smoking increase blood pressure, recordings taken after a few hours of gap in smoking reflect lower blood pressure as compared to non-smokers [Box 2]. [39]



The use of smokeless tobacco has received relatively lesser attention in the scientific literature as compared to smoking. However, the use of smokeless forms of tobacco is not uncommon. In fact while there is a decline in smoking rates in many developed countries, prevalence of smokeless tobacco use continues to rise. [40],[41] In India prevalence of use of smokeless tobacco among adult males and females is 33% and 18%, respectively.

Smokeless tobacco use has been associated with various metabolic and hemodynamic derangements associated with metabolic syndrome. These include hypertension, dyslipidemia, and impaired glycemic control. Role of smokeless tobacco in platelet dysfunction [42] and derangement of factors of coagulation cascade [43] has not been well established.


   Tobacco and Insulin Resistance Top


Insulin resistance has been postulated to play a significant role in development of metabolic syndrome. [44] Insulin resistance directly contributes to other metabolic risk factors as well. Increased insulin resistance might underlie the metabolic and hemodynamic abnormalities contributing to metabolic syndrome. Tobacco use has been associated with reduced insulin sensitivity and development of insulin resistance. [45] Even a short-term tobacco use also leads to development of insulin resistance. [46] Smoking increases the circulating levels of hormones such as cortisol, catecholamines, and growth hormone which have insulin antagonistic actions. High circulating levels of free fatty acids also interfere with insulin medicated glucose uptake. Autonomic dysfunction as reflected in the increased heart rate has also been associated with insulin resistance. [47] Additionally, the heart rate has been found to be linearly associated with an increased risk of metabolic syndrome. [29] A higher heart rate has also been found to be an independent risk factor for hypertension. Tobacco use is associated with increased heart rate.

Smokeless tobacco use has been associated with hyperinsulinemia. However, the mechanism of insulin resistance induced by smokeless tobacco use might be different from that of smoking as the level of growth hormone (an insulin counter-regulatory hormone) has not been found to be raised among users of smokeless tobacco forms. [48]


   Tobacco and Dyslipidemia Top


Smoking leads to increase in triglyceride levels and reduction in HDL cholesterol by increasing sympathetic activity. Smoking causes higher fasting plasma cortisol concentrations, resulting in an increase in visceral adipose tissue. [49]

Studies assessing the impact of smokeless tobacco use on lipid profile have come up with contradictory findings. While higher blood cholesterol, higher triglyceride and lower high-density lipoprotein levels have been reported in some studies, [50],[51] others have failed to find such associations. [52]


   Tobacco and Adiposity Top


As mentioned above smoking is related to high WHR in a dose-dependent manner. Smokers tend to have a higher waist and lower hip circumference compared to non-smokers. [32] Waist circumference is closely related to the visceral adipose tissue distribution. The visceral adipose tissue distribution, in turn, is influenced by the serum cortisol [53] and sex hormone concentrations (low estrogen and testosterone). [54] Low levels of total and free testosterone have been associated with development of visceral obesity and metabolic syndrome. Testosterone facilitates lipolysis and inhibits fatty acid formation. The effect of testosterone on metabolic syndrome is independent to that of risk of obesity. [55] Smokeless tobacco use has also been shown to lead to obesity development. [56]


   Tobacco and Hypertension Top


Smoking as a hypertension risk factor is not well established. Smoking leads to an acute increase in blood pressure. Nicotine acts as an adrenergic agonist, mediating local and systemic catecholamine release. Additionally, it causes release of vasopressin. Smoking also causes an increase in the heart rate. A higher heart rate has also been found to be an independent risk factor for hypertension. [29]

However, several epidemiological studies have found that blood pressure levels among cigarette smokers are the same as or lower than those of non-smokers. This observation has been attributed to the methodology employed in these studies. The studies assessing 24-h ambulatory blood pressure monitoring have found that smokers tend to maintain a higher mean daytime ambulatory systolic blood pressure than nonsmokers. [57] The use of smokeless tobacco has been associated with an increase in blood pressure consequent to its effect on sympathetic system. [58] These findings have been reported in studies from India as well. [59],[60] High sodium content, nicotine and licorice present in smokeless tobacco are responsible for this effect. Users' age, level of physical activity, and total duration of effect seem to mediate the long-term effect on blood pressure. [16] Also, it is associated with an increase in the heart rate.

Similarly acute response of blood pressure to environmental tobacco smoke exposure is uncertain with studies reporting either an increase [61] or no effects [62] following the passive smoking.


   Tobacco and Proinflammatory State and Prothrombotic State Top


Smoking has been associated with increased levels of inflammatory markers such as C reactive protein and fibrinogen. [63] It triggers an immunologic response to vascular injury, which is associated with increased levels of inflammatory markers. These markers have a dose-dependent and temporal relationship to smoking and smoking cessation. [64]

Smoking alters the coagulation-fibrinolysis system in favor of thrombosis. [65] It influences coagulation-fibrinolysis cascade at many levels. Its primary action is on endothelium, platelets, and fibrinogen. [66]


   Persistence of Effect of Tobacco use on Metabolic Syndrome Top


Tobacco use cessation lowers the risk of developing metabolic syndrome. However, the increased risk of metabolic syndrome among smokers tends to persist for years after quitting. This risk is reduced as compared to the risk during smoking years, but is still higher than those who have never smoked. [23] The possible underlying mechanisms for the long-lasting effects of smoking on insulin resistance include vascular changes leading to decreased glucose uptake by skeletal muscle, proinflammatory effect (as evidenced by increased circulating white blood cell count, cytokines) and decreased plasma levels of adiponectin. [67]


   Management of Tobacco use Top


Effective management of tobacco use requires an individualized comprehensive intervention plan. All users should be advised to quit. Those who have not yet started should be advised not to initiate. All patients seeking medical help should be asked about their tobacco use-both smoking and smokeless forms. Additionally, they should be assessed about the exposure to SHS. Severity of tobacco dependence can be assessed suing the Fagerstrom Test for Nicotine Dependence (FTND) scale. Separate versions are available for smoking and smokeless forms.

Various pharmacological and nonpharmacological interventions are available for treatment of tobacco dependence. The medications approved for treatment of tobacco dependence include the Nicotine Replacement Therapy (NRT), bupropion-sustained release (bupropion-SR), varenicline, clonidine, and nortryptiline. [68]

NRT is one of the most commonly used first-line therapy for tobacco dependence. It prevents the withdrawals associated with abstinence from tobacco products and addressed craving. It avoids the harmful consequence of the non-nicotine ingredients of tobacco products. It is freely available as a gum. Other delivery forms include patch, inhaler, lozenges, and nasal spray. The dose of nicotine is determined by the amount of tobacco product used by the individual.

Bupropion-SR acts by blockage of reuptake of dopamine and norepinephrine in the central nervous system. Its use is preferred if there is co-morbid depression. Additionally, it has been found to be effective for quitting associated weight gain. Varenicline is a partial agonist at the nicotinic cholinergic receptors. Recently, there are some reports about cardiovascular adverse effects associated with its use.

Clonidine and nortryptiline constitute the second-line therapies that are not frequently used. Along with the medications each individual should be offered nonpharmacological interventions. It has been shown that a combination of pharmacological and nonpharmacological interventions is associated with best results for tobacco dependence treatment. [69] Some of the nonpharmacological interventions commonly used include motivation enhancement therapy, brief intervention, and relapse prevention.


   Impact of Smoking Cessation on Metabolic Syndrome Top


Tobacco use cessation lowers the risk of developing metabolic syndrome. It has been associated with a reduction in the triglyceride level and improved HDL level. [34] It improves insulin sensitivity as well. [70]

However, increase in body weight subsequent to quitting tobacco use could contribute to the increase risk of metabolic syndrome. The possible mechanisms of weight gain after quitting tobacco use include increased energy intake, decreased resting metabolic rate, decreased physical activity, and increased lipoprotein lipase activity. [71] Additionally, nicotine, through its antiestrogenic effects, induces lipolysis by stimulating the sympathetic nervous system. [72] An imbalance between lipid intake and lipid oxidation consequent to smoking cessation can also contribute to increased body fat. NRT has been reported to be associated with hyperinsulinemia and insulin resistance. This association has been found to be independent of the postcessation weight gain among these individuals. [73]

However, the potential benefits of tobacco use cessation are multiple. Hence, it is important to advise all users to quit. An appropriate dietary and exercise schedule should be formulated for those interested in quitting tobacco use to address quitting associated weight gain.

Exposure to tobacco-smoking, smokeless forms and SHS-is a contributor to the various core components of metabolic syndrome. Tobacco acts at multiple levels in the etiopathogenesis of metabolic syndrome. Appropriate management of tobacco use and prevention of exposure to SHS can help reduce the risk of metabolic syndrome.

 
   References Top

1.Smoking and health: Joint report of the Study Group on Smoking and Health. Science 1957;125:1129-33.  Back to cited text no. 1
    
2.Lopez AD, Mathers CD, Ezzati M, Jamison DT, Murray CJ. Global burden of disease and risk factors. Washington, DC: Oxford University Press and The World Bank; 2006.  Back to cited text no. 2
    
3.Woodward A, Laugesen M. How many deaths are caused by second-hand cigarette smoke? Tob Control 2001;10:383-8.  Back to cited text no. 3
    
4.Öberg M, Jaakkola MS, Woodward A, Peruga A, Prüss-Ustün A. Worldwide burden of disease from exposure to second-hand smoke: A retrospective analysis of data from 192 countries. Lancet 2011;377:139-46.  Back to cited text no. 4
    
5.WHO report on the global tobacco epidemic, 2009: Implementing smoke-free environments. Geneva: World Health Organisation; 2009, France.  Back to cited text no. 5
    
6.International Institute for Population Sciences. National Family Health Survey (NFHS-3) 2005-06, Mumbai, 2007..  Back to cited text no. 6
    
7.Ministry of Health and Family Welfare, Government of India. Global Adult Tobacco Survey, GATS India, 2005-2006.  Back to cited text no. 7
    
8.Kahn R, Buse J, Ferrannini E, Stern M; American Diabetes Association; European Association for the Study of Diabetes. The metabolic syndrome: Time for a critical appraisal: Joint statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care 2005;28:2289-304.  Back to cited text no. 8
    
9.Grundy SM, Brewer HB, Cleeman JJ, Smith SC, Lenfant C, American Heart Association; National Heart, Lung, and Blood Institute. Definition of Metabolic Syndrome Report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Circulation 2004;109:433-8.  Back to cited text no. 9
    
10.Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, et al. Harmonizing the metabolic syndrome. A joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation 2009;120:1640-5.  Back to cited text no. 10
    
11.Vega GL. Obesity, the metabolic syndrome, and Cardiovascular disease. Am Heart J 2001;142:1108-16.  Back to cited text no. 11
    
12.Kotronen A, Yki-Jarvinen H. Fatty liver: A novel component of the metabolic syndrome. Arterioscler Thromb Vasc Biol 2008;28:27-38.  Back to cited text no. 12
    
13.Chen J, Muntner P, Hamm LL, Jones DW, Batuman V, Fonseca V, et al. The metabolic syndrome and chronic kidney disease in U.S. adults. Ann Intern Med 2004;140:167-74.  Back to cited text no. 13
    
14.Fabbri LM, Rabe KF. From COPD to chronic systemic inflammatory syndrome? Lancet 2007;370:797-9.  Back to cited text no. 14
    
15.International Diabetes Foundation. The IDF consensus worldwide definition of the metabolic syndrome. Brussels, Belgium: IDF Communications; 2006.  Back to cited text no. 15
    
16.Deepa R, Shantiram CS, Premalatha G, Sastry 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. 16
    
17.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. 17
    
18.Prabhakaran D, Chaturvedi V, Shah P, Manhapra A, Jeemon P, Shah B, et al. Differences in the prevalence of metabolic syndrome in urban and rural India: A problem of urbanization. Chronic Illn 2007;3:8-19.  Back to cited text no. 18
    
19.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. 19
    
20.Wilsgaard T, Jacobsen BK. Lifestyle factors and incident metabolic syndrome. The Tromsø Study 1979-2001. Diabetes Res Clin Pract 2007;78:217-24.  Back to cited text no. 20
    
21.Miyatake N, Wada J, Kawasaki Y, Nishii K, Makino H, Numata T. Relationship between metabolic syndrome and cigarette smoking in the Japanese population. Intern Med 2006;45:1039-43.  Back to cited text no. 21
    
22.Nakanishi N, Takatorige T, Suzuki K. Cigarette smoking and the risk of the metabolic syndrome in middle-aged Japanese male office workers. Ind Health 2005;43:295-301.  Back to cited text no. 22
    
23.Ishizaka N, Ishizaka Y, Toda E, Hashimoto H, Nagai R, Yamakado M. Association between cigarette smoking, metabolic syndrome, and carotid arteriosclerosis in Japanese individuals. Atherosclerosis 2005;181:381-8.  Back to cited text no. 23
    
24.Wada T, Urashima M, Fukumoto T. Risk of metabolic syndrome persists twenty years after the cessation of smoking. Intern Med 2007;46:1079-82.  Back to cited text no. 24
    
25.Park YW, Zhu 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, 1988-1994. Arch Intern Med 2003;163:427-36.  Back to cited text no. 25
    
26.Weitzman M, Cook S, Auinger P, Florin TA, Daniels S, Nguyen M, et al. Tobacco Smoke Exposure Is Associated With the Metabolic Syndrome in Adolescents. Circulation 2005;112:862-9.  Back to cited text no. 26
    
27.Lechuga EN, Moranth RV. Metabolic syndrome in the southeast of Barranquilla (Colombia). Salud Uninorte 2008;24:40-52.  Back to cited text no. 27
    
28.Sawant A, Mankeshwar R, Shah S, Raghavan R, Dhongde G, Raje H, et al. Prevalence of metabolic syndrome in urban india. Cholesterol 2011;2011;920983.  Back to cited text no. 28
    
29.Xie B, Palmer PH, Pang Z, Sun P, Duan H, Johnson CA. Environmental tobacco use and indicators of metabolic syndrome in Chinese adults. Nicotine Tob Res 2010;12:198-206.  Back to cited text no. 29
    
30.Oda E, Kawai R. Significance of heart rate in the prevalence of metabolic syndrome and its related risk factors in Japanese. Circ J 2009;73:1431-6.  Back to cited text no. 30
    
31.Nakashita Y, Nakamura M, Kitamura A, Kiyama M, Ishikawa Y, Mikami H. Relationships of cigarette smoking and alcohol consumption to metabolic syndrome in Japanese Men. J Epidemiol 2010;20:391-7.  Back to cited text no. 31
    
32.Panagiotakos DB, Pitsavos C, Chrysohoou C, Skoumas J, Masoura C, Toutouzas P, et al. Effect of exposure to secondhand smoke on markers of inflammation: The ATTICA study. Am J Med 2004;116:145-50.  Back to cited text no. 32
    
33.Canoy D, Wareham N, Luben R, Welch A, Bingham S, Day N, et al. Cigarette smoking and fat distribution in 21,828 British men and women: A population-based study. Obes Res 2005;13:1466-75.  Back to cited text no. 33
    
34.Rosmond R, Bjorntorp P. Psychosocial and socio-economic factors in women and their relationship to obesity and regional body fat distribution. Int J Obes Relat Metab Disord 1999;23:138-45.  Back to cited text no. 34
    
35.Chen CC, Li TC, Chang PC, Liu CS, Lin WY, Wu MT, et al. Association among cigarette smoking, metabolic syndrome, and its individual components: The metabolic syndrome study in Taiwan. Metabolism 2008;57:544-8.  Back to cited text no. 35
    
36.Ferrence R, Slade J, Room R, Pope M. Nicotine and Public Health. Washington DC: American Public Health Association; 2000.  Back to cited text no. 36
    
37.Oh SW, Yoon YS, Lee ES, Kim WK, Park C, Lee S, et al. Association between cigarette smoking and metabolic syndrome: The Korea National Health and Nutrition Examination Survey. Diabetes Care 2005;28:2064-6.  Back to cited text no. 37
    
38.Dzien A, Dzien-Bischinger C, Hoppichler F, Lechleitner M. The metabolic syndrome as a link between smoking and cardiovascular disease. Diabetes Obes Metab 2004;6:127-32.  Back to cited text no. 38
    
39.Takeuchi T, Nakao M, Nomura K, Yano E. Association of metabolic syndrome with smoking and alcohol intake in Japanese men. Nicotine Tob Res 2009;11:1093-8.  Back to cited text no. 39
    
40.Gupta R, Gurm H, Bartholomew JR. Smokeless tobacco and cardiovascular risk. Arch Intern Med 2004;164:1845-9.  Back to cited text no. 40
    
41.Lindahl B, Stegmayr B, Johansson I, Weinehall L, Hallmans G. Trends in lifestyle 1986-99 in a 25- to 64-year-old population of the Northern Sweden MONICA project. Scand J Public Health Suppl 2003;61:31-7.  Back to cited text no. 41
    
42.Yildiz D, Liu YS, Ercal N, Armstrong DW. Comparison of pure nicotine- and smokeless tobacco extract-induced toxicities and oxidative stress. Arch Environ Contam Toxicol 1999;37:434-9.  Back to cited text no. 42
    
43.Eliasson M, Asplund K, Evrin PE, Lundblad D. Relationship of cigarette smoking and snuff dipping to plasma fibrinogen, fibrinolytic variables and serum insulin: The Northern Sweden MONICA study. Atherosclerosis 1995;113:41-53.  Back to cited text no. 43
    
44.Ferrannini E, Haffner SM, Mitchell BD, Stern MP. Hyperinsulinaemia: The key feature of a cardiovascular and metabolic syndrome. Diabetologia 1991;34:416-22.  Back to cited text no. 44
    
45.Filozof C, Fernández Pinilla MC, Fernández-Cruz A. Smoking cessation and weight gain. Obes Rev 2004;5:95-103.  Back to cited text no. 45
    
46.Frati AC, Iniestra F, Ariza CR. Acute effect of cigarette smoking on glucose tolerance and other cardiovascular risk factors. Diabetes Care 1996;19:112-8.  Back to cited text no. 46
    
47.Palatini P, Casiglia E, Pauletto P, Staessen J, Kaciroti N, Julius S. Relationship of tachycardia with high blood pressure and metabolic abnormalities: A study with mixture analysis in three populations. Hypertension 1997;30:1267-73.  Back to cited text no. 47
    
48.Attvall S, Fowelin J, Lager I, Von Schenck H, Smith U. Smoking induces insulin resistance-a potential link with the insulin resistance syndrome. J Intern Med 1993;233:327-32.  Back to cited text no. 48
    
49.Chiolero A, Faeh D, Paccaud F, Cornuz J. Consequences of smoking for body weight, body fat distribution, and insulin resistance. Am J Clin Nutr 2008;87:801-9.  Back to cited text no. 49
    
50.Tucker LA. Use of smokeless tobacco, cigarette smoking and hypercholesterolemia. Am J Public Health 1989;79:1048-50.  Back to cited text no. 50
    
51.Khurana M, Sharma D, Khandelwal PD. Lipid profile in smokers and tobacco chewers-a comparative study. J Assoc Physicians India 2000;48:895-7.  Back to cited text no. 51
    
52.Bolinder G, Noren A, de Faire U, Wahren J. Smokeless tobacco use and atherosclerosis: An ultrasonographic investigation of carotid intima media thickness in healthy middle-aged men. Atherosclerosis 1997;132:95-103.  Back to cited text no. 52
    
53.Pasquali R, Vicennati V. Activity of the hypothalamic-pituitaryadrenal axis in different obesity phenotypes. Int J Obes Relat Metab Disord 2000;24(suppl 2):S47-9.  Back to cited text no. 53
    
54.Haarbo J, Marslew U, Gotfredsen A, Christiansen C. Postmenopausal hormone replacement therapy prevents central distribution of body fat after menopause. Metabolism 1991;40:1323- 6.  Back to cited text no. 54
    
55.Wang C, Jackson G, Jones TH, Matsumoto AM, Nehra A, Perelman MA, et al. Low testosterone associated with obesity and the metabolic syndrome contributes to sexual dysfunction and cardiovascular disease risk in men with type 2 diabetes. Diabetes Care 2011;34:1669-75.  Back to cited text no. 55
    
56.Norberg M, Stenlund H, Lindahl B, Boman K, Weinehall L. Contribution of Swedish moist snuff to the metabolic syndrome: A wolf in sheep's clothing? Scand J Public Health 2006;34:576-83.  Back to cited text no. 56
    
57.Primatesta P, Falaschetti E Gupta S, Marmot MG, Poulter NR. Association between smoking and blood pressure: Evidence from the health survey for England. Hypertension 2001;37:187-93.  Back to cited text no. 57
    
58.Westman EC. Does smokeless tobacco cause hypertension? South Med J 1995;88:716-20.  Back to cited text no. 58
    
59.Hazarika NC, Biswas D, Narain K, Kalita HC, Mahanta J. Hypertension and its risk factors in tea garden workers of Assam. Natl Med J India 2002;15:63-8.  Back to cited text no. 59
    
60.Pandey A, Patni N, Sarangi S, Singh M, Sharma K, Vellimana AK, et al. Association of exclusive smokeless tobacco consumption with hypertension in an adult male rural population of India. Tob Induc Dis 2009;5:15.  Back to cited text no. 60
    
61.Mahmud A, Feely J. Effects of passive smoking on blood pressure and aortic pressure waveform in healthy young adults - influence of gender. Br J Clin Pharmacol 2004;57:37-43.  Back to cited text no. 61
    
62.Kato M, Roberts-Thomson P, Philips BG, Narkiewicz K, Haynes WG, Pesek CA, et al. The effects of short-term passive smoke exposure on endothelium-dependent and independent vasodilatation. J Hypertens 1999;17:1395-401.  Back to cited text no. 62
    
63.Woodward M, Rumley A, Lowe GD, Tunstall-Pedoe H. C-reactive protein: Associations with haematological variables, cardiovascular risk factors and prevalent cardiovascular disease. Br J Haematol 2003;122:135-41.  Back to cited text no. 63
    
64.Bakhru A, Erlinger TP. Smoking cessation and cardiovascular disease risk factors: Results from the Third National Health and Nutrition Examination Survey. PLoS Med 2005;2:e160.  Back to cited text no. 64
    
65.Pretorius E, Oberholzer HM, van der Spuy WJ, Meiring JH. Smoking and coagulation: The sticky fibrin phenomenon. Ultrastruct Pathol 2010;34:236-9.  Back to cited text no. 65
    
66.Leone A. Smoking, haemostatic factors, and cardiovascular risk. Curr Pharm Des 2007;13:1661-7.  Back to cited text no. 66
    
67.Ishizakaa N, Ishizakab Y, Toda E, Hashimoto H, Nagaia R, Yamakado M. Association between cigarette smoking, metabolic syndrome, and carotid arteriosclerosis in Japanese individuals. Atherosclerosis 2005;181:381-8.  Back to cited text no. 67
    
68.Grief SN. Nicotine dependence: Health consequences, smoking cessation therapies, and pharmacotherapy. Prim Care 2011;38:23-39, 5.  Back to cited text no. 68
    
69.Grandes G, Cortada JM, Arrazola A, Laka JP. Predictors of long-term outcome of a smoking cessation programme in primary care. Br J Gen Pract 2003;487:101-7.  Back to cited text no. 69
    
70.He Y, Lam TH, Jiang B, Wang J, Sai X, Fan L, et al. Combined effects of tobacco smoke exposure and metabolic syndrome on cardiovascular risk in older residents of China. J Am Coll Cardiol 2009;53:363-71.  Back to cited text no. 70
    
71.Hishida A, Koyama A, Tomota A, Katase S, Asai Y, Hamajima1 N. Smoking cessation, alcohol intake and transient increase in the risk of metabolic syndrome among Japanese smokers at one health checkup institution. BMC Public Health 2009;9:263.  Back to cited text no. 71
    
72.Corella D, Guillén ME, Sáiz C, Portolés O, Sabater A, Folch J, et al. Associations of LPL and APOC3 gene polymorphisms on plasma lipids in a Mediterranean population: Interaction with tobacco smoking and the APOE locus. J Lipid Res 2002;43:416-27.  Back to cited text no. 72
    
73.Eliasson B, Taskinen MR, Smith U. Long-term use of nicotine gum is associated with hyperinsulinaemia and insulin resistance. Circulation 1996;94:878-81.  Back to cited text no. 73
    



 
 
    Tables

  [Table 1]


This article has been cited by
1 The relationship between hypovitaminosis D and metabolic syndrome: a cross sectional study among employees of a private university in Lebanon
Rachelle Ghadieh,Jocelyne Mattar Bou Mosleh,Sibelle Al Hayek,Samar Merhi,Jessy El Hayek Fares
BMC Nutrition. 2018; 4(1)
[Pubmed] | [DOI]
2 Resveratrol and pterostilbene ameliorate the metabolic derangements associated with smokeless tobacco in estrogen deficient female rats
Abhijit Nirwane,Anuradha Majumdar
Journal of Functional Foods. 2016; 23: 261
[Pubmed] | [DOI]
3 Lifestyle Factors and Metabolic Syndrome among Workers: The Role of Interactions between Smoking and Alcohol to Nutrition and Exercise
Jui-Hua Huang,Ren-Hau Li,Shu-Ling Huang,Hon-Ke Sia,Yu-Ling Chen,Feng-Cheng Tang
International Journal of Environmental Research and Public Health. 2015; 12(12): 15967
[Pubmed] | [DOI]
4 The Metabolic Syndrome among Postmenopausal Women in Rural Canton: Prevalence, Associated Factors, and the Optimal Obesity and Atherogenic Indices
Huiying Liang,Xi Chen,Qiaozhu Chen,Yulin Wang,Xueji Wu,Yaohui Li,Bingying Pan,Huazhang Liu,Ming Li,Chiara Bolego
PLoS ONE. 2013; 8(9): e74121
[Pubmed] | [DOI]
5 Hormonal, metabolic and nutritional alterations in smokers: emergency for smoking abstinence
Gláucia Renata Souza Rodrigues,Marcela Melquíades,Maria Alvim Leite,Maíra Barros Louro,Carmen Perches,Ana Lúcia de Almeida Vargas,Sheila Cristina Potente Dutra Luquetti,Aline Silva de Aguiar Nemer
Jornal Brasileiro de Psiquiatria. 2013; 62(4): 261
[Pubmed] | [DOI]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
    Abstract
   Introduction
    Tobacco and Meta...
    Epidemiological ...
    Type of Tobacco ...
    Association of T...
    Tobacco and Insu...
    Tobacco and Dysl...
    Tobacco and Adip...
    Tobacco and Hype...
    Tobacco and Proi...
    Persistence of E...
    Management of To...
    Impact of Smokin...
    References
    Article Tables

 Article Access Statistics
    Viewed1827    
    Printed73    
    Emailed0    
    PDF Downloaded478    
    Comments [Add]    
    Cited by others 5    

Recommend this journal