The Korean Journal of Medicine

The Korean Association of Internal Medicine (대한내과학회)
권호 표지

Effects of smoking, alcohol, exercise, level of education, and family history on the metabolic syndrome in Korean adults

한국 성인에서 흡연, 음주, 운동, 교육정도 및 가족력이 대사증후군에 미치는 영향

Jung, Chan-Hee;Park, Jeong-Sik;Lee, Won-Young;Kim, Sun-Woo
정찬희;박정식;이원영;김선우

  • Published : 20020000
⟨ Previous Next ⟩

Abstract

Background : People with the metabolic syndrome are at increased risk for cardiovascular mortality. Metabolic syndrome is caused by interplay between genetic and many environmental factors. Although several environmental factors have diverse effect on the development of metabolic syndrome, few studies have examined their relation in Koreans. This study was performed to estimate the effects of smoking, alcohol consumption, exercise, education level and family history on the components of metabolic syndrome in Korean adults and to observe the relative risk of developing metabolic syndrome defined by NCEP-ATP III according to these factors. Methods : This study was performed in 4341 subjects (2059 men, 2282 women, mean age 42.3$\pm$10.4). We gathered the smoking, alcohol drinking, exercise, family history and education level by self-administered questionnaire at the health promotion center. Height, weight, waist circumference, blood pressure were examined. Fasting serum triglyceride, high density lipoprotein cholesterol, fasting glucose were measured. Results : Multivariate-adjusted odds ratio of hypertriglyceridemia was 1.4 (95% CI 1.0-1.8) and low HDL-C (high density lipoprotein cholesterol) was 1.9 (95% CI 1.3-2.6) in subjects who smoked more than 20 PYS compared to nonsmokers. Also relative risk of developing metabolic syndrome in smokers (more than 20 PYS) was 1.9 (95% CI 1.1-3.7) compared to nonsmokers. Alcohol consumption had a significant protective effect against low HDL-C in all categories compared to nondrinkers (adjusted OR 0.6-0.2). In people with lack of exercise, the odds ratio of high waist circumference was 4.1 (95% CI 1.31-8.6), high triglyceride was 1.3 (95% CI 1.0-1.8), low HDL-C was 1.5 (95% CI 1.5-2.0) when compared to subjects with regular exercise. Relative risk for metabolic syndrome was 1.7 (95% CI 0.9-2.8). The adjusted odds ratio of high blood pressure was 1.3 (95% CI 1.1-1.6) and high fasting glucose was 1.7 (95% CI 1.1-2.5) in subjects with family history compared to subjects without family history. Relative risk for the metabolic syndrome was 1.5 (95% CI 1.1-2.1) in subjects with family history. Relative risk for the presence of the metabolic syndrome in subjects with lowest education level was 2.0 (95% CI 1.2-3.4) when compared to subjects with the highest education level. Significant associations were found between low education and high waist circumference (OR 4.5, 95% CI 1.5-14.0) and low HDL-C (OR 1.2, 95% CI 1.0-1.4) and high blood pressure (OR 2.1, 95% CI 1.6-2.9). Conclusion : Smoking was associated with dyslipidemia. Alcohol consumption increased HDL-C and was associated with abdominal obesity. Lack of exercise was associated with obesity and dyslipidemia. Family history was associated with hypertension and diabetes. Low education level was strongly associated with hypertension and abdominal obesity. Since subjects with low education level and family history were associated with increased risk for metabolic syndrome and thus developing cardiovascular disease, particular attention should be paid in these subjects.

배경 : 대사증후군은 심혈관 질환의 이환율과 이로인한 사망률을 증가시키는 것으로 알려져 있어 이에 대한 치료의 중요성이 강조 되고 있다. 이러한 대사증후군은 유전적인 요소뿐 아니라 많은 환경적 요소들의 작용으로 발생하며 특히 흡연, 음주, 운동, 교육정도 등의 환경적인 요소들이 대사증후군에 미치는 영향은 다양하게 보고 되어 왔다. 그러나 한국인을 대상으로 한 연구는 많지 않은 실정이다. 본 연구는 한국인 성인을 대상으로 NCEP-ATP III에 의한 새로운 대사증후군의 기준을 적용하여 이들 환경적 인자들이 대사증후군의 구성인자들 및 대사증후군 자체에 미치는 영향을 알아보고자 시행 되었다. 방법 : 2001년 12월에 성균관대학교 의과대학 강북삼성병원 건강검진센터에서 건강검진을 받은 20세 이상 (평균 연령 42.3$\pm$10.4세)의 성인 남녀 4,341명(남자 2,059명, 여자 2,282명)을 대상으로 하였다. 흡연, 음주, 운동, 교육수준, 가족력(당뇨병, 고혈압, 심혈관계 질환, 뇌졸중) 유무를 조사하였고, NCEP ATP Ⅲ (National Cholesterol Education Program, Adults Treatment Panel Ⅲ)에 의한 대사증후군의 새로운 진단기준에 근거하여 대사증후군 인자들과의 연관성을 측정하였다. 결과 : 연령, 성별, 체질량지수를 포함한 다변수 보정을 하여 무흡연자군과 비교해서 20갑년 이상의 흡연자군의 혈중 고중성지방혈증(high TG)과 저고밀도지단백 콜레스테롤(low HDL-C)의 비교위험도는 각각 1.4(95% CI 1.0-1.8), 1.9(95% CI 1.3->2.6)이였다. 그리고 대사증후군 발생의 비교위험도는 1.9(95% CI 1.1-3.7)이였다. 같은 보정방법으로 무음주자군과 비교하여 주당 400 g 이상의 알콜섭취군의 복부비만의 비교위험도는 5.0(95% CI 1.2-21.5)이었고 혈중 저고밀도지단백 콜레스테롤 (low HDL-C)에 대해서는 0.2(95% CI 0.1-0.4)였다. 그러나 대사증후군 발생의 비교위험도는 0.8(95% CI 0.5-2.2)였다. 운동정도에 따라서 분석하였을 때 주당 5회 이상 운동을 하는 군에 비해 운동을 하지 않는 군의 혈중고중성지방혈증(high TG), 저고밀도지단백 콜레스테롤 (low HDL-C)의 비교위험도는 각각 1.3(95% CI 1.0-1.8), 1.5(95% CI 1.2-2.0)였고, 복부비만의 위험도는 4.1(95% CI 1.3-18.6)이었으며 대사증후군 발생의 비교 위험도는 1.7(95% CI 0.9-2.8)이었다. 가족력 유무에 따라, 가족력이 없는 군에 비해 당뇨병, 고혈압, 심혈관계질환, 뇌졸중의 가족력이 있는 군에서 고혈압 및 고혈당의 비교위험도는 각각 1.3(95% CI 1.1-1.6), 1.7(95% CI 1.1-2.5)이었고, 대사증후군 발생의 비교위험도는 1.5 (95% CI 1.1-2.1)이였다. 교육정도에 따라 분석하였을때, 전문대 이상의 학력군에 비해 초등학교 이하 학력군의 복부비만과 고혈압의 비교위험도는 각각 4.5(95% CI 1.5-14.0), 2.1(95% CI 0.4-1.8)이었고 대사증후군 발생 위험도도 2.0(95% CI 1.2-3.4)으로 높았다. 결론 : 지질대사 이상과 관련이 있는 위험인자로 흡연 및 운동부족이 관련되었고, 복부비만에 대해서는 음주 및 저학력이 위험인자로 고혈압에 대해서는 가족력과 저학력이 유의한 위험인자로서 대사증후군에 영향을 주는 것을 알 수 있었다. 특히 가족력이 있고 교육정도가 낮은 사람들에서 대사증후군의 발생위험율이 유의하게 증가함을 알 수 있었고, 심혈관 질환의 발생이 높을 것으로 예상되므로 특히 이들 군에서 대사증후군의 예방과 인자들에 대한 적극적인 치료가 필요할 것으로 사료된다.

Keywords

References

  1. Isomaa B, Almgren P, Tuomi T, Forsen B, Lahti K, Nissen M, Taskinen MR, Groop L. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care 24:683-689, 2001. https://doi.org/10.2337/diacare.24.4.683
  2. Trevisan M, Liu J, Bahsas FB, Menotti A. Syndrome X and mortality: a population-based study. Am J Epidemiol 148:958-966, 1998. https://doi.org/10.1093/oxfordjournals.aje.a009572
  3. Groop L, Orho-Melander M. The dysmetabolic syndrome. J Intern Med 250:105-120, 2001. https://doi.org/10.1046/j.1365-2796.2001.00864.x
  4. Alberti KG, Zimmet PZ. Definition, diagnosis and classification of diabetes mellitus and its complications: part 1. diagnosis and classification of diabetes mellitus, provisional report of a WHO consultation. Diabet Med 15:539-553, 1998. https://doi.org/10.1002/(SICI)1096-9136(199807)15:7<539::AID-DIA668>3.0.CO;2-S
  5. National Cholesterol Education Program. Executive summary of the third report of the national cholesterol education program (NCEP) expert panel on detection, evaluation and treatment of high blood cholesterol in adults (adult treatment panel Ⅲ). JAMA 285:2486-2497, 2001. https://doi.org/10.1001/jama.285.19.2486
  6. Liese AD, Mayer-Davis EJ, Tyroler HA, Davis CE, Keil U, Schmidt MI, Brancati FL, Heiss G. Familial components of the multiple metabolic syndrome. Diabetologia 40:963-970, 1997. https://doi.org/10.1007/s001250050775
  7. Hong Y, Pedersen NL, Brismar K, de Faire U. Genetic and environmental architecture of the features of the insulin-resistance syndrome. Am J Hum Genet 60:143-152, 1997.
  8. Mjos OD. Lipid effects of smoking. Am Heart J 115:272-275, 1988. https://doi.org/10.1016/0002-8703(88)90649-7
  9. Shimokata H, Muller DC, Andres R. Studies in the distribution of body fat. JAMA 261:1169-1173, 1989. https://doi.org/10.1001/jama.261.8.1169
  10. Lee KS, Park CY, Meng KH, Bush A, Lee SH, Lee WC, Koo JW, Chung CK. The association of cigarette smoking and alcohol consumption with other cardiovascular risk factors in men from Seoul, Korea. Ann Epidemiol 8:31-38, 1998. https://doi.org/10.1016/S1047-2797(97)00113-0
  11. Facchini F, Chen YD, Reaven GM. Light-tomoderate alcohol intake is associated with enhanced insulin sensitivity. Diabetes Care 17:115-119, 1994. https://doi.org/10.2337/diacare.17.2.115
  12. Gaziano JM, Buring JE, Breslow JL, Goldhaber SZ, Rosner B, Vandenburgh M, Willett W, Hennekens CH. Moderate alcohol intake, increased levels of high-density lipoprotein and its subfractions and decreased risk of myocardial infarction. N Engl J Med 329:1829-1834, 1993. https://doi.org/10.1056/NEJM199312163292501
  13. Dyer AR, Stamler J, Paul O, Berkson DM, Shekelle RB, Lepper MH, Mckean H, Lindberg HA, Garside D, Tokich T. Alcohol, cardiovascular risk factors and mortality. Circulation 64:III20-27, 1981.
  14. Keil U, Chambless L, Filipiak B, Hartel U. Alcohol and blood pressure and its interaction with smoking and other behavioural variables: results from the MONICA augsburg survey 1984-1985. J Hypertens 9:491-498, 1991. https://doi.org/10.1097/00004872-199106000-00003
  15. Valek J, Vlasakova Z. The metabolic syndrome, its heredity, methods of detection and clinical significance. Vnitr Lek 43:566-573, 1997.
  16. Hunt KJ, Heiss G, Sholinsky PD, Province MA. Familial history of metabolic disorders and the multiple metabolic syndrome: the NHLBI family heart study. Genet Epidemiol 19:395-409, 2000. https://doi.org/10.1002/1098-2272(200012)19:4<395::AID-GEPI10>3.0.CO;2-3
  17. Wamala SP, Lynch J, Horsten M, Mittleman MA, Schench-Gustafsson K, Orth-Gomer K. Education and the metabolic syndrome in women. Diabetes Care 22:1999-2003, 1999. https://doi.org/10.2337/diacare.22.12.1999
  18. Laporte R, Valvo-Gerard L, Kuller L, Dai W, Bates M, Cresanta J, Williams K, Palkin D. The relationship between alcohol consumption, liver enzymes and high-density lipoprotein cholesterol. Circulation 64:III67-72, 1981.
  19. Linn S, Carroll M, Johnson C, Fulwood R, Kalsbeek W, Briefel R. High-density lipoprotein cholesterol and alcohol consumption in US white and black adults: data from NHANES Ⅱ. Am J Public Health 83:811-816, 1993. https://doi.org/10.2105/AJPH.83.6.811
  20. Suh I, Shaten BJ, Cutler JA, Kuller LH. Alcohol use and mortality from coronary heart disease: the role of high-density lipoprotein cholesterol. Ann Intern Med 116:881-887, 1992. https://doi.org/10.7326/0003-4819-116-11-881
  21. Seidell JC, Cigolini M, Deslypere JP, Charzewska J, Ellsinger BM, Cruz A. Body fat distribution in relation to physical activity and smoking habits in 38-year-old European men. Am J Epidemiol 133:257-265, 1991. https://doi.org/10.1093/oxfordjournals.aje.a115870
  22. Williams RR, Hunt SC, Wu LL, Hopkins PN, Hasstedt SJ, Schumacher MC, Stults BM, Kuida H. Concordance dyslipidemia, hypertension and early coronary disease in Utah families. Klin Wochenschr 68:53, 1990.
  23. Molarius A, Seidell JC, Sans S, Tuomilehto J, Kuulasmaa K. Educational level, relative body weight, and changes in their association over 10 years: an international perspective from the WHO MONICA project. Am J Public Health 90:1260-1268, 2000. https://doi.org/10.2105/AJPH.90.8.1260
  24. Cirera L, Tormo MJ, Chirlaque MD, Navarro C. Cardiovascular risk factors and educational attainment in southern Spain: a study of a random sample of 3091 adults. Eur J Epidemiol 14:755-763, 1998.
  25. Bjorntorp P. Behavior and metabolic disease. Int J Behav Med 3:285-302, 1996. https://doi.org/10.1207/s15327558ijbm0304_1
  26. Bjorntorp P. Visceral fat accumulation: the missing link between psychosocial factors and cardiovascular disease. J Intern Med 230:195-201, 1991. https://doi.org/10.1111/j.1365-2796.1991.tb00431.x
  27. Goldbourt U, Medalie JH. Characteristics of smokers, non-smokers and ex-smokers among 10,000 adult males in Israel. Am J Epidemiol 105:75-86, 1977. https://doi.org/10.1093/oxfordjournals.aje.a112358
  28. Museat JE, Harris RE, Haley NJ, Wynder EL. Cigarette smoking and plasma cholesterol. Am Heart J 121:141-147, 1991. https://doi.org/10.1016/0002-8703(91)90967-M
  29. Cryer PE, Haymond MW, Santiago JV, Shah SD. Norepinephrine and epinephrine release and adrenergic mediation of smoking-associated hemodynamic and metabolic events. N Engl J Med 295:573-577, 1976. https://doi.org/10.1056/NEJM197609092951101
  30. Green MS, Jucha E, Luz Y. Blood pressure in smokers and nonsmokers: epidemiologic findings. Am Heart J 111:932-940, 1986. https://doi.org/10.1016/0002-8703(86)90645-9
  31. Facchini FS, Hollenbeck CB, Jeppensen J, Chen I, Reaven GM. Insulin resistance and cigarette smoking. Lancet 339:1128-1130, 1992. https://doi.org/10.1016/0140-6736(92)90730-Q