건강한 한국 남성에서 음주와 흡연의 결합효과 혈중 지질에 미치는 영향: 제4기 국민건강영양조사
Original Article
김알렉산드라, 이윤미, 김태성, 이지원*, 김 수*
연세대학교 의과대학 세브란스병원 가정의학과
Combined Impact of Cigarette Smoking and Alcohol Consumption on Serum Lipoprotein Profiles in Healthy Korean Men: The 2007–2009 Korea National Health and Nutrition Examination Survey
Aleksandra Kim, Yoon Mi Lee, Tae Sung Kim, Ji Won Lee*, Sue Kim*
Departments of Family Medicine, Severence Hospital, Yonsei University College of Medicine, Seoul, Korea
Background: Several previous studies have reported independent eff ects of smoking and alcohol consumption in the literature.
However, there are few studies on joint impact and interaction of smoking and alcohol consumption, and the results are inconsistent to this point. Th erefore, this study was conducted to investigate the interactive impact of alcohol and smoking consumption on serum lipoproteins in Korean men.
Methods: Participants were composed of 4,254 healthy Korean males, aged 19 years or older, from the Forth Korea National Health and Nutrition Examination Surveys. Alcohol and smoking consumption were assessed by face-to-face interview with questionnaires. Lipid profi les and atherogenic indices were analyzed.
Results: Th e lipoprotein profi les and atherogenic indices were in favorable levels in drinkers in smoking group than those in non-smoking group. In addition, unfavorable levels of lipid profiles were seen in smokers, in non-drinking group than in drinking group.
Conclusion: This study shows that combined impact of smoking and alcohol consumption on the atherogenic lipoprotein profi les. Further studies are needed to clarify the mechanism and signifi cance of our fi ndings.
Keywords: Smoking; Alcohol Drinking; Serum Lipoprotein Profi le
INTRODUCTION
Ischemic heart disease and stroke are continuously increasing worldwide, leading to high morbidity and mortality. It is reported that more than 23 million people will die annually from cerebro- and cardiovascular diseases by 2030.1) Among life style habits affecting the incidence of cardiovascular disease, smoking, and excessive alcohol consumption are major risk factors known to facilitate the atherosclerotic progression.2,3)
According to previous studies, coronary attacks and mortality Received: August 31, 2013, Accepted: July 9, 2014
*Corresponding Author: Sue Kim
Tel: 02-2228-2330, Fax: 02-362-2473 E-mail: [email protected]
*Corresponding Author: Ji Won Lee
Tel: 02-2228-2330, Fax: 02-362-2473 E-mail: [email protected]
Korean Journal of Family Practice
Copyright © 2014 by Th e Korean Academy of Family Medicine
were distinctly higher in smokers than in non-smokers.4,5) The association between dose-dependent cigarette smoking and lower high density lipoprotein cholesterol (HDL-C) is considered to explain this atherosclerotic outcome.6,7) On the other hand, recent studies showed moderate alcohol consumption may protect risks of coronary disease and stroke,8) due to strong positive relationship between alcohol and HDL-C, unlike with smoking.9,10) In addition, alcohol consumption is thought not only to modify the lipoprotein level, but also to affect the basic intracellular and intercellular signaling of vascular cells, thereby promoting the formation of atherosclerotic lesions.11)
However, only a few studies reported the combined impact of smoking and alcohol consumption, and there still are controversies on this issue to this point. Xu et al.12) reported that moderate alcohol consumption reduced mortality from cardiovascular diseases, but this beneficial effect was offset by cigarette smoking. On the other hand, Wakabayashi and Groschner13) and Wakabayashi14) suggested that anti-atherogenic action of alcohol drinking through cholesterol metabolism is facilitated by smoking. Furthermore, Wu et al.15) suggested that strong positive effect of alcohol consumption on HDL-C level was independent from amount of cigarette smoking. Accordingly, evaluating the combined impact of smoking and alcohol consumption on lipid metabolic profiles with larger sample is necessary to determine whether it is possible to predict the atherosclerotic diseases associated with these life style factors combined.
Therefore, the aim of this study was to investigate the combined impact of smoking and alcohol consumption on serum lipoproteins and atherogenic indices in healthy Korean men.
METHODS
This study analyzed pooled data from the 2007–2009 Forth Korea National Health and Nutrition Examination Surveys (KNHANES IV). KNHANES is a nationally representative survey, which is performed by the Korean Ministry of Health and Welfare.
The survey questions were prepared by the Korea Institute for Health and Social Affairs and Korea Centers for Disease Control (KCDC), which were approved by the ethics committee at the KCDC. The subjects of this study were Korean adult males aged 19 years and older. This study started from a total of 24,871 participants who responded to the health interview survey in items about smoking
and alcohol consumption. Those, who had any illness or had been receiving medication for dyslipidemia, hypertension, diabetes mellitus, cardiovascular disease, cerebra-vascular accident were excluded from the study. After the exclusion, 4,254 healthy males were included in the final analyses.
1. Data Collection
Data on smoking status, alcohol consumption and other medical and lifestyle information were collected by face-to-face interviews with the participants. Prior to the interview, all participants com- pleted an informed consent form.
Alcohol consumption was assessed by questioning the subjects about their drinking behavior during the year preceding the interview. According to 2005 National Institute on Alcohol Abuse and Alcoholism guideline,16) participants were divided into the following groups: (1) non-drinkers: individuals who reported never drinking or not drinking for about 1 year; (2) drinkers: individuals who reported drinking. Furthermore, drinkers were grouped as follows: moderate drinker and heavy drinker. Heavy drinker was defined for participants drinking more than three or four drinks on a single occasion, or drinking more than seven drinks per week or more.
Cigarette smoking habit was also assessed using the questio- nnaire, and participants were classified into the following groups according to their answers: (1) nonsmokers (individuals who reported never having a cigarette or ex-smoker); (2) smokers (individuals who reported smoking every day now). For smokers, the smoking dose was questioned: how many cigarette smoked and the smokers were grouped as follows: light (<20 cigarettes per day), heavy (≥20 cigarettes per day) according to their answers on average cigarette consumption in the self-report questionnaire.
Individuals were considered to participate in structured regular physical activity (exercise), if exercised moderately more than five times weekly for over 30 minutes per session, or engaged in vigorous exercise more than three times weekly for over 20 minutes per session, through International Physical Activity Questionnaire Korean version.17)
Body mass index (BMI) was calculated using the formula: body weight (kg)/height2 (m2). Body weight and height were measured to the nearest 0.1 kg and 0.1 cm, respectively. Blood pressure was assessed twice at a 5-minute interval on the right arm using a standard mercury sphygmomanometer (Baumanometer; Baum, Copiague,
NY, USA) and recorded as an average of the two readings.
Blood samples were taken after fasting for eight or more hours and were immediately refrigerated before transporting via cold storage to the Central Testing Institute in Seoul, Korea. All samples were analyzed within 24 hours. Fasting plasma glucose, total cholesterol (TC), triglyceride (TG), and HDL-C concentrations were measured with a Hitachi Automatic Analyzer 7600 (Hitachi, Tokyo, Japan) by enzymatic methods using commercially available kits (Daiichi, Tokyo, Japan). Low density lipoprotein cholesterol (LDL-C) levels were calculated using Friedewald’s formula in participants with TG <400 mg/dL. When TG levels ≥400 mg/dL, LDL-C levels were measured directly using a commercially available kit (Cholestest LDL; Sekisui Medical, Tokyo, Japan). Non high density lipoprotein cholesterol (non-HDL-C) levels were calculated by subtracting HDL-C levels from serum TC levels. TC/HDL ratio and LDL/HDL ratio were calculated based on the measured data.
Previous study considered that for cardiovascular diseases prediction, using TC/HDL-C and LDL-C/HDL-C ratio is a superior measure of risk for cardiovascular diseases compared with LDL-C.18)
2. Statistical Analyses
For analyses, we used the KNHANES stratification variables and sampling weights designated by the Korean Centers for Disease Control and Prevention, which were based on the sample design of each different survey. The data were presented as weighted means and standard errors. Mean values of each variable in different drinking or smoking groups were calculated after adjustment for age, BMI and regular physical activity and were compared among groups using analysis of covariance with pair comparison Bonferroni correction.
Data were analyzed using SAS ver. 9.2 (SAS Institute Inc., Cary, NC, USA). P-value<0.05 was considered to be statistically significant.
The statistical comparison was performed between non-smokers and smokers at each degree of alcohol consumption and between non- drinkers and drinkers at each degree of smoking consumption. The rationale was to minimize the use of numerous statistical tests and it was expected that the difference between combined and separate effect of smoking and alcohol consumption can be determined at maximum changes in serum lipid profiles. The observed values and change in serum lipid profiles for each group were presented.
RESULTS
1. General Characteristics of the Study Subjects
Table 1 shows basic characteristics of the participants. The average age and BMI were approximately 39 years and 23.79 kg/m2. Among the total participants, 26.96% of men reported to be light to moderate drinkers, and 62.05% of men reported to be heavy alcohol consumers. In addition, 27.11% of men reported smoking cigarettes lightly, and 22.80% of men reported to be heavy smokers.Table 1. General characteristics of the subjects
Characteristic Male (n=11,593,375)
Age (y) 39.3±0.3
Body mass index (kg/m2) 23.8±0.1
Blood pressure (mm Hg)
Systolic 116.3±0.3
Diastolic 78.5±0.2
Fasting plasma glucose (mg/dL) 93.5±0.3 Cholesterol (mg/dL)
TC 183.6±0.7
HDL-C 48.1±0.3
LDL-C 108.7±0.6
Non-HDL-C 135.5±0.7
TC to HDL-C ratio 4.0±0.1
LDL to HDL-C ratio 0.8±0.1
Triglyceride (mg/dL) 135.2±1.4
Alcohol consumption
Non-drinkers 1,273,886 (11.0)
Light to moderate drinkers 3,125,493 (27.0)
Heavy drinkers 7,193,996 (62.1)
Smoking
Non-smokers 5,807,779 (50.1)
Light smokers 3,142,898 (27.1)
Heavy smokers 2,642,698 (22.8)
Regular physical activity (exercise)
No 7,168,902 (61.8)
Yes 4,424,473 (38.2)
Values are presented as mean±standard error or number (%).
TC: total cholesterol, HDL-C: high density lipoprotein cholesterol, LDL-C: low density lipoprotein cholesterol.
2. Independent Impact of Cigarette Smoking on Serum Lipoproteins and Atherogenic Indices
The relationship of cigarette smoking with serum lipoproteins was analyzed by examining the difference of serum lipoproteins between non-smokers, light smokers and heavy smokers. Heavy smokers had significantly higher level of serum TC, TG, LDL-C (mean difference, 5.684, 24.152, 2.891, respectively) and significantly lower level of HDL-C (mean difference, 1.684) than non-smokers.In addition, non HDL-C and TC/HDL ratio showed significantly higher levels in heavy smokers, and especially, non HDL-C had a great difference (mean difference, 7.368) between heavy smokers
and non-smokers (Table 2).
3. Independent Impact of Alcohol Consumption on Serum Lipoproteins and Atherogenic Indices
The relationship of alcohol consumption with serum lipids among the participants, categorized as non-drinkers, moderate drinkers, and heavy drinkers, was examined with the difference of serum lipoproteins between the three groups. Heavy drinkers had significantly higher level of serum TG and HDL-C (mean difference, 17.282, 5.303, respectively) and significantly lower level of serum
Table 2. Independent impact of cigarette smoking on serum lipoproteins and atherogenic indices
Variable Non-smokers
(n=5,807,779)
Light smokers (n=3,142,898)
Heavy smokers (n=2,642,698)
Mean diff erence in smokers (heavy drinkers vs. non-drinkers)
TC (mg/dL) 183.9±0.8 185.1±1.1 189.6±1.3 5.7*
Triglyceride (mg/dL) 129.6±1.8 139.2±2.7 153.7±2.9 24.2*
HDL cholesterol (mg/dL) 48.4±0.4 48.2±0.4 46.7±0.4 -1.7*
LDL cholesterol (mg/dL) 109.7±0.7 109.5±1.0 112.6±1.2 2.9
Non-HDL cholesterol (mg/dL) 135.5±0.8 137.0±1.1 142.9±1.2 7.4*
TC/HDL ratio 4.0±0.1 4.1±0.1 4.3±0.1 0.3*
LDL/HDL ratio 0.8±0.1 0.8±0.1 0.8±0.1 0.1*
Values are presented as mean±standard error.
TC: total cholesterol, HDL: high density lipoprotein, LDL: low density lipoprotein.
*P<0.05 was used as the signifi cant diff erence between groups of cigarette smoking. P-values are calculated by the analysis of covariance test with compare main eff ect with Bonferroni correction, after adjustment for age, body mass index, regular physical activity, and alcohol consumption.
Table 3. Independent impact of alcohol consumption on serum lipoproteins and atherogenic indices
Non-drinkers (n=1,273,886)
Moderate drinkers (n=3,125,493)
Heavy drinkers (n=7,193,996)
Mean diff erence in drinkers (heavy smokers vs. non-smokers)
TC (mg/dL) 184.7±1.7 184.7±1.0 186.2±0.8 1.5
Triglyceride (mg/dL) 126.9±3.0 128.9±2.1 144.2±1.9 17.3*
HDL cholesterol (mg/dL) 44.2±0.6 46.7±0.4 49.5±0.3 5.3*
LDL cholesterol (mg/dL) 115.2±1.5 112.3±0.9 108.2±0.7 -6.9*
Non-HDL cholesterol (mg/dL) 140.5±1.6 138.0±1.0 136.7±0.8 -3.8
TC/HDL ratio 4.4±0.1 4.2±0.1 4.0±0.1 -0.4*
LDL/HDL ratio 0.8±0.1 0.8±0.1 0.8±0.1 -0.1*
Values are presented as mean±standard error.
TC: total cholesterol, HDL: high density lipoprotein, LDL: low density lipoprotein.
*P<0.05 was used as the signifi cant diff erence between groups of alcohol consumption. P-values are calculated by the analysis of covariance test with compare main eff ect with Bonferroni correction, after adjustment for age, body mass index, regular physical activity, and cigarette smoking.
LDL-C (mean difference, 6.930) than non-drinkers. Non HDL-C, TC/HDL and LDL/HDL ratio, significantly showed lower levels according to amount of alcohol consumption (Table 3).
4. Combined Impact of Cigarette Smoking and Alcohol Consumption on Serum Lipoproteins and Atherogenic Indices
The adjusted mean and standard error (SE) of serum lipoprotein levels and atherogenic indices at each degree of alcohol consumption in non-smokers and smokers are presented in the Table 4, and the mean differences between heavy drinkers and non-drinkers in different smoking groups are shown in Table 5. TC and TG levels
were higher in heavy drinkers than non-drinkers with significant mean difference in non-smoker group. HDL-C was higher in heavy drinkers than non-drinkers, and the mean differences were both significant in non-smoking and smoking groups. LDL-C, non-HDL, TC/HDL and LDL/HDL ratio were all lower in heavy drinkers than non-drinkers in smokers, and mean differences were greater in smokers group than in non-smokers group.
The adjusted mean and SE of serum lipoprotein level and atherogenic indices at each degree of smoking consumption in non- drinkers and drinkers are presented in the Table 6, and the mean difference between smokers and non-smokers in different alcohol consumption groups are shown in Table 5. TC and TG levels were
Table 4. Th e means of serum lipoproteins and atherogenic indices in non-smokers and smokers at each degree of alcohol consumption
Variable
Non-smokers (n=5,807,779) Smokers (n=5785596)
Non-drinkers (n=892,411)
Moderate drinkers (n=1,903,841)
Heavy drinkers (n=3,011,527)
Non-drinkers (n=381,475)
Moderate drinkers (n=1,221,652)
Heavy drinkers (n=4,182,469)
TC (mg/dL) 180.3±1.6 183.1±1.3 188.0±1.1 194.5±3.7 186.8±1.5 185.2±1.0
Triglyceride (mg/dL) 117.5±3.3 125.9±2.8 137.6±2.8 142.5±6.6 130.2±3.3 151.5±2.6
HDL cholesterol (mg/dL) 45.4±0.7 47.2±0.5 49.6±0.5 41.9±0.8 46.1±0.6 49.2±0.4
LDL cholesterol (mg/dL) 111.4±1.4 110.8±1.1 110.9±1.1 124.0±3.1 114.6±1.4 106.4±0.9
Non-HDL cholesterol (mg/dL) 134.9±1.6 135.9±1.2 138.4±1.1 152.5±3.5 140.6±1.6 136.0±0.9
TC/HDL ratio 4.2±0.1 4.1±0.1 4.0±0.1 4.8±0.1 4.3±0.1 4.0±0.1
LDL/HDL ratio 0.8±0.1 0.8±0.1 0.8±0.1 0.8±0.1 0.8±0.1 0.8±0.1
Values are presented as mean±standard error.
TC: total cholesterol, HDL: high density lipoprotein, LDL: low density lipoprotein.
Table 5. Maximum amount of change in serum lipoproteins and atherogenic indices between combine and separate effect of alcohol consumption and cigarette smoking
Variable Mean diff erence of heavy drinkers vs. non-drinkers Mean diff erence heavy smokers vs. non-smokers
Non-smoker Smoker Non-drinkers Drinker
TC (mg/dL) 7.7±1.9* -9.0±3.8 17.7±5.6* 4.0±1.4*
Triglyceride (mg/dL) 20.1±4.3* 10.1±7.2 26.7±9.4* 23.1±3.7*
HDL cholesterol (mg/dL) 4.2±0.8* 7.1±0.9* -3.7±1.1* -1.5±0.5
LDL cholesterol (mg/dL) -0.5±1.7 -17.±3.1* 16.0±4.5* 1.3±1.3
Non-HDL cholesterol (mg/dL) 3.5±1.9 -16.1±3.7* 21.3±5.4* 5.5±1.5*
TC/HDL ratio -0.2±0.1* -0.8±0.1* 0.7±0.2* 0.3±0.1*
LDL/HDL ratio -0.1±0.1* -0.1±0.1* -0.1±0.1 -0.1±0.1*
Values are presented as mean±standard error.
TC: total cholesterol, HDL: high density lipoprotein, LDL: low density lipoprotein.
*P<0.05 was used as the signifi cant diff erence between means diff erences between comparison groups. P-values are calculated by the analysis of covariance test with compare main eff ect with Bonferroni correction, after adjustment for age, body mass index, and regular physical activity.
higher in heavy smokers than non-smokers with significant greater mean differences in non-drinkers group. HDL-C was lower, and LDL-C was higher in smokers in non-drinkers group compared with drinkers group, with significant mean differences only in non- drinkers group. Atherogenic indices were higher in smokers than in non-smokers, and the mean differences were greater in non-drinkers group.
DISCUSSION
This study focuses on combined impact of smoking and alcohol consumption assessed by comparing mean differences of lipoprotein profiles in groups according to smoking or alcohol consumption, in relations with different drinking or smoking behavior, respectively.
The lipoprotein profiles and atherogenic indices were in favorable levels in drinkers in smoking group than in non-smoking group. In addition, unfavorable levels of lipid profiles were seen in smokers, in non-drinking group than in drinking group.
Our results confirmed the previously reported independent effect of smoking and alcohol consumption. Heavy smokers had significantly higher TG, LDL-C and lower HDL-C level, than non-smokers. In addition, atherogenic indices were significantly higher in heavy smokers than in non-smokers groups. Previous research reported smoking alone decreases HDL-C that explains the atherosclerosis risk1.6,7,18-20) Also, there was a significant increase in TC and LDL-C in smokers.21,22) Recent studies have revealed new mechanisms that smoking triggers acute atherothrombosis by endothelial dysfunction,23,24) plaque composition,25-27) blood
coagulation,28) leading to the increased risk of cardiovascular death in smokers.
Furthermore, alcohol is also known to be an important factor in anti-atherosclerosis, influencing lipid metabolism.15,28,29) In this study, heavy drinkers had significantly higher TG, HDL-C level and significantly lower LDL-C than non-drinkers. Atherogenic indices, such as non HDL-C, TC/HDL and LDL/HDL ratio were significantly lower in heavy drinkers than non-drinkers, which were in line with previous studies. Alcohol drinking is found not only to alter the quantity of circulating lipoproteins, but also modify their molecular structure and physicochemical characteristics in a way that may affect the basic intracellular and intercellular signaling of vascular cells. These changes may have a significant impact on the arterial wall and atherosclerotic lesions.30)
We found that TC and TG levels were higher in heavy drinkers in non-smokers than in smokers, HDL-C was higher in heavy drinkers in smokers group, and LDL-C, non-HDL, TC/HDL and LDL/HDL ratio were all lower in heavy drinkers than non-drinkers, with mean differences greater in smokers group than in non-smokers group. Moreover, TC, TG, and LDL-C levels were higher, HDL-C was lower, and atherogenic indices were all higher in heavy smokers in non-drinkers than in drinkers, with mean differences greater in non-drinkers group. Thus, the anti-atherogenic impact of alcohol consumption was aggravated in smokers group, and atherogenic action of smoking through cholesterol metabolism was suppressed by alcohol drinking. These findings suggest that drinkers with smoking may have larger quantities of alcohol intake and the increase in HDL-C, and decrease in LDL-C became the predominant Table 6. Th e means of serum lipoproteins and atherogenic indices in non-drinkers and drinkers at each degree of cigarette smoking
Variable
Non-drinkers (n=1,273,886) Drinkers (n=10,319,489)
Non-smokers (n=892,411)
Light smokers (n=152,032)
Heavy smokers (n=229,443)
Non-smokers (n=4,915,368)
Light smokers (n=2,990,866)
Heavy smokers (n=2,413,255)
TC (mg/dL) 181.0±1.7 195.2±4.4 198.7±5.3 184.5±0.8 184.6±1.1 188.5±1.2
Triglyceride (mg/dL) 118.6±3.5 151.8±10.8 145.3±8.4 131.4±1.9 139.5±2.8 154.5±3.1
HDL cholesterol (mg/dL) 45.1±0.6 41.1±1.4 41.5±0.9 48.8±0.4 48.9±0.5 47.4±0.5
LDL cholesterol (mg/dL) 112.2±1.5 123.7±4.0 128.1±4.3 109.4±0.8 108.2±1.0 110.7±1.2
Non-HDL cholesterol (mg/dL) 135.9±1.6 154.1±4.4 157.2±5.1 135.6±0.8 135.7±1.1 141.1±1.2
TC/HDL ratio 4.2±0.1 4.9±0.2 5.0±0.1 4.0±0.1 4.0±0.1 4.2±0.1
LDL/HDL ratio 0.8±0.1 0.8±0.1 0.8±0.1 0.8±0.1 0.8±0.1 0.8±0.1
Values are presented as mean±standard error.
TC: total cholesterol, HDL: high density lipoprotein, LDL: low density lipoprotein.
features.29) The protection against atherosclerosis by lower LDL-C and higher HDL-C can explain anti-atherogenic effect of alcohol consumption in smokers.14,30,31)
Previous studies with joint impact of smoking and alcohol consumption on lipoprotein levels have shown inconsistent results.
Our study is in line with the study of Wakabayashi and Groschner13) and Wakabayashi14) that reported favorable levels of lipoprotein profiles in drinkers in smoking group. They reported lower levels of LDL in alcohol consumers were more prominent in smokers in 2008, and lower levels of non-HDL-C and HDL-C were seen in both smoking and alcohol consuming participants in 2010. The results reported in similar characteristics of the participants who were middle-aged healthy Asian males, in similar environmental condition for exposure to smoking and alcohol consumption may explain for this similarity. But in addition, we compared and reported atherogenic indices, such as TC/HDL and LDL/HDL ratio and showed not only age, BMI, but also physical activity status adjusted means with standard errors in each variable of cigarette smoking and alcohol consumption groups.
However, Wu et al.15) study suggested a strong positive influence of alcohol on HDL-C concentration regardless of levels of cigarette smoking. This discrepancy with the result of our study may have occurred since the results were analyzed only after adjustment for age and BMI only, while our study calculated mean values after adjustment for factors that strongly influence lipid metabolism, such as age, BMI, and regular physical activity status. Furthermore, Xu et al.12) study reported that smoking diminish the protective effect of moderate alcohol consumption on cardiovascular diseases (CVD) mortality, according to the amount of alcohol and smoking consumed. The study was based on the data of only married elderly men, with outcome of death records, which may have led to discrepant results with our study. Indeed, more prospective longitudinal study on the follow-up of the influence of smoking and alcohol on CVD related mortality is necessary in the future.
This study has several limitations. First, the study was cross- sectional designed, making it difficult to determine the causal relationship. Second, the influence of genetic factors on lipid metabolism was not taken into account. Finally, there is a possibility of recall bias for cigarette smoking and alcohol consumption.
Despite these limitations, our study has several strengths. First, this is large population-based study among Korean men using nationally representative data.32-34) This study also assessed various atherogenic
indices including non-HDL-C, TC/HDL and LDL/HDL ratio.
Finally, lifestyle-related risk factors, including dietary intake (BMI) and physical activity were taken into account and adjusted in the analyses.
In conclusion, this study reports the combined impact of smoking and alcohol consumption on serum lipoprotein levels and atherogenic lipid indices in healthy Korean men. Subsequently in the future, prospective studies are required to further determine the relationship precisely and clarify the mechanism and significance of our findings.
ACKNOWLEDGMENTS
This study was supported by a faculty research Grant from Yonsei University College of Medicine for 2013 (6-2013-0021) and the Bio & Medical Technology Development Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT and Future Planning (NRF- 2013M3A9B6046413). This work was supported by the Biomedical Technology Development Research Program through the NRF funded by the Ministry of Science, ICT and Future Planning (NRF- 2013M3A9B6046413).
요약
연구배경: 흡연과 음주는 심혈관계 질환의 주요한 위험인자 인 혈중 지질 농도에 각각 다양한 영향을 미치는 것으로 잘 알 려져 있다. 그러나 흡연과 음주가 함께 혈중 지질 농도에 미치 는 결합적 영향에 대해서는 연구사례가 많지 않다. 따라서 본 연구는 국민건강영양조사를 바탕으로 한국 남성에서 혈중 지 질에 끼치는 흡연과 음주의 결합효과를 고찰하고자 하였다.
방법: 제4기 국민건강영양조사자료 중 고지혈증, 고혈압, 심 혈관질환 및 약물 복용자를 제외한 만 19세 이상의 건강한 한 국 남성 4,254명(가중치 적용 후 11,593,375명)을 대상으로 연 령, 체질량지수, 평소 운동량, 음주력, 흡연력을 보정하여 혈중 지질, 심혈관질환의 지표인자와 흡연과 알코올 결합적 영향 간의 관계를 analysis of covariance 방법을 통해 분석하였다.
결과: 혈중 지질 수치와 심혈관질환의 지표인자는 음주-금연 군보다 음주-흡연군에서 더 낮은 것으로 나타났다. 또한 혈중 지질 수치와 심혈관질환 지표인자는 흡연-금주군보다는 흡 연-음주군에서 더 낮은 결과를 보였다.
결론: 이 연구를 통해 흡연과 음주의 결합적 영향의 결론은 흡
연과 음주의 결합이 혈중 지질 수치에 이로운 영향을 주는 관 계를 보이고 있음을 확인할 수 있었다. 향후 이에 대한 비교 연 구 및 장기적 효과, 그 작용원리를 명확하게 하기 위해 추가 적 인 연구가 필요할 것으로 생각된다.
중심단어: 흡연; 음주; 혈중 지질
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