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Effects of smoking and alcohol consumption on lipid profile in male adults in northwest rural China
p u b l i c h e a l t h 1 5 7 ( 2 0 1 8 ) 7 e1 3
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Original Research
Effects of smoking and alcohol consumption on lipid profile in male adults in northwest rural China X.X. Li, Y. Zhao, L.X. Huang, H.X. Xu, X.Y. Liu, J.J. Yang, P.J. Zhang, Y.H. Zhang* Department of Epidemiology and Health Statistics, School of Public Health and Management, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, PR China
article info
abstract
Article history:
Objectives: To determine the individual and combined influences of smoking and alcohol
Received 26 July 2017
consumption on lipid profile in male adults in northwest rural China.
Received in revised form
Design: Cross-sectional study.
4 November 2017
Methods: In total, 4614 subjects were enrolled in the cross-sectional study, performed be-
Accepted 9 January 2018
tween 2008 and 2012. The present study examined males aged 18 years from northwest rural China (n ¼ 707). Data on current smoking and drinking status were collected. Logistic regression was used to estimate the individual and combined influences of smoking and
Keywords:
alcohol consumption on lipid profile. Age, ethnic group, educational background, smoking
Smoking
(or alcohol consumption), waist circumference, body mass index, blood pressure and
Alcohol consumption
fasting blood glucose were adjusted as confounders.
Dyslipidaemia
Results: Total cholesterol (TC)/high-density lipoprotein cholesterol (HDL-C) ratio, tri-
Lipid profile
glycerides (TG)/HDL-C ratio, low-density lipoprotein cholesterol (LDL-C)/HDL-C ratio and
Chinese
visceral adiposity index (VAI) were significantly higher in smokers than in non-smokers, whereas HDL-C was lower in smokers. TG/HDL-C ratio, LDL-C/HDL-C ratio, TG, lipid accumulation product and VAI were significantly higher in drinkers than non-drinkers. After adjustment for confounders, significant relationships were observed between smoking status and any dyslipidemia, low HDL-C and high VAI (odds ratios [ORs]: 2.53 [95% confidence interval {CI}: 1.25e5.15], 6.13 [95% CI: 2.84e13.25] and 4.39 [95% CI: 2.02 e9.54], respectively). The OR for any dyslipidaemia was 1.94 (95% CI: 1.09e3.48) for subjects who smoke and drank alcohol compared with subjects who did not smoke or drink alcohol. Conclusions: Abnormalities in lipid profile are correlated with smoking and alcohol consumption, which calls for intervention strategies to prevent dyslipidaemia and control risk factors for cardiovascular disease. © 2018 The Royal Society for Public Health. Published by Elsevier Ltd. All rights reserved.
* Corresponding author. Department of Epidemiology and Health Statistics, School of Public Health and Management, Ningxia Medical University, 1160 Shengli Street, Yinchuan, Ningxia Hui Autonomous Region, PR China. Tel./fax: þ86 951 6980144. E-mail address: [email protected] (Y.H. Zhang). https://doi.org/10.1016/j.puhe.2018.01.003 0033-3506/© 2018 The Royal Society for Public Health. Published by Elsevier Ltd. All rights reserved.
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Introduction
Methods
Dyslipidaemia is defined as an abnormal level of lipid in the blood and is characterised by increased levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG) and a decreased level of high-density lipoprotein cholesterol (HDL-C). Dyslipidaemia is prevalent among adults worldwide; for example, 53% (105.3 million) of adults in the United States have lipid abnormalities.1 In China, it has been reported that the prevalence of dyslipidaemia is 34.0% in the total population and 26.3% in rural areas.2 In addition, in China, the prevalence of dyslipidaemia is significantly higher in males (41.9%) than females (32.5%).2 Dyslipidaemia is an important risk factor for cardiovascular disease.3,4 A study reported that the hazard ratio for coronary heart disease was 2.52 (95% confidence interval [CI]: 1.15e5.07) in males with high TC compared with males with low TC.5 A cohort study comprised of 15,335 patients showed that high TG is independently associated with increased all-cause mortality in patients with coronary heart disease.6 LDL-C is a strong independent predictor of coronary heart disease in individuals with diabetes.7 An inverse relationship has been reported between HDL-C and coronary heart disease, and an isolated low HDL-C was more prevalent among Asian populations.8 The body of research suggesting that the TG/HDL-C ratio is a powerful independent predictor of all-cause mortality and cardiovascular events is growing.9 In addition to a malfunction of lipid metabolism, many epidemiological studies have found that a small number of modifiable behavioural risk factors (e.g. smoking and alcohol consumption) are major contributors to the development of cardiovascular disease. Research has shown that smoking and alcohol consumption are strong risk factors for dyslipidaemia. Smoking decreases HDL-C and increases TG, whereas alcohol consumption increases both HDL-C and TG.10 Smoking cessation improves lipid metabolism.11 A study among Chinese nonagenarians/centenarians found that smoking habits were not associated with increased risk of dyslipidaemia, which differed from the results found in the general population.12 It has been reported that alcohol consumption increases TC and HDL-C but has no significant effect on TG, except at high levels of consumption.13 Some animal experiments and epidemiological studies found that chronic alcohol intake increased serum HDL-C significantly.14 Smoking and drinking behaviours often coincide, which has a reciprocal influence on potentiating tendency.15 Most previous studies have focused on evaluating the influences of smoking and alcohol consumption on dyslipidaemia. However, their combined influence remains unclear. Therefore, the present study was undertaken to explore the influences of smoking and alcohol consumption, individually and in combination, on lipid profile and dyslipidaemia among the rural Chinese population, among whom the prevalence rates of overweight and obesity are substantially lower than in Western populations, largely due to differences in dietary and lifestyle factors.
Study design and participants A cross-sectional survey was carried out from 2008 to 2012 in Yuanzhou District, Qingtongxia City and Pingluo County in Ningxia Hui Autonomous Region, China. This cross-sectional survey has been described previously.16 In brief, the survey enrolled 4614 subjects who were rural residents in northwest China, aged 18e75 years. During the study period, 4614 subjects (3591 females and 1023 males) provided general demographic and lifestyle data via interview and underwent a physical examination. According to the mechanical sampling (k ¼ 1), 2393 subjects donated a blood sample voluntarily. As the rates of smoking and alcohol consumption were low in females, the present study was limited to males. Three hundred and sixteen male subjects were excluded, including 28 subjects who reported a history of coronary heart disease, 91 subjects with hypertension, 23 subjects with diabetes, 55 subjects who had quit smoking, 23 subjects who had quit drinking and 96 subjects who did not meet the required level of serum lipid. After these exclusions, the study population consisted of 707 male subjects. The study was approved by the Research Ethics Committee of the Ningxia Medical University, and all participants gave their written consent.
Data collection and measurements All subjects were interviewed by a trained research assistant with a closed-ended questionnaire, which solicited information on demographic characteristics including age, ethnic group, educational background, smoking and drinking status, personal and family history of disease, etc. The interviewers filled in the questionnaires and self-checked their accuracy and completeness on the spot. In terms of smoking and drinking status, subjects were classified into the following groups: (1) Non-smokers: individuals who claimed that they had never smoked a cigarette. (2) Smokers: individuals who claimed that they smoked every day and had smoked for more than six months. Based on smoking quantification, smokers were subclassified as light smokers (1e20 cigarettes/day) or heavy smokers (>20 cigarettes/day). Based on smoking duration, smokers were subclassified as 1e10 years, 11e20 years and >20 years. (3) Ex-smokers: individuals who claimed that they had quit smoking at least six months before the interview. In terms of alcohol consumption, subjects were classified into the following groups: (1) Non-drinkers: individuals who claimed that they had never consumed alcohol. (2) Drinkers: individuals who claimed that they drank alcohol every day and had done so for more than six months. Based on drinking duration, alcohol drinkers were subclassified as 1e20 years and >20 years.
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(3) Ex-drinkers: individuals who claimed that they had quit drinking at least six months before the interview. The methods used for anthropometric measurements and collection/preservation of blood samples have been described previously.16 Blood glucose was measured using One Touch Ultra 2 (Life Scan, Wayne, PA, USA) immediately after blood collection. Serum HDL-C, TC and TG were measured using an automatic biochemical analyser (COBASE 501, Roche Diagnostics GmbH, Switzerland). Serum LDL-C was calculated using the Friedewald formula.17 Dyslipidaemia was defined using the criteria of the International Diabetes Federation (2005): TC 5.72 mmol/l, TG 1.7 mmol/l, LDL-C 3.4 mmol/l and HDL-C < 0.9 mmol/l. It has been reported that the TG/HDLC ratio is a powerful independent predictor of all-cause mortality and is a risk factor for cardiovascular events,18 and a high TG/HDL-C ratio was defined as 3.75.19 The visceral adiposity index (VAI) and lipid accumulation product (LAP) were calculated by anthropometric and metabolic index.20 Epidemiological studies suggest that VAI and LAP have wellvalidated predictive power for the risk of cardiovascular disease and diabetes.21e24 The following formulae were used:
Table 1 e Characteristics of subjects according to smoking status. Parameters
Smoker
Non-smoker
n ¼ 330
n ¼ 377
Age (years) Ethnic group (Han/Hui, n) Body mass index (kg/m2) Waist circumference (cm) Fasting glucose (mmol/l) TC (mmol/l) TG (mmol/l) LDL-C (mmol/l) HDL-C (mmol/l) TC/HDL-C ratio TG/HDL-C ratio LDL-C/HDL-C ratio LAPa VAIa
46.2 (11.6) 239/91 22.9 (3.3) 81.3 (9.2) 5.4 (0.6) 3.88 (0.79) 1.40 (0.82) 2.02 (0.67) 1.21 (0.30) 3.37 (1.09) 1.30 (1.05) 1.77 (0.77) 1.24 (0.42) 1.77 (0.30)
49.0 (12.6) 148/229 23.2 (3.1) 82.2 (9.1) 5.5 (0.5) 3.89 (0.82) 1.30 (0.89) 2.00 (0.65) 1.30 (0.33) 3.11 (0.86) 1.09 (0.90) 1.62 (0.66) 1.24 (0.39) 1.71 (0.28)
P-value
0.003 <0.001 0.28 0.17 0.12 0.84 0.11 0.68 <0.001 <0.001 0.004 0.006 0.83 0.005
TC, total cholesterol; TG, triglycerides; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; LAP, lipid accumulation product; VAI, visceral adiposity index. Values are given as mean (standard deviation) unless otherwise indicated. a Log-transformed values were used in the analysis.
LAP ¼ [WC (cm) 65] [TG (mmol/l)] VAI ¼ [WC/39.68 þ (1.88 BMI)] (TG/1.03) (1.31/HDL-C) where both TG and HDL-C are expressed in mmol/l. WC and BMI represent mean waist circumference and body mass index, respectively. Subjects in the highest tertile for VAI and LAP were defined as subjects with high VAI and LAP.
Statistical analysis All statistical analyses in this study were performed using SPSS, version 14.0 (IBM Corp., Armonk, NY, USA). P < 0.05 was considered to indicate statistical significance. LAP and VAI were log-transformed due to their skewed distributions. The results are shown as mean (standard deviation [SD]) and odds ratio (OR) and 95% CI. Differences between mean values were evaluated using Student's t-test. Differences between groups were analysed by analysis of variance. Logistic regression was used to estimate OR (95% CI) of smoking and drinking status and lipid profile. Age, ethnic group, educational background, smoking (or drinking), waist circumference, body mass index, blood pressure and fasting blood glucose were adjusted as confounders.
Results Of the 707 subjects, 330 were classified as smokers and 377 were classified as non-smokers; mean ages were 46.2 (SD: 11.6) years and 49.0 (SD: 12.6) years, respectively. As shown in Table 1, HDL-C was significantly lower in smokers than in non-smokers. Also, smokers had significantly higher TC/HDLC, TG/HDL-C and LDL-C/HDL-C ratios and VAI than nonsmokers (all P < 0.05). Table 2 shows that the TG/HDL-C and LDL-C/HDL-C ratios and TG, LAP and VAI were significantly higher in drinkers than
in non-drinkers. A significant positive association was found between TG and LAP and years of drinking. Table 3 shows the adjusted OR (95% CI) of dyslipidaemia and abnormal lipid-related indices by smoking status (non-smokers vs light smokers vs heavy smokers). A significant association was found between smoking status and any dyslipidaemia, low HDL-C and high VAI; ORs were 2.53 (95% CI: 1.25e5.15), 6.13 (95% CI: 2.84e13.25) and 4.39 (95% CI: 2.02e9.54), respectively, after adjusting for potential confounders including age, ethnic group, educational background, alcohol consumption, waist circumference, body mass index, blood pressure and fasting blood glucose. In addition, the relationships between co-smoking and drinking and lipid profile were analysed in subject groups, as shown in Table 4. The OR for dyslipidaemia was 1.94 (95% CI: 1.09e3.48) when comparing co-smoking and drinking subjects with subjects who smoked but did not drink, and subjects who did not drink or smoke. The subjects who co-smoked and drank alcohol were associated with increased risk of higher TG, but this association was no longer significant after adjustment for age, ethnic group, educational background, waist circumference, body mass index, blood pressure and fasting blood glucose. The ORs for low HDL-C and high VAI were significantly higher than the reference level of 1.00 in subjects who smoked but did not drink. The OR for a high TG/HDL-C ratio was significantly higher than the reference level of 1.00 in subjects who smoked but did not drink and tended to be higher in cosmoking and drinking subjects in Model 2, but this was not significantly different from the reference level. Compared with the reference level of 1.00, ORs for high LAP and high VAI in subjects who smoked but did not drink were 1.89 (95% CI: 1.03e3.48) and 2.39 (95% CI: 1.46e3.92), respectively.
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Table 2 e Variations of lipid profile indices according to drinking status. Drinking status (n ¼ 707)
Lipid profile variables
Non-drinker (n ¼ 552) TC (mmol/l) TG (mmol/l) LDL-C (mmol/l) HDL-C (mmol/l) TC/HDL-C ratio TG/HDL-C ratio LDL-C/HDL-C ratio LAPa VAIa
3.87 (0.78) 1.26 (0.76) 2.04 (0.64) 1.26 (0.32) 3.23 (0.97) 1.12 (0.89) 1.55 (0.67) 1.21 (0.40) 1.71 (0.28)
3.94 1.65 1.89 1.28 3.24 1.44 1.73 1.34 1.82
Years of drinking (n ¼ 330)
P-value
Drinker (n ¼ 155) (0.89) (1.10) (0.71) (0.33) (1.02) (1.21) (0.72) (0.42) (0.31)
1e20 (n ¼ 70) 0.31 <0.001* 0.11 0.34 0.98 0.002* 0.006* <0.001* <0.001*
3.82 (0.87) 1.47 (0.72) 1.86 (0.77) 1.23 (0.31) 3.27 (1.12) 1.31 (0.93) 1.60 (0.72) 1.24 (0.43) 1.80 (0.28)
P-value
>20 (n ¼ 85) 4.04 1.80 1.91 1.33 3.19 1.55 1.50 1.42 1.83
(0.90) (1.31) (0.65) (0.34) (0.94) (1.40) (0.60) (0.40) (0.34)
0.12 0.047* 0.70 0.08 0.62 0.23 0.40 0.008* 0.51
TC, total cholesterol; TG, triglycerides; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; LAP, lipid accumulation product; VAI, visceral adiposity index. Values are given as mean (standard deviation). * Indicates statistically significant (P < 0.05). a Log-transformed values were used in the analysis.
Discussion This study explored the individual and combined effects of smoking and alcohol consumption on lipid profile. TC/HDL-C, TG/HDL-C and LDL-C/HDL-C ratios and VAI were higher in smokers compared with non-smokers, whereas HDL-C was
lower in smokers. TG/HDL-C and LDL-C/HDL-C ratios, TG, LAP and VAI were higher in drinkers than in non-drinkers. The OR for any dyslipidaemia was 1.94 (95% CI: 1.09e3.48) for comparing the co-smoking and drinking subjects with subjects who did not smoke or drink alcohol.
Table 4 e Odds ratio of lipid profile according to smoking and alcohol consumption status. Table 3 e Odds ratio (OR) of lipid profile according to smoking status. Lipid profile variables Any dyslipidemiaa Model 1 OR (95% CI) Model 2 OR (95% CI) High TG Model 1 OR (95% CI) Model 2 OR (95% CI) High LDL-C Model 1 OR (95% CI) Model 2 OR (95% CI) Low HDL-C Model 1 OR (95% CI) Model 2 OR (95% CI) High TG/HDL-C ratio Model 1 OR (95% CI) Model 2 OR (95% CI) High LAP Model 1 OR (95% CI) Model 2 OR (95% CI) High VAI Model 1 OR (95% CI) Model 2 OR (95% CI)
Lipid profile variables
NonLight smoker Heavy smoker smokerb 1 1
1.24 (0.88e1.74) 1.30 (0.88e1.92)
2.25 (1.19e4.24) 2.53 (1.25e5.15)
1 1
1.09 (0.75e1.58) 0.99 (0.64e1.54)
1.95 (1.00e3.82) 1.82 (0.84e3.94)
1 1
0.99 (0.41e2.38) 1.18 (0.45e3.11)
2.23 (0.60e8.21) 2.48 (0.61e10.06)
1 1
1.49 (0.96e2.32) 1.66 (1.01e2.73)
3.92 (1.95e7.87) 6.13 (2.84e13.25)
1 1
2.52 (0.99e6.39) 1.23 (0.15e10.23) 3.74 (1.21e11.52) 1.39 (0.14e14.22)
1 1
1.11 (0.78e1.59) 1.24 (0.72e2.14)
1.65 (0.85e3.21) 2.11 (0.76e5.86)
1 1
1.35 (0.94e1.93) 1.68 (1.08e2.63)
2.78 (1.46e5.29) 4.39 (2.02e9.54)
TG, triglycerides; LDL-C, low-density lipoprotein cholesterol; HDLC, high-density lipoprotein cholesterol; LAP, lipid accumulation product; VAI, visceral adiposity index; light smoker, 20 cigarettes/ day; heavy smoker, >20 cigarettes/day; CI, confidence interval. Model 2: adjusted for age, ethnic group, educational background, alcohol consumption, waist circumference, body mass index, blood pressure and fasting blood glucose. a Any dyslipidemia is defined as high total cholesterol, low HDL-C, high LDL-C or high TG. b Significantly higher ORs compared with a reference level of 1.00.
Any dyslipidemiaa Model 1 OR (95% CI) Model 2 OR (95% CI) High TG Model 1 OR (95% CI) Model 2 OR (95% CI) High LDL-C Model 1 OR (95% CI) Model 2 OR (95% CI) Low HDL-C Model 1 OR (95% CI) Model 2 OR (95% CI) High TG/HDL-C ratio Model 1 OR (95% CI) Model 2 OR (95% CI) High LAP Model 1 OR (95% CI) Model 2 OR (95% CI) High VAI Model 1 OR (95% CI) Model 2 OR (95% CI)
Nonsmoker, nondrinkerb
Smoker, non-drinker
Co-smoker and drinker
1 1
1.50 (1.03e2.20) 1.77 (1.11e2.82) 1.82 (1.18e2.80) 1.94 (1.09e3.48)
1 1
1.26 (0.82e1.94) 2.08 (1.26e3.42) 1.40 (0.85e2.29) 1.84 (0.97e3.47)
1 1
1.71 (0.65e4.50) 1.14 (0.30e4.37) 2.64 (0.89e7.86) 2.55 (0.50e13.15)
1 1
1.70 (1.07e2.72) 1.49 (0.82e2.69) 1.85 (1.10e3.09) 1.70 (0.83e3.47)
1 1
1.77 (0.59e5.33) 3.71 (1.22e11.28) 2.62 (0.73e9.39) 3.52 (0.74e16.76)
1 1
1.26 (0.84e1.90) 1.97 (1.22e3.19) 1.89 (1.03e3.48) 2.24 (1.00e5.00)
1 1
1.66 (1.11e2.47) 1.81 (1.10e2.95) 2.39 (1.46e3.92) 1.95 (0.99e3.83)
TG, triglycerides; LDL-C, low-density lipoprotein cholesterol; HDLC, high-density lipoprotein cholesterol; LAP, lipid accumulation product; VAI, visceral adiposity index; CI, confidence interval; OR, odds ratio. Model 2: adjusted for age, ethnic group, educational background, waist circumference, body mass index, blood pressure and fasting blood glucose. a Any dyslipidemia is defined as high total cholesterol, low HDL-C, high LDL-C or high TG. b Significantly higher ORs compared with a reference level of 1.00.
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The results of previous studies regarding the influences of smoking and alcohol consumption on lipid profile and its association with serum lipid/lipoprotein among Chinese populations were generally consistent with the results of the present study.25e27 Prenatal exposure to cigarette smoke has been shown to induce a lipid profile in the offspring and alter the offspring's risk of developing cardiovascular disease in future.28 A previous study reported that the OR of higher TG was 1.30 (95% CI: 1.09e1.55), the OR of lower HDL-C was 1.29 (95% CI: 1.08e1.54), the OR of higher LDL-C was 1.30 (95% CI: 1.07e1.56) and the OR of higher TG was 1.40 (95% CI: 1.16e1.68) in males who smoked 21e30 cigarettes per day compared with non-smokers.29 Furthermore, several studies have reported an effective improvement in lipid profile after smoking cessation. In particular, HDL-C levels increased,30,31 and individuals of working age who quit smoking may thus reduce the calculated risk of cardiovascular disease to nearly the same level as individuals who have never smoked.32 This mechanism may be due to the effects of smoking on oxidative stress and inflammation.33 Most previous studies have focused on the effects of alcohol consumption on dyslipidaemia, and an association between higher risk of dyslipidaemia and alcohol consumption has been reported.34,35 However, several studies have identified a negative association between alcohol consumption and dyslipidaemia. For example, compared with nondrinkers, consumption of 90 g of alcohol per week had a significant protective effect against lower HDL-C.29 Moreover, there was an inverse association between light-to-moderate alcohol consumption and lipid-related indices in patients with diabetes.19 Although most previous studies have focused on the effect of daily alcohol consumption (amount) on dyslipidaemia, little is known about the association between patterns of alcohol consumption and dyslipidaemia. The relationship between alcohol consumption and lipid profile remains unclear and complex.34 Unfortunately, the present study did not investigate the influence of drinking cessation or the duration of drinking cessation on dyslipidaemia. In reality, many subjects who smoke also drink alcohol.36 The neurochemical mechanisms of action of nicotine and alcohol appear to be mutually reinforcing.37 Some studies have analysed the potential combined effects of smoking and alcohol consumption on some diseases.38,39 A 30-year cohort study of 5771 male participants found that current smokers had a high relative rate for coronary heart disease mortality, while alcohol consumption in never smokers was a possible protective effect against heart disease mortality; smoking and drinking >15 units/week was the riskiest behaviour for all causes of death.40 Although the interactions between smoking and alcohol consumption are complex, evaluated tobacco use can be a clinical indicator for alcohol misuse.41 Neuronal nicotinic acetylcholine receptor systems play an important role in the behavioural effects of alcohol.42 These results suggest that subjects who smoke and drink alcohol may be at greater risk of dyslipidaemia compared with subjects who do not smoke or drink alcohol. There is a need for more intervention strategies to prevent dyslipidaemia and control risk factors for cardiovascular disease. The results of this study show that there is an increase in lipid profile in subjects who smoke and drink alcohol, and co-
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smoking and drinking subjects had a higher risk of dyslipidaemia. Smokers had low HDL-C, and drinkers had high HDLC. However, this study has potential limitations. As it was a cross-sectional survey, no temporal relationship could be established, and it was not possible to establish causal conclusions for the associations between smoking and alcohol consumption habits and dyslipidaemia. Prospective observation studies are needed to observe the causal variation of lipid profile in smokers and drinkers. Meanwhile, there is a need to gather detailed data regarding smoking cessation and drinking cessation, and the drinking data need to be quantified. In addition, diet and physical exercise are extremely important factors and should be considered. Evidence shows that the effects of smoking take time to be detected,43 which suggests a need for more follow-up studies with large samples to explore the time effect of smoking and dyslipidaemia.
Author statements Acknowledgements The authors would like to thank the village doctors of all participating villages for their support with subject recruitment, and the study participants for their willingness to be interviewed and donate blood samples. Finally, the authors wish to thank all investigators for their contributions to the research.
Ethical approval This study was approved by the Medical Ethics Review Committee of Ningxia Medical University.
Funding This work was supported by Natural Science Foundation of China (No. 81160358).
Competing interests None declared.
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21. Chen HY, Chiu YL, Chuang YF, Hsu SP, Pai MF, Yang JY, et al. Visceral adiposity index and risks of cardiovascular events and mortality in prevalent hemodialysis patients. Cardiovasc Diabetol 2014;13:136e45. 22. Chen C, Xu Y, Guo ZR, Yang J, Wu M, Hu XS. The application of visceral adiposity index in identifying type 2 diabetes risks based on a prospective cohort in China. Lipids Health Dis 2014;13:108e16. 23. Bozorgmanesh M, Hadaegh F, Azizi F. Diabetes prediction, lipid accumulation product, and adiposity measures; 6-year follow-up: Tehran lipid and glucose study. Lipids Health Dis 2010;9:45. 24. Kahn HS. The “lipid accumulation product” performs better than the body mass index for recognizing cardiovascular risk: a population-based comparison. BMC Cardiovasc Disord 2005;5:26. 25. Tan XJ, Jiao GP, Ren YJ, Gao XR, Ding Y, Wang XR, et al. Relationship between smoking and dyslipidemia in western Chinese elderly males. J Clin Lab Analy 2008;22:159e63. 26. Wang S, Xu L, Jonas JB, You QS, Wang YX, Yang H. Prevalence and associated factors of dyslipidemia in the adult Chinese population. PLoS One 2011;6:e17326. 27. Shen Z, Munker S, Wang C, Xu L, Ye H, Chen H, et al. Association between alcohol intake, overweight, and serum lipid levels and the risk analysis associated with the development of dyslipidemia. J Clin Lipidol 2014;8:273e8. 28. Ng SP, Conklin DJ, Bhatnagar A, Bolanowski DD, Lyon J, Zelikoff JT. Prenatal exposure to cigarette smoke induces dietand sex-dependent dyslipidemia and weight gain in adult murine offspring. Environ Health Perspect 2009;117:1042e8. 29. Lee KS, Park CY, Meng KH, Bush A, Lee SH, Lee WC, et al. The association of cigarette smoking and alcohol consumption with other cardiovascular risk factors in men from Seoul, Korea. Ann Epidemiol 1998;8:31e8. 30. Stubbe I, Eskilsson J, Nilsson-Ehle P. High-density lipoprotein concentrations increase after stopping smoking. Br Med J (Clin Res Ed) 1982;284:1511e3. 31. Maeda K, Noguchi Y, Fukui T. The effects of cessation from cigarette smoking on the lipid and lipoprotein profiles: a meta-analysis. Prev Med 2003;37:283e90. 32. Keto J, Ventola H, Jokelainen J, Linden K, KeinanenKiukaanniemi S, Timonen M, et al. Cardiovascular disease risk factors in relation to smoking behaviour and history: a population-based cohort study. Open Heart 2016;3:e000358. 33. Van der Vaart H, Postma D, Timens W, Ten H. Acute effects of cigarette smoke on inflammation and oxidative stress: a review. Thorax 2004;59:713e21. 34. Kwon YJ, Kim SE, Park BJ, Bae JW, Kang HT. High-risk drinking is associated with dyslipidemia in a different way, based on the 2010e2012 KNHANES. Clin Chima Acta 2016;456:170e5. 35. Wakabayashi I. Associations between heavy alcohol drinking and lipid-related indices in middle-aged men. Alcohol 2013;47:637e42. 36. Room R. Smoking and drinking as complementary behaviours. Biomed Pharmacother 2004;58:111e5. 37. Larsson A, Engel JA. Neurochemical and behavioral studies on ethanol and nicotine interactions. Neurosci Biobehav Rev 2004;27:713e20. 38. Hashibe M, Brennan P, Chuang SC, Boccia S, Castellsague X, Chen C, et al. Interaction between tobacco and alcohol use and the risk of head and neck cancer: pooled analysis in the International Head and Neck Cancer Epidemiology Consortium. Cancer Epidemiol Biomarkers Prev 2009;18:541e50. 39. Petti S, Masood M, Scully C. The magnitude of tobacco smoking-betel quid chewing-alcohol drinking interaction effect on oral cancer in South-East Asia. A meta-analysis of observational studies. PLoS One 2013;8:e78999.
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Original Research
Effects of smoking and alcohol consumption on lipid profile in male adults in northwest rural China X.X. Li, Y. Zhao, L.X. Huang, H.X. Xu, X.Y. Liu, J.J. Yang, P.J. Zhang, Y.H. Zhang* Department of Epidemiology and Health Statistics, School of Public Health and Management, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, PR China
article info
abstract
Article history:
Objectives: To determine the individual and combined influences of smoking and alcohol
Received 26 July 2017
consumption on lipid profile in male adults in northwest rural China.
Received in revised form
Design: Cross-sectional study.
4 November 2017
Methods: In total, 4614 subjects were enrolled in the cross-sectional study, performed be-
Accepted 9 January 2018
tween 2008 and 2012. The present study examined males aged 18 years from northwest rural China (n ¼ 707). Data on current smoking and drinking status were collected. Logistic regression was used to estimate the individual and combined influences of smoking and
Keywords:
alcohol consumption on lipid profile. Age, ethnic group, educational background, smoking
Smoking
(or alcohol consumption), waist circumference, body mass index, blood pressure and
Alcohol consumption
fasting blood glucose were adjusted as confounders.
Dyslipidaemia
Results: Total cholesterol (TC)/high-density lipoprotein cholesterol (HDL-C) ratio, tri-
Lipid profile
glycerides (TG)/HDL-C ratio, low-density lipoprotein cholesterol (LDL-C)/HDL-C ratio and
Chinese
visceral adiposity index (VAI) were significantly higher in smokers than in non-smokers, whereas HDL-C was lower in smokers. TG/HDL-C ratio, LDL-C/HDL-C ratio, TG, lipid accumulation product and VAI were significantly higher in drinkers than non-drinkers. After adjustment for confounders, significant relationships were observed between smoking status and any dyslipidemia, low HDL-C and high VAI (odds ratios [ORs]: 2.53 [95% confidence interval {CI}: 1.25e5.15], 6.13 [95% CI: 2.84e13.25] and 4.39 [95% CI: 2.02 e9.54], respectively). The OR for any dyslipidaemia was 1.94 (95% CI: 1.09e3.48) for subjects who smoke and drank alcohol compared with subjects who did not smoke or drink alcohol. Conclusions: Abnormalities in lipid profile are correlated with smoking and alcohol consumption, which calls for intervention strategies to prevent dyslipidaemia and control risk factors for cardiovascular disease. © 2018 The Royal Society for Public Health. Published by Elsevier Ltd. All rights reserved.
* Corresponding author. Department of Epidemiology and Health Statistics, School of Public Health and Management, Ningxia Medical University, 1160 Shengli Street, Yinchuan, Ningxia Hui Autonomous Region, PR China. Tel./fax: þ86 951 6980144. E-mail address: [email protected] (Y.H. Zhang). https://doi.org/10.1016/j.puhe.2018.01.003 0033-3506/© 2018 The Royal Society for Public Health. Published by Elsevier Ltd. All rights reserved.
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Introduction
Methods
Dyslipidaemia is defined as an abnormal level of lipid in the blood and is characterised by increased levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG) and a decreased level of high-density lipoprotein cholesterol (HDL-C). Dyslipidaemia is prevalent among adults worldwide; for example, 53% (105.3 million) of adults in the United States have lipid abnormalities.1 In China, it has been reported that the prevalence of dyslipidaemia is 34.0% in the total population and 26.3% in rural areas.2 In addition, in China, the prevalence of dyslipidaemia is significantly higher in males (41.9%) than females (32.5%).2 Dyslipidaemia is an important risk factor for cardiovascular disease.3,4 A study reported that the hazard ratio for coronary heart disease was 2.52 (95% confidence interval [CI]: 1.15e5.07) in males with high TC compared with males with low TC.5 A cohort study comprised of 15,335 patients showed that high TG is independently associated with increased all-cause mortality in patients with coronary heart disease.6 LDL-C is a strong independent predictor of coronary heart disease in individuals with diabetes.7 An inverse relationship has been reported between HDL-C and coronary heart disease, and an isolated low HDL-C was more prevalent among Asian populations.8 The body of research suggesting that the TG/HDL-C ratio is a powerful independent predictor of all-cause mortality and cardiovascular events is growing.9 In addition to a malfunction of lipid metabolism, many epidemiological studies have found that a small number of modifiable behavioural risk factors (e.g. smoking and alcohol consumption) are major contributors to the development of cardiovascular disease. Research has shown that smoking and alcohol consumption are strong risk factors for dyslipidaemia. Smoking decreases HDL-C and increases TG, whereas alcohol consumption increases both HDL-C and TG.10 Smoking cessation improves lipid metabolism.11 A study among Chinese nonagenarians/centenarians found that smoking habits were not associated with increased risk of dyslipidaemia, which differed from the results found in the general population.12 It has been reported that alcohol consumption increases TC and HDL-C but has no significant effect on TG, except at high levels of consumption.13 Some animal experiments and epidemiological studies found that chronic alcohol intake increased serum HDL-C significantly.14 Smoking and drinking behaviours often coincide, which has a reciprocal influence on potentiating tendency.15 Most previous studies have focused on evaluating the influences of smoking and alcohol consumption on dyslipidaemia. However, their combined influence remains unclear. Therefore, the present study was undertaken to explore the influences of smoking and alcohol consumption, individually and in combination, on lipid profile and dyslipidaemia among the rural Chinese population, among whom the prevalence rates of overweight and obesity are substantially lower than in Western populations, largely due to differences in dietary and lifestyle factors.
Study design and participants A cross-sectional survey was carried out from 2008 to 2012 in Yuanzhou District, Qingtongxia City and Pingluo County in Ningxia Hui Autonomous Region, China. This cross-sectional survey has been described previously.16 In brief, the survey enrolled 4614 subjects who were rural residents in northwest China, aged 18e75 years. During the study period, 4614 subjects (3591 females and 1023 males) provided general demographic and lifestyle data via interview and underwent a physical examination. According to the mechanical sampling (k ¼ 1), 2393 subjects donated a blood sample voluntarily. As the rates of smoking and alcohol consumption were low in females, the present study was limited to males. Three hundred and sixteen male subjects were excluded, including 28 subjects who reported a history of coronary heart disease, 91 subjects with hypertension, 23 subjects with diabetes, 55 subjects who had quit smoking, 23 subjects who had quit drinking and 96 subjects who did not meet the required level of serum lipid. After these exclusions, the study population consisted of 707 male subjects. The study was approved by the Research Ethics Committee of the Ningxia Medical University, and all participants gave their written consent.
Data collection and measurements All subjects were interviewed by a trained research assistant with a closed-ended questionnaire, which solicited information on demographic characteristics including age, ethnic group, educational background, smoking and drinking status, personal and family history of disease, etc. The interviewers filled in the questionnaires and self-checked their accuracy and completeness on the spot. In terms of smoking and drinking status, subjects were classified into the following groups: (1) Non-smokers: individuals who claimed that they had never smoked a cigarette. (2) Smokers: individuals who claimed that they smoked every day and had smoked for more than six months. Based on smoking quantification, smokers were subclassified as light smokers (1e20 cigarettes/day) or heavy smokers (>20 cigarettes/day). Based on smoking duration, smokers were subclassified as 1e10 years, 11e20 years and >20 years. (3) Ex-smokers: individuals who claimed that they had quit smoking at least six months before the interview. In terms of alcohol consumption, subjects were classified into the following groups: (1) Non-drinkers: individuals who claimed that they had never consumed alcohol. (2) Drinkers: individuals who claimed that they drank alcohol every day and had done so for more than six months. Based on drinking duration, alcohol drinkers were subclassified as 1e20 years and >20 years.
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(3) Ex-drinkers: individuals who claimed that they had quit drinking at least six months before the interview. The methods used for anthropometric measurements and collection/preservation of blood samples have been described previously.16 Blood glucose was measured using One Touch Ultra 2 (Life Scan, Wayne, PA, USA) immediately after blood collection. Serum HDL-C, TC and TG were measured using an automatic biochemical analyser (COBASE 501, Roche Diagnostics GmbH, Switzerland). Serum LDL-C was calculated using the Friedewald formula.17 Dyslipidaemia was defined using the criteria of the International Diabetes Federation (2005): TC 5.72 mmol/l, TG 1.7 mmol/l, LDL-C 3.4 mmol/l and HDL-C < 0.9 mmol/l. It has been reported that the TG/HDLC ratio is a powerful independent predictor of all-cause mortality and is a risk factor for cardiovascular events,18 and a high TG/HDL-C ratio was defined as 3.75.19 The visceral adiposity index (VAI) and lipid accumulation product (LAP) were calculated by anthropometric and metabolic index.20 Epidemiological studies suggest that VAI and LAP have wellvalidated predictive power for the risk of cardiovascular disease and diabetes.21e24 The following formulae were used:
Table 1 e Characteristics of subjects according to smoking status. Parameters
Smoker
Non-smoker
n ¼ 330
n ¼ 377
Age (years) Ethnic group (Han/Hui, n) Body mass index (kg/m2) Waist circumference (cm) Fasting glucose (mmol/l) TC (mmol/l) TG (mmol/l) LDL-C (mmol/l) HDL-C (mmol/l) TC/HDL-C ratio TG/HDL-C ratio LDL-C/HDL-C ratio LAPa VAIa
46.2 (11.6) 239/91 22.9 (3.3) 81.3 (9.2) 5.4 (0.6) 3.88 (0.79) 1.40 (0.82) 2.02 (0.67) 1.21 (0.30) 3.37 (1.09) 1.30 (1.05) 1.77 (0.77) 1.24 (0.42) 1.77 (0.30)
49.0 (12.6) 148/229 23.2 (3.1) 82.2 (9.1) 5.5 (0.5) 3.89 (0.82) 1.30 (0.89) 2.00 (0.65) 1.30 (0.33) 3.11 (0.86) 1.09 (0.90) 1.62 (0.66) 1.24 (0.39) 1.71 (0.28)
P-value
0.003 <0.001 0.28 0.17 0.12 0.84 0.11 0.68 <0.001 <0.001 0.004 0.006 0.83 0.005
TC, total cholesterol; TG, triglycerides; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; LAP, lipid accumulation product; VAI, visceral adiposity index. Values are given as mean (standard deviation) unless otherwise indicated. a Log-transformed values were used in the analysis.
LAP ¼ [WC (cm) 65] [TG (mmol/l)] VAI ¼ [WC/39.68 þ (1.88 BMI)] (TG/1.03) (1.31/HDL-C) where both TG and HDL-C are expressed in mmol/l. WC and BMI represent mean waist circumference and body mass index, respectively. Subjects in the highest tertile for VAI and LAP were defined as subjects with high VAI and LAP.
Statistical analysis All statistical analyses in this study were performed using SPSS, version 14.0 (IBM Corp., Armonk, NY, USA). P < 0.05 was considered to indicate statistical significance. LAP and VAI were log-transformed due to their skewed distributions. The results are shown as mean (standard deviation [SD]) and odds ratio (OR) and 95% CI. Differences between mean values were evaluated using Student's t-test. Differences between groups were analysed by analysis of variance. Logistic regression was used to estimate OR (95% CI) of smoking and drinking status and lipid profile. Age, ethnic group, educational background, smoking (or drinking), waist circumference, body mass index, blood pressure and fasting blood glucose were adjusted as confounders.
Results Of the 707 subjects, 330 were classified as smokers and 377 were classified as non-smokers; mean ages were 46.2 (SD: 11.6) years and 49.0 (SD: 12.6) years, respectively. As shown in Table 1, HDL-C was significantly lower in smokers than in non-smokers. Also, smokers had significantly higher TC/HDLC, TG/HDL-C and LDL-C/HDL-C ratios and VAI than nonsmokers (all P < 0.05). Table 2 shows that the TG/HDL-C and LDL-C/HDL-C ratios and TG, LAP and VAI were significantly higher in drinkers than
in non-drinkers. A significant positive association was found between TG and LAP and years of drinking. Table 3 shows the adjusted OR (95% CI) of dyslipidaemia and abnormal lipid-related indices by smoking status (non-smokers vs light smokers vs heavy smokers). A significant association was found between smoking status and any dyslipidaemia, low HDL-C and high VAI; ORs were 2.53 (95% CI: 1.25e5.15), 6.13 (95% CI: 2.84e13.25) and 4.39 (95% CI: 2.02e9.54), respectively, after adjusting for potential confounders including age, ethnic group, educational background, alcohol consumption, waist circumference, body mass index, blood pressure and fasting blood glucose. In addition, the relationships between co-smoking and drinking and lipid profile were analysed in subject groups, as shown in Table 4. The OR for dyslipidaemia was 1.94 (95% CI: 1.09e3.48) when comparing co-smoking and drinking subjects with subjects who smoked but did not drink, and subjects who did not drink or smoke. The subjects who co-smoked and drank alcohol were associated with increased risk of higher TG, but this association was no longer significant after adjustment for age, ethnic group, educational background, waist circumference, body mass index, blood pressure and fasting blood glucose. The ORs for low HDL-C and high VAI were significantly higher than the reference level of 1.00 in subjects who smoked but did not drink. The OR for a high TG/HDL-C ratio was significantly higher than the reference level of 1.00 in subjects who smoked but did not drink and tended to be higher in cosmoking and drinking subjects in Model 2, but this was not significantly different from the reference level. Compared with the reference level of 1.00, ORs for high LAP and high VAI in subjects who smoked but did not drink were 1.89 (95% CI: 1.03e3.48) and 2.39 (95% CI: 1.46e3.92), respectively.
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Table 2 e Variations of lipid profile indices according to drinking status. Drinking status (n ¼ 707)
Lipid profile variables
Non-drinker (n ¼ 552) TC (mmol/l) TG (mmol/l) LDL-C (mmol/l) HDL-C (mmol/l) TC/HDL-C ratio TG/HDL-C ratio LDL-C/HDL-C ratio LAPa VAIa
3.87 (0.78) 1.26 (0.76) 2.04 (0.64) 1.26 (0.32) 3.23 (0.97) 1.12 (0.89) 1.55 (0.67) 1.21 (0.40) 1.71 (0.28)
3.94 1.65 1.89 1.28 3.24 1.44 1.73 1.34 1.82
Years of drinking (n ¼ 330)
P-value
Drinker (n ¼ 155) (0.89) (1.10) (0.71) (0.33) (1.02) (1.21) (0.72) (0.42) (0.31)
1e20 (n ¼ 70) 0.31 <0.001* 0.11 0.34 0.98 0.002* 0.006* <0.001* <0.001*
3.82 (0.87) 1.47 (0.72) 1.86 (0.77) 1.23 (0.31) 3.27 (1.12) 1.31 (0.93) 1.60 (0.72) 1.24 (0.43) 1.80 (0.28)
P-value
>20 (n ¼ 85) 4.04 1.80 1.91 1.33 3.19 1.55 1.50 1.42 1.83
(0.90) (1.31) (0.65) (0.34) (0.94) (1.40) (0.60) (0.40) (0.34)
0.12 0.047* 0.70 0.08 0.62 0.23 0.40 0.008* 0.51
TC, total cholesterol; TG, triglycerides; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; LAP, lipid accumulation product; VAI, visceral adiposity index. Values are given as mean (standard deviation). * Indicates statistically significant (P < 0.05). a Log-transformed values were used in the analysis.
Discussion This study explored the individual and combined effects of smoking and alcohol consumption on lipid profile. TC/HDL-C, TG/HDL-C and LDL-C/HDL-C ratios and VAI were higher in smokers compared with non-smokers, whereas HDL-C was
lower in smokers. TG/HDL-C and LDL-C/HDL-C ratios, TG, LAP and VAI were higher in drinkers than in non-drinkers. The OR for any dyslipidaemia was 1.94 (95% CI: 1.09e3.48) for comparing the co-smoking and drinking subjects with subjects who did not smoke or drink alcohol.
Table 4 e Odds ratio of lipid profile according to smoking and alcohol consumption status. Table 3 e Odds ratio (OR) of lipid profile according to smoking status. Lipid profile variables Any dyslipidemiaa Model 1 OR (95% CI) Model 2 OR (95% CI) High TG Model 1 OR (95% CI) Model 2 OR (95% CI) High LDL-C Model 1 OR (95% CI) Model 2 OR (95% CI) Low HDL-C Model 1 OR (95% CI) Model 2 OR (95% CI) High TG/HDL-C ratio Model 1 OR (95% CI) Model 2 OR (95% CI) High LAP Model 1 OR (95% CI) Model 2 OR (95% CI) High VAI Model 1 OR (95% CI) Model 2 OR (95% CI)
Lipid profile variables
NonLight smoker Heavy smoker smokerb 1 1
1.24 (0.88e1.74) 1.30 (0.88e1.92)
2.25 (1.19e4.24) 2.53 (1.25e5.15)
1 1
1.09 (0.75e1.58) 0.99 (0.64e1.54)
1.95 (1.00e3.82) 1.82 (0.84e3.94)
1 1
0.99 (0.41e2.38) 1.18 (0.45e3.11)
2.23 (0.60e8.21) 2.48 (0.61e10.06)
1 1
1.49 (0.96e2.32) 1.66 (1.01e2.73)
3.92 (1.95e7.87) 6.13 (2.84e13.25)
1 1
2.52 (0.99e6.39) 1.23 (0.15e10.23) 3.74 (1.21e11.52) 1.39 (0.14e14.22)
1 1
1.11 (0.78e1.59) 1.24 (0.72e2.14)
1.65 (0.85e3.21) 2.11 (0.76e5.86)
1 1
1.35 (0.94e1.93) 1.68 (1.08e2.63)
2.78 (1.46e5.29) 4.39 (2.02e9.54)
TG, triglycerides; LDL-C, low-density lipoprotein cholesterol; HDLC, high-density lipoprotein cholesterol; LAP, lipid accumulation product; VAI, visceral adiposity index; light smoker, 20 cigarettes/ day; heavy smoker, >20 cigarettes/day; CI, confidence interval. Model 2: adjusted for age, ethnic group, educational background, alcohol consumption, waist circumference, body mass index, blood pressure and fasting blood glucose. a Any dyslipidemia is defined as high total cholesterol, low HDL-C, high LDL-C or high TG. b Significantly higher ORs compared with a reference level of 1.00.
Any dyslipidemiaa Model 1 OR (95% CI) Model 2 OR (95% CI) High TG Model 1 OR (95% CI) Model 2 OR (95% CI) High LDL-C Model 1 OR (95% CI) Model 2 OR (95% CI) Low HDL-C Model 1 OR (95% CI) Model 2 OR (95% CI) High TG/HDL-C ratio Model 1 OR (95% CI) Model 2 OR (95% CI) High LAP Model 1 OR (95% CI) Model 2 OR (95% CI) High VAI Model 1 OR (95% CI) Model 2 OR (95% CI)
Nonsmoker, nondrinkerb
Smoker, non-drinker
Co-smoker and drinker
1 1
1.50 (1.03e2.20) 1.77 (1.11e2.82) 1.82 (1.18e2.80) 1.94 (1.09e3.48)
1 1
1.26 (0.82e1.94) 2.08 (1.26e3.42) 1.40 (0.85e2.29) 1.84 (0.97e3.47)
1 1
1.71 (0.65e4.50) 1.14 (0.30e4.37) 2.64 (0.89e7.86) 2.55 (0.50e13.15)
1 1
1.70 (1.07e2.72) 1.49 (0.82e2.69) 1.85 (1.10e3.09) 1.70 (0.83e3.47)
1 1
1.77 (0.59e5.33) 3.71 (1.22e11.28) 2.62 (0.73e9.39) 3.52 (0.74e16.76)
1 1
1.26 (0.84e1.90) 1.97 (1.22e3.19) 1.89 (1.03e3.48) 2.24 (1.00e5.00)
1 1
1.66 (1.11e2.47) 1.81 (1.10e2.95) 2.39 (1.46e3.92) 1.95 (0.99e3.83)
TG, triglycerides; LDL-C, low-density lipoprotein cholesterol; HDLC, high-density lipoprotein cholesterol; LAP, lipid accumulation product; VAI, visceral adiposity index; CI, confidence interval; OR, odds ratio. Model 2: adjusted for age, ethnic group, educational background, waist circumference, body mass index, blood pressure and fasting blood glucose. a Any dyslipidemia is defined as high total cholesterol, low HDL-C, high LDL-C or high TG. b Significantly higher ORs compared with a reference level of 1.00.
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The results of previous studies regarding the influences of smoking and alcohol consumption on lipid profile and its association with serum lipid/lipoprotein among Chinese populations were generally consistent with the results of the present study.25e27 Prenatal exposure to cigarette smoke has been shown to induce a lipid profile in the offspring and alter the offspring's risk of developing cardiovascular disease in future.28 A previous study reported that the OR of higher TG was 1.30 (95% CI: 1.09e1.55), the OR of lower HDL-C was 1.29 (95% CI: 1.08e1.54), the OR of higher LDL-C was 1.30 (95% CI: 1.07e1.56) and the OR of higher TG was 1.40 (95% CI: 1.16e1.68) in males who smoked 21e30 cigarettes per day compared with non-smokers.29 Furthermore, several studies have reported an effective improvement in lipid profile after smoking cessation. In particular, HDL-C levels increased,30,31 and individuals of working age who quit smoking may thus reduce the calculated risk of cardiovascular disease to nearly the same level as individuals who have never smoked.32 This mechanism may be due to the effects of smoking on oxidative stress and inflammation.33 Most previous studies have focused on the effects of alcohol consumption on dyslipidaemia, and an association between higher risk of dyslipidaemia and alcohol consumption has been reported.34,35 However, several studies have identified a negative association between alcohol consumption and dyslipidaemia. For example, compared with nondrinkers, consumption of 90 g of alcohol per week had a significant protective effect against lower HDL-C.29 Moreover, there was an inverse association between light-to-moderate alcohol consumption and lipid-related indices in patients with diabetes.19 Although most previous studies have focused on the effect of daily alcohol consumption (amount) on dyslipidaemia, little is known about the association between patterns of alcohol consumption and dyslipidaemia. The relationship between alcohol consumption and lipid profile remains unclear and complex.34 Unfortunately, the present study did not investigate the influence of drinking cessation or the duration of drinking cessation on dyslipidaemia. In reality, many subjects who smoke also drink alcohol.36 The neurochemical mechanisms of action of nicotine and alcohol appear to be mutually reinforcing.37 Some studies have analysed the potential combined effects of smoking and alcohol consumption on some diseases.38,39 A 30-year cohort study of 5771 male participants found that current smokers had a high relative rate for coronary heart disease mortality, while alcohol consumption in never smokers was a possible protective effect against heart disease mortality; smoking and drinking >15 units/week was the riskiest behaviour for all causes of death.40 Although the interactions between smoking and alcohol consumption are complex, evaluated tobacco use can be a clinical indicator for alcohol misuse.41 Neuronal nicotinic acetylcholine receptor systems play an important role in the behavioural effects of alcohol.42 These results suggest that subjects who smoke and drink alcohol may be at greater risk of dyslipidaemia compared with subjects who do not smoke or drink alcohol. There is a need for more intervention strategies to prevent dyslipidaemia and control risk factors for cardiovascular disease. The results of this study show that there is an increase in lipid profile in subjects who smoke and drink alcohol, and co-
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smoking and drinking subjects had a higher risk of dyslipidaemia. Smokers had low HDL-C, and drinkers had high HDLC. However, this study has potential limitations. As it was a cross-sectional survey, no temporal relationship could be established, and it was not possible to establish causal conclusions for the associations between smoking and alcohol consumption habits and dyslipidaemia. Prospective observation studies are needed to observe the causal variation of lipid profile in smokers and drinkers. Meanwhile, there is a need to gather detailed data regarding smoking cessation and drinking cessation, and the drinking data need to be quantified. In addition, diet and physical exercise are extremely important factors and should be considered. Evidence shows that the effects of smoking take time to be detected,43 which suggests a need for more follow-up studies with large samples to explore the time effect of smoking and dyslipidaemia.
Author statements Acknowledgements The authors would like to thank the village doctors of all participating villages for their support with subject recruitment, and the study participants for their willingness to be interviewed and donate blood samples. Finally, the authors wish to thank all investigators for their contributions to the research.
Ethical approval This study was approved by the Medical Ethics Review Committee of Ningxia Medical University.
Funding This work was supported by Natural Science Foundation of China (No. 81160358).
Competing interests None declared.
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