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increasing evidence shows that cigarette smoking is a risk factor for the development of chronic liver disease and liver cancer [ 18.0.co;2-m. href=/articles/10.1186/1471-230x-12-145#ref-cr13 id=ref-link-section-a8cc8e6cdd97>13.]. many studies have focused on the effects of smoking on lfts. in most studies, a significant increase in alt levels has been reported in smokers [ 19.co;2-r.1186/1471-230x-12-145#ref-cr14 id=ref-link-section-5c3038c875c8>14]. however, some other studies have reported no such effect [ 20.co;2-k.1186/1471-230x-12-145#ref-cr15 id=ref-link-section-7b9d64e8b50d>15.

the most interesting result of this study is the interactive influence of alcohol drinking and smoking on lfts. first, when we looked at the effects of alcohol drinking in various smoking statuses, it appeared that alcohol consumption has a synergistic effect with smoking on ggt and alp levels, particularly in the young male (table 4). in addition, the alp level was increased by alcohol consumption in the past-smokers, a subgroup in which the alp level was the most drastically increased by alcohol drinking among all three lfts. because the liver is the organ to metabolize alcohol, the effects of alcohol on the liver function are directly linked with alcohol metabolism. the liver function may be impaired by alcohol consumption in a dose-dependent manner as the liver is particularly vulnerable to the effects of alcohol consumption [ 27 ]. in addition, the results of a study on the association between the level of alcohol consumption and alcohol-related disorders found that the risk of developing alcohol-related disorders was increased in the individuals with ggt levels greater than 44 u/l [ 28 ]. previous studies documented that individuals with high ggt levels drank more [ 29 ] or had a higher risk of developing alcohol-related disorders [ 28 ]. thus, the effects of alcohol consumption on the liver function may be more dramatic when the ggt level is high. these synergistic effects of alcohol drinking and smoking on ggt levels were more pronounced in the young male than in the young female group. however, the effect of smoking on the alp level was the most pronounced in the young female group. the mechanism of the synergistic effect of alcohol drinking and smoking on lfts remains to be clarified. however, the enhanced hepatic oxidative stress by smoking may be a possible explanation. some studies have reported that oxidative stress is induced by smoking and alcohol consumption, and it may be associated with the development of alcoholic liver injury and steatosis [ 30 ]. in addition, the effects of smoking on lfts may be exacerbated by alcohol consumption, as smoking may enhance the alcohol-related oxidative stress and may result in the development of alcoholic liver injury and steatosis [ 31 ].

several mechanisms are suggested to explain the effect of smoking on the alcohol-induced liver dysfunction. for example, it is suggested that smoking reduces the ethanol metabolism or increases the production of acetaldehyde [ 35 ]. in addition, it has been reported that smoking affects the blood flow of the liver [ 36 ], which might affect the alcohol metabolism. although the evidence of these mechanisms is still in the preliminary stage, it is suggested that smoking lowers the liver blood flow, which may be a possible mechanism for the lowered alcohol metabolism or increased acetaldehyde. it is reported that the health risk of alcohol consumption is determined by the amount and duration of drinking [ 37 ]. however, in this study, it was interesting to observe that the risk of cvd mortality was not altered by smoking, while the risk of alcohol-induced liver disease was not attenuated by smoking.
based on the world health organization’s definition of non-communicable diseases [ 13 ], many studies have identified the lft abnormalities and investigated the associations between lfts and various diseases and lifestyle habits [ 14 – 23 ]. however, the major strength of the present study was to include all of the lft items in the lifestyle-related variables. however, some limitations should be noted. first, our study has a cross-sectional design and some significant lft changes induced by smoking or alcohol drinking habits might not be apparent. in addition, the results of the present study did not apply to the general population and should be interpreted cautiously. second, as the sample size of our study was relatively small, our findings should be interpreted cautiously until the results are confirmed in large population studies. third, the present study does not provide any causal inferences. fourth, we did not consider the effect of coffee drinking status in this study, since coffee consumption might be associated with some diseases and/or some lifestyle habits [ 24, 25 ]. therefore, we need to focus on these issues in the future. however, in spite of these limitations, the present study is a good example of how to analyze the associations of various lifestyle habits including the habits of coffee drinking, smoking and alcohol drinking using the comprehensive set of lft items.