To investigate the influence on plasma lipid levels of alcohol and a common polymorphism in the human apolipoprotein AI gene promoter at a position 75?bp upstream of the transcription start site Methods For this study, 742 healthy Yi and Han subjects all above 15 years old formed the total population which was divided into three groups: the Yi farmer group, the Yi emigrant group and the Han resident group All estimates of plasma lipids and apolipoproteins were performed using an auto analyzer Genetic DNA was prepared from the blood clots using the Triton X 100 lysis technique Amplification of a 432?bp fragment of the apoAI gene promoter was performed using PCR followed by restriction digestion, electrophoresis and identification of the genotypes involved Results The samples were divided on the basis of alcohol consumption: non drinkers, 1-25?g/day, 26-75?g/day and >75?g/day Comparing the four alcohol consumption groups, plasma HDLC and apoAI levels were increased as the alcohol consumption increased with no evidence of threshold effects in the Yi farmers and the Han people groups A similar association was found in the Yi emigrant group, but was not statistically significant The frequencies of the A allele in the three populations were similar, and no significant difference of lipid and apolipoprotein levels was found between subjects with and without the A allele in the three populations But, in Han and Yi emigrant samples, the drinkers with the GG genotype had higher plasma HDLC and apoAI levels than non drinkers with the same genotype, while the drinkers with the A allele had lower plasma HDLC and apoAI levels than drinkers without the A allele Non drinkers with the A allele had higher levels of apoAI than non drinkers with GG genotypes It was estimated that 18% of the variability of plasma apoAI level could be explained by the G to A polymorphism in non drinkers of Yi emigrants ( F =8 94, P <0 01) Conclusions The present data suggest that moderate alcohol consumption and the G to A substitution could lower the risk of coronary heart disease (CHD), but the beneficial effects of one will be negated by the other To investigate the influence on plasma lipid levels of alcohol and a common polymorphism in the human apolipoprotein AI gene promoter at a position 75? Bp upstream of the transcription start site Methods For this study, 742 healthy Yi and Han subjects all above 15 years old formed the total population which was divided into three groups: the Yi farmer group, the Yi emigrant group and the Han resident group All estimates of plasma lipids and apolipoproteins were performed using an auto analyzer Genetic DNA was prepared from the blood clots using the Triton X 100 lysis technique Amplification of a 432? bp fragment of the apoAI gene promoter was performed using PCR followed by restriction digestion, electrophoresis and identification of the genotypes involved Results of the samples were divided on the basis of alcohol consumption: non drinkers, 1-25? g / day, 26-75 μg / day and> 75 μg / day Comparing the four alcohol consumption groups, plasma HDLC and apoAI levels were in creased as the alcohol consumption increased with no evidence of threshold effects in the Yi farmers and the Han people groups A similar association was found in the Yi emigrant group, but was not significant significant The frequencies of the A allele in the three populations were similar, and no significant difference of lipid and apolipoprotein levels was found between subjects with and without the A allele in the three populations But, in Han and Yi emigrant samples, the drinkers with the GG genotype had higher plasma HDLC and apoAI levels than non drinkers with the same genotype, while the drinkers with the A allele had lower plasma HDLC and apoAI levels than drinkers without the A allele Non drinkers with the A allele had higher levels of apoAI than non drinkers with GG genotypes It was estimated that 18% of the variability of plasma apoAI level could be explained by the G to A polymorphism in non-drinkers of Yi emigrants (F = 8 94, P <0 01) Conclusions The present data suggest that moderate alcohol consumption and the G to A substitution could lower the risk of coronary heart disease (CHD), but the beneficial effects of one will be negated by the other