The present study showed that the levels of serum TG, HDL-C, ApoA1, and the ratio of ApoA1 to ApoB were higher in drinkers than in nondrinkers. There were no significant differences in the levels of TC, LDL-C and ApoB between the two groups. These results suggest that the great majority of our study populations are beneficial from alcohol consumption. Low to middle amounts of alcohol when taken on a regular basis have been shown to protect against CAD and death [12, 13]. A moderate intake of alcohol is associated with protection against CAD, probably due in part to a dose-dependent increase in HDL-C and ApoA1 levels [14–17]. According to a previous meta-analysis, a daily dose of 30 g alcohol results in an average HDL-C level rise of 3.99 mg/dl, and an ApoA1 level rise of 8.82 mg/dl . The harmful effects of heavy alcohol consumption on serum lipid profiles may be due to an increase in plasma TG levels [14, 18]. In the previous meta-analysis, 30 g of alcohol daily was associated with a plasma TG increase of 5.69 mg/dl . The alcohol intake of 60 g/day increases the TG levels by about 0.19 mg/dl per 1 gram of alcohol consumed . The effects of alcohol consumption on LDL-C are inconsistent. A recent study in older Italian subjects (65-84 years old) has found that alcohol intake increases serum LDL-C levels . Another recent study of Turks also found increases in LDL-C, as well as in ApoB and TG, with alcohol in men, while women had decreased TG and no change in LDL-C or ApoB with alcohol . A decrease in LDL-C with increased alcohol intake has also been reported in some studies, but this effect is less consistent and probably depends on the combination of one or more unmeasured factors .
The genotypic and allelic frequencies of PPARD +294T > C polymorphism were different in diverse populations. Several previous studies have showed that the frequency of the rare allele (+294C) was 18.3% in Russian endurance-oriented athletes and 12.1% in controls (P < 0.0001) , 32.0% in Tunisian CAD patients and 18.9% in healthy volunteers (P = 0.001) , and 30.8% in Chinese CAD patients and 19.5% in normal controls (P < 0.05) . Other studies, however, showed that there was no difference in its frequency between the patients with type 2 diabetes and the non-diabetic controls (18.7% vs 19.2%) , or among the patients with metabolic syndrome, essential hypertension and type 2 diabetes . In the present study, we showed that the frequency of +294C alleles was 25.8% in nondrinkers, and 23.8% in drinkers (P > 0.05). There was no significant difference in the genotypic and allelic frequencies between males and females in both groups. However, the frequency of PPARD +294C allele was higher in our study population than in 543 healthy 50-year-old-men (15.6%) from the northern part of the greater Stockholm area , in normal controls (19.5%) from Chinese Anhui Province , in healthy Tunisian population (18.9%) , and in non-diabetic Germany controls (19.2%) ; but it was lower than in Tunisian CAD patients (32.0%)  and Chinese CAD patients (30.8%) . These results indicate that the prevalence of the C allele variants of PPARD +294T > C polymorphism may have an ethnic or disease specificity.
The association of PPARD +294T > C polymorphism and serum lipid levels is inconsistent. Skogsberg et al.  demonstrated that homozygotes for the rare C allele had a higher LDL-C concentration than homozygotes for the common T allele. There were no associations with the HDL-C levels. In another study in Scottish men, they found that the +294C allele did not influence LDL-C concentrations but was associated with lower HDL-C levels . Aberle et al.  also showed a highly significant association between the rare C allele and lower HDL-C levels in dyslipidemic female subjects. In addition, metabolic syndrome patients with CC genotype had significantly higher TC and LDL-C levels than those with TT and TC genotypes . The PPARD +294T > C polymorphism was associated with HDL-C and was dependent on sex among subjects with and without type 2 diabetes . The risk variant of PPARD +294T > C marker was associated with higher LDL-C and increased serum TC . However, Gouni-Berthold et al.  found that the presence of the C allele had no effect on TG, HDL-C, and LDL-C levels, both in diabetic and non-diabetic German controls, or both in men and in women. The same result was found by Jguirim-Souissi et al.  both in CAD patients and healthy controls. In the present study, we showed that the levels of TC in nondrinkers were different among the three genotypes, the C allele carriers had higher serum TC levels than the C allele noncarriers. But the levels of all seven lipid traits in drinkers were not different among the three genotypes. Serum TC, HDL-C, LDL-C, ApoA1, and ApoB levels were correlated with genotypes in drinkers but not in nondrinkers. These results suggest that the effects of PPARD +294T > C polymorphism on serum lipid levels are different between nondrinkers and drinkers.
The interactions between PPARD +294T > C polymorphism and alcohol consumption on serum lipid levels have not been previously explored. In a previous study, Brand-Herrmann et al.  showed that alcohol consumption modulates the relation between the PPAR-gamma 2 (PPARG) Pro12Ala and HDL-C. They randomly recruited 251 nuclear families (433 parents and 493 offspring) in the framework of the European Project on Genes in Hypertension study and genotyped 926 participants in whom all serum lipid variables and information on alcohol consumption were available for PPAR-gamma 2 Pro12Ala. The results showed that the Ala12 allele was more frequent in Novosibirsk (17%) than in Cracow (12%) and Mirano (11%, P < 0.01). Italian offspring carrying the Ala12 allele had higher serum HDL-C than noncarriers (P < 0.05). HDL-C levels were on average 0.086 mmol/L (P = 0.001) higher in drinkers than in nondrinkers. As compared with Pro12 homozygotes, Ala12 allele carriers consuming alcohol had higher serum total and HDL-C, with the opposite trend occurring in nondrinkers. This genotype-alcohol interaction was independent of the type of alcoholic beverage and more pronounced in moderate than in heavy drinkers. In the present study, however, we found no interaction between the PPARD +294T > C genotypes and alcohol consumption on serum lipid levels in the drinkers. These findings suggest that increased levels of TG, HDL-C, ApoA1, and the ratio of ApoA1 to ApoB in drinkers were not influenced by the interactions of PPARD +294T > C polymorphism and alcohol consumption. The effect of different kinds of wine on serum lipid profiles is not well known. In the present study, 90% of the wine drunk by the subjects was corn wine, rice wine or rum, in which the alcohol content is low. Thus, the effects of different kinds of alcohol consumption on serum lipid levels still need to be determined [44, 45].