ABSTRACT
OBJECTIVES@#Cigarette smoking is an established, strong, and modifiable risk factor for coronary heart disease (CHD). However, little research has investigated CHD risk in former smokers who continue to be exposed to others’ cigarette smoke (former & secondhand smokers). @*METHODS@#In the Tehran Lipid and Glucose Study, a prospective population-based cohort (n=20,069) was followed up for a median period of 14.6 years. A subset of 8,050 participants of 30 years of age and older was analyzed, with first CHD events as the study outcome. Participants were categorized as never, former, current, secondhand, and former & secondhand smokers. Data on smoking intensity (cigarette/d) were also collected. A Cox proportional hazards regression model was applied to estimate the risk of CHD, taking into account the main potential confounders. @*RESULTS@#The mean age of participants was 46.10 ±11.38 years, and they experienced 1,118 first CHD events (with most CHD cases in former smokers) during the follow-up period. The risk of CHD was highest in current smokers, followed in order by former & secondhand, former, and secondhand smokers (hazard ratio [HR], 1.99; 95% confidence interval [CI], 1.65 to 2.39; HR, 1.55; 95% CI, 1.15 to 2.08; HR, 1.39; 95% CI, 1.12 to 1.72; HR, 1.27; 95% CI, 1.07 to 1.51, respectively), compared to never smokers. The risk of CHD increased with smoking intensity, which has been proposed as a preferable measure of smoking, indicating a dose-response pattern. @*CONCLUSIONS@#The elevated risk of CHD in former & secondhand smokers was a noteworthy finding, with possible implications for health policy; however, further research is needed.
ABSTRACT
OBJECTIVES@#Cigarette smoking is an established, strong, and modifiable risk factor for coronary heart disease (CHD). However, little research has investigated CHD risk in former smokers who continue to be exposed to others’ cigarette smoke (former & secondhand smokers). @*METHODS@#In the Tehran Lipid and Glucose Study, a prospective population-based cohort (n=20,069) was followed up for a median period of 14.6 years. A subset of 8,050 participants of 30 years of age and older was analyzed, with first CHD events as the study outcome. Participants were categorized as never, former, current, secondhand, and former & secondhand smokers. Data on smoking intensity (cigarette/d) were also collected. A Cox proportional hazards regression model was applied to estimate the risk of CHD, taking into account the main potential confounders. @*RESULTS@#The mean age of participants was 46.10 ±11.38 years, and they experienced 1,118 first CHD events (with most CHD cases in former smokers) during the follow-up period. The risk of CHD was highest in current smokers, followed in order by former & secondhand, former, and secondhand smokers (hazard ratio [HR], 1.99; 95% confidence interval [CI], 1.65 to 2.39; HR, 1.55; 95% CI, 1.15 to 2.08; HR, 1.39; 95% CI, 1.12 to 1.72; HR, 1.27; 95% CI, 1.07 to 1.51, respectively), compared to never smokers. The risk of CHD increased with smoking intensity, which has been proposed as a preferable measure of smoking, indicating a dose-response pattern. @*CONCLUSIONS@#The elevated risk of CHD in former & secondhand smokers was a noteworthy finding, with possible implications for health policy; however, further research is needed.
ABSTRACT
Background: the aim of this study was to examine the interaction of dietary food groups and genetic variants of APOA1/APOC3, relative to Metabolic Syndrome [MetS] risk in adults
Methods: in this matched nested case-control study, 414 MetS subjects and 414 controls were selected from among participants of Tehran Lipid and Glucose Study. Dietary intake was assessed with the use of a valid and reliable semi-quantitative food frequency questionnaire. Single Nucleotide Polymorphisms [SNPs], APOA1 [rs670, -75G>A and rs5069,+83C>T/APOC3 rs5128 C3238>G] were genotyped by the conventional polymerase chain reaction and restriction fragment length polymorphism
Results: the mean [SD] of age was 40.7 [13] and 41.2 [13] years in male cases and controls versus 44.0 [11] and 44.0 [12] years in female case and controls. A significant interaction between intake quartiles of the sugar group and APOA1 combined group [GA+AA/CT+TT] SNPs was found; The ORs for these genotype carriers were [1, 0.44, 0.36, 0.23; P trend<0.001] in quartiles of intake, relative to other combined genotypes [P interaction=0.02]. MetS risk appeared to be increased significantly in higher quartiles of sweet beverages and fish intakes in the GA+AA/CT+TT/CC genotypes of APOA1/APOC3 SNPs, compared to other genotypes [P interaction=0.01]. The combined effect of genotypes of APOC3/APOA1 showed further decrease in MetS risk in higher quartiles of sugar group intakes [OR: 1, 0.24, 0.26, 0.14, P trend=0.001] relative to other combinations [P interaction=0.008]
Conclusion: results obtained demonstrate that some dietary food groups [sugar, fish, and sweet beverages] modulate the effect of APOA1/APOC3 SNPs in relation to MetS risk