BackgroundData regarding the impact of different lipid measures on cardiovascular diseases (CVD) and mortality events is not consistent. We aimed to evaluate the relationship between different lipid parameters and incident CVD and mortality events in an Iranian population over a median follow-up of 11.9 years.MethodsThe study was conducted on 2532 men and 2986 women aged ≥ 40 years. Multivariate adjusted hazard ratios (HRs), using age as time scale, were calculated for every 1 standard deviation (SD) increase in total cholesterol (TC), logarithm-transformed triglycerides (ln-TGs), low density lipoprotein-cholesterol (LDL-C), high density lipoprotein-cholesterol (HDL-C), non-HDL-C, TC/HDL-C and ln-TGs/HDL-C. Covariates included gender (female as reference), body mass index, education status, low physical activity, smoking, blood pressure status (normotension, prehypertension and hypertension), glucose tolerance status (normal glucose tolerance, prediabetes and diabetes) and lipid lowering drugs. The same analyses were also repeated for tertiles of all lipid measures. Considering the absence of interaction between gender and lipid parameters, we used a sex-adjusted analysis. For analyses of mortality events, prevalent CVD was adjusted as well (All p for interactions > 0.1).ResultsA total of 789 new CVD events, 279 cardiovascular (CV) and 270 non-CV deaths occurred. In multivariate analysis, all lipid measures except HDL-C showed significant risk for new CVD events with HRs ranged from 1.14 to 1.27 for ln-TGs/HDL-C and LDL-C, respectively (all p-values ≤ 0.001). Considering CV mortality, there were significant positive associations between TC, LDL-C, non-HDL-C, TC/HDL-C and CV mortality events in sex-adjusted analysis; however after multivariate analysis, these associations attenuated and reached to null. Applying lipid measures as categorical variables, only TC displayed a positive association with CV mortality in multivariate analysis [TC ≥ 6.14 mmol/L: HR 1.43 (1.04–1.98)].In multivariate analysis, there were negative significant associations between all lipid measures except HDL-C and non-CV mortality; every 1-SD increase in TC, LDL-C, non-HDL-C, ln-TGs ,TC/HDL-C and ln-TGs/HDL-C was associated with 24, 25, 27, 19, 23 and 17 % decreased risk in non-CV mortality (all p-values ≤ 0.01).ConclusionsThese findings indicate divergent associations of TC, LDL-C, non-HDL-C, TC/HDL-C, TGs and TGs/HDL-C with CVD vs non-CV mortality, demonstrating a higher risk for the former and lower risk for the latter.Electronic supplementary materialThe online version of this article (doi:10.1186/s12986-016-0102-1) contains supplementary material, which is available to authorized users.

Purpose Impaired fasting glucose (IFG) is associated with incident diabetes, cardiovascular risk, and markers of atherosclerosis in early adulthood. We aimed to explore the 10‐year change in IFG prevalence among adolescent participants of the Tehran Lipid and Glucose Study, a population‐based study from Iran. Methods For our study, we used data on fasting plasma glucose (FPG), anthropometric, and demographic information of 11 to 19‐year‐old adolescents in study periods I (1999‐2005; 1415 boys, 1583 girls) and II (2011‐2014; 477 boys, 469 girls). Sex‐adjusted and sex‐stratified multivariable logistic regression models were used to assess the relationship of the study period (reference: study period I) with IFG. Results The prevalence of IFG, general obesity, and central obesity increased from 7%, 13.3%, and 18.8% in study period I to 16.6%, 24%, and 37.4% in study period II; while a favorable trend was seen for blood pressure, triglycerides, and high‐density lipoprotein cholesterol. In the fully adjusted model, being older (age group 15‐19 vs 11‐14 years) and female sex were associated with lower risk. Being overweight and obese increased the risk by risk ratios (confidence interval) of 1.57 (1.17‐2.11) and 1.63 (1.15‐2.30), respectively. Central adiposity did not remain as an independent risk factor. Nevertheless, study period persisted as a significant factor despite all adjustments [2.20 (1.81‐2.68)]. Results in the sex‐stratified models were generally the same. Conclusion Our results demonstrated that the over 2‐fold rise in IFG prevalence among adolescents was not solely dependent on general and central obesity.