Tobacco, physical exercise and lipid profile

Abstract

A group of 572 young cadets from the General Military Academy in Zaragoza (AGEMZA) with a mean age of 19.9 years was studied in two different situations: on admission to the AGEMZA, when physical activity was very intensive (A) and after 8 months, by which time they had all received identical diets and physical activity was considerably reduced (B). On both occasions they were asked about their smoking habits and their personal and family histories. Their height and weight were recorded and a sample of venous blood was taken to determine the lipid, biochemical and haematological profiles. We found that more smokers had a family history of sudden death or acute myocardial infarction than the non-smokers. The smokers also showed a lower HDL cholesterol level (54.3 +/- 9.8 mg.dl-1 +/- SD) than the non-smokers (59.4 +/- 10.9) (P less than 0.0001) and a higher level of triglycerides (75.4 +/- 24.7 mg.dl-1) than the non-smokers (65.4 +/- 21.1 mg.dl-1). The smokers had a higher white cell count (8194 +/- 1981 vs 7332 +/- 1672 cells. 10mm-3) (P less than 0.001), a higher haemoglobin value (14.9 +/- 0.9 vs 14.6 +/- 0.9 g.dl-1) (P less than 0.004) and a higher haematocrit value (44.2 +/- 2.3 vs 43.6 +/- 2.7%) (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Association of endothelial function and vascular data with LDL-c and HDL-c in a homogeneous population of middle-aged, healthy military men: Evidence for a critical role of optimal lipid levels

“…A cohort of military men underwent a thorough preventive cardiovascular examination in the AGEMZA study [9,10]. In this group, the population's age was around 35 years.…”

Smoking and apolipoprotein levels: A meta-analysis of published data

“…1 . For the analyses of smoking status and its association to apolipoprotein levels, a total of 66 publications that assessed the effect of smoking status on any of the following parameters were identified: 39 studies on apolipoprotein AI [23] , [24] , [25] , [26] , [27] , [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] , [36] , [37] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [45] , [46] , [47] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] , [59] , [60] , [61] , ten studies on apolipoprotein AII [23] , [24] , [26] , [32] , [34] , [36] , [43] , [47] , [53] , [55] , 40 studies on apolipoprotein B [23] , [24] , [27] , [28] , [29] , [30] , [32] , [34] , [35] , [37] , [38] , [39] , [40] , [41] ...…”

“…Using influence diagnostics, four studies (Casasnovas et al [27] , Pasupathi et al [60] , Sirisali et al [59] , and Sharma et al [67] ) were identified as having a large impact on between-study heterogeneity. Thus, sensitivity analyses were conducted excluding these studies.…”

“…The pooled mean levels of apolipoprotein AI were 1.48 ± 0.009 g/L in smokers and 1.54 ± 0.007 g/L in nonsmokers. The meta-analysis for apolipoprotein AI levels between smokers and nonsmokers was performed using data from 39 studies including 59 estimates [23] , [24] , [25] , [26] , [27] , [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] , [36] , [37] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [45] , [46] , [47] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] , [59] , [60] , [61] . The fixed-effects model mean difference was − 0.038 (95% CI: −0.041, −0.035 g/L, I 2 =90%).…”

“…The pooled mean ratios of apolipoprotein B to AI were 0.62 ± 0.002 in smokers and 0.65 ± 0.001 in nonsmokers. The meta-analysis assessing the effects of smoking on the apolipoprotein B: AI ratio included 31 studies with 46 estimates [23] , [24] , [27] , [28] , [29] , [30] , [32] , [34] , [35] , [37] , [38] , [39] , [40] , [41] , [42] , [44] , [45] , [46] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] , [62] , [70] . The fixed-effects model showed an increased ratio in smokers (mean difference= 0.047, 95% CI: 0.047, 0.048 g/L, I 2 =99%).…”