Influence of worksite environmental tobacco smoke on serum lipoprotein profiles of female nonsmokers

The purpose of this study was to examine the influence of environmental tobacco smoke (ETS) in the workplace on high-density lipoprotein cholesterol (HDL-C), HDL-C subfractions, and apolipoprotein (apo) A-I and apo B in female workers. Premenopausal women free from factors known to influence HDL-C (cigarette smoking, vigorous physical exercise, etc) who were not taking oral contraceptives, were moderate consumers of alcohol, caffeine, and dietary fat, and were between the ages of 21 and 50 years participated in one of two groups: (1) nonsmokers who had never smoked cigarettes and were generally free from ETS exposure (nonsmokers), and (2) nonsmokers who had never smoked but were subjected to concentrated doses of ETS at least 6 hours per day, 4 days per week, for at least the past 6 consecutive months (ETS-exposed). A third group consisting of current cigarette smokers who smoked a minimum of 20 cigarettes per day for at least the past 5 consecutive years served as smoking controls (smokers). Subjects were matched by group as closely as possible with regard to criteria that can influence blood lipoprotein levels. Participants were solicited from taverns and restaurants where they were employed. It was hypothesized that individuals chronically exposed to ETS would demonstrate unfavorable lipoprotein profiles. Results showed that HDL-C, HDL₂, and apo A-I were significantly (P < .05) depressed for ETS-exposed and smokers as compared with nonsmokers. Values for ETS-exposed were not different from those for smokers. Total cholesterol, triglycerides, HDL₃, and apo B did not differ among the three groups. It was concluded that excessive exposure to ETS in female workers can have deleterious effects on HDL-C, HDL₂, and apo A-I in nonsmokers that are similar to effects observed in cigarette smokers. It is possible that these effects increase coronary artery disease (CAD) risk.     

Clinical significance of measurements of serum apolipoprotein A-I, A-II and B in hypertriglyceridemic male patients with and without coronary artery disease

To examine the relationship of hypertriglyceridemia to coronary artery disease (CAD), we measured serum cholesterol, triglyceride, high density lipoprotein cholesterol (HDL-C) and apolipoproteins (apo) A-I, A-II and B in 82 male patients with angiographically defined CAD and 140 age-matched healthy controls. The CAD patients had significantly lower apo A-I and A-II and HDL-C levels, but had higher apo B and triglyceride levels than the controls. After adjustments of apolipoproteins for serum triglyceride, CAD patients had significantly higher apo B and lower apo A-I and A-II levels than the controls. Discriminant analysis showed that apo B was the best discriminator and that apo A-I was next. In the normotriglyceridemic subgroup HDL-C also had a sufficient power for discrimination between CAD patients and the controls, but in the hypertriglyceridemic subgroup HDL-C had no discriminative power. Both apo A-I and B had significant discriminative power between CAD patients and the controls, independently of the serum triglyceride level. These results indicate that measurements of serum apo A-I and apo B are useful for the study of coronary risk factor in hypertriglyceridemic subjects. Finally, it is necessary to sub-classify dyslipoproteinemia by serum apolipoprotein levels for predicting the future occurrence of CAD in the general population.     

Effects of age and cigarette smoking on serum concentrations of lipids and apolipoproteins in a male military population

The effects of age and cigarette smoking on lipids and apolipoproteins were studied in men, 20-65 years old, randomly selected from a military population in the Madrid area, Spain. Subjects were classified as non-smokers, medium smokers (10-20 cigarettes/day) and heavy smokers (more than 20 cigarettes/day). Smoking prevalence was 58%. Serum apolipoprotein A-I and HDL-cholesterol (HDL-C) were not age-dependent, while total cholesterol (TC), triglycerides (TG), LDL-cholesterol (LDL-C) and the TC/HDL-C ratio increased with age. None of the variables studied was age-dependent over 30 years. The effects of smoking on TC, TG, LDL-C, HDL-C, TC/HDL-C ratio, apolipoprotein A-I, apolipoprotein B, and apo A-I/apo B ratio in the 20-29-year-old group appeared to be prominent in heavy smokers (P values less than 0.001, less than 0.05, less than 0.01, less than 0.05, less than 0.001, less than 0.05, less than 0.01 and less than 0.05, respectively) but not in medium smokers, in which only TG increased significantly (P less than 0.001). Few differences were noted between non-smokers and smokers over 30 although the TC/HDL-C ratio did increase in heavy smokers (P less than 0.05).     

Lipoproteins and apolipoproteins in young male survivors of myocardial infarction

Plasma and lipoprotein cholesterol, triglycerides, apolipoproteins (apo) A-I, A-II, B and phospholipid concentrations were measured at 10 days and 4 months after myocardial infarction (MI) in 60 young Kuwaiti male MI survivors below the age of 40 years. Controls were matched for age, relative weights, smoking, dietary habits and physical activities. The young MI survivors had significantly higher levels of total and LDL-cholesterol, and ratios of LDL/HDL- and LDL/HDL2-cholesterol. Total VLDL and LDL triglycerides, and phospholipids were also elevated in MI survivors compared to controls. Similarly, plasma and LDL-apo B as well as the ratios of apo B/apo A-I were higher in the MI group. There was no significant change in the levels of VLDL and HDL3-cholesterol and of apo A-II in these patients compared to their controls. Concentrations of HDL- and HDL2-cholesterol and of plasma and HDL apo A-I were significantly lower in the young MI survivors compared to the control subjects. The better discriminating lipoproteins and apolipoproteins in MI patients in descending order were HDL2-cholesterol greater than apo B greater than apo A-I greater than VLDL-triglyceride greater than HDL-cholesterol greater than LDL/HDL2-cholesterol greater than triglycerides. The data indicate that measurement of HDL2-cholesterol, apo B and apo A-I may be useful indicators in assessing coronary artery disease risk than triglycerides (TG), total cholesterol (TC), LDL-cholesterol and HDL-cholesterol.     

Levels of serum lipids, apolipoproteins A-I and B and pseudocholinesterase activity and their discriminative values in patients with coronary by-pass operation

Serum lipids and apoproteins A-I and B were measured in 115 male patients and serum pseudocholinesterase activity (PChE) was determined in 83 patients with 3 vessel coronary artery disease (CAD). The control subjects were matched according to sex, smoking, relative weight and age and were free from heart disease. The CAD patients had significantly higher serum VLDL cholesterol and triglyceride levels and lower HDL cholesterol and apo A-I levels and lower HDL to total cholesterol ratio than the controls. The concentrations of serum total cholesterol and LDL cholesterol were only slightly (6.4% and 8.8%, on an average) higher in CAD patients than in controls. The apo B levels of CAD patients were also slightly lower in patients than in controls. The CAD patients had slightly higher PChE activities than controls. The ratios of apo A-I to PChE and HDL cholesterol to PChE were significantly (about 30%, P less than 0.001) lower in patients than in controls. In discriminant analysis between the groups HDL cholesterol and apo A-I showed the best (74% success in reclassifying the patients to correct groups), and total cholesterol, triglycerides, LDL cholesterol and apo B remarkably weak discriminating power among the single variables of serum lipids and lipoproteins. In discriminating analysis the apo A-I/PChE and HDL cholesterol/PChE ratios showed relatively high (77.1 and 71.1% success from the patients to correct groups) and serum PChE activity weak discriminating power. These results indicate that low levels of HDL cholesterol and apo A-I and the low ratio of HDL cholesterol to total cholesterol are the most potent metabolic risk factors for 3 vessel coronary artery disease in a population with relatively high serum total cholesterol level. The determinations of apo A-I/PChE and HDL cholesterol/PChE ratios may be an additional, valuable tool in discriminating the risk for CAD.     

Association between plasma lipids, and apolipoproteins and coronary artery disease: a cross-sectional study in a low-risk Korean population

BACKGROUND: Due to the lower level of the traditional lipid profiles in Koreans than in the series of patients from the western countries, the need to investigate other lipid parameters to help identify the individuals at high risk of CAD has been emphasized. AIM AND METHODS: To investigate whether apolipoprotein B (apo B), apolipoprotein A-I (apo A-I) and their ratio give additional information to the traditional lipid risk factors for discriminating the individuals at high-risk for coronary artery disease (CAD), 544 subjects, who met the lipid criteria of total cholesterol (TC) <230 mg/dl, low-density lipoprotein cholesterol (LDL-C) <120 mg/dl and high-density lipoprotein cholesterol (HDL-C) >40 mg/dl were recruited. Patients were considered to be CAD(+) if they had > or =50% stenosis in at least one coronary artery. RESULTS: In men, TC and apo B/apo A-I ratio were significantly different between groups with and without CAD after adjusting for age and diabetes (P = 0.037 and 0.035), and in women, triglyceride (TG), HDL-C and apo B/apo A-I ratio were significantly different after adjusting for age, diabetes and smoking status (P = 0.006, 0.007 and 0.030, respectively). In the lowest quartile of TC, TG and LDL-C, and the highest quartile of HDL-C, only apo B/apo A-I ratio was associated with CAD in both men and women. The only variable showing a significant difference between patients with and without CAD was apo B/apo A-I ratio. In models assessing whether apolipoproteins give additional information to traditional lipid risk factors, HDL-C, LDL-C, apo B/apo A-I ratio and in women but not in men, TG and apo B were all independent markers for the presence of CAD. Among the nontraditional lipid factors, only apo B/apo A-I ratio showed its additional value for identifying the presence of CAD. CONCLUSION: Apo B/apo A-I ratio is the only variable that differentiates the patients with CAD from those without and, furthermore, gives additional information to that supplied by traditional lipid risk factors in a low-risk Korean population.     

Homocysteine as a risk factor for coronary heart diseases and its association with inflammatory biomarkers, lipids and dietary factors

The causal relation of total Homocysteine (tHcy) to coronary heart diseases (CHD) is unclear. In vitro studies suggest a proinflammatory effect. Among 32,826 women from the Nurses' Health Study who provided blood samples in 1989-1990, 237 CHD events were documented during 8 years of follow-up. The cases (1:2) were matched to controls on age, smoking, and month of blood draw. Plasma tHcy was inversely associated with blood levels of folate (partial r = -0.3, P < 0.0001) and B1(2) (r = -0.2, P < 0.0001) and with dietary intake of folate (r = -0.1, P < 0.01) and B(2) vitamin (r = -0.1, P = 0.01). tHcy was positively associated with soluble tumor necrosis receptor (sTNF-R) 1 and 2 (partial r = 0.2, P < 0.0001). In a multivariate model adjusted for age, smoking, BMI, parental history, hypertension, diabetes, postmenopausal hormone use, physical activity and alcohol intake, the relative risk of CHD between the extreme quartiles of tHcy was 1.66 (95% CI; 1.05-2.64, P trend = 0.02). The association was not appreciably attenuated after further adjustments for sTNF-R1, sTNF-R2, CRP, or Total Cholesterol:/HDL-c ratio. tHcy is an independent risk predictor of CHD and modestly associated with TNF-receptors. However, the inflammatory biomarkers measured could not explain its role in CHD.     

Effect of mild aerobic exercise on serum lipids and apolipoproteins in patients with coronary artery disease

The effects of mild aerobic exercise on serum lipids, apolipoproteins and lecithin-cholesterol acyltransferase (LCAT) activity were examined in 11 male patients with coronary artery disease and 4 healthy male controls. The mild aerobic exercise program involved exercise intensity at 50% of maximal oxygen uptake, as determined from the blood lactate threshold, for 60 min periods 3 times per week for 10 weeks. Following mild aerobic exercise, serum levels of high density lipoprotein cholesterol (HDL-C) were increased significantly from 50 +/- 7 mg/dl to 59 +/- 11 mg/dl (p less than 0.05) with a simultaneous increase in apolipoprotein A-I (apo A-I) in normal controls. The LCAT activity was significantly increased from 65 +/- 22 nmol/ml/hr to 99 +/- 30 nmol/ml/hr in normal controls (p less than 0.05). Furthermore, maximal oxygen uptake (VO2max) was significantly increased in normal controls. In contrast, no significant changes were found in HDL-C, apo A-I, apo B, VO2max and body weight in patients with coronary artery disease. There was significant correlation between the initial HDL-C level and the change in HDL-C level following the exercise program in the combined group of normal controls and patients with coronary artery disease.     

Lifestyle factors affecting intrapair differences of serum apoproteins and cholesterol concentrations in adult identical twins

83 pairs of twins, aged 50-74 years, were studied with respect to their serum apoproteins (A-I, A-II, B, C-II, C-III and E) and cholesterol concentrations. Each of the variables showed a higher intraclass correlation in the MZ twins than in the DZ twins. HDL cholesterol showed the highest intraclass correlation among the variables and indicated strong heritability. In the MZ pairs discordant for alcohol consumption, the higher consumers within the pair showed a significantly higher level of apo A-I and HDL cholesterol, and a lower level of apo B concentration. In the MZ pairs discordant for cigarette smoking, the higher consumers within the pair showed a significantly lower level of apo C-III. In the MZ pairs discordant for obesity, the heavier twins within the pair showed higher levels of non-HDL cholesterol, total cholesterol, apo B, apo C-II and apo C-III. In the MZ pairs discordant, for occupation, the twins of 'heavy work' showed significantly higher levels of apo B, total cholesterol and non-HDL cholesterol than the twins of 'light work'.     

Influence of triglyceride concentration on the relationship between lipoprotein cholesterol and apolipoprotein B and A-I levels

A sample of 2,103 men aged 47 to 76 years from the Québec Cardiovascular Study cohort was examined to quantify the influence of plasma triglyceride (TG) levels on the relationship between plasma lipoprotein cholesterol and either apolipoprotein A-I (apo A-I) or apo B concentrations. Regression analyses between high-density lipoprotein cholesterol (HDL-C) and apo A-I through TG tertiles showed highly significant correlations (.62 < or = r < or = .75, P < .0001) in all TG tertiles between these 2 variables. The associations for plasma apo B versus low-density lipoprotein cholesterol (LDL-C) and non-HDL-C levels were also studied on the basis of TG concentrations, and correlation coefficients between either LDL-C or non-HDL-C and apo B were essentially similar among TG tertiles (.78 < or = r < or = .85 and .83 < or = r < or = .86 for LDL-C and non-HDL-C, respectively, P < .0001). Regression analyses also showed that lower HDL-C levels were found for any given apo A-I concentration among men in the 2 upper TG tertiles, whereas lower LDL-C concentrations were observed at any given apo B level among subjects in the upper TG tertile. We further investigated whether there were synergistic alterations in the HDL-C/apo A-I and LDL-C/apo B ratios as a function of increasing plasma TG. A significant association was noted between these 2 ratios (r = .37; P < .0001). Mean HDL-C/apo A-I and LDL-C/apo B ratios were then calculated across quintiles of plasma TG concentrations. Increased TG concentrations were first associated with a reduced HDL-C/apo A-I ratio, followed by a decreased LDL-C/apo B ratio. These results suggest that a relatively modest increase in TG may rapidly alter the relative cholesterol content of HDL particles. Finally, the cholesterol content of the non-HDL fraction appears to be influenced less by TG levels than HDL-C and LDL-C fractions. Thus, the plasma apo B-containing lipoprotein cholesterol level may provide a better index of number of atherogenic particles than the LDL-C concentration, particularly in the presence of hypertriglyceridemia (HTG).     

Multivariate genetic analysis of high density lipoprotein particles.

The aim of this study was to investigate the effect of genetic factors on three components of plasma high density lipoproteins, HDL-cholesterol (HDL-C), apolipoprotein A-I (apo A-I) and lipoprotein particle Lp A-I (Lp A-I), which contains apo A-I but not apo A-II. These analyses were carried out on 106 nuclear families with one or more children (407 subjects) who volunteered for health screening at the Center for Preventive Medicine, Vandoeuvre, France. After adjustment by stepwise multiple linear regression analysis for age, gender, weight, height, ponderosity, alcohol consumption, smoking habits, and hormonal treatment in females, a multifactorial model (considering the effect of polygenes, individual, specific, environmental and common household factors) was fitted to each variable separately. The hypothesis of no common household effects was accepted for each of the traits. The contribution of genetic factors to inter-individual variance was larger than the contribution of environmental factors for apo A-I (h2 = 0.81) and Lp A-I (h2 = 0.63) but not for HDL-C (h2 = 0.44). Bivariate analyses were carried out by parameterizing covariance components between traits. The genetic correlations were always significantly different from zero. They were estimated to be 0.73 between HDL-C and apo A-I, 0.40 between HDL-C and Lp A-I, 0.51 between apo A-I and Lp A-I. These results suggest that HDL-C, apo A-I and Lp A-I are only in part affected by the same genes and that the measurement of lipids as well as the apo A-I and Lp A-I gives complementary and different information on the metabolic and genetic aspects.     

Cigarette smoking,physical activity,and alcohol consumption: Relationship to blood lipids and lipoproteins in premenopausal females

A total of 164 premenopausal female subjects were randomly selected for evaluation from a much larger pool of volunteers. The relationships between blood lipid and lipoprotein levels as dependent variables and cigarette smoking, physical activity, and alcohol consumption were determined from partial regression coefficients. A lower HDL-C level (10.1 mg/dL) was seen in smokers v nonsmokers. For each ounce of alcohol consumed, HDL-C level was higher by 2.8 mg/dL, and greater physical activity was associated with a higher HDL-C level of 8.6 mg/dL. An analysis of covariance with covariance adjustments for age and body fat revealed that smokers who regularly exercise or consume alcohol had significantly lower HDL-C levels than nonsmokers with similar habits. Subjects who both exercise and consume alcohol demonstrated higher HDL-C levels than those who indulge in one or the other separately. Results suggest that cigarette smoking may attenuate the effects of chronic exercise or alcohol consumption, or of both, to raise HDL-C levels. Also, chronic exercise and alcohol consumption may exert an additive effect, raising HDL-C level.     

Interactions between fibrinolysis, lipoproteins and leptin related to a first myocardial infarction.

BACKGROUND: The summarized importance of haemostatic and metabolic variables (insulin, lipids including lipoprotein (a) [Lp(a)] and leptin) in predicting first myocardial infarction, as well as possible interactions among these variables, have not been reported. DESIGN: A prospective case-control study nested within the Northern Sweden Health and Disease Cohort. METHODS: Sixty-two men diagnosed with a first myocardial infarction were sex- and age-matched with 124 controls. Conditional logistic regression was conducted including established risk factors, plasma levels of plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (tPA) mass concentration, von Willebrand factor, insulin, proinsulin, specific insulin, apolipoprotein A-I (apo A-I), Lp(a), and leptin. Interaction analysis was also performed for tPA, apo A-I, Lp(a), leptin and proinsulin. RESULTS: Smoking, low plasma levels of apo A-I and high plasma levels of cholesterol, Lp(a), tPA, PAI-1, proinsulin and leptin were associated with myocardial infarction in univariate conditional logistic regression analysis. High tPA [odds ratio (OR), 21.3; 95% confidence interval (CI), 2.04-222] and Lp(a) (OR, 7.21; 95% CI, 1.31-39.8) and low apo A-I (OR, 0.15; 95% CI, 0.02-0.93) remained significant risk determinants in multivariate analysis with smoking habits, body mass index, hypertension, cholesterol, and diabetes included as covariates. There were non-significant synergic interactions between high Lp(a) and leptin and tPA, respectively, and between high Lp(a) and low apo A-I. CONCLUSION: Plasma levels of tPA, Lp(a), and apo A-I are independently associated with subsequent development of a first myocardial infarction in men.     

Lipids, lipoproteins, apolipoproteins, and other risk factors in Chinese men and women with and without myocardial infarction

One hundred and fifty-four male and 69 female Chinese patients, aged between 40 and 60 years, who had suffered myocardial infarction (MI) were investigated and compared with 216 men and 219 women who had no history or ECG evidence of coronary heart disease. The male MI patients had significantly raised levels of triglycerides (160 mg/dl), cholesterol (194 mg/dl), VLDL-CH (31 mg/dl), apolipoprotein B (122 mg/dl) and apolipoprotein E (4.7 mg/dl) and a lower apolipoprotein A-I level (126 mg/dl) than the control group (triglycerides 131, cholesterol 179, VLDL-CH 26, apo B 102, apo E4.2, and apo A-I 138 mg/dl). The women with MI also had higher values for the atherogenic lipids than the control group (triglycerides 175 vs. 134 mg/dl, cholesterol 218 vs. 186 mg/dl, LDL-CH 128 vs. 104 mg/dl, VLDL-CH 32 vs. 26 mg/dl, apo B 121 vs. 103 mg/dl and apo E 5.4 vs. 4.3 mg/dl), as well as lowered apolipoprotein A-I (128 vs. 144 mg/dl). The Lp(a) levels (men and women considered together) were significantly higher for the MI patients (34.3 mg/dl vs. 26.2 mg/dl). Anti-atherogenic lipoproteins such as HDL-cholesterol, HDL2-CH, HDL3-CH, phospholipids and apolipoprotein A-II, C-II and C-III showed no difference between the groups.     

Enhanced fractional catabolic rate of apo A-I and apo A-II in heterozygous subjects for apo A-I(Zaragoza) (L144R)

We have recently reported a new apolipoprotein (apo) A-I variant (apo A-I(Zaragoza) L144R) in a Spanish family with HDL-C levels below the 5th percentile for age and sex and low apo A-I concentrations. All the apo A-I(Zaragoza) subjects were heterozygous and none of them showed evidence of coronary artery disease (CAD). Mean plasma HDL-C, apo A-I, and apo A-II levels were lower in apo A-I(Zaragoza) carriers as compared to control subjects (40, 60, and 50%, respectively). Lipid composition analysis revealed that apo A-I(Zaragoza) carriers had HDL particles with a higher percentage of HDL triglyceride and a lower percentage of HDL esterified cholesterol as compared to those of control subjects. Lecithin:cholesterol acyltransferase (LCAT) activity and cholesterol esterification rate of apo A-I(Zaragoza) carriers were normal. Apo A-I and apo A-II metabolic studies were performed on two heterozygous apo A-I(Zaragoza) carriers and on six control subjects. We used a primed constant infusion of [5,5,5-2H3]leucine and HDL apo A-I and apo A-II tracer/tracee ratios were determined by gas chromatography mass spectrometry and fitted to a monoexponential equation using SAAM II software. Both subjects carrying apo A-I(Zaragoza) variant showed mean apo A-I fractional catabolic rate (FCR) values more than two-fold higher than mean FCR values of their controls (0.470+/-0.0792 vs. 0.207+/-0.0635 x day(-1), respectively). Apo A-I secretion rate (SR) of apo A-I(Zaragoza) subjects was slightly increased compared with controls (17.32+/-0.226 vs. 12.76+/-3.918 mg x kg(-l) x day(-1), respectively). Apo A-II FCR was also markedly elevated in both subjects with apo A-I(Zaragoza) when compared with controls (0.366+/-0.1450 vs. 0.171+/-0.0333 x day(-1), respectively) and apo A-II SR was normal (2.31+/-0.517 vs. 2.1+/-0.684 mg x kg(-l) x day(-1), respectively). Our results show that the apo A-I(Zaragoza) variant results in heterozygosis in abnormal HDL particle composition and in enhanced catabolism of apo A-I and apo A-II without affecting significantly the secretion rates of these apolipoproteins and the LCAT activation.     

Smoking and plasma homocysteine.

BACKGROUND: Smoking is known to be associated with an increased plasma homocysteine level. Both are associated with an increased risk of cardiovascular disease. B-vitamins modulate plasma homocysteine levels. AIMS: To investigate the relationships between smoking, plasma homocysteine, nutrient levels and risk of cardiovascular disease. METHODS: The European Concerted Action Project case control study of 750 cases and 800 age- and sex-matched controls aged less than 60 years from 19 centres in 10 European countries. RESULTS: Smokers were at increased risk of vascular disease. This risk was greatly increased in the presence of a raised plasma homocysteine; cigarette smokers with a plasma homocysteine above 12 micromol.l(-1) had a 12-fold increased risk of cardiovascular disease (OR 12.4 95% CI 7.3 to 21.2) compared with non-smokers with a normal plasma homocysteine. In both cases and controls the current smokers had a higher plasma homocysteine level than the never smokers (11.7 micromol.l(-1) vs 10.07 micromol.l(-1), P<0.05 cases; 9.90 micromol.l(-1) vs 9.53 micromol.l(-1)P value non significant controls). Current smokers tended to have lower levels of folate, and vitamin B6 and vitamin B12 than never smokers. The risk of cardiovascular disease associated with smoking was not significantly altered by adjustment for levels of B-vitamins using a conditional regression model (OR for current smoker >20.day(-1) 8.19, after adjustment for B6, B12, folate OR 7.09). CONCLUSIONS: This case control study suggests that smokers with high plasma homocysteine are at greatly increased risk of cardiovascular disease and should therefore be offered intensive advice to help them cease smoking. They also have reduced levels of those B-vitamins (folate, vitamin B6 and vitamin B12) that modulate homocysteine metabolism. While this finding may reflect a direct effect of smoking or reduced B-vitamin intake, supplementation of these nutrients may be appropriate in smokers with high homocysteine levels.     

Influence of cholesteryl ester transfer protein, peroxisome proliferator-activated receptor α, apolipoprotein E, and apolipoprotein A-I polymorphisms on high-density lipoprotein cholesterol, apolipoprotein A-I, lipoprotein A-I, and lipoprotein A-I:A-II concentrations: the Prospective Epidemiological Study of Myocardial Infarction study

The plasma level of high-density lipoprotein cholesterol (HDL-C) is known to be inversely associated with cardiovascular risk. However, besides lifestyle, gene polymorphism may influence the HDL-C concentration. The aim of this study was to investigate the possibility of interactions between CETP, PPARA, APOE, and APOAI polymorphisms and HDL-C, apolipoprotein (apo) A-I, lipoprotein (Lp) A-I, and Lp A-I:A-II in a sample selected from the Prospective Epidemiological Study of Myocardial Infarction (PRIME) study population who remained free of cardiovascular events over 5 years of follow-up. Healthy individuals (857) were randomly selected for genotyping the PRIME study subjects. The population was selected so as to provide 25% of subjects in the lowest tertile of HDL-C (≤28 mg/dL) in the whole PRIME study sample, 25% of subjects in the highest tertile of HDL-C (≥73 mg/dL), and 50% of subjects in the medium tertile of HDL-C (28-73 mg/dL). Genotyping was performed by using a polymerase chain reaction system with predeveloped TaqMan allelic discrimination assay. The CETP A373P rare allele c was less frequent in the group of subjects with high HDL-C, apo A-I, Lp A-I, and Lp A-I:A-II concentrations. Apolipoprotein A-I and Lp A-I were also found to be higher in the presence of the ?2 allele coding for APOE. The effect of the CETP A373P rare allele c on HDL-C was independent of all tested parameters except triglycerides. The respective effect of these polymorphisms and triglycerides on cardiovascular risk should be evaluated prospectively.     

Impact of alcohol intake on measures of lipid metabolism depends on context defined by gender,body mass index,cigarette smoking,and apolipoprotein E genotype

Hyperlipidemia, smoking, and obesity are well-known risk factors for cardiovascular disease. Conversely, moderate alcohol intake is associated with lower atherosclerosis risk. However, the influence of taking alcohol on the interrelationships of these factors in a particular context has not been thoroughly investigated. In this study, we asked whether the association between plasma measures of lipid metabolism and alcohol intake is dependent on context defined by gender, age, body mass index (BMI), smoking, and apolipoprotein E (APOE) genotype. Data were obtained in a sample of 869 women and 824 men who participated in the Quebec Heart Health Survey. There was no evidence that variation among APOE genotypes influenced the association between LDL cholesterol (LDL-C) or HDL cholesterol (HDL)-C and alcohol, after adjustment for age and BMI. Further, the positive (LDL-C and BMI) and the negative (HDL-C and BMI) associations that were observed in men and women with the epsilon3/2 and epsilon3/3 genotypes were not modified by alcohol intake. However, in women with the epsilon4/3 genotype only, we found a significant influence of an alcohol by BMI interaction on the prediction of total cholesterol, LDL-C, HDL-C, apoA-I, and apoB, and this interaction was influenced by the status of smoking. Whereas the influence of an alcohol by BMI interaction on total cholesterol and LDL-C was significant in smokers, its influence on HDL-C was significant only in non-smokers. This study emphasizes the context dependency of the influence of alcohol on lipid metabolism and demonstrates how biological, environmental, and genetic factors interact to determine cardiovascular disease risk.     

Relationships of serum lipoproteins and apoproteins to sex hormones and to the binding capacity of sex hormone binding globulin in healthy Finnish men

We have determined the levels of serum sex hormones, the binding capacity of sex hormone binding globulin (SHBG), urinary estrogens, serum lipids, lipoproteins, and apolipoproteins A-I, A-II, and B in 30 healthy middle-aged Finnish men with similar dietary habits. Serum levels of total testosterone, free testosterone, 5 alpha-dihydrotestosterone (5 alpha-DHT), and the binding capacity of SHBG were all positively correlated to high density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I (apo A-I) (r = .43 to .80, P less than 0.05 to 0.001). Total testosterone and 5 alpha-DHT showed a positive correlation to the ratio of apo A-I to Apo A-II (r = .37, P less than 0.05 and r = .58, P less than 0.01, respectively). Serum estradiol levels were negatively correlated to serum total cholesterol, low density lipoprotein cholesterol (LDL), and Apo B (r = -.51 to -.56, P less than 0.01). Moreover, serum free estradiol was negatively correlated to HDL-C and Apo A-I (r = -.46 and r = -.50, P less than 0.01). In multiple linear regression analysis, 5 alpha-DHT was the most significant independent determinant of HDL-C and apo A-I levels when androgens, luteinizing hormone, estradiol, binding capacity of SHBG, and exogenous factors such as age, body mass index (BMI), smoking, alcohol consumption, and diet were taken into account. Multivariate analysis also demonstrated that both total and free estradiol were inversely related to serum Apo B levels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Association among cigarette smoking, metabolic syndrome, and its individual components: the metabolic syndrome study in Taiwan

Insulin resistance is a common feature of metabolic syndrome. Smokers are at great risk of developing insulin resistance. Theoretically, smoking status should be associated with metabolic syndrome. This study aimed to explore the association among cigarette smoking, metabolic syndrome, and its individual components. Information of participants regarding previous and current diseases, family history of disease, smoking habits, alcohol consumption, betel nut chewing, and physical activity status were gathered from self-reported nutrition and lifestyle questionnaires. The fasting plasma glucose, triglyceride level, high-density lipoprotein cholesterol (HDL-C) level, blood pressure, and anthropometric indices in each patient were measured. Data of 1146 male subjects were analyzed. Individuals who currently smoked had a higher prevalence of metabolic syndrome than those who had never smoked and those who had quit smoking. The adjusted odds ratios of current smoking amount showed a statistically significant dose-dependent association with metabolic syndrome, high triglyceride level, and low HDL-C level. Current smokers who smoke > or =20 pack-years have a significantly increased risk of developing metabolic syndrome, high triglyceride level, and low HDL-C level. The higher risk of development of metabolic syndrome, high triglyceride level, and low HDL-C level was insignificant in former smokers. In conclusion, this community-based study supports the view that smoking is associated with metabolic syndrome and its individual components. Smoking cessation is beneficial to metabolic syndrome and its individual components.