Effects of ethanol intake on lipoproteins and atherosclerosis.
ABSTRACT This article reviews published studies regarding effects of ethanol intake on lipoprotein levels and function as they relate to atherosclerosis, with special emphasis on recent publications in the past 2 years.
Some recent studies have explored novel mechanisms of ethanol on atherogenesis via effects on HDL composition and function. Other studies have focused on changes in levels of LDL cholesterol (LDL-C), triglyceride, and other factors such as inflammatory markers C-reactive protein (CRP) and lipoprotein-associated phospholipase A2 (LpPLA2). Other areas of emphasis have been the effects within specific populations and between genders, as well as contributions of genetic polymorphisms in prediction of response to ethanol. Surprisingly, results of recent studies are often at odds with prior, seemingly well established findings.
The association between moderate ethanol consumption and favorable changes in lipoproteins and lipoprotein-related factors in atherosclerosis continues to become better established with the publication of new studies in this field. Continued progress is being achieved in understanding the well established link between moderate intake and reduced risk of cardiovascular disease (CVD). Nevertheless, it remains difficult to implement these findings in clinical practice due to the ongoing lack of randomized, blinded clinical trial data, and the well known hazards of excess ethanol consumption.
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ABSTRACT: The existence of an independent association between elevated triglyceride (TG) levels, cardiovascular (CV) risk and mortality has been largely controversial. The main difficulty in isolating the effect of hypertriglyceridemia on CV risk is the fact that elevated triglyceride levels are commonly associated with concomitant changes in high density lipoprotein (HDL), low density lipoprotein (LDL) and other lipoproteins. As a result of this problem and in disregard of the real biological role of TG, its significance as a plausible therapeutic target was unfoundedly underestimated for many years. However, taking epidemiological data together, both moderate and severe hypertriglyceridaemia are associated with a substantially increased long term total mortality and CV risk. Plasma TG levels partially reflect the concentration of the triglyceride-carrying lipoproteins (TRL): very low density lipoprotein (VLDL), chylomicrons and their remnants. Furthermore, hypertriglyceridemia commonly leads to reduction in HDL and increase in atherogenic small dense LDL levels. TG may also stimulate atherogenesis by mechanisms, such excessive free fatty acids (FFA) release, production of proinflammatory cytokines, fibrinogen, coagulation factors and impairment of fibrinolysis. Genetic studies strongly support hypertriglyceridemia and high concentrations of TRL as causal risk factors for CV disease. The most common forms of hypertriglyceridemia are related to overweight and sedentary life style, which in turn lead to insulin resistance, metabolic syndrome (MS) and type 2 diabetes mellitus (T2DM). Intensive lifestyle therapy is the main initial treatment of hypertriglyceridemia. Statins are a cornerstone of the modern lipids-modifying therapy. If the primary goal is to lower TG levels, fibrates (bezafibrate and fenofibrate for monotherapy, and in combination with statin; gemfibrozil only for monotherapy) could be the preferable drugs. Also ezetimibe has mild positive effects in lowering TG. Initial experience with en ezetimibe/fibrates combination seems promising. The recently released IMPROVE-IT Trial is the first to prove that adding a non-statin drug (ezetimibe) to a statin lowers the risk of future CV events. In conclusion, the classical clinical paradigm of lipids-modifying treatment should be changed and high TG should be recognized as an important target for therapy in their own right. Hypertriglyceridemia should be treated.Cardiovascular Diabetology 12/2014; 13(1):159. DOI:10.1186/PREACCEPT-2085133501150912 · 3.71 Impact Factor
Article: Secondary dyslipidaemiaOfficial journal of the South African Academy of Family Practice/Primary Care 08/2014; 53(4):317-323. DOI:10.1080/20786204.2011.10874107
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ABSTRACT: Objective The aim of this study was to assess the prevalence of atherogenic dyslipidemia (AD) and the lipid triad (LT) in the working population in Spain, their associated variables and how far they are linked to cardiovascular risk (CVR). Methods Observational cross-sectional study of 70,609 workers (71.5% male (M), 28.5% female (F), mean age 39.2 ± 10), who attended medical checkups and agreed to participate. Plasma samples were analysed in a central laboratory. AD definition used was: triglycerides ≥150 mg/dl and HDL cholesterol <40 mg/dl (M)/<50 mg/dl (F) and LT when LDL cholesterol > 160 mg/dl is further added. Univariate comparisons in the absence and presence of AD and LT and the probability of AD according to different parameters and their possible association with CVR were assessed. CVR was stratified following the European SCORE model for low risk-population. Results 5.7% (95% CI 4.7–6.9) of the working population have AD and 1.1% (95% CI 1.0–1.2) LT. In univariate analysis, workers with AD and LT had a higher prevalence of obesity, hypertension, smoking and diabetes than those who had not (p < 0.001). In multivariate analysis, BMI, sex, age 40–49, diabetes, tobacco, uric acid, LDL or blood pressure significantly influenced the risk of AD. AD was significantly associated with CVR after adjusting for alcohol and obesity. However, most of the AD subjects (91.8%) were classified as low risk. Conclusions About 6% of the working population in Spain meets AD criteria. Assuming that these subjects have increased CVR, AD allows to identify additional 5% of subjects with increased CVR to that one the SCORE model detects, helping to improve cardiovascular risk stratification.Atherosclerosis 08/2014; 235(2):562–569. DOI:10.1016/j.atherosclerosis.2014.05.960 · 3.71 Impact Factor