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Introduction: Different alcoholic beverages exert different effects on inflammation and oxidative stress but these results are controversial and scanty in some aspects. We analyze the effect of different alcoholic beverages after a fat-enriched diet on lipid profile, inflammatory factors and oxidative stress in healthy people in a controlled environment., Methods: We have performed a cross-over design in five different weeks. Sixteen healthy volunteers have received the same oral fat-enriched diet (1486kcal/m(2)) and a daily total amount of 16g/m(2) of alcohol, of different beverages (red wine, vodka, brandy or rum) and equivalent caloric intakes as sugar with water in the control group. We have measured the levels of serum lipids, high sensitivity C-reactive protein (hsCRP), tumor necrosis factor α (TNFα), interleukin 6 (IL-6), soluble phospholipase A2 (sPLA2), lipid peroxidation (LPO) and total antioxidant capacity (TAC)., Results: Red wine intake was associated with decreased of mean concentrations of hsCRP, TNFα and IL-6 induced by fat-enriched diet (p<0.05); nevertheless, sPLA2 concentrations were not significantly modified. After a fat-enriched diet added with red wine, TAC increased as compared to the same diet supplemented with rum, brandy, vodka or the control (water with sugar) (p<0.05)., Conclusions: Moderate red wine intake, but not other alcoholic beverages, decreased pro-inflammatory factors and increased total antioxidant capacity despite a fat-enriched diet intake in healthy young volunteers., (Copyright © 2015 Elsevier España, S.L.U. y Sociedad Española de Medicina Interna (SEMI). All rights reserved.)

An investigation was conducted on the effects of pravastatin, an inhibitor of the HMG CoA reductase, on lipoproteins concentrations and degradation of LDL (low density lipoproteins) in 14 patients with familial hypercholesterolemia (FH). Therapy with pravastatin for twelve weeks, 20 mg every 12 hours, and a low fat (30% calories) and cholesterol (less than 300 mg/daily) diet decreased serum concentrations of LDL cholesterol and apolipoprotein B by 35.5% and 24%, respectively (p < 0.001 for both parameters). On the other hand, apolipoprotein A-1 concentrations increased by 15.1% (p < 0.05) and HDL cholesterol (high density lipoproteins) by 6.8%; concentrations of apolipoprotein A-II did not change. LDL degradation in peripheral lymphocytes increased by 41.3% (p < 0.05) and a correlation was observed (p < 0.05) between percentage of LDL degradation and percentage in the LDL cholesterol decrease. Likewise, a positive trend (p = 0.057) was observed between increases in LDL degradation and aging. These findings indicate that pravastatin favorably influences the lipoprotein profile and that this effect is mediated, at least partly, by an increase in cellular capacity of LDL degradation.