The Effect Of Alcohol On Cardiovascular Risk Factors: Is There New Information? PMC

pubmed oxidized cholesterol and alcohol

Macrophages uptake oxLDL via CD36, which results in the intracellular nucleation of cholesterol crystals in lysosomes. This process activates inflammasome with the same result as when the cholesterol page crystals are phagocytosed (Poznyak et al., 2020b). The risks increase with the amount of alcohol a person drinks, according to the Centers for Disease Control and Prevention (CDC).

pubmed oxidized cholesterol and alcohol

Sample size calculations show that 60,000 individuals are needed to detect the expected risk of any alcohol-related cancer, and when aiming to investigate specific forms of cancer, such as breast cancer, up to five times bigger samples are needed [7]. Since in observational studies, limited alcohol consumption has no beneficial association with most cancers, a RCT specifically to prove alcohol causes cancer is ethically dubious. Secondly, the fear of falsely extrapolating results from a specific and high-risk study population to a more general public has been expressed. However, we argue that if a protective effect is observed in a high-risk population, these effects are likely to be physiologically generalizable to a lower risk population, albeit with a smaller absolute risk reduction. Ultimately, we emphasize that alcohol is consumed by half of the world’s population, and to date, there is a nearly complete lack of causal evidence on its long-term effects. Therefore, obtaining highest level of evidence in an appropriate way is in everyone’s benefit.

Moreover, the difference in the atherosclerosis pathogenesis between various species was not fully investigated. In a recent review, Wakabayashi investigated the relationship between platelet count and alcohol intake in 6508 middle-aged men who were either non-drinkers or drank less than 66 g/day. He described that there was no significant correlation between these two variables and concluded that further studies are needed to evaluate this association in heavier drinkers [40].

Moreover, pneumococcal immunization resulted in decreased atherosclerosis development rate in the low-density lipoprotein receptor (LDLR)-deficient mice (Shekhar et al., 2018). The results of the 5-years follow-up from the large trials of the pneumococcal polysaccharide vaccine efficacy for the primary prevention of acute coronary syndromes and ischemic strokes are on the way. This investigation called AUSPICE (Australian Study for the Prevention through Immunization of Cardiovascular Events) involved 55 60 years old human subjects (Ren et al., 2016). A human phase I-IIa of GLACIER (Goal of oxidized LDL and ACtivated macrophage Inhibition by Exposure to a Recombinant antibody) is another trial involved subjects suffering from stable carotid artery or aortic disease.

Interestingly, a direct angiogenic cytokine, SGC2, which is also crucial for AP-1 regulation, appeared to be a direct miRNA-155 target. Changes in SGC2 expression violate the expression of adhesion molecules (Feinberg and Moore, 2016). These effects lead to decreased cholesterol click this link now loading and inhibition of inflammatory factors (IL-6, IL-8, MCP-1, CCL2, and MMP-9) expression (Maa et al., 2011). Interestingly, Nox5 is not presented in the rodent genome that hinders the investigation of the role of Nox5 in atherosclerosis progression.

The role of oxidative stress as a major contributor to the atherogenic process has been elegantly reviewed [3, 4]. Thus, oxidation of LDL to form oxidized LDL (OxLDL) results in its massive uptake by peripheral macrophages (i.e. scavenger pathway), his response leading to the formation of foam cells. The accumulation of these foam cells in the intima of the arterial wall results in a gradual decrease in arterial lumen and eventually occlusion of the artery causing myocardial infarction (MI).

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