13 October 2020 In Phenolic compounds
Polyphenols are antioxidants contained in plants as olive and grape. As part of the Mediterranean diet, they may decrease the risk of cancer, of chronic and neurodegenerative diseases. Alcohol consumption plays a detrimental effect on health, causing tissue damage and disrupting the metabolism of Neurotrophins (NTs). NTs are crucial proteins for the life cycle of neuronal and non-neuronal cells. Alcohol abuse elicits changes in NTs levels in the brain and in other target organs, however, it was observed minor damage in animals early exposed to red wine, probably due to the antioxidant effects of polyphenols. Indeed, data show that resveratrol or other polyphenols extracted from the olive can effectively counteract serum free radicals’ formation caused by chronic alcohol intake, contrasting also alcohol-induced NTs liver elevation. The aim of the present review is to update pieces of evidences about the antioxidant properties of polyphenols and their role in counteracting alcohol-induced damage.
13 October 2020 In Liver Disease
Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease worldwide, with a prevalence of 25-30%. Since its first description in 1980, NAFLD has been conceived as a different entity from alcohol-related fatty liver disease (ALD), despite that, both diseases have an overlap in the pathophysiology, share genetic-epigenetic factors, and frequently coexist. Both entities are characterized by a broad spectrum of histological features ranging from isolated steatosis to steatohepatitis and cirrhosis. Distinction between NAFLD and ALD is based on the amount of consumed alcohol, which has been arbitrarily established. In this context, a proposal of positive criteria for NAFLD diagnosis not considering exclusion of alcohol consumption as a prerequisite criterion for diagnosis had emerged, recognizing the possibility of a dual etiology of fatty liver in some individuals. The impact of moderate alcohol use on the severity of NAFLD is ill-defined. Some studies suggest protective effects in moderate doses, but current evidence shows that there is no safe threshold for alcohol consumption for NAFLD. In fact, given the synergistic effect between alcohol consumption, obesity, and metabolic dysfunction, it is likely that alcohol use serves as a significant risk factor for the progression of liver disease in NAFLD and metabolic syndrome. This also affects the incidence of hepatocellular carcinoma. In this review, we summarize the overlapping pathophysiology of NAFLD and ALD, the current data on alcohol consumption in patients with NAFLD, and the effects of metabolic dysfunction and overweight in ALD.
13 October 2020 In Diabetes
It is well known that alcohol consumption is associated with type 2 diabetes. However, the association between age of alcohol onset (AAO) and drinking duration with type 2 diabetes among Chinese adults is not fully understood. Our study was based on the data from the China Kadoorie Biobank, which included 512,712 participants aged 30-79 years in China from 2004-2008. Cox proportional-hazard model was used to estimate the association between AAO and drinking duration with type 2 diabetes. After adjustment for potential covariates, 18.1 = AAO = 29.0, 29.1 = AAO = 39.0 and AAO > 39.0 were associated with 22% (95%CI: 14%, 30%), 25% (95%CI: 17%, 33%) and 32% (95%CI: 24%, 39%) lower hazard ratio of type 2 diabetes, compared with abstainer, respectively. Drinking duration 30.0 were associated with 18% (95%CI: 9%, 33%) and 20% (95%CI: 3%, 40%) higher hazard ratio of type 2 diabetes, compared with 18.1 = AAO = 29.0 and drinking duration
13 October 2020 In Cancer
Oral cancer (OC) is among the top twenty occurring cancers in the world, with a mortality rate of 50%. A shift to a functionally inflammatory or a 'disease state' oral microbiome composition has been observed amongst patients with premalignant disorders and OC, with evidence suggesting alcohol could be exacerbating the inflammatory influence of the oral microorganisms. Alcohol dehydrogenase (ADH, EC 1.1.1.1) converts alcohol into a known carcinogenic metabolite, acetaldehyde and while ADH levels in oral mucosa are low, several oral commensal species possess ADH and could produce genotoxic levels of acetaldehyde. With a direct association between oral microbiome status, alcohol and poor oral health status combining to induce chronic inflammation with increased acetaldehyde levels - this leads to a tumour promoting environment. This new disease state increases the production of reactive oxygen species (ROS), while impairing anti-oxidant systems thus activating the redox signalling required for the promotion and survival of tumours. This review aims to highlight the evidence linking these processes in the progression of oral cancer.
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