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1.
Alcohol and Cancer: Epidemiology and Biological Mechanisms.
Rumgay, H, Murphy, N, Ferrari, P, Soerjomataram, I
Nutrients. 2021;(9)
Abstract
Approximately 4% of cancers worldwide are caused by alcohol consumption. Drinking alcohol increases the risk of several cancer types, including cancers of the upper aerodigestive tract, liver, colorectum, and breast. In this review, we summarise the epidemiological evidence on alcohol and cancer risk and the mechanistic evidence of alcohol-mediated carcinogenesis. There are several mechanistic pathways by which the consumption of alcohol, as ethanol, is known to cause cancer, though some are still not fully understood. Ethanol's metabolite acetaldehyde can cause DNA damage and block DNA synthesis and repair, whilst both ethanol and acetaldehyde can disrupt DNA methylation. Ethanol can also induce inflammation and oxidative stress leading to lipid peroxidation and further DNA damage. One-carbon metabolism and folate levels are also impaired by ethanol. Other known mechanisms are discussed. Further understanding of the carcinogenic properties of alcohol and its metabolites will inform future research, but there is already a need for comprehensive alcohol control and cancer prevention strategies to reduce the burden of cancer attributable to alcohol.
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2.
Consensus and Controversy in the Debate over the Biphasic Impact of Alcohol Consumption on the Cardiovascular System.
Stătescu, C, Clement, A, Șerban, IL, Sascău, R
Nutrients. 2021;(4)
Abstract
In the past few decades, research has focused on the importance of addressing modifiable risk factors as a means of lowering the risk of cardiovascular disease (CVD), which represents the worldwide leading cause of death. For quite a long time, it has been considered that ethanol intake has a biphasic impact on the cardiovascular system, mainly depending on the drinking pattern, amount of consumption, and type of alcoholic beverage. Multiple case-control studies and meta-analyses reported the existence of a "U-type" or "J-shaped" relationship between alcohol and CVD, as well as mortality, indicating that low to moderate alcohol consumption decreases the number of adverse cardiovascular events and deaths compared to abstinence, while excessive alcohol use has unquestionably deleterious effects on the circulatory system. However, beginning in the early 2000s, the cardioprotective effects of low doses of alcohol were abnegated by the results of large epidemiological studies. Therefore, this narrative review aims to reiterate the association of alcohol use with cardiac arrhythmias, dilated cardiomyopathy, arterial hypertension, atherosclerotic vascular disease, and type 2 diabetes mellitus, highlighting literature disagreements over the risk and benefits of low to moderate drinking on the cardiovascular system.
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3.
Alcohol Drinking, Apolipoprotein Polymorphisms and the Risk of Cardiovascular Diseases.
Ceci, FM, Ceccanti, M, Petrella, C, Vitali, M, Messina, MP, Chaldakov, GN, Greco, A, Ralli, M, Lucarelli, M, Angeloni, A, et al
Current neurovascular research. 2021;(1):150-161
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Abstract
Lipoprotein disorders are a major risk factor for atherosclerotic neuro-cardiovascular disease (ACVD) and are heavily influenced by lifestyle, including alcohol drinking. Moderate drinkers have a lower ACVD risk than abstainers due to their higher levels of high-density lipoprotein (HDL) cholesterol, an important protective factor against ACVD. On the contrary, heavy drinking increases ACVD risk. According to an extensive literature body, ethanol intoxication modifies lipid serum profile and induces endothelial dysfunction. Single nucleotide polymorphisms may influence the relationship between alcohol drinking, HDL cholesterol level, and atherosclerotic risk. The risk of ACVD in heavy drinkers seems enhanced in patients with apolipoprotein E4 allele, interleukin- 6-174 polymorphism, and cholesteryl ester transfer protein TaqIB polymorphism. Apolipoprotein E4 is a known risk factor for ACVD, while apolipoprotein E2 has mixed effects. Therefore, even if a "protective role" may be attributed to moderate drinking, this effect cannot be extended to everyone.
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4.
Alcohol Consumption in Rheumatoid Arthritis: A Path through the Immune System.
Azizov, V, Zaiss, MM
Nutrients. 2021;(4)
Abstract
Benefits and harms of different components of human diet have been known for hundreds of years. Alcohol is one the highest consumed, abused, and addictive substances worldwide. Consequences of alcohol abuse are increased risks for diseases of the cardiovascular system, liver, and nervous system, as well as reduced immune system function. Paradoxically, alcohol has also been a consistent protective factor against the development of autoimmune diseases such as type 1 diabetes, multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis (RA). Here, we focused on summarizing current findings on the effects of alcohol, as well as of its metabolites, acetaldehyde and acetate, on the immune system and RA. Heavy or moderate alcohol consumption can affect intestinal barrier integrity, as well as the microbiome, possibly contributing to RA. Additionally, systemic increase in acetate negatively affects humoral immune response, diminishing TFH cell as well as professional antigen-presenting cell (APC) function. Hence, alcohol consumption has profound effects on the efficacy of vaccinations, but also elicits protection against autoimmune diseases. The mechanism of alcohol's negative effects on the immune system is multivariate. Future studies addressing alcohol and its metabolite acetate's effect on individual components of the immune system remains crucial for our understanding and development of novel therapeutic pathways.
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5.
Alcohol and the Brain.
Nutt, D, Hayes, A, Fonville, L, Zafar, R, Palmer, EOC, Paterson, L, Lingford-Hughes, A
Nutrients. 2021;(11)
Abstract
Alcohol works on the brain to produce its desired effects, e.g., sociability and intoxication, and hence the brain is an important organ for exploring subsequent harms. These come in many different forms such as the consequences of damage during intoxication, e.g., from falls and fights, damage from withdrawal, damage from the toxicity of alcohol and its metabolites and altered brain structure and function with implications for behavioral processes such as craving and addiction. On top of that are peripheral factors that compound brain damage such as poor diet, vitamin deficiencies leading to Wernicke-Korsakoff syndrome. Prenatal alcohol exposure can also have a profound impact on brain development and lead to irremediable changes of fetal alcohol syndrome. This chapter briefly reviews aspects of these with a particular focus on recent brain imaging results. Cardiovascular effects of alcohol that lead to brain pathology are not covered as they are dealt with elsewhere in the volume.
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Dose-Response Relationships between Levels of Alcohol Use and Risks of Mortality or Disease, for All People, by Age, Sex, and Specific Risk Factors.
Rehm, J, Rovira, P, Llamosas-Falcón, L, Shield, KD
Nutrients. 2021;(8)
Abstract
Alcohol use has been causally linked to more than 200 disease and injury conditions, as defined by three-digit ICD-10 codes. The understanding of how alcohol use is related to these conditions is essential to public health and policy research. Accordingly, this study presents a narrative review of different dose-response relationships for alcohol use. Relative-risk (RR) functions were obtained from various comparative risk assessments. Two main dimensions of alcohol consumption are used to assess disease and injury risk: (1) volume of consumption, and (2) patterns of drinking, operationalized via frequency of heavy drinking occasions. Lifetime abstention was used as the reference group. Most dose-response relationships between alcohol and outcomes are monotonic, but for diabetes type 2 and ischemic diseases, there are indications of a curvilinear relationship, where light to moderate drinking is associated with lower risk compared with not drinking (i.e., RR < 1). In general, women experience a greater increase in RR per gram of alcohol consumed than men. The RR per gram of alcohol consumed was lower for people of older ages. RRs indicated that alcohol use may interact synergistically with other risk factors, in particular with socioeconomic status and other behavioural risk factors, such as smoking, obesity, or physical inactivity. The literature on the impact of genetic constitution on dose-response curves is underdeveloped, but certain genetic variants are linked to an increased RR per gram of alcohol consumed for some diseases. When developing alcohol policy measures, including low-risk drinking guidelines, dose-response relationships must be taken into consideration.
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Margin of Exposure Analyses and Overall Toxic Effects of Alcohol with Special Consideration of Carcinogenicity.
Okaru, AO, Lachenmeier, DW
Nutrients. 2021;(11)
Abstract
Quantitative assessments of the health risk of the constituents of alcoholic beverages including ethanol are reported in the literature, generally with hepatotoxic effects considered as the endpoint. Risk assessment studies on minor compounds such as mycotoxins, metals, and other contaminants are also available on carcinogenicity as the endpoint. This review seeks to highlight population cancer risks due to alcohol consumption using the margin of exposure methodology. The individual and cumulative health risk contribution of each component in alcoholic beverages is highlighted. Overall, the results obtained consistently show that the ethanol contributes the bulk of harmful effects of alcoholic beverages, while all other compounds only contribute in a minor fashion (less than 1% compared to ethanol). Our data provide compelling evidence that policy should be focused on reducing total alcohol intake (recorded and unrecorded), while measures on other compounds should be only secondary to this goal.
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'Joining the Dots': Individual, Sociocultural and Environmental Links between Alcohol Consumption, Dietary Intake and Body Weight-A Narrative Review.
Fong, M, Scott, S, Albani, V, Adamson, A, Kaner, E
Nutrients. 2021;(9)
Abstract
Alcohol is energy-dense, elicits weak satiety responses relative to solid food, inhibits dietary fat oxidation, and may stimulate food intake. It has, therefore, been proposed as a contributor to weight gain and obesity. The aim of this narrative review was to consolidate and critically appraise the evidence on the relationship of alcohol consumption with dietary intake and body weight, within mainstream (non-treatment) populations. Publications were identified from a PubMed keyword search using the terms 'alcohol', 'food', 'eating', 'weight', 'body mass index', 'obesity', 'food reward', 'inhibition', 'attentional bias', 'appetite', 'culture', 'social'. A snowball method and citation searches were used to identify additional relevant publications. Reference lists of relevant publications were also consulted. While limited by statistical heterogeneity, pooled results of experimental studies showed a relatively robust association between acute alcohol intake and greater food and total energy intake. This appears to occur via metabolic and psychological mechanisms that have not yet been fully elucidated. Evidence on the relationship between alcohol intake and weight is equivocal. Most evidence was derived from cross-sectional survey data which does not allow for a cause-effect relationship to be established. Observational research evidence was limited by heterogeneity and methodological issues, reducing the certainty of the evidence. We found very little qualitative work regarding the social, cultural, and environmental links between concurrent alcohol intake and eating behaviours. That the evidence of alcohol intake and body weight remains uncertain despite no shortage of research over the years, indicates that more innovative research methodologies and nuanced analyses are needed to capture what is clearly a complex and dynamic relationship. Also, given synergies between 'Big Food' and 'Big Alcohol' industries, effective policy solutions are likely to overlap and a unified approach to policy change may be more effective than isolated efforts. However, joint action may not occur until stronger evidence on the relationship between alcohol intake, food intake and weight is established.
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Alcohol Use and Abuse Conspires With HIV Infection to Aggravate Intestinal Dysbiosis and Increase Microbial Translocation in People Living With HIV: A Review.
Yan, J, Ouyang, J, Isnard, S, Zhou, X, Harypursat, V, Routy, JP, Chen, Y
Frontiers in immunology. 2021;:741658
Abstract
The intestinal microbiome is an essential so-called human "organ", vital for the induction of innate immunity, for metabolizing nutrients, and for maintenance of the structural integrity of the intestinal barrier. HIV infection adversely influences the richness and diversity of the intestinal microbiome, resulting in structural and functional impairment of the intestinal barrier and an increased intestinal permeability. Pathogens and metabolites may thus cross the "leaky" intestinal barrier and enter the systemic circulation, which is a significant factor accounting for the persistent underlying chronic inflammatory state present in people living with HIV (PLWH). Additionally, alcohol use and abuse has been found to be prevalent in PLWH and has been strongly associated with the incidence and progression of HIV/AIDS. Recently, converging evidence has indicated that the mechanism underlying this phenomenon is related to intestinal microbiome and barrier function through numerous pathways. Alcohol acts as a "partner" with HIV in disrupting microbiome ecology, and thus impairing of the intestinal barrier. Optimizing the microbiome and restoring the integrity of the intestinal barrier is likely to be an effective adjunctive therapeutic strategy for PLWH. We herein critically review the interplay among HIV, alcohol, and the gut barrier, thus setting the scene with regards to development of effective strategies to counteract the dysregulated gut microbiome and the reduction of microbial translocation and inflammation in PLWH.
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10.
Role of Diet in Colorectal Cancer Incidence: Umbrella Review of Meta-analyses of Prospective Observational Studies.
Veettil, SK, Wong, TY, Loo, YS, Playdon, MC, Lai, NM, Giovannucci, EL, Chaiyakunapruk, N
JAMA network open. 2021;(2):e2037341
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Abstract
IMPORTANCE Several meta-analyses have summarized evidence for the association between dietary factors and the incidence of colorectal cancer (CRC). However, to date, there has been little synthesis of the strength, precision, and quality of this evidence in aggregate. OBJECTIVE To grade the evidence from published meta-analyses of prospective observational studies that assessed the association of dietary patterns, specific foods, food groups, beverages (including alcohol), macronutrients, and micronutrients with the incidence of CRC. DATA SOURCES MEDLINE, Embase, and the Cochrane Library were searched from database inception to September 2019. EVIDENCE REVIEW Only meta-analyses of prospective observational studies with a cohort study design were eligible. Evidence of association was graded according to established criteria as follows: convincing, highly suggestive, suggestive, weak, or not significant. RESULTS From 9954 publications, 222 full-text articles (2.2%) were evaluated for eligibility, and 45 meta-analyses (20.3%) that described 109 associations between dietary factors and CRC incidence were selected. Overall, 35 of the 109 associations (32.1%) were nominally statistically significant using random-effects meta-analysis models; 17 associations (15.6%) demonstrated large heterogeneity between studies (I2 > 50%), whereas small-study effects were found for 11 associations (10.1%). Excess significance bias was not detected for any association between diet and CRC. The primary analysis identified 5 (4.6%) convincing, 2 (1.8%) highly suggestive, 10 (9.2%) suggestive, and 18 (16.5%) weak associations between diet and CRC, while there was no evidence for 74 (67.9%) associations. There was convincing evidence of an association of intake of red meat (high vs low) and alcohol (≥4 drinks/d vs 0 or occasional drinks) with the incidence of CRC and an inverse association of higher vs lower intakes of dietary fiber, calcium, and yogurt with CRC risk. The evidence for convincing associations remained robust following sensitivity analyses. CONCLUSIONS AND RELEVANCE This umbrella review found convincing evidence of an association between lower CRC risk and higher intakes of dietary fiber, dietary calcium, and yogurt and lower intakes of alcohol and red meat. More research is needed on specific foods for which evidence remains suggestive, including other dairy products, whole grains, processed meat, and specific dietary patterns.