Modest Alcohol Research Articles

Precision medicine in alcohol use disorder: Mapping etiologic and maintenance mechanisms to mechanisms of behavior change to improve patient outcomes.

Precision medicine has been advanced as a potential solution to the problem of alcohol use disorder heterogeneity and modest alcohol use disorder treatment efficacy. The success of precision medicine lies in our ability to first identify the etiologic and maintenance mechanisms at play for a given person and then choose the treatment that is most likely to address such mechanisms. There exist several frameworks that describe empirically supported substance use disorder (SUD) etiologic and maintenance mechanisms (e.g., the Etiologic, Theory-based, Ontogenetic, Hierarchical [ETOH] Framework). There also exists a large literature on mechanisms of behavior change in alcohol use disorder treatment. However, the mechanism of behavior change literature on alcohol use disorder treatments has focused broadly on mechanisms of change rather than more specifically on core alcohol use disorder etiologic and maintenance mechanisms. Thus, the two types of mechanisms have never been integrated or systematically evaluated for their overlap. As such, the aim of the present brief review is to demonstrate how commonly used alcohol use disorder treatments may overlap with and directly target certain alcohol use disorder etiologic and maintenance mechanisms (specifically those described by the ETOH framework). We delineate empirically plausible overlapping mechanisms and theoretically plausible overlapping mechanisms that warrant more research. Last, based on the identification of empirically and theoretically plausible overlapping mechanisms, we elaborate on how ongoing work related to alcohol use disorder precision medicine may test specific hypotheses regarding which treatments work best for whom. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Dose-dependent Association of Alcohol Consumption With Obesity and Type 2 Diabetes: Mendelian Randomization Analyses.

Effects of modest alcohol consumption remain controversial. Mendelian randomization (MR) can help to mitigate biases due to confounding and reverse causation in observational studies, and evaluate the potential causal role of alcohol consumption. This work aimed to evaluate dose-dependent effect of alcohol consumption on obesity and type 2 diabetes. Assessing 408 540 participants of European ancestry in the UK Biobank, we first tested the association between self-reported alcohol intake frequency and 10 anthropometric measurements, obesity, and type 2 diabetes. We then conducted MR analyses both in the overall population and in subpopulations stratified by alcohol intake frequency. Among individuals having more than 14 drinks per week, a 1-drink-per-week increase in genetically predicted alcohol intake frequency was associated with a 0.36-kg increase in fat mass (SD = 0.03 kg), a 1.08-fold increased odds of obesity (95% CI, 1.06-1.10), and a 1.10-fold increased odds of type 2 diabetes (95% CI, 1.06-1.13). These associations were stronger in women than in men. Furthermore, no evidence was found supporting the association between genetically increased alcohol intake frequency and improved health outcomes among individuals having 7 or fewer drinks per week, as MR estimates largely overlapped with the null. These results withstood multiple sensitivity analyses assessing the validity of MR assumptions. As opposed to observational associations, MR results suggest there may not be protective effects of modest alcohol consumption on obesity traits and type 2 diabetes. Heavy alcohol consumption could lead to increased measures of obesity as well as increased risk of type 2 diabetes.

Any alcohol use in NAFLD patients is associated with significant changes to the intestinal virome.

The prevalence of alcohol use disorder (AUD) and metabolic dysfunction-associated fatty liver disease (MAFLD) are increasing worldwide, leading to the increasing likelihood of both etiologies contributing to a patient's liver disease. However, the effects of modest alcohol use in NAFLD are controversial and more studies are needed. We compared the intestinal viromes of patients with AUD and NAFLD in order to evaluate the effect of alcohol consumption on the intestinal viromes of NAFLD patients by extracting virus-like particles and performing metagenomic sequencing. Viral nucleic acids were extracted from fecal samples and subjected to metagenomic sequencing. We demonstrate significant differences in the intestinal viromes of NAFLD and AUD patients, and that alcohol use in NAFLD patients reclassified to MAFLD accounted for significant differences in the intestinal viromes. The relative abundance of several Lactococcus phages was more similar between AUD patients and alcohol-consuming MAFLD patients than non-alcohol-consuming MAFLD patients and control subjects, and multivariate modeling using the most discriminating Lactococcus phages could better predict alcohol use in the MAFLD population than the alcohol-associated liver disease/NAFLD Index. Significant differences in the viral composition and diversity were also seen between MAFLD patients with low and moderate alcohol consumption compared with no alcohol consumption. The intestinal virome of MAFLD patients who consume low to moderate amounts of alcohol are significantly different from those who do not, and many features of the intestinal virome of alcohol-consuming MAFLD patients resemble that of AUD patients.

Assessing maternal alcohol consumption in pregnancy: does phosphatidylethanol measured from day 5 newborn blood spot cards have any value? An observational, population-based study

ObjectivePrenatal alcohol exposure (PAE) places children at risk of fetal alcohol spectrum disorder (FASD) but ascertainment of PAE is problematic. Early intervention for children at risk of FASD may help...

Complete alcohol abstinence increases the risk of NAFLD but not severity. A population analysis with transient elastography

Background & Aims As the global prevalence of non-alcoholic fatty liver disease (NAFLD) continues to rise, ubiquity of alcohol use has also prompted discussion regarding the potential interactions between the two. This study aims to examine the effects of modest alcohol consumption on the prevalence and complications of NAFLD in a multi-ethnic population. Methods This study analyses the 2017–2018 cycles of NHANES that examined liver fibrosis and steatosis with vibration controlled transient elastography. A coarsened exact matching was conducted to reduce confounding. Logistic regression was done with a multivariate model to assess the relationship between alcohol consumption (modest drinkers and non-drinkers) and risk of NAFLD and its complications. Results 2,067 individuals were found to have NAFLD and 284 NAFLD patients had a total history of alcohol abstinence. After coarsened exact matching, the prevalence of NAFLD was 49% (CI: 0.41 − 0.58) in non-drinkers and 33% (CI: 0.26 − 0.41) in modest drinkers. Non-drinkers had twice the odds of NAFLD compared to modest drinkers (OR: 1.99, CI: 1.22 − 3.22, p<.01) after adjustment for confounders. There were no significant differences in the odds of significant fibrosis, advance fibrosis, cirrhosis, cardiovascular disease and stroke between non-drinkers and modest drinkers. The odds of malignancy in non-drinkers were almost significantly less than modest drinkers (OR: 0.28, CI:0.08 − 1.02, p=.053). Conclusion Interestingly, modest alcohol consumption is associated with decreased odds of NAFLD. Further investigations are required to examine the relationship between alcohol consumption and NAFLD and subsequently the potential impact on NAFLD management.

Very low event rate and few device implants in drug-induced brugada. A seven-year experience of ajmaline challenge at a district general hospital

Abstract Funding Acknowledgements Type of funding sources: None. Background Patients with a drug-induced Brugada electrocardiogram (ECG) are thought to have a lower risk of sudden cardiac death than those with a spontaneous type 1 ECG. Despite having a Brugada ECG, most patients do not need an implantable cardioverter defibrillator (ICD). Purpose To report a district general hospital experience on referral and outcomes of ajmaline challenge (AC) with medium term follow up. Methods 92 consecutive patients (50 males, mean age 41 ±17) had an AC in a single centre from 2014-2021. High ventricular leads were used from 2015. Ajmaline (1m/kg) was administered intravenously over 10-minutes. Data were collected from the electronic health record. Results The AC was positive in 18 (20%) patients. The yield from high leads was higher (7% vs 22%) p=0.28) but not statistically significant. There were no deaths or documented ventricular arrhythmias (VA) in AC positive patients during a median follow up of 3.2 years (1.7-4.9). The resting ECG was normal in 46.7%. A type 1 pattern had been provoked by fever or electrolyte derangements in 3.3%, type 2 pattern in 8.7% and a type 3 pattern in 5.4%. An RSR pattern (not in keeping with a BrS ECG) was seen in 26.4%. The test was stopped prematurely due to QRS widening &amp;gt;150ms in 1 patient. No adverse arrhythmic events occurred (table 1). In our cohort, positive AC patients were older (48y vs 37y p= 0.05) and more likely to have a type 2 (28% vs 4% p=0.007) or type 3 ECG (17% vs 3% p=0.05). Asymptomatic patients were more likely to have a normal ECG (22% vs 78% p=0.05) Of those with a positive AC, nine patients had symptoms of palpitations or syncope (table 2). A subcutaneous ICD (S-ICD) was implanted for syncope in two patients. No device therapies have occurred during a follow up of 2.5 years and 3.9 years respectively. Of those with a positive AC but asymptomatic, one S-ICD was initially implanted due to patient preference. A second S-ICD was implanted in a patient who experienced a collapse and brief seizure in the context of modest alcohol consumption. In seven positive patients (39%) and 18 negative patients (23%) an ILR was implanted. 1 episode of complete heart block was detected in an ajmaline negative patient during a median follow up of 2.7 years (1.7-3.9). There were no device related complications or adverse events. Conclusion AC is safe with a low number of device implants and ICD shocks. The yield from ILR implants was very low. A single patient had a potentially adverse outcome after consuming alcohol, a known trigger for VA in BrS. Our findings are in keeping with contemporary evidence that suggests the risk of adverse cardiac events in drug-induced BrS is low. However, time to first ICD shock may occur after ten years or more from diagnosis so long term follow up is required.

Association of Habitual Alcohol Intake With Risk of Cardiovascular Disease

Observational studies have consistently proposed cardiovascular benefits associated with light alcohol consumption, while recent genetic analyses (ie, mendelian randomization studies) have suggested a possible causal link between alcohol intake and increased risk of cardiovascular disease. However, traditional approaches to genetic epidemiology assume a linear association and thus have not fully evaluated dose-response estimates of risk across different levels of alcohol intake. To assess the association of habitual alcohol intake with cardiovascular disease risk and to evaluate the direction and relative magnitude of cardiovascular risk associated with different amounts of alcohol consumption. This cohort study used the UK Biobank (2006-2010, follow-up until 2016) to examine confounding in epidemiologic associations between alcohol intake and cardiovascular diseases. Using both traditional (ie, linear) and nonlinear mendelian randomization, potential associations between alcohol consumption and cardiovascular diseases (eg, hypertension and coronary artery disease) as well as corresponding association shapes were assessed. Data analysis was conducted from July 2019 to January 2022. Genetic predisposition to alcohol intake. The association between alcohol consumption and cardiovascular diseases, including hypertension, coronary artery disease, myocardial infarction, stroke, heart failure, and atrial fibrillation. This study included 371 463 participants (mean [SD] age, 57.0 [7.9] years; 172 400 [46%] men), who consumed a mean (SD) 9.2 (10.6) standard drinks per week. Overall, 121 708 participants (33%) had hypertension. Light to moderate alcohol consumption was associated with healthier lifestyle factors, adjustment for which attenuated the cardioprotective epidemiologic associations with modest intake. In linear mendelian randomization analyses, a 1-SD increase in genetically predicted alcohol consumption was associated with 1.3-fold (95% CI, 1.2-1.4) higher risk of hypertension (P < .001) and 1.4-fold (95% CI, 1.1-1.8) higher risk of coronary artery disease (P = .006). Nonlinear mendelian randomization analyses suggested nonlinear associations between alcohol consumption and both hypertension and coronary artery disease: light alcohol intake was associated with minimal increases in cardiovascular risk, whereas heavier consumption was associated with exponential increases in risk of both clinical and subclinical cardiovascular disease. In this cohort study, coincident, favorable lifestyle factors attenuated the observational benefits of modest alcohol intake. Genetic epidemiology suggested that alcohol consumption of all amounts was associated with increased cardiovascular risk, but marked risk differences exist across levels of intake, including those accepted by current national guidelines.

Modest alcohol intake and mortality in individuals with elevated alanine aminotransferase levels: a nationwide cohort study

BackgroundAlanine aminotransferase (ALT) levels are widely used to screen liver disease, and many asymptomatic individuals show elevated ALT levels. As elevated ALT level indicates liver injury, even a small amount of alcohol intake may be harmful in subjects with elevated ALT levels, but there is limited evidence of the effect of light to moderate amount of alcohol intake in this subgroup.MethodsA cohort of 367,612 men and women without established liver diseases (including chronic viral hepatitis, alcohol-associated liver disease, cirrhosis, liver transplantation, or rare forms of liver disease) who underwent at least 1 health screening exam between 2009 and 2015 were assessed for liver-related and all-cause mortality. Elevated ALT levels were defined as ≥ 34 U/L for men and 25 U/L for women.ResultsIn participants with normal ALT levels, the fully-adjusted hazard ratios (95% CI) for liver-related mortality comparing light and moderate drinkers to non-drinkers were 0.73 (0.51–1.05), and 1.06 (0.73–1.52), respectively. In participants with elevated ALT levels, the corresponding hazard ratios were 1.57 (1.08–2.28), and 2.09 (CI 1.46–2.99), respectively (p value for alcohol intake by ALT interaction < 0.01). For all-cause mortality, the fully-adjusted hazard ratios comparing light and moderate drinkers to non-drinkers in participants with normal ALT levels were 0.72 (0.66–0.77), and 0.89 (0.82–0.97), respectively. In participants with elevated ALT levels, the corresponding hazard ratios were 0.93 (0.81–1.08), and 1.31 (1.14–1.50), respectively (p value for alcohol intake by ALT interaction < 0.01).ConclusionsSmall amounts of alcohol intake were associated with increased liver-related and all-cause mortality among individuals with elevated ALT levels. Subjects with elevated ALT levels should be advised complete abstinence from alcohol.

Variant Aldehyde Dehydrogenase 2 (ALDH2*2) as a Risk Factor for Mechanical LA Substrate Formation and Atrial Fibrillation with Modest Alcohol Consumption in Ethnic Asians.

Aldehyde dehydrogenase 2 (ALDH2) rs671 polymorphism is a common genetic variant in Asians that is responsible for defective toxic aldehyde and lipid peroxidation metabolism after alcohol consumption. The extent to which low alcohol consumption may cause atrial substrates to trigger atrial fibrillation (AF) development in users with ALDH2 variants remains to be determined. We prospectively enrolled 249 ethnic Asians, including 56 non-drinkers and 193 habitual drinkers (135 (70%) as ALDH2 wild-type: GG, rs671; 58 (30%) as ALDH2 variants: G/A or A/A, rs671). Novel left atrial (LA) mechanical substrates with dynamic characteristics were assessed using a speckle-tracking algorithm and correlated to daily alcohol consumption and ALDH2 genotypes. Despite modest and comparable alcohol consumption by the habitual alcohol users (14.3 [8.3~28.6] and 12.3 [6.3~30.7] g/day for those without and with ALDH2 polymorphism, p = 0.31), there was a substantial and graded increase in the 4-HNE adduct and prolonged PR, and a reduction in novel LA mechanical parameters (including peak atrial longitudinal strain (PALS) and phasic strain rates (reservoir, conduit, and booster pump functions), p < 0.05), rather than an LA emptying fraction (LAEF) or LA volume index across non-drinkers, and in habitual drinkers without and with ALDH2 polymorphism (all p < 0.05). The presence of ALDH2 polymorphism worsened the association between increasing daily alcohol dose and LAEF, PALS, and phasic reservoir and booster functions (all Pinteraction: <0.05). Binge drinking superimposed on regular alcohol use exclusively further worsened LA booster pump function compared to regular drinking without binge use (1.66 ± 0.57 vs. 1.97 ± 0.56 1/s, p = 0.001). Impaired LA booster function further independently helped to predict AF after consideration of the CHARGE-AF score (adjusted 1.68 (95% CI: 1.06–2.67), p = 0.028, per 1 z-score increment). Habitual modest alcohol consumption led to mechanical LA substrate formation in an ethnic Asian population, which was more pronounced in subjects harboring ALDH2 variants. Impaired LA booster functions may serve as a useful predictor of AF in such populations.

Abstract 056: Alcohol Increases Risk Of Cardiovascular Disease At All Levels Of Intake

Genetic analyses have suggested a causal association between alcohol intake and cardiovascular diseases, questioning the purported cardioprotective effects of modest intake. Though traditional approaches to genetic epidemiology are limited in ability to assess association shapes, we hypothesized that any alcohol may increase risk of cardiovascular disease. In 371,463 participants from the UK Biobank, we first examined for confounding in epidemiological associations between alcohol intake and cardiovascular diseases. Next, using traditional and non-linear genetic approaches (Mendelian randomization), we assessed for causal links of alcohol consumption with several cardiovascular diseases and evaluated the shapes of all causal associations identified. Study participants consumed 9.2 (SD, 10.6) standard drinks per week on average; 121,708 (32.8%) and 27,667 (7.5%) subjects had hypertension and CAD, respectively. Modest consumers of alcohol demonstrated healthier lifestyles - such as lower BMI and greater physical activity - than abstainers, and adjustment for lifestyle factors attenuated the observed benefits of light alcohol intake. Traditional and non-linear Mendelian randomization demonstrated consistently risk-increasing and quadratic associations between alcohol consumption and both clinical and subclinical cardiovascular disease, with exponential increases in risk across levels of drinking; relative to abstainers, consumption of 7, 14, 21, and 28 drinks per week conferred 1.2, 1.7, 3.4, and 8.9-fold odds of hypertension and 1.2, 2.3, 6.2, and 25.9-fold odds of CAD, respectively (both models p&lt;0.001). In conclusion, coincident, favorable lifestyle factors may mediate the observational benefits of modest alcohol intake. All amounts of alcohol intake increase cardiovascular risk, but marked absolute and relative risk differences exist across levels of intake, which should inform public health recommendations around habitual alcohol consumption.

Alcohol consumption, cardiac biomarkers, and risk of atrial fibrillation and adverse outcomes.

Aims There is inconsistent evidence on the relation of alcohol intake with incident atrial fibrillation (AF), in particular at lower doses. We assessed the association between alcohol consumption, biomarkers, and incident AF across the spectrum of alcohol intake in European cohorts.Methods and results In a community-based pooled cohort, we followed 107 845 individuals for the association between alcohol consumption, including types of alcohol and drinking patterns, and incident AF. We collected information on classical cardiovascular risk factors and incident heart failure (HF) and measured the biomarkers N-terminal pro-B-type natriuretic peptide and high-sensitivity troponin I. The median age of individuals was 47.8 years, 48.3% were men. The median alcohol consumption was 3 g/day. N = 5854 individuals developed AF (median follow-up time: 13.9 years). In a sex- and cohort-stratified Cox regression analysis alcohol consumption was non-linearly and positively associated with incident AF. The hazard ratio for one drink (12 g) per day was 1.16, 95% CI 1.11–1.22, P < 0.001. Associations were similar across types of alcohol. In contrast, alcohol consumption at lower doses was associated with reduced risk of incident HF. The association between alcohol consumption and incident AF was neither fully explained by cardiac biomarker concentrations nor by the occurrence of HF.Conclusions In contrast to other cardiovascular diseases such as HF, even modest habitual alcohol intake of 1.2 drinks/day was associated with an increased risk of AF, which needs to be considered in AF prevention.

Modest alcohol consumption and risk of advanced liver fibrosis in nonalcoholic fatty liver disease: a systematic review and meta-analysis.

BackgroundRecent studies have suggested an association between modest alcohol consumption and a decreased risk of advanced liver fibrosis among patients with nonalcoholic fatty liver disease (NAFLD) although the results are inconsistent. The current systematic review and meta-analysis was conducted to comprehensively investigate this possible association by identifying all the relevant studies and combining their results.MethodsA comprehensive literature review was conducted utilizing the MEDLINE and EMBASE databases through February 2019 to identify all cross-sectional studies that compared the prevalence of advanced liver fibrosis among NAFLD patients who were modest alcohol drinkers to NAFLD patients who were non-drinkers. Effect estimates from each study were extracted and combined together using the random-effect, generic inverse variance method of DerSimonian and Laird.ResultsA total of 6 studies with 8,936 participants fulfilled the eligibility criteria and were included in the meta-analysis. The risk of advanced liver fibrosis among patients with NAFLD who were modest alcohol drinkers was significantly lower compared to patients with NAFLD who were non-drinkers with a pooled odds ratio of 0.51 (95% confidence interval [CI] 0.35-0.75; I2 47%). The funnel plot was symmetric and was not suggestive of publication bias.ConclusionA significantly lower risk of advanced liver fibrosis was observed among NAFLD patients who were modest alcohol drinkers compared to non-drinkers in this meta-analysis.

Modest alcohol intake not associated with significant hepatic steatosis or more severe liver disease among patients with diabetes mellitus.

The effect of modest alcohol intake on prevalence of significant hepatic steatosis and severity of liver disease in patients with type 2 diabetes mellitus (T2DM) is unclear. This is a cross-sectional study on T2DM patients. Modest alcohol intake was defined as alcohol intake ≤21units/week in men and ≤14units/week in women. Significant hepatic steatosis was diagnosed on the basis of controlled attenuation parameter>263dB/m, while advanced fibrosis was diagnosed on the basis of liver stiffness measurement≥9.6kPa using M probe or ≥9.3kPa using XL probe. Patients with liver stiffness measurement≥8.0kPa were offered liver biopsy. Five hundred fifty-seven patients underwent transient elastography, and 71 patients underwent liver biopsy. The prevalence of modest drinking was 16.5%. Modest drinking was equally prevalent among ethnic Indians and Chinese at 22.9% and 23.3%, respectively, but uncommon among ethnic Malays at 1.7%. Modest drinkers were more likely to be male, smoked, and had significantly lower glycated hemoglobin, total cholesterol, low-density lipoprotein cholesterol, alkaline phosphatase, and platelet count. There was no significant difference in the prevalence of significant hepatic steatosis or advanced fibrosis based on transient elastography and steatohepatitis or advanced fibrosis between modest drinkers and nondrinkers. The prevalence of significant hepatic steatosis was higher among ethnic Malays and Indians compared with ethnic Chinese, but the Chinese did not have a lower prevalence of more severe liver disease. Modest alcohol intake is not associated with higher prevalence of significant hepatic steatosis or more severe liver disease among patients with T2DM.

Bile acids associate with specific gut microbiota, low-level alcohol consumption and liver fibrosis in patients with non-alcoholic fatty liver disease.

Bile acids (BAs) are synthesized by the liver and modified by gut bacteria, and may play an intermediary role between the gut microbiome and liver in promoting fibrosis in non-alcoholic fatty liver disease (NAFLD). We investigated the associations between serum and faecal BAs, gut microbiome and fibrosis in patients with and without NAFLD and examined the impact of diet and alcohol consumption on these relationships. Adult patients (n=122) underwent liver biopsy and BAs characterization by high-performance liquid chromatography/mass spectrometry. Gut microbiome composition was analysed using next-generation 16S rRNA sequencing. Diet and alcohol intake were determined by 3-day food diary. Serum and faecal BA concentrations increased progressively among non-NAFLD controls (n=55), NAFLD patients with no/mild fibrosis (F0-2, n=58) and NAFLD with advanced fibrosis (F3/4, n=9). Progressive increases in serum BAs were driven by primary conjugated BAs including glycocholic acid [GCA] and secondary conjugated BAs. In contrast, faecal BA increase was driven by secondary unconjugated BAs (predominately deoxycholic acid [DCA]). Serum GCA levels and faecal DCA levels correlated with the abundance of Bacteroidaceae and Lachnospiraceae, and stool secondary BAs with an unclassifiable family of the order Bacteroidales (Bacteroidales;other). These bacterial taxa were also associated with advanced fibrosis. Modest alcohol consumption was positively correlated with faecal DCA levels and relative abundance of Lachnospiracaea and Bacteroidales;other. Higher serum and faecal BA levels are associated with advanced fibrosis in NAFLD. Specific gut bacteria link alterations in BA profiles and advanced fibrosis, and may be influenced by low-level alcohol consumption.

Moderate Alcohol Intake in Non-Alcoholic Fatty Liver Disease: To Drink or Not to Drink?

Nonalcoholic fatty liver disease (NAFLD) is defined by hepatic steatosis in the presence of alcohol intake within safe limits, defined by guidelines of scientific associations (usually 20 g or 2 units/day in women, 30 g or 3 units in men). The diagnosis is usually followed by medical counseling of total abstinence, in order to prevent disease progression. This policy has been challenged by epidemiological studies, suggesting that the risk of liver disease and disease progression is lower in modest drinkers than in total abstainers. We revised the literature on the effects of modest alcohol intake on disease burden. Epidemiological data may suffer from several potential biases (recall bias for retrospective analyses, difficulties in the calculation of g/day), limiting their validity. Prospective data suggest that NAFLD patients with regular alcohol intake, although within the safe thresholds, are at higher risk of liver disease progression, including hepatocellular carcinoma; a detrimental effect of modest alcohol drinking is similarly observed in liver disease of viral etiology. Alcohol intake is also a risk factor for extrahepatic cancers, particularly breast, oral, and pharyngeal cancers, with gender difference and no floor effect, which outweigh the possible beneficial effects on cardiovascular system, also derived from retrospective studies. Finally, the negative effects of the calorie content of alcohol on dietary restriction and weight loss, the pivotal intervention to reduce NAFLD burden, should be considered. In summary, the policy of counseling NAFLD patients for alcohol abstinence should be maintained.

Effect of alcohol consumption on nonalcoholic fatty liver disease

The prevalence of nonalcoholic fatty liver disease (NAFLD) is estimated to be 26.3% among the US population. A subset of this population exhibits an aggressive histological phenotype, nonalcoholic steatohepatitis (NASH) with ≥ stage 2 fibrosis, which may progress to cirrhosis. The definition of NAFLD excludes excessive alcohol intake, which is well known to cause alcoholic liver disease and will not be discussed here. Most NAFLD clinical trials use ~14 drinks per week as the cutoff for excessive alcohol intake. Alcohol consumption below this threshold, which we define as moderate alcohol consumption, is common in the US. According to the 2012 Behavioral Risk Factor Surveillance System (BRFSS), 56% of the US adult population consume alcohol, but only 8.2% report drinking heavily and 18.3% report binge drinking. The American Association for the Study of Liver Diseases (AASLD) Practice Guidance of 2018 states that there are insufficient data to make a recommendation with regard to moderate alcohol consumption in patients with NAFLD, citing a lack of longitudinal studies that examine the impact of moderate alcohol consumption on disease progression and its extrahepatic harms versus benefits, specifically in individuals with established NAFLD. NAFLD prevalence studies have generally noted a negative correlation between modest alcohol consumption and NAFLD. However, prevalence studies have limited application to patients with established NAFLD who present to the clinic. There can also be many confounding factors, because modest alcohol consumption is also negatively associated with some NAFLD risk factors, and those risk factors may not be adequately adjusted for in analyses. The prevalence of NASH with significant fibrosis (≥ F2) is more important because this is the group that is believed to have progressive disease. Thus, cohort studies of disease progression are more important from the patient's standpoint. Because these patients have already developed NAFLD or NASH, their interest lies in their odds of disease progression if they have moderate alcohol consumption compared to abstinence. It is also noteworthy that cardiovascular disease is the most important cause of death among patients with NAFLD. Moderate alcohol consumption has been associated with a reduction in overall mortality, but mostly in cardiovascular mortality. However, this protective effect has not been demonstrated specifically in patients with NAFLD.

31-Year-Old Woman With Jaundice and Abdominal Pain

31-Year-Old Woman With Jaundice and Abdominal Pain

MODEST ALCOHOL CONSUMPTION IS ASSOCIATED WITH FAVORABLE FINDINGS ON ECHOCARDIOGRAPHY

The effects of modest alcohol consumption on cardiovascular structure and function remains unclear. We hypothesized that modest alcohol consumption would be associated with no changes in comparison to non-drinkers. We examined 7,163 individuals undergoing echocardiography and compared findings

Abstract ES8-3: Does breast cancer prevention need an 18th amendment? New evidence on alcohol and breast cancer

Abstract Epidemiological studies have consistently supported an association between alcohol consumption and breast cancer risk for many years. Breast cancer guidelines from many societies, including the American Cancer Society, have also discussed reducing alcohol consumption to help prevent breast cancer. So why aren't more women aware of this association? This talk will review the latest evidence, including more recent mechanistic studies, about the association between alcohol intake and breast cancer as well as newer data about the lack of cardio protective benefit of modest alcohol intake. What evidence do we now have about whether the association with breast cancer risk and outcomes after diagnosis varies by time in life and intensity of drinking patterns? Citation Format: Terry M. Does breast cancer prevention need an 18th amendment? New evidence on alcohol and breast cancer [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr ES8-3.

Effect of alcohol consumption on food energy intake: a systematic review and meta-analysis.

The relationship between alcohol consumption and body weight is complex and inconclusive being potentially mediated by alcohol type, habitual consumption levels and sex differences. Heavy and regular alcohol consumption has been positively correlated with increasing body weight, although it is unclear whether this is due to alcohol consumption per se or to additional energy intake from food. This review explores the effects of alcohol consumption on food energy intake in healthy adults. CINAHL Plus, EMBASE, Medline and PsycINFO were searched through February 2018 for crossover and randomised controlled trials where an alcohol dose was compared with a non-alcohol condition. Study quality was assessed using the Effective Public Health Practice Project tool. A total of twenty-two studies involving 701 participants were included from the 18 427 papers retrieved. Studies consistently demonstrated no compensation for alcoholic beverage energy intake, with dietary energy intake not decreasing due to alcoholic beverage ingestion. Meta-analyses using the random-effects model were conducted on twelve studies and demonstrated that alcoholic beverage consumption significantly increased food energy intake and total energy intake compared with a non-alcoholic comparator by weighted mean differences of 343 (95 % CI 161, 525) and 1072 (95 % CI 820, 1323) kJ, respectively. Generalisability is limited to younger adults (18-37 years), and meta-analyses for some outcomes had substantial statistical heterogeneity or evidence of small-study effects. This review suggests that adults do not compensate appropriately for alcohol energy by eating less, and a relatively modest alcohol dose may lead to an increase in food consumption.