Alcohol consumption in patients with nonalcoholic fatty liver disease: yes, or no?
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SUBMITTER: Protopapas AA
PROVIDER: S-EPMC8276351 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:AimTo examine the association between lifetime alcohol consumption and significant liver disease in type 2 diabetic patients with NAFLD.MethodsA cross-sectional study assessing 151 patients with NAFLD at risk of clinically significant liver disease. NAFLD fibrosis severity was classified by transient elastography; liver stiffness measurements ≥8.2 kPa defined significant fibrosis. Lifetime drinking history classified patients into nondrinkers, light drinkers (always ≤20 g/day), and moderate drinkers (any period with intake >20 g/day).ResultCompared with lifetime nondrinkers, light and moderate drinkers were more likely to be male (p = 0.008) and to be Caucasian (p = 0.007) and to have a history of cigarette smoking (p = 0.000), obstructive sleep apnea (p = 0.003), and self-reported depression (p = 0.003). Moderate drinkers required ≥3 hypoglycemic agents to maintain diabetic control (p = 0.041) and fibrate medication to lower blood triglyceride levels (p = 0.044). Compared to lifetime nondrinkers, light drinkers had 1.79 (95% CI: 0.67-4.82; p = 0.247) and moderate drinkers had 0.91 (95% CI: 0.27-3.10; p = 0.881) times the odds of having liver stiffness measurements ≥8.2 kPa (adjusted for age, gender, and body mass index).ConclusionsIn diabetic patients with NAFLD, light or moderate lifetime alcohol consumption was not significantly associated with liver fibrosis. The impact of lifetime alcohol intake on fibrosis progression and diabetic comorbidities, in particular obstructive sleep apnea and hypertriglyceridemia, requires further investigation.
| S-EPMC5687130 | biostudies-literature
Project description: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.
| S-EPMC6789297 | biostudies-literature
Project description:Background & aimsCardiovascular disease (CVD) is the leading cause of death among patients with nonalcoholic fatty liver disease (NAFLD). Moderate drinking (vs abstinence) is associated with lower risk of CVD in the general population. We assessed whether alcohol use is associated with CVD risk in patients with NAFLD.MethodsWe analyzed data from participants in the Coronary Artery Risk Development in Young Adults longitudinal cohort study of 5115 black and white young adults, 18-30 years old, recruited from 4 cities in the United States from 1985 through 1986. Participants self-reported alcohol use at study entry and then again after 15, 20, and 25 years. At year 25 (2010-2011), participants underwent computed tomography examination of the thorax and abdomen and tissue Doppler echocardiography with myocardial strain measured by speckle tracking. Coronary artery calcification was defined as an Agatston score above 0. NAFLD was defined as liver attenuation <51 Hounsfield Units after exclusions. Drinkers reported 1-21 (men) or 1-14 (women) standard drinks/week at years 15, 20, or 25. Nondrinkers reported no alcohol use at years 15, 20, and 25.ResultsOf the 570 participants with NAFLD (mean age, 50 years; 54% black; 46% female), 332 (58%) were drinkers; significantly higher proportions of drinkers were white, male, and with higher levels of education compared with nondrinkers (P < .05 for all). Higher proportions of drinkers had obesity, diabetes, and metabolic syndrome compared with nondrinkers (P < .01). There was no difference in liver attenuation between groups (P = .12). After multivariable adjustment, there was no association between alcohol use and CVD risk factors (diabetes, hypertension, hyperlipidemia) or subclinical CVD measures (coronary artery calcification, early transmitral velocity/late (atrial) transmitral velocity (E/A) ratio, global longitudinal strain).ConclusionsIn a population-based sample of individuals with NAFLD in midlife, prospectively assessed alcohol use is not associated with significant differences in risk factors for CVD or markers of subclinical CVD. In contrast to general population findings, alcohol use may not reduce the risk of CVD in patients with NAFLD.
| S-EPMC5669829 | biostudies-literature
Project description:Whether moderate alcohol intake is beneficial remains an unsolved issue. Recent studies have suggested that moderate alcohol consumption is associated with beneficial effects related to the prevention of cardiovascular diseases. Moderate alcohol consumption leads to a higher risk of hepatocellular carcinoma in patients with chronic viral liver diseases. However, the effects of moderate alcohol intake in patients with nonalcoholic fatty liver disease are unclear. In this review, we analyzed, from various perspectives, the effect of moderate alcohol consumption in patients with nonalcoholic fatty liver disease. We reviewed four cohort studies and seven cross-sectional studies. The results showed that moderate alcohol consumption was negatively related to the incidence of nonalcoholic steatohepatitis and liver fibrosis. However, moderate alcohol consumption was positively associated with the incidence of hepatocellular carcinoma in patients with nonalcoholic fatty liver disease. The results of the analysis of the relationship between moderate alcohol consumption and the levels of triglycerides, total cholesterol, high-density lipoprotein, and hypertension were diverse. More clinical data are needed to draw a conclusion about the effects of moderate alcohol consumption in patients with nonalcoholic fatty liver disease.
| S-EPMC6529167 | biostudies-literature
Project description:Fatty liver disease constitutes a spectrum of liver diseases which begin with simple steatosis and may progress to advance stages of steatohepatitis, cirrhosis, and hepatocellular carcinoma (HCC). The two main etiologies are-alcohol related fatty liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD). NAFLD is a global health epidemic strongly associated with modern dietary habits and life-style. It is the second most common cause of chronic liver disease in the US after chronic hepatitis C virus (HCV) infection. Approximately 100 million people are affected with this condition in the US alone. Excessive intakes of calories, saturated fat and refined carbohydrates, and sedentary life style have led to explosion of this health epidemic in developing nations as well. ALD is the third most common cause of chronic liver disease in the US. Even though the predominant trigger for onset of steatosis is different in these two conditions, they share common themes in progression from steatosis to the advance stages. Oxidative stress (OS) is considered a very significant contributor to hepatocyte injury in these conditions. Mitochondrial dysfunction contributes to this OS. Role of mitochondrial dysfunction in pathogenesis of fatty liver diseases is emerging but far from completely understood. A better understanding is essential for more effective preventive and therapeutic interventions. Here, we discuss the pathogenesis and therapeutic approaches of NAFLD and ALD from a mitochondrial perspective.
| S-EPMC7792990 | biostudies-literature
Project description:The fungal microbiota plays an important role in the pathogenesis of alcohol-associated liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD). In this study, we aimed to compare changes of the fecal fungal microbiota between patients with ALD and NAFLD and to elucidate patterns in different disease stages between the two conditions. We analyzed fungal internal transcribed spacer 2 (ITS2) sequencing using fecal samples from a cohort of 48 patients with ALD, 78 patients with NAFLD, and 34 controls. The fungal microbiota differed significantly between ALD and NAFLD. The genera Saccharomyces, Kluyveromyces, Scopulariopsis, and the species Candida albicans (C. albicans), Malassezia restricta (M. restricta), Scopulariopsis cordiae (S. cordiae) were significantly increased in patients with ALD, whereas the genera Kazachstania and Mucor were significantly increased in the NAFLD cohort. We identified the fungal signature consisting of Scopulariopsis, Kluyveromyces, M. restricta, and Mucor to have the highest discriminative ability to detect ALD vs NAFLD with an area under the curve (AUC) of 0.93. When stratifying the ALD and NAFLD cohorts by fibrosis severity, the fungal signature with the highest AUC of 0.92 to distinguish ALD F0-F1 vs NAFLD F0-F1 comprised Scopulariopsis, Kluyveromyces, Mucor, M. restricta, and Kazachstania. For more advanced fibrosis stages (F2-F4), the fungal signature composed of Scopulariopsis, Kluyveromyces, Mucor, and M. restricta achieved the highest AUC of 0.99 to differentiate ALD from NAFLD. This is the first study to identify a fungal signature to differentiate two metabolic fatty liver diseases from each other, specifically ALD from NAFLD. This might have clinical utility in unclear cases and might hence help shape treatment approaches. However, larger studies are required to validate this fungal signature in other populations of ALD and NAFLD.
| S-EPMC10841010 | biostudies-literature
Project description:Nonalcoholic fatty liver disease represents a spectrum of pathology that ranges from benign steatosis to potentially-progressive steatohepatitis and affects more than 30% of US adults. Advanced NAFLD is associated with increased morbidity and mortality from cirrhosis, primary liver cancer, cardiovascular disease and extrahepatic cancers. Accurate identification of patients at risk for advanced NAFLD is challenging. The aims of this study were to define the liver gene expression patterns that distinguish mild from advanced NAFLD and to develop a gene expression profile associated with advanced NAFLD. We analyzed total RNA from 72 patients with NAFLD (40 with mild NAFLD, fibrosis stage 0-1 and 32 with advanced NAFLD, fibrosis stage 3-4) and developed a gene profile associated with advanced NAFLD. This dataset is part of the TransQST collection.
2013-08-30 | E-GEOD-49541 | biostudies-arrayexpress
Project description:Background & aimsAlcohol dehydrogenase 1B (ADH1B) is involved in alcohol metabolism. The allele A (ADH1B∗2) of the rs1229984: A>G variant in ADH1B is associated with a higher alcohol metabolizing activity compared to the ancestral allele G (ADH1B∗1). Moderate alcohol consumption is associated with reduced severity of nonalcoholic fatty liver disease (NAFLD), based on histologic analysis, compared with no alcohol consumption. However, it is unclear whether ADH1B∗2 modifies the relationship between moderate alcohol consumption and severity of NAFLD. We examined the association between ADH1B∗2 and moderate alcohol consumption and histologic severity of NAFLD.MethodsWe collected data from 1557 multiethnic adult patients with biopsy-proven NAFLD enrolled into 4 different studies conducted by the Nonalcoholic Steatohepatitis (NASH) Clinical Research Network. Histories of alcohol consumption were obtained from answers to standardized questionnaires. Liver biopsy samples were analyzed by histology and scored centrally according to the NASH Clinical Research Network criteria. We performed covariate adjusted logistic regressions to identify associations between histologic features of NAFLD severity and moderate alcohol consumption and/or ADH1B∗2.ResultsA higher proportion of Asians/Pacific Islanders/Hawaiians carried the ADH1B∗2 allele (86%) than other racial groups (4%-13%). However, the study population comprised mostly non-Hispanic whites (1153 patients, 74%), so the primary analysis focused on this group. Among them, 433 were moderate drinkers and 90 were ADH1B∗2 carriers. After we adjusted for confounders, including alcohol consumption status, ADH1B∗2 was associated with lower frequency of steatohepatitis (odds ratio [OR], 0.52; P < .01) or fibrosis (odds ratio, 0.69; P = .050) compared with ADH1B∗1. Moderate alcohol consumption (g/d) reduced the severity of NAFLD in patients with ADH1B∗1 or ADH1B∗2. However, ADH1B∗2, compared to ADH1B∗1, was associated with a reduced risk of definite NASH (ADH1B∗2: OR, 0.80; P < .01 vs ADH1B∗1: OR, 0.96; P = .036) and a reduced risk of an NAFLD activity score of 4 or higher (ADH1B∗2: OR, 0.83; P = .012 vs ADH1B∗1: OR, 0.96; P = .048) (P < .01 for the difference in the effect of moderate alcohol consumption between alleles). The relationship between body mass index and NAFLD severity was significantly modified by ADH1B∗2, even after we controlled for alcohol consumption.ConclusionsADH1B∗2 reduces the risk of NASH and fibrosis in adults with NAFLD regardless of alcohol consumption status. ADH1B∗2 might modify the association between high body mass index and NAFLD severity.
| S-EPMC7502531 | biostudies-literature
Project description:Nonalcoholic fatty liver disease represents a spectrum of pathology that ranges from benign steatosis to potentially-progressive steatohepatitis and affects more than 30% of US adults. Advanced NAFLD is associated with increased morbidity and mortality from cirrhosis, primary liver cancer, cardiovascular disease and extrahepatic cancers. Accurate identification of patients at risk for advanced NAFLD is challenging. The aims of this study were to define the liver gene expression patterns that distinguish mild from advanced NAFLD and to develop a gene expression profile associated with advanced NAFLD.
2013-08-30 | GSE49541 | GEO
Project description: Not available
| S-EPMC10446130 | biostudies-literature