Nutritional effects of alcoholism

Falck‐Ytter, Yngve; McCullough, Arthur J.

doi:10.1007/s11894-000-0028-6

Cited by 19 publications

(7 citation statements)

References 47 publications

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“…Also, the proven direct hepatotoxic effects of ethanol have undermined the observation that the hepatic disease of alcoholism is due to the contribution of malnutrition to the liver injury of alcoholism and evolution of alcoholic cirrhosis was defined (Zimmerman, 1955). The efficiency of alcohol as a substrate for energy production appears to be influenced by the amount of both alcohol and fat consumption as well as by gender (Falck-Ytter and McCullough, 2000). Frenzer et al (2002) also described the polymorphism in alcoholmetabolizing enzymes, glutathione S-transferases and apolipoprotein E that increases susceptibility to alcohol-induced cirrhosis and chronic pancreatitis.…”

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Alcohol, microbiome, life style influence alcohol and non-alcoholic organ damage

Neuman

French

Zakhari³

et al. 2017

Experimental and Molecular Pathology

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This paper is based upon the "8th Charles Lieber's Satellite Symposium" organized by Manuela G. Neuman at the Research Society on Alcoholism Annual Meeting, on June 25, 2016 at New Orleans, Louisiana, USA. The integrative symposium investigated different aspects of alcohol-induced liver disease (ALD) as well as non-alcohol-induced liver disease (NAFLD) and possible repair. We revealed the basic aspects of alcohol metabolism that may be responsible for the development of liver disease as well as the factors that determine the amount, frequency and which type of alcohol misuse leads to liver and gastrointestinal diseases. We aimed to (1) describe the immuno-pathology of ALD, (2) examine the role of genetics in the development of alcoholic hepatitis (ASH) and NAFLD, (3) propose diagnostic markers of ASH and non-alcoholic steatohepatitis (NASH), (4) examine age and ethnic differences as well as analyze the validity of some models, (5) develop common research tools and biomarkers to study alcohol-induced effects, 6) examine the role of alcohol in oral health and colon and gastrointestinal cancer and (7) focus on factors that aggravate the severity of organ-damage. The present review includes pre-clinical, translational and clinical research that characterizes ALD and NAFLD. Strong clinical and experimental evidence lead to recognition of the key toxic role of alcohol in the pathogenesis of ALD with simple fatty infiltrations and chronic alcoholic hepatitis with hepatic fibrosis or cirrhosis. These latter stages may also be associated with a number of cellular and histological changes, including the presence of Mallory's hyaline, megamitochondria, or perivenular and perisinusoidal fibrosis. Genetic polymorphisms of ethanol metabolizing enzymes and cytochrome p450 (CYP) 2E1 activation may change the severity of ASH and NASH. Other risk factors such as its co-morbidities with chronic viral hepatitis in the presence or absence of human deficiency virus were discussed. Dysregulation of metabolism, as a result of ethanol exposure, in the intestine leads to colon carcinogenesis. The hepatotoxic effects of ethanol undermine the contribution of malnutrition to the liver injury. Dietary interventions such as micro and macronutrients, as well as changes to the microbiota have been suggested. The clinical aspects of NASH, as part of the metabolic syndrome in the aging population, have been presented. The symposium addressed mechanisms and biomarkers of alcohol induced damage to different organs, as well as the role of the microbiome in this dialog. The microbiota regulates and acts as a key element in harmonizing immune responses at intestinal mucosal surfaces. It is known that microbiota is an inducer of proinflammatory T helper 17 cells and regulatory T cells in the intestine. The signals at the sites of inflammation mediate recruitment and differentiation in order to remove inflammatory inducers and promote tissue homeostasis restoration. The change in the intestinal microbiota also influences the change in obesity and regress...

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confidence: 99%

Alcohol, microbiome, life style influence alcohol and non-alcoholic organ damage

Neuman

French

Zakhari³

et al. 2017

Experimental and Molecular Pathology

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“…Accordingly, associated factors like odour, taste, and energy content (calories) can play a role in alcohol consumption, and their contribution has been considered (Kampov‐Polevoy et al . 1999; Falck‐Ytter & McCullough 2000). Another evolutionary aspect derives from the pharmacological interference with the neural substrates of the ‘pleasure’ or ‘reward’ system of the brain (Wise 1996).…”

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confidence: 99%

“…One evolutionary aspect of alcoholism may be an historical association with the food consumption behaviour of frugivor primates, because localization of ripe and decaying fruit via volatilized alcohols, and consumption of nutrients may have adaptive values (Dudley 2000). Accordingly, associated factors like odour, taste, and energy content (calories) can play a role in alcohol consumption, and their contribution has been considered (Kampov-Polevoy et al 1999;Falck-Ytter & McCullough 2000). Another evolutionary aspect derives from the pharmacological interference with the neural substrates of the 'pleasure' or 'reward' system of the brain (Wise 1996).…”

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Strain and sex differences in repeated ethanol treatment‐induced motor activity in quasi‐congenic mice

Sershen

Hashim

Vadász³

2002

Genes Brain and Behavior

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The B6.C quasi-congenic Recombinant QTL Introgression (RQI) strains of the b4i5 series have similar genetic background, but differ in about 5% of their genome from the C57BL/6ByJ (B6) background strain because they carry short chromosome segments introgressed from the BALB/cJ (C) donor strain. These RQI strains were derived from mouse lines selectively bred for high activity of mesencephalic tyrosine hydroxylase (TH/MES), therefore genetic variation in dopamine system-related behaviours, such as ethanol-induced motor activity, can be expected. Males and females of 17 RQI and two progenitor strains were tested for initial motor activity for 15 min after a habituating injection of saline, which was followed by an i.p. injection of saline or ethanol (2 g/kg) and an additional test of motor activity for 30 min. This procedure was repeated during 4 subsequent days. In all strains, the first-day ethanol treatment showed an inhibitory effect. With repetition of the treatment the inhibitory effect decreased, and a stimulatory effect could be observed with significant strain-and sex-dependent variation. Females exhibited higher activity in the saline group than males, and reached an equilibrium of inhibition and stimulation sooner than males with repetition of the ethanol treatment. The highest (Ͼ 25-fold) difference in activity after repeated ethanol treatment was detected between females of the two strains B6.Cb4i5-Alpha4/Vad and B6.Cb4i5-Beta13/Vad. These results firstly suggest that females are more sensitive to repeated ethanol exposure than males, secondly they support the observations that ethanol has both inhibitory and stimulatory effects on motor activity, which are affected by sex, genotype, and repetition of treatment, and thirdly offer new quasi-congenic animal models with highly different responses to ethanol allowing one to more quickly move to gene detection.

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“…A LCOHOL (ETOH) ACCOUNTS for 4 -6% of the average energy intake in most Western countries and is affected by both environmental and inherited biological mechanisms (1,2). As a nutrient, it influences the metabolism of most tissues in the body, with marked effects on glucose (G) homeostasis (3).…”

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Glucose Tolerance during Moderate Alcohol Intake: Insights on Insulin Action from Glucose/Lactate Dynamics

Avogaro

Watanabe

Gottardo

et al. 2002

The Journal of Clinical Endocrinology & Metabolism

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Moderate alcohol (ETOH) intake has been associated with a significant reduction in risk for infarction among general populations. In this study, we assessed the effects of low-dose ETOH (40 g over 3-h period as vodka) on the interaction between glucose (G), insulin, and lactate (L) during the insulin-modified frequently sampled i.v. glucose tolerance test (FSIGT) (0.3 U/kg body weight between 20-25 min) in eight normal volunteers. In the control (C) study, water was administered. An insulin-independent two-compartment model was used to describe G and L kinetics. Insulin sensitivity (S(I)) was significantly higher in the ETOH study than in the C study (2.49 +/- 0.52 vs. 0.92 +/- 0.20 10(-4) min(-1)microU(-1)ml, C vs. ETOH; P = 0.0391). No significant differences were observed in G effectiveness (0.029 +/- 0.004 vs. 0.033 +/- 0.004 min(-1)). Blood L levels were higher during FSIGT when ETOH was administered [area under the curve (AUC), 201 plus minus 16 vs. 123 +/- 23 mmol/liter in 240 min; P = 0.0001]. The dynamic analysis of blood L concentrations showed that ETOH also significantly decreased L clearance (0.0016 +/- 0.0011 vs. 0.0029 +/- 0.0002 min(-1); P = 0.0156), whereas no difference was observed for the fractional conversion of the rate of G disappearance to L (0.0033 +/- 0.0012 vs. 0.0031 +/- 0.0005 min(-1)). ETOH decreased baseline plasma FFA concentration; AUC of FFA was markedly reduced with ETOH (65 +/- 14 vs. 109 plus minus 17 mmol/liter in 240 min; P = 0.0063) and inversely correlated with S(I) (r = 0.693; P = 0.0029). The amount of C-peptide in 240 min as well as the amounts before and after insulin administration were not different between the two tests. We concluded that G and L kinetics derived from FSIGT shows that moderate ETOH intake: 1) improves insulin action; 2) decreases L clearance; and 3) does not affect beta cell function. Because ETOH at moderate doses has a marked antilipolytic action, it might improve insulin action by improving substrate competition. The present findings suggest that moderate alcohol consumption in the diet should not be discouraged.

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Nutritional effects of alcoholism

Cited by 19 publications

References 47 publications

Alcohol, microbiome, life style influence alcohol and non-alcoholic organ damage

Alcohol, microbiome, life style influence alcohol and non-alcoholic organ damage

Strain and sex differences in repeated ethanol treatment‐induced motor activity in quasi‐congenic mice

Glucose Tolerance during Moderate Alcohol Intake: Insights on Insulin Action from Glucose/Lactate Dynamics

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