Abstention Group Research Articles

Mediterranean Alcohol-Drinking Patterns and All-Cause Mortality in Women More Than 55 Years Old and Men More Than 50 Years Old in the "Seguimiento Universidad de Navarra" (SUN) Cohort.

Most of the available epidemiological evidence on alcohol and chronic disease agrees on recommending alcohol abstention to young people, but some controversy exists about the most appropriate recommendation for alcohol abstention for people of older ages. A growing body of evidence suggests that the pattern of alcohol consumption is likely to be a strong effect modifier. The Mediterranean Alcohol Drinking Pattern (MADP) represents a score integrating several dimensions of drinking patterns (moderation, preference for red wine, drinking with meals, and avoiding binge drinking). Our aim was to clarify this issue and provide more precise recommendations on alcohol consumption. We prospectively followed-up 2226 participants (men older than 50 years and women older than 55 years at baseline) in the Seguimiento Universidad de Navarra (SUN) cohort. We classified participants into three categories of adherence to the MADP score (low, moderate, and high), and we added a fourth category for abstainers. Cox regression models estimated multivariable-adjusted hazard ratios (HR) of all-cause death and 95% confidence intervals (CI) using low MADP adherence as the reference category. The strongest reduction in risk of mortality was observed for those with high adherence to the MADP, with an HR of 0.54 (95% CI: 0.37-0.80). The moderate adherence group (HR = 0.65, 95% CI: 0.44-0.96) and the abstention group (HR = 0.60, 95% CI: 0.36-0.98) also exhibited lower risks of mortality than the low MADP adherence group. based on the available evidence, a public health message can be provided to people older than 50 years as follows: among those who drink alcohol, high adherence to the MADP score could substantially reduce their risk of all-cause mortality.

Similarity Measures between Temporal Complex Intuitionistic Fuzzy Sets and Application in Pattern Recognition and Medical Diagnosis

This work addresses the issue of similarity measures between two temporal complex Atanassov’s intuitionistic fuzzy sets, many measures of similarity between complex Atanassov’s intuitionistic fuzzy sets. What was proposed before did not consider the abstention group influence, which may lead to counterintuitive results in some cases. A new structure of temporal complex Atanassov’s intuitionistic fuzzy sets is obtained. This set is formally generalized from a conventional Atanassov’s intuitionistic complex fuzzy sets. Here we analyze the limitations of the existing similarity measures. Then, a new similarity measure of temporal complex Atanassov’s intuitionistic fuzzy sets is proposed and several numeric examples are given to demonstrate the validity of the proposed measure. Finally, the proposed similarity measure is applied to pattern recognition and medical diagnosis.

A New Similarity Measure of Intuitionistic Fuzzy Sets Considering Abstention Group Influence and Its Applications

AbstractThe issue of similarity measures of intuitionistic fuzzy sets (IFSs) is considered in this paper. Many existing similarity measures for two IFSs fail to take the abstention group influence into consideration and may lead to counterintuitive results in some cases. To deal with the problem, this paper first discusses the limitations of the existing similarity measures by some numerical examples, then, by considering the influence of abstention group, a new similarity measure of intuitionistic fuzzy sets is proposed, and the same numerical examples are given to demonstrate the validity of the proposed measure. Finally, the proposed similarity measure is applied to pattern recognition, multicriteria group decision making, and medical diagnosis.

Ascorbic acid supplementation enhances recovery from ethanol induced inhibition of Leydig cell steroidogenesis than abstention in male guinea pigs

The impact of ascorbic acid supplementation against ethanol induced Leydig cell toxicity was studied in guinea pigs. Male guinea pigs were exposed to ethanol (4g/kgb.wt.) for 90 days. After 90 days, ethanol administration was completely stopped and animals in the ethanol group were divided into abstention group and ascorbic acid supplemented group (25mg/100gb.wt.) and those in control group were maintained as control and control+ascorbic acid group. Ethanol administration reduced the serum testosterone and LH (luteinising hormone) levels and elevated estradiol levels. Cholesterol levels in Leydig cell were increased whereas the mRNA and protein expressions of StAR (steroidogenic acute regulatory) protein, cytochrome P450scc (cytochrome p450side chain cleavage enzyme), 3β-HSD (3β-hydroxysteroid dehydrogenase), 17β-HSD (17β-hydroxysteroid dehydrogenase) and LH receptor were drastically reduced. Administration of ascorbic acid resulted in alteration of all these parameters indicating enhanced recovery from ethanol induced inhibition of Leydig cell steroidogenesis. Although abstention could also reduce the inhibition of steroidogenesis, this was lesser in comparison with ascorbic acid supplemented group.

Ascorbic acid is superior to silymarin in the recovery of ethanol-induced inflammatory reactions in hepatocytes of guinea pigs

Both oxidative stress and inflammatory reactions play a major role in alcoholic liver fibrosis. We evaluated the efficacy of ascorbic acid (AA) and silymarin in the regression of alcohol-induced inflammation in hepatocytes of guinea pigs (Cavia porcellus). Animals were administered with ethanol at a daily dose of 4 g/kg body weight (b.wt) for 90 days. On the ninety-first day, ethanol administration was stopped and animals were divided into alcohol abstention group and silymarin- (25 mg/100 g b.wt) and AA- (25 mg/100 g b.wt) supplemented groups and maintained for 30 days. There was a significant increase in the activities of alanine aminotransferase, aspartate aminotransferase, and γ-glutamyl transpeptidase in the serum of the ethanol group. The intracellular reactive oxygen species (ROS) and expressions of cytochrome P4502E1 and nuclear factor κB1, tumor necrosis factor-α, and transforming growth factor-β(1) in hepatocytes were significantly increased in ethanol group. The fibrotic markers α-smooth muscle actin and α(1)(I) collagen and activity of cytotoxicity marker caspase-3 were significantly increased and AA content was significantly reduced in hepatocytes of alcohol-treated guinea pigs. But the AA and silymarin supplementation significantly reduced these changes in comparison with alcohol abstention group. AA could induce greater reduction of inflammatory and fibrotic markers in hepatocytes than silymarin. This indicates that AA is superior to silymarin in inhibiting intracellular ROS generation and thereby reducing the ethanol-induced inflammation in hepatocytes.

Ascorbic acid supplementation causes faster restoration of reduced glutathione content in the regression of alcohol-induced hepatotoxicity in male guinea pigs

Alcoholic liver disease is caused mainly by free radicals. Ascorbic acid (AA) and glutathione (GSH) are the major water-soluble antioxidants in the liver. The impact of AA supplementation on GSH, AA and activities of GSH-dependent enzymes in alcoholic guinea pigs was studied and was compared with alcohol abstention. Guinea pigs were administered ethanol at a dose of 4 g/kg body weight (b.wt)/day for 90 days. After 90 days, alcohol administration was stopped and one-half of the ethanol-treated animals were supplemented with AA (25 mg/100 g b.wt) for 30 days and the other half was maintained as the abstention group. There was a significant increase in the activities of alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transpeptidase in the serum of the ethanol group. In addition, a significant decrease in the GSH content, activities of GSH peroxidase, GSH reductase, and increased activity of GSH-S-transferase were observed in the liver of the ethanol group. Histopathological analysis and triglycerides content in the liver of the ethanol group showed induction of steatosis. But AA supplementation and abstention altered the changes caused by ethanol. However, maximum protective effect was observed in the AA-supplemented group indicating the ameliorative effect of AA in the liver.

Ascorbic acid supplementation down-regulates the alcohol induced oxidative stress, hepatic stellate cell activation, cytotoxicity and mRNA levels of selected fibrotic genes in guinea pigs

Both oxidative stress and endotoxins mediated immunological reactions play a major role in the progression of alcoholic hepatic fibrosis. Ascorbic acid has been reported to reduce alcohol-induced toxicity and ascorbic acid levels are reduced in alcoholics. Hence, we investigated the hepatoprotective action of ascorbic acid in the reversal of alcohol-induced hepatic fibrosis in male guinea pigs (n = 36), and it was compared with the animals abstenting from alcohol treatment. In comparison with the alcohol abstention group, there was a reduction in the activities of toxicity markers and levels of lipid and protein peroxidation products, expression of α-SMA, caspase-3 activity and mRNA levels of CYP2E1, TGF-β1, TNF-α and α1(I) collagen in liver of the ascorbic acid-supplemented group. The ascorbic acid content in liver was significantly reduced in the alcohol-treated guinea pigs. But it was reversed to normal level in the ascorbic acid-supplemented group. The anti-fibrotic action of ascorbic acid in the rapid regression of alcoholic liver fibrosis may be attributed to decrease in the oxidative stress, hepatic stellate cells activation, cytotoxicity and mRNA expression of fibrotic genes CYP2E1, TGF-β1, TNF-α and α1 (I) collagen in hepatic tissues.

Comparative Study of the Efficacy of Ascorbic Acid, Quercetin, and Thiamine for Reversing Ethanol-Induced Toxicity

This study compares the curative effect of three antioxidants-ascorbic acid, quercetin, and thiamine-on ethanol-induced toxicity in rats. Administration of ethanol at a dose of 4 g/kg of body weight/day for 90 days initiated chronic alcohol-induced oxidative stress as shown by increased malondialdehyde level and DNA fragmentation in liver and brain. Ethanol administration also led to a decrease in DNA content. Activities of toxicity marker enzymes-alanine aminotransferase, aspartate aminotransferase, and γ-glutamyltranspeptidase-in liver and serum increased progressively upon ethanol administration. After ethanol administration for 90 days, the efficacy of antioxidant treatment of the alcohol-induced toxicity was studied by supplementing ascorbic acid (200 mg/100 g of body weight/day), quercetin (50 mg/kg of body weight/day), and thiamine (25 mg/kg of body weight/day) for 30 days. These groups were compared with the abstention group (not treated with ethanol). All the alterations induced by alcohol were reduced significantly by the supplementation of antioxidants and also with abstention. The regression by antioxidants was greater that of abstention. Antioxidants significantly reduced the oxidative stress induced by ethanol intoxication, increased membrane integrity, and also increased organ regeneration. Ascorbic acid was shown to be more effective than quercetin and thiamine in treating both hepatotoxicity and neurotoxicity induced by alcohol administration. This may be due to the higher antioxidant potential of ascorbic acid in physiological conditions.

Protective effect of quercetin in the regression of ethanol-induced hepatotoxicity

This study examined the protective effects of quercetin on chronic ethanol-induced liver injury. Rats were treated with ethanol at a dose of 4 g/100 g/day for 90 days. After ethanol intoxication, levels of serum amino transferases were significantly elevated. Decreased activity of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase was also observed on ethanol administration. Increased amounts of lipid peroxidation products viz. hydroperoxides, conjugated dienes and malodialdehyde were observed on ethanol intoxication. Ethanol administration resulted in significant decrease in liver glutathione content. After 90 days, the control animals were divided into two groups, the control group and the control+quercetin group. Ethanol-treated group was divided into two groups, abstention group and quercetin-supplemented group. After 30 days, the animals were sacrificed and various biochemical parameters were analyzed. The changes in enzyme activities as well as levels of lipid peroxidation products were reversed to a certain extent by quercetin. Quercetin supplementation resulted in increase of glutathione content to a significant level compared to normal abstention group. Quercetin supplemented group showed a faster recovery than abstention group. This shows the protective effect of quercetin against chronic ethanol induced hepatotoxicity. Histopathological study is also in line with these results.

Oxidative DNA Damage is Induced by Chronic Cigarette Smoking, but Repaired by Abstention

The association of chronic cigarette smoking and abstention with oxidative DNA damage was studied. The serum level of an oxidative DNA damage marker, 8-hydroxy-2′-deoxyguanosine (8-OHdG), was measured in 20 healthy male smokers and 8 healthy male non-smokers. The 8-OHdG level was significantly higher in the smokers than in the non-smokers (0.22 ± 0.05 vs. 0.07 ± 0.02 ng/ml, p < 0.001). Ten of 20 smokers abstained from smoking for 4 weeks. Their 8-OHdG levels were significantly reduced by the smoking abstention (0.27 ± 0.05 to 0.14 ± 0.02 ng/ml, p < 0.001). The remaining 10 not only abstained from smoking, but also received 2g /day of oral vitamin C. Their 8-OHdG levels were also significantly reduced (0.27 ± 0.05 to 0.13 ± 0.02 ng/ml, p < 0.001). However, there was no significant difference in the serial changes in 8-OHdG level between the smoking abstention group and the smoking abstention with vitamin C supplementation group. These results suggest that chronic cigarette smoking enhanced oxidative DNA damage, but the damage was repaired by smoking abstention, and that vitamin C supplementation might not enhance the repair. In light of the DNA damage, smoking abstention should be encouraged.

The Effect of Cessation and Resumption of Moderate Alcohol Intake on Serum High-Density-Lipoprotein Subfractions

High-density lipoproteins (HDL) in plasma may be divided into two subfractions: less dense HDL2, the concentration of which appears to be negatively associated with coronary heart disease, and more dense HDL3, which is reportedly unrelated to coronary disease. Alcohol consumption correlates with both reduced coronary heart disease and increased plasma HDL cholesterol concentrations; however, the relation of moderate alcohol intake to HDL2 and HDL3 is obscure. To study the effect of alcohol on these HDL subfractions, we randomly assigned 24 men who were moderate drinkers to an abstention group (n = 12) or a control drinking group (n = 12). After six weeks, concentrations of HDL cholesterol and HDL3 mass were decreased in abstainers but not in drinkers (P less than or equal to 0.05), whereas HDL2 mass was unchanged. Resumption of drinking increased the levels of HDL cholesterol and HDL3 mass (P less than or equal to 0.05) without affecting HDL2 mass. These data suggest that the association of alcohol with coronary disease is not mediated by increases in plasma HDL2 levels. Furthermore, the HDL3 fraction may not be "inert" with respect to coronary heart disease, or the association of alcohol with coronary disease may operate through mechanisms unrelated to HDL.