Capsaicin Reduces Ethanol Consumption in C57BL/6 but not DBA/2 Mice

Rise in oral cancer risk factors associated with the COVID-19 pandemic mandates a more diligent approach to oral cancer screening and treatment

AHA Science Advisory: Wine and your heart: a science advisory for healthcare professionals from the Nutrition Committee, Council on Epidemiology and Prevention, and Council on Cardiovascular Nursing of the American Heart Association.

Angiotensin-Converting Enzyme Inhibitors and Risk of Esophageal and Gastric Cancer: A Nested Case-Control Study

For the purpose of investigating the determinants of preference for alcohol, it would be advantageous to use a procedure in which the subjects had concurrent access to alcohol and an isocaloric food. However, in widely used animal models, the introduction of a weak sucrose solution markedly reduced alcohol consumption. In contrast, when alcohol was sweetened, rats defended high baseline levels of alcohol intake despite access to chow, 10% sucrose, and increases in body weight that markedly reduced food consumption. Under these conditions, certain pharmacological treatments selectively reduced alcohol consumption. The present experiment further tests the generality of the contrast between food and sweetened alcohol consumption in rats. To test if rats will defend baseline levels of alcohol consumption when (1) the competing reinforcer is an isocaloric, preferred food and (2) when the cost of defending alcohol entails a decrease in food consumption as well as an increase in response output. The rats had access to a 10% alcohol plus 0.25% saccharin solution and an isocaloric, 14.8% Polycose solution in a two-lever, choice procedure. In the initial condition, the response requirement for each drink was set at five responses (variable-ratio 5); in subsequent conditions the variable-ratio values were increased to 7.5, 10, 15, and 30 responses. In the initial condition, the rats drank twice as much Polycose as alcohol. However, with increases in the variable-ratio requirements, Polycose consumption systematically decreased, whereas sweetened alcohol consumption remained at its baseline level or above in all but the variable-ratio 30 condition. Rats defended baseline alcohol consumption but not baseline food consumption. As alcohol and food consumption can be dissociated in humans, research on the mechanisms that mediate alcohol regulated preference in rats may shed light on the mechanisms that control human alcohol consumption.

This prospective study was performed in order to investigate the effect of baseline body mass index (BMI), BMI changes, baseline alcohol consumption, and changes in alcohol consumption on liver enzyme activity. This study population consisted of 6846 male workers in a steel manufacturing company who had undergone health examinations in 1994 and 1998. The risk for elevated both aspartate aminotransferase (AST) and alanine aminotransferase (ALT) values over the four years increased with the baseline BMI and BMI changes, but not with alcohol consumption. Compared with the subject BMI < 20, the adjusted odds ratios (OR) for those with baseline BMI 20-21.9, 22-24.9, 25- were 1.2, 1.6, 1.7 in AST and 1.4, 2.4, 2.8 in ALT, respectively. Compared with subjects who either lost or maintained their weight, the adjusted OR for men with slight, moderate, and heavy weight gain were 1.7, 2.6, 6.8 in AST and 2.4, 3.9, 11.3 in ALT, respectively. However gamma-glutamyl transferase (GGT) was associated with BMI changes and baseline alcohol consumption, not with baseline BMI and changes in alcohol consumption. Compared with subjects who lost or maintained weight, the adjusted OR for men with slight, moderate, and heavy weight gain were 2.4, 4.4 and 8.5, respectively. In comparison with non-drinkers, the adjusted OR for light, moderate and heavy drinkers were 1.8, 2.1 and 5.8, respectively. These data suggest that body weight, rather than alcohol consumption, may be the major factor in determining the serum level of liver enzymes. Even when body weight was not generally considered to be overweight, slight to moderate gains in weight were associated with increases in serum liver enzymes.

Higher susceptibility to sunburn is associated with decreased plasma glutamine and increased plasma glutamate levels among US women: An analysis of the Nurses' Health Study I and II

Background and Purpose-The association of light to moderate alcohol consumption with risk of ischemic stroke remains uncertain, as are the roles of potentially mediating factors and modification by apolipoprotein E (apoE) genotype. Methods-We studied the prospective association of alcohol consumption and risk of ischemic stroke among 4410 participants free of cardiovascular disease at baseline in the Cardiovascular Health Study, a population-based cohort study of older adults from 4 US communities. Participants reported their consumption of alcoholic beverages yearly. Results-During an average follow-up period of 9.2 years, 434 cases of incident ischemic stroke occurred. Compared with long-term abstainers, the multivariate relative risks of ischemic stroke were 0.85 (95% CI, 0.63 to 1.13), 0.75 (95% CI, 0.53 to 1.06), 0.82 (95% CI, 0.51 to 1.30), and 1.03 (95% CI, 0.68 to 1.57) among consumers of 1, 1 to 6, 7 to 13, and 14 drinks per week (P quadratic trend 0.06). ApoE genotype appeared to modify the alcohol-ischemic stroke relationship (P interaction 0.08), with generally lower risks among drinkers than abstainers in apoE4-negative participants but higher risks among drinkers than abstainers among apoE4-positive participants. We could not identify candidate mediators among lipid, inflammatory, and prothrombotic factors. Conclusions-In this study of older adults, the association of alcohol use and risk of ischemic stroke was U-shaped, with modestly lower risk among consumers of 1 to 6 drinks per week. However, apoE genotype may modify this association, and even moderate alcohol intake may be associated with an increased risk of ischemic stroke among apoE4-positive older adults. (Stroke.

Background: Liver cancer is a significant disease burden, with metabolic factors potentially influencing its risk. Diabetics, due to metabolic abnormalities, may be more sensitive to environmental exposures. Beverages like tea and alcohol could impact liver cancer risk and may influence prevention in diabetics. Methods: This study included 30,289 diabetics and 482,292 non-diabetics aged 30–79 years from the China Kadoorie Biobank. Baseline alcohol and tea consumption during the past year was collected through questionnaires, including frequency, amount, duration, and types. Incident liver cancer cases were identified from the national health insurance system and local disease registries. Cox proportional hazards regression models estimated hazard ratios (HRs) and 95% confidence intervals (CIs). Results: During a median follow-up of 9.6 years for diabetics and 10.1 years for non-diabetics, 193 (0.69 cases/1000 person-years) and 398 (0.45 cases/1000 person-years) incident liver cancer cases were documented, respectively. Weekly alcohol consumption was associated with higher liver cancer risk in both groups, stronger in diabetics (HR = 1.62; 95% CI: 1.12, 2.34) than in non-diabetics (HR = 1.20, 95% CI: 1.07, 1.35). Among diabetics, the risk was higher in some weekly alcohol consumption subgroups: high-level intake (HR = 2.21; 95% CI: 1.28, 3.80), ≥30 years (HR = 1.70; 95% CI: 1.06, 2.71), or spirit (≥50% alcohol) alcohol-specific consumption (HR = 1.91; 95% CI: 1.20, 3.04), and these associations were stronger than those in non-diabetics. For weekly tea consumption, low-level intake (HR = 0.82; 95% CI: 0.68, 0.99), <10 years (HR = 0.74; 95% CI: 0.58, 0.93), 10–29 years (HR = 0.84; 95% CI: 0.71, 0.99), and green tea-specific consumption (HR = 0.86; 95% CI: 0.75, 0.98) were associated with reduced liver cancer risk in non-diabetics. However, these associations were not significant in those with diabetes. Conclusions: Weekly alcohol consumption is significantly associated with an increased risk of liver cancer, especially in diabetics, while tea consumption appears to lower risk only in non-diabetics, highlighting the need for alcohol reduction in diabetics.

Sex differences and the lack of effects of chemogenetic manipulation of pro-opiomelanocortin (POMC) neurons on alcohol consumption in male and female mice

Alcoholic Liver Disease: Pathogenesis and New Therapeutic Targets

In order to describe the relation between snoring, cardiovascular risk factors, metabolic factors and sympathetitic activity, 804 70-year-old males and females were classified according to snoring habits and life-style factors (alcohol and tobacco consumption), blood pressure, body mass index (BMI), plasma lipids (triglycerides, cholesterol, high density lipoprotein), plasma catecholamines (epinephrine, norepinephrine), fasting blood glucose and glucose tolerance test (1 gram glucose per kg body weight given and blood glucose was measured 1 and 2 hours thereafter) were evaluated in all participants. Self-reported snoring was associated with gender (males showed higher prevalence than females, p < 0.05), alcohol consumption (p < 0.01), BMI (p < 0.001), systolic (p < 0.01) and diastolic (p < 0.05) blood pressure, glucose tolerance test (p < 0.01), plasma norepinephrine (p < 0.05) and partly with tobacco consumption (p = 0.08). No associations were found between snoring and fasting glucose, plasma lipids, plasma epinephrine or in the use of antihypertensive medication. In multivariate analysis, with forced entry of gender, BMI, physical activity, alcohol and tobacco consumption, the relation between snoring and blood pressure ceased; only systolic blood pressure was associated with snoring (p < 0.05). Snoring was still associated with plasma norepinephrine (p < 0.001) and abnormal glucose tolerance (p < 0.001). We conclude that, in a 70-year-old population, snoring is associated with gender, BMI and alcohol consumption. Snores showed higher plasma norepinephrine and abnormal glucose tolerance.

Combined alcoholic and non-alcoholic steatohepatitis.

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.

Stopping smoking results in weight gain. Avoidance of alcohol is often advocated to reduce cues to smoking, but the effect of alcohol consumption on body weight is unclear. We used regression models to examine weight change by baseline alcohol consumption in quitting and continuing smokers. Weight was measured at baseline and at 8 years, and weekly alcohol consumption was reported at baseline in participants from the Oxfordshire general practices nicotine patch/placebo trial. Of 698 smokers attempting to stop smoking, 85 were abstinent for 8 years and 613 continued to smoke. The association between baseline alcohol consumption and weight change depended upon smoking status (p for interaction = .019). In smokers, there was no association with weight change, 0.005 (95% CI: -0.037 to 0.056) kg per UK unit (U) (8 g of ethanol) consumed each week. This was unmodified by gender and baseline body mass index (BMI). In quitters, there was a negative association with weight change, -0.174 (95% CI: -0.315 to -0.034) kg per U consumed each week (unmodified by gender and baseline BMI). Quitters who consumed 14 U (112 g ethanol) a week weighed a mean 2.4 kg less than quitters who did not drink. Quitting smokers who drink more alcohol appear to gain less weight after quitting than those who do not drink. This is consistent across studies, it may be accounted for by unmeasured confounders or it may be that alcohol reduces weight gain. If alcohol reduces weight gain, the advice for quitting smokers must balance the benefits and hazards of alcohol consumption. However, there is currently insufficient evidence to advise quitters who drink little or no alcohol to increase consumption.

ContextReduced insulin sensitivity is one of the traditional risk factors for chronic diseases such as type 2 diabetes. Reduced insulin sensitivity leads to insulin resistance, which in turn can lead to the development of type 2 diabetes. Few studies have examined factors such as blood pressure, tobacco and alcohol consumption that influence changes in insulin sensitivity over time especially among young adults.PurposeTo examine temporal changes in insulin sensitivity in young adults (18-30 years of age at baseline) over a period of 20 years by taking into account the effects of tobacco and alcohol consumptions at baseline. In other words, the purpose of the present study is to examine if baseline tobacco and alcohol consumptions can be used in predicting lowered insulin sensitivity.MethodThis is a retrospective study using data collected by the Coronary Artery Risk Development in Young Adults (CARDIA) study from the National Heart, Lung, and Blood Institute. Participants were enrolled into the study in 1985 (baseline) and followed up to 2005. Insulin sensitivity, measured by the quantitative insulin sensitivity check index (QUICKI), was recorded at baseline and 20 years later, in 2005. The number of participants included in the study was 3,547. The original study included a total of 5,112 participants at baseline. Of these, 54.48% were female, and 45.52% were male; 45.31% were 18 to 24 years of age, and 54.69% were 25 to 30 years of age. Ordinal logistic regression was used to assess changes in insulin sensitivity.Changes in insulin sensitivity from baseline were calculated and grouped into three categories (more than 15%, more than 8.5% to at most 15%, and at most 8.5%), which provided the basis for employing ordinal logistic regression to assess changes in insulin sensitivity. The effects of alcohol and smoking consumption at baseline on the change in insulin sensitivity were accounted for by including these variables in the model.ResultsDaily alcohol consumption (ml/day) at baseline was not associated with changes in insulin sensitivity (OR = 0.998, 95% CI 0.995-1.001), while the number of cigarettes consumed per day at baseline was statistically significantly associated with changes in insulin sensitivity (OR = 1.016, 95% CI 1.007-1.025). Covariates such as age (OR = 1.05, 95% CI 1.031-1.071), mean arterial blood pressure (OR = 0.986, 95% CI 0.977-0.994), body-mass index (OR = 0.951, 95% CI 0.936-0.965), race (OR = 0.840, 95% CI 0.735-0.960), and sex (OR = 0.561, 95% CI 0.483-0.652) were significantly associated with changes in insulin sensitivity.ConclusionAfter adjusting for relevant covariates, the daily tobacco consumption at baseline was independently associated with changes in insulin sensitivity. But we were not able to replicate the association between daily alcohol consumption at baseline and changes in insulin resistance reported by other studies. Further studies in different populations and settings are warranted to examine the association between alcohol consumption and changes in insulin resistance.