Global melanoma correlations with obesity, smoking, and alcohol consumption.
Ontology highlight
ABSTRACT:
SUBMITTER: Batta N
PROVIDER: S-EPMC9387903 | biostudies-literature | 2021 Jul-Dec
REPOSITORIES: biostudies-literature
Publications
Global melanoma correlations with obesity, smoking, and alcohol consumption.
Batta Nisha N Shangraw Sarah S Nicklawsky Andrew A Yamauchi Takeshi T Zhai Zili Z Ravindran Menon Dinoop D Gao Dexiang D Dellavalle Robert P RP Fujita Mayumi M
JMIR dermatology 20210701 2
Similar Datasets
Project description:This study aimed to analyze colorectal polyp prevalence associated with health behavior. Data from 1180 Korean men (young adult (YA), aged 40-49; middle age (MA) aged 50-59; old aged (OA), aged 60-79 years) were collected. Health behavior included alcohol consumption, smoking status, and obesity. Obesity was determined using body mass index (BMI) and waist circumference (WC). Odds ratio (OR) was calculated by logistic regression. The prevalence of polyps increased for current smokers by 2.642 times in the YA group, 3.468 times in the MA group, and 3.104 times in the OA group compared to the never-smokers. The OR for WC increased in subjects with obesity by 1.514 in the MA and 1.451 in the OA group compared to normal. The prevalence of three or more polyps increased with WC obesity by 2.3 times in YA, 2.2 times in MA, and 1.9 times in OA compared to normal WC. Therefore, smoking cessation and obesity management may reduce the risk of colorectal polyps.
| S-EPMC7177673 | biostudies-literature
Project description:Recreational alcohol intake is a widespread activity globally and alcohol energy (7 kcal/g) can be a contributing factor to weight gain if not compensated for. Given that both excessive alcohol intake and obesity are of public health interest, the present paper provides an update on the association between alcohol consumption and body weight. In general, recent prospective studies show that light-to-moderate alcohol intake is not associated with adiposity gain while heavy drinking is more consistently related to weight gain. Experimental evidence is also mixed and suggests that moderate intake of alcohol does not lead to weight gain over short follow-up periods. However, many factors can explain the conflicting findings and a better characterization of individuals more likely to gain weight as a result of alcohol consumption is needed. In particular, individuals who frequently drink moderate amounts of alcohol may enjoy a healthier lifestyle in general that may protect them from weight gain. In conclusion, despite the important limitations of current studies, it is reasonable to say that alcohol intake may be a risk factor for obesity in some individuals, likely based on a multitude of factors, some of which are discussed herein.
| S-EPMC4338356 | biostudies-literature
Project description:Background: Tobacco smoking and alcohol consumption have been associated with frailty in observational studies. We sought to examine whether these associations reflect causality using the two-sample Mendelian randomization (MR) design. Methods: We used summary genome-wide association statistics for smoking initiation (N = 2,669,029), alcohol consumption (N = 2,428,851), and the frailty index (FI, N = 175,226) in participants of European ancestry. Both univariable and multivariable MR were performed to comprehensively evaluate the independent effects of smoking and alcohol consumption on the FI, accompanied by multiple sensitivity analyses. Results were verified using lifetime smoking and alcohol use disorder. Reverse direction MR was undertaken to assess the potential for reverse causation. Results: Genetic predisposition to smoking initiation was significantly associated with increased FI (univariable MR: β = 0.345; 95% confidence interval [CI] = 0.316 to 0.374; p = 1.36E-113; multivariable MR: β = 0.219; 95% CI = 0.197 to 0.241; p = 2.44E-83). Genetically predicted alcohol consumption showed a suggestive association with the FI (univariable MR: β = −0.090; 95% CI = −0.151 to −0.029; p = 0.003; multivariable MR β = −0.153; 95% CI = −0.212 to −0.094; p = 2.03E-07), with inconsistent results in sensitivity analyses. In complementary analysis, genetic predicted lifetime smoking, but not alcohol use disorder was associated with the FI. There is no convincing evidence for reverse causation. Conclusion: The present MR study supported smoking as a causal risk factor of frailty. Further research is warranted to investigate whether alcohol consumption has a causal role in frailty.
| S-EPMC9935614 | biostudies-literature
Project description:The aim of this study was to investigate the association of body mass index (BMI), alcohol consumption, and smoking status with the occurrence of Bell's palsy. The Korean National Health Insurance Service-Health Screening Cohort of a ≥ 40-year-old population from 2000-2003 was used. A total of 5,632 Bell's palsy participants were matched with 22,528 control participants in terms of age, sex, income, region of residence, and past medical histories of hypertension, diabetes, and dyslipidemia. Bell's palsy was classified by a history of ≥2 diagnoses with ICD-10 code (G510) and steroid treatment. BMI (kg/m2) was classified as <18.5 (underweight), ≥18.5 to <23 (normal), ≥23 to <25 (overweight), ≥25 to <30 (obese I), and ≥30 (obese II). Alcohol consumption was divided into non-drinkers and those who drank 2-3 times a month, 1-2 times a week, and ≥3 times a week. Smoking status was categorized as current smokers, past smokers, and non-smokers. The odds of obesity, alcohol consumption, and smoking with Bell's palsy were analyzed using logistic regression analysis. BMI showed proportionally positive associations with Bell's palsy (adjusted OR [95% CI] = 0.61 [0.47-0.79] for underweight, 1.16 [1.08-1.26] for normal, 1.24 [1.15-1.33] for obese I, and 1.61 [1.38-1.88] for obese II, P < 0.001). The odds of alcohol consumption with Bell's palsy were 0.90 (95% confidence interval [CI] = 0.82-0.99) for 2-3 times a month, 0.77 (95% CI = 0.69-0.85) for 1-2 times a week, and 0.79 (95% CI = 0.71-0.88) for ≥3 times a week compared to nondrinkers (P < 0.001). Smoking did not show a relationship with the occurrence of Bell's palsy. Obesity was related to the risk of Bell's palsy in the population over 40 years old. On the other hand, alcohol consumption was negatively associated with the occurrence of Bell's palsy.
| S-EPMC7060281 | biostudies-literature
Project description:We investigate whether the serotonin transporter-linked polymorphic region (5HTTLPR), a gene associated with environmental sensitivity, moderates the association between smoking and drinking patterns at adolescents' schools and their corresponding risk for smoking and drinking themselves. Drawing on the school-based design of the National Longitudinal Study of Adolescent Health in conjunction with molecular genetic data for roughly 15,000 respondents (including over 2,000 sibling pairs), we show that adolescents smoke more cigarettes and consume more alcohol when attending schools with elevated rates of tobacco and alcohol use. More important, an individual's susceptibility to school-level patterns of smoking or drinking is conditional on the number of short alleles he or she has in 5HTTLPR. Overall, the findings demonstrate the utility of the differential susceptibility framework for medical sociology by suggesting that health behaviors reflect interactions between genetic factors and the prevalence of these behaviors in a person's context.
| S-EPMC3659161 | biostudies-literature
Project description:BackgroundWhether the positive associations of smoking and alcohol consumption with gastrointestinal diseases are causal is uncertain. We conducted this Mendelian randomization (MR) to comprehensively examine associations of smoking and alcohol consumption with common gastrointestinal diseases.MethodsGenetic variants associated with smoking initiation and alcohol consumption at the genome-wide significance level were selected as instrumental variables. Genetic associations with 24 gastrointestinal diseases were obtained from the UK Biobank, FinnGen study, and other large consortia. Univariable and multivariable MR analyses were conducted to estimate the overall and independent MR associations after mutual adjustment for genetic liability to smoking and alcohol consumption.ResultsGenetic predisposition to smoking initiation was associated with increased risk of 20 of 24 gastrointestinal diseases, including 7 upper gastrointestinal diseases (gastroesophageal reflux, esophageal cancer, gastric ulcer, duodenal ulcer, acute gastritis, chronic gastritis, and gastric cancer), 4 lower gastrointestinal diseases (irritable bowel syndrome, diverticular disease, Crohn's disease, and ulcerative colitis), 8 hepatobiliary and pancreatic diseases (non-alcoholic fatty liver disease, alcoholic liver disease, cirrhosis, liver cancer, cholecystitis, cholelithiasis, and acute and chronic pancreatitis), and acute appendicitis. Fifteen out of 20 associations persisted after adjusting for genetically predicted alcohol consumption. Genetically predicted higher alcohol consumption was associated with increased risk of duodenal ulcer, alcoholic liver disease, cirrhosis, and chronic pancreatitis; however, the association for duodenal ulcer did not remain statistically significant after adjustment for genetic predisposition to smoking initiation.ConclusionsThis study provides MR evidence supporting causal associations of smoking with a broad range of gastrointestinal diseases, whereas alcohol consumption was associated with only a few gastrointestinal diseases.FundingThe Natural Science Fund for Distinguished Young Scholars of Zhejiang Province; National Natural Science Foundation of China; Key Project of Research and Development Plan of Hunan Province; the Swedish Heart Lung Foundation; the Swedish Research Council; the Swedish Cancer Society.
| S-EPMC10017103 | biostudies-literature
Project description:The purpose of this study was to evaluate the relationships of smoking, alcohol consumption, and obesity with thyroid cancer in Korean residents. The Korean National Health Insurance Service-Health Screening Cohort includes individuals ≥ 40 years who were assessed from 2002 to 2013. In total, 4977 thyroid cancer participants were matched with respect to age, sex, income, and region of residence with 19,908 controls at a ratio of 1:4. Crude and adjusted (for the Charlson comorbidity index, smoking status, frequency of alcohol consumption, and obesity) odds ratios (ORs) were analyzed using conditional logistic regression analyses. Additionally, 95% confidence intervals (CIs) were calculated. The adjusted OR of smoking for thyroid cancer was 0.62 (95% CI 0.54-0.72, P < 0.001), and that of alcohol consumption was 0.83 (95% CI 0.75-0.92, P < 0.001). The adjusted ORs of the BMI categories were 1.13 (95% CI 1.05-1.22, P = 0.002) for obese I, and 1.24 (95% CI 1.04-1.47, P = 0.014) for obese II. The ORs of smoking and alcohol consumption were lower, and those of overweight and obesity were higher in thyroid cancer patients than in individuals in the control group.
| S-EPMC7648098 | biostudies-literature
Project description:PurposeTo investigate the role of consumption phenotypes as genetic proxies for alcohol misuse and nicotine dependence.MethodsWe leveraged GWAS data from well-powered studies of consumption, alcohol misuse, and nicotine dependence phenotypes measured in individuals of European ancestry from the UK Biobank (UKB) and other population-based cohorts (largest total N = 263,954), and performed genetic correlations within a medical-center cohort, BioVU (N = 66,915). For alcohol, we used quantitative measures of consumption and misuse via AUDIT from UKB. For smoking, we used cigarettes per day from UKB and non-UKB cohorts comprising the GSCAN consortium, and nicotine dependence via ICD codes from UKB and Fagerström Test for Nicotine Dependence from non-UKB cohorts.ResultsIn a large phenome-wide association study, we show that smoking consumption and dependence phenotypes show similar strongly negatively associations with a plethora of diseases, whereas alcohol consumption shows patterns of genetic association that diverge from those of alcohol misuse.ConclusionsOur study suggests that cigarette smoking consumption, which can be easily measured in the general population, may be good a genetic proxy for nicotine dependence, whereas alcohol consumption is not a direct genetic proxy of alcohol misuse.
| S-EPMC8026738 | biostudies-literature
Project description:BackgroundThe global impact of alcohol consumption on deaths due to cardiomyopathy (CM) has not been quantified to date, even though CM contains a subcategory for alcoholic CM with an effect of heavy drinking over time as the postulated underlying causal mechanism. In this feasibility study, a model to estimate the alcohol-attributable fraction (AAF) of CM deaths based on alcohol exposure measures is proposed.MethodsA two-step model was developed based on aggregate-level data from 95 countries, including the most populous (data from 2013 or last available year). First, the crude mortality rate of alcoholic CM per 1,000,000 adults was predicted using a negative binomial regression based on prevalence of alcohol use disorders (AUD) and adult alcohol per capita consumption (APC) (n = 52 countries). Second, the proportion of alcoholic CM among all CM deaths (i.e., AAF) was predicted using a fractional response probit regression with alcoholic CM crude mortality rate (from Step 1), AUD prevalence, APC per drinker, and Global Burden of Disease region as predictions. Additional models repeated these steps by sex and for the wider Global Burden of Disease study definition of CM.ResultsThere were strong correlations (>0.9) between the crude mortality rate of alcoholic CM and the AAFs, supporting the modeling strategy. In the first step, the population-weighted mean crude mortality rate was estimated at 8.4 alcoholic CM deaths per 1,000,000 (95% CI: 7.4-9.3). In the second step, the global AAFs were estimated at 6.9% (95% CI: 5.4-8.4%). Sex-specific figures suggested a lower AAF among females (2.9%, 95% CI: 2.3-3.4%) as compared to males (8.9%, 95% CI: 7.0-10.7%). Larger deviations between observed and predicted AAFs were found in Eastern Europe and Central Asia.ConclusionsThe model proposed promises to fill the gap to include AAFs for CM into comparative risk assessments in the future. These predictions likely will be underestimates because of the stigma involved in all fully alcohol-attributable conditions and subsequent problems in coding of alcoholic CM deaths.
| S-EPMC5445448 | biostudies-literature
Project description:This article investigates alcohol consumption attributable burden of diseases. The present study considers the overall effect of Human Development Index (HDI), Socio Demographic Index (SDI) and Gross Domestic Product (GDP) for income to measure how these variables impact Global Burden of Diseases (GDB), bringing a different perspective to the results. Data from over 177 countries mainly including European, Asian, North American, South American, African and Australian regions were analysed from 2000 to 2019. A Panel regression technique was applied, and Fixed Effects (FE) and Random Effects (RE) estimations were chosen to derive outcomes of the Hausman test. The findings reflected that alcohol consumption (wine, beer, spirit and other alcohol) has a positive significant relationship with the Global Burden of Diseases (GBD) globally and in the African continent excluding North America and South America. Human Development Index (HDI) have a negative impact on GBD on all countries. Particularly HDI have a negative impact on GBD in African continent except other continents. Also, in the African continent and globally, GBD has a significant positive and in Europe, a significant negative impact on the Socio Demographic Index (SDI). The findings demonstrate the overall picture of the impact of alcohol consumption and other variables on GBD and provide suggestions on how these variables should be tackled in the future to reduce GBD. This is the initial empirical study that investigates the impact of alcohol consumption, analysing the combined effect of HDI, SDI and income on the GBD of continent wise and globally.
| S-EPMC9333294 | biostudies-literature