Recently the cases after drinking are increasing, but the systematic studys on ethanol content in vivo and correlative problems are still absent. According to the measured results of ethanol content in vivo, ethanol metabolic distributed rules, mechanisms of ethanol toxicological effect and its production in vivo, this study analysed systematically the time after drinking, total quantity of absorbed ethanol, psychological situations, behavioral dominated ability, death causes and manners in order to find out the implied forensic medical information and provide the reference for colleague.
Alcohol Drinking/metabolism* ; Alcohol-Induced Disorders ; Ethanol/metabolism* ; Forensic Medicine ; Humans ; Postmortem Changes ; Substance Abuse Detection/methods* ; Time Factors

Alcohol Drinking ; adverse effects ; Fatty Liver ; metabolism ; physiopathology ; Fatty Liver, Alcoholic ; metabolism ; physiopathology ; Female ; Humans ; Male

Alcohol Drinking ; adverse effects ; Ethanol ; adverse effects ; metabolism ; Humans ; Liver Diseases, Alcoholic ; immunology ; physiopathology

Alcohol consumption is a serious health issue in Korea in terms of the amount consumed and the behavior related to its consumption. Aldehyde dehydrogenase 2 (ALDH2) is a key enzyme in alcohol metabolism that degrades acetaldehyde to nontoxic acetic acid. The enzyme is coded by the ALDH2 gene, which is commonly polymorphic in East Asian populations. A point mutation in the ALDH2 gene (the rs671 allele) yields an inactive form of ALDH2 that causes acetaldehyde accumulation in the body after alcohol consumption, thereby inhibiting normal alcohol metabolism. Individuals who are homozygous for polymorphism in ALDH2 tend to refrain from drinking alcohol, decreasing their chances of developing alcoholism and exposure to the associated risks. Mendelian randomization (MR) studies have demonstrated that alcohol consumption predicted by ALDH2 genotype is causally related to cardiovascular risks. Moreover, recent MR studies suggest that the ALDH2 variant has mechanistic effects on some disease outcomes or mortality through increased blood levels of acetaldehyde, showing differences therein between heterozygotes (ALDH2*2*2) and homozygotes (ALDH2*1*2) in those who consume alcohol. Accordingly, consideration of ALDH2 genotype in alcohol prevention programs is warranted. In conclusion, strategies that incorporate genetic information and provide an evidential basis from which to help people make informed decisions on alcohol consumption are urgently required.
Acetaldehyde ; Acetic Acid ; Alcohol Drinking* ; Alcoholism ; Aldehyde Dehydrogenase* ; Asian Continental Ancestry Group ; Drinking ; Genotype ; Heterozygote ; Homozygote ; Humans ; Korea* ; Mendelian Randomization Analysis ; Metabolism ; Mortality ; Point Mutation ; Random Allocation

Alcohol-induced asthma is defined as exacerbation of asthmatic symptoms after drinking alcoholic beverages. This phenomenon is rare in Caucasians and is more specific to Asians. It has been observed among 50% of Japanese asthmatic patients and genetic predisposition in acetal-dehyde metabolism is thought to be a main factor in alcohol-induced asthma. Although the genetic predisposition of acetaldehyde metabolism in Koreans may be similar to the Japanese, alcohol-induced asthma has not been reported in Korea. We experienced two cases of alcohol-induced asthma which were confirmed by oral ethanol provocation test. In the first case, a 60-year-old male asthma patient presenting a recurrent episode of wheezing and dyspnea after alcohol consumption visited our clinic. After an oral challenge with 300ml of 10% ethanol solution dissolved in 5% glucose solution, dyspnea and wheezing episode were reproduced and 23% decrease in FEV1 compared to basal level was also shown at 20 minutes after ingestion. In the second case, a 32-year-old female asthma patient was presented with the same symptoms. After oral challenge, dyspnea and wheezing episode were reproduced and 30% decrease in FEV1 compared to basal level was shown at 60 minutes after ingestion. Short acting bronchodilator was applied and 21% increase in FEV1 resulted. They were instructed to avoid alcohol consumption with good results.
Acetaldehyde ; Adult ; Alcohol Drinking ; Alcoholic Beverages ; Asian Continental Ancestry Group ; Asthma* ; Drinking ; Dyspnea ; Eating ; Ethanol ; Female ; Genetic Predisposition to Disease ; Glucose ; Humans ; Korea ; Male ; Metabolism ; Middle Aged ; Respiratory Sounds

Objective To understand the prevalence and metabolic abnormalities of fatty liver disease among adults in Mianyang City,Sichuan Province,and to analyze their influencing factors.Methods Totally 294 603 adults aged 18 years and older were enrolled by using a multi-stage stratified random sampling method in Mianyang City from November 1,2014 to September 30,2015.Fatty liver was diagnosed by abdominal ultrasound.The general demographic characteristics,smoking history,drinking history,and history of chronic disease were collected through questionnaires.Meanwhile,10 217 subjects were randomly selected for biochemical tests[fasting plasma gluose(FPG),triacylglycerol(TG),total cholesterol(TC),and alanine aminotransferase(ALT)].Results Of these 294 603 subjects,17 105(5.81%)had fatty liver.After having been age-adjusted based on the results of the sixth national census in 2010,the standardized prevalence was 5.32%.The prevalence was significantly higher in males(6.76%;standardized prevalence:7.24%)than in females(5.09%;standardized prevalence:4.08%)(=365.814,<0.001)。The prevalence of fatty liver disease was significantly higher in people with current smokers(8.52%)/ex-smokers(8.89%),occasional alcohol users(6.79%)/regular alcohol users(10.51%)/daily alcohol users(10.62%),and patients with hypertension(12.14%)/diabetes(15.19%)/coronary heart disease(10.22%)than those without corresponding characteristics(all <0.001).Abnormal increase in body mass index,diastolic blood pressure,FPG,TG,TC,and ALT were risk factors for fatty liver in Logistic regression model.Conclusions The prevalence of fatty liver in adults is relatively low in Mianyang City.Patients with fatty liver usually have varying degrees of abnormal increase in blood lipids,blood glucose,blood pressure,and ALT.Healthy lifestyles and comprehensively assessment of metabolic status are conducive to the prevention and treatment of fatty liver and extrahepatic complications.
Alcohol Drinking ; Body Mass Index ; China ; Fatty Liver ; metabolism ; physiopathology ; Female ; Humans ; Hypertension ; Male ; Prevalence ; Risk Factors ; Smoking

OBJECTIVE: To explore alcohol pharmacokinetics as well as acetaldehyde level in peripheral blood in human subjects with different ALDH2 genotypes after drinking. METHODS: Venous blood samples of 14 unrelated volunteers were collected. Polymerase chain reaction-restriction fragment length polymorphism technology was adopted for DNA extraction and ALDH2 genotyping. The volunteers were asked to drink beer at certain doses. The concentration of alcohol and acetaldehyde were assayed by headspace gas chromatography method at different time. The pharmacokinetic parameters were calculated. RESULTS: According to the results of electrophoresis, 5 people carried ALDH2*1/*1 as wild group and 9 people carried ALDH2*1/*2 as mutation group. The good linear range of alcohol and acetaldehyde were 0-1 570.7 microg/mL and 0-5.1772 microg/mL, respectively. The AUC values of alcohol and acetaldehyde and the t1/2Z value of alcohol were higher in the mutation group than that in the wild group. But the CL/F value of alcohol was lower in the mutation group than that in the wild group (P<0.05). CONCLUSION After the consumption of alcohol, alcohol and acetaldehyde metabolism in blood slow down in ALDH2*1/*2 mutation group influenced by the inhibition of enzyme activity, leading to the accumulation of acetaldehyde in peripheral blood, thus reinforcing their effects in the body.
Alcohol Drinking ; Aldehyde Dehydrogenase/genetics* ; Aldehyde Dehydrogenase, Mitochondrial ; Ethanol/metabolism* ; Genotype ; Humans ; Polymerase Chain Reaction ; Polymorphism, Genetic

Objective To explore the change rules of blood ethanol and blood acetaldehyde concentration, the impairment of psychomotor functions of different acetaldehyde dehydrogenase （ALDH） 2 genotype individuals after alcohol consumption and the relationship among them. Methods The ALDH2 genotypes in seventy-nine healthy volunteers were obtained by SNaPshot^TM method, then divided into ALDH2*1/*1 （wild type） and ALDH2*1/*2 （mutant type） group. After volunteers consumed 1.0 g/kg of alcohol, blood ethanol concentration and blood acetaldehyde concentration at a series of time points before and after alcohol consumption and psychomotor functions, such as, visual selective response time, auditory simple response time and tracking experiment were detected. Biphasic alcohol response questionnaires were collected. Results After alcohol consumption, ALDH2*1/*2 group's blood ethanol and blood acetaldehyde concentration reached the peak earlier than ALDH2*1/*1 group. Its blood acetaldehyde concentration was higher than that of ALDH2*1/*1 group, 1-6 h after alcohol consumption. The psychomotor functions, such as visual selective response time and auditory simple response time in ALDH2*1/*2 group were more significantly impaired than those in ALDH2*1/*1 group after alcohol consumption. There was no statistical significance between the two groups in excitement or sedation reactions （P>0.05）. Pearson correlation coefficient test showed that blood acetaldehyde concentration was related with psychomotor function. Conclusion There are significant differences between the psychomotor function of ALDH2 wild type and mutant type individuals after alcohol consumption estimated to be related to the difference in blood acetaldehyde concentration after alcohol consumption.
Acetaldehyde/metabolism* ; Alcohol Drinking/blood* ; Aldehyde Dehydrogenase/genetics* ; Aldehyde Dehydrogenase, Mitochondrial ; Aldehyde Oxidoreductases ; Ethanol/metabolism* ; Genotype ; Humans ; Polymorphism, Genetic/genetics* ; Psychomotor Performance/physiology*

Rhabdomyolysis is defined as skeletal muscle injury with release of muscle cell constituents into the plasma and may lead to acute renal failure secondary to myoglobinuria. The causes of rhabdomyolysis is diverse:alcohol abuse, primary muscle disease, disturbance of muscle metabolism, sustained seizure, infection, drugs, tox ins, trauma, severe exercise, CO intoxication etc. Rhabdomyolysis may cause acute derangement in electrolyte balance and death. It should be diagnosed earlier and managed properly. We experienced a 49 year-old woman developed acute renal failure and myoglobinuria after alcohol drinking. A kidney biopsy revealed acute interstitial nephritis. In the presence of otherwise unexplained acute renal failure in alcoholic patients, rhabdomyolysis should be considered in the differential diagnosis.
Acute Kidney Injury ; Alcohol Drinking* ; Alcoholics ; Biopsy ; Diagnosis, Differential ; Female ; Humans ; Kidney ; Metabolism ; Middle Aged ; Muscle Cells ; Muscle, Skeletal ; Myoglobinuria* ; Nephritis, Interstitial* ; Plasma ; Rhabdomyolysis ; Seizures ; Water-Electrolyte Balance

BACKGROUND: Decreased antioxidant defense mechanisms and over-generated free radicals by either normal or aberrant metabolism play an important role in the pathogenesis of cardiovascular disease and cancer. And the life style and diet including antioxidant vitamin A and E have been thought an important factor in antioxidant systems. Recently, Total Antioxidant Status kit (TAS; Randox, UK) has been developed for measuring the total antioxidant capacity of blood. So we evaluated the association of life style and total antioxidant capacity in patients with chronic cardiovascular disease. METHODS: Sixty six cases of chronic cardiovascular disease and sixty three normal controls were evaluated. Serum total antioxidant capacity was measured by Hitachi 747 (Hitachi Ltd, Japan) with TAS kit, vitamin A and E were measured by high performance liquid chromatography method, and serum lipid profile by Hitachi 7060 (Hitachi Ltd, Japan). RESULTS: The mean total antioxidant capacity did not show difference between patients and controls. After 3 months, we detected significant increase of total antioxidant capacity, high-density lipoprotein cholesterol and mild increase of antioxidant vitamins and significant decrease of total cholesterol, triglyceride, lipoprotein (a). The heavy alcohol consumption group showed significant difference with other groups (P<0.05). CONCLUSIONS: The measurement of total antioxidant capacity for the cardiovascular disease patients was thought to be useful to evaluate oxidative stress and antioxidant status. Alcohol consumption and supplementation with antioxidant vitamins could have an effect on total antioxidant capacity.
Alcohol Drinking ; Antioxidants ; Cardiovascular Diseases* ; Cholesterol ; Chromatography, Liquid ; Defense Mechanisms ; Diet* ; Free Radicals ; Humans ; Life Style* ; Lipoprotein(a) ; Lipoproteins ; Metabolism ; Oxidative Stress ; Triglycerides ; Vitamin A ; Vitamins