Research In Nursing

Introduction to Alcoholism and Liver Disease

Alcoholic liver disease (ALD) is induced by hepatic damage through years of heavy alcoholism. Years of alcohol consumption can lead the liver to swell and get enlarged. A known disease like Liver cirrhosis can cause scarring as well. Cirrhosis is the last stage of liver disease. ALD is an important public health concern (Seitz et al., 2018). Approximately 8 to 10 percent of Americans drink excessive alcohol. Excessive drinking is regarded as over eight alcoholic drinks per week for women, and more than 15 for men. Liver disease is one of the many effects of heavy consumption of alcohol. It is particularly serious because liver disease can be lethal. With more than 500 functionalities, the liver is among the most diverse organs of the body. The functions involve filtering away plasma toxins, energy storage, processing hormones and protein, and controlling sugar levels and cholesterol (Osna et al., 2017).

 Damage done to the liver can affect the entire body. As even the liver is usually highly efficient in regenerating and restoring itself, it can take a very long time to become apparent once harm starts. Often it is irreversible by the time the damage is found. In 2014, the number of fatalities from alcohol-related liver illness in the united states was 19,388, as per the Centers for Disease Control and Prevention (CDC), while all causes of liver disease and cirrhosis are projected to contribute to 12 deaths per 100,000 people a year (Salarian et al., 2019). In this assessment, the critical appraisal of few journal articles on the effect of alcohol consumption on the liver will be done under few headings.

Article 1- Risk Behaviors Associated with Alcohol Consumption Predict Future Severe Liver Disease (Hagström et al., 2019).


This article was written by Hannes Hagström, Tomas Hemmingsson, Andrea Discacciati, and Anna Andreasson. Hannes Hagström’s research focus has mostly been on liver-related epidemiology, with a strong interest in liver fatty disease. His workgroup specializes in the long-term effects of fatty liver disease and defining risk factors for the progression of the disease. He was instrumental in the creation of one of the largest observational cohorts of fatty liver disease worldwide. There is no conflict of interest involved of the authors in the study.

Research question of the article

Excess alcohol intake can lead to cirrhosis, but it's unclear if this risk is affected by the type of alcohol and consumption pattern (Simpson et al., 2019). In this direction, the study was aimed at exploring whether the form and duration of alcohol intake could predict the occurrence of serious liver disease early in life. There is a dose-response effect on the likelihood of developing cirrhosis from the overall amount of alcohol consumed. In addition to the overall cumulative dose of alcohol ingested, genetic, and environmental factors can affect the risk of developing cirrhosis. For certain trials, wine intake was associated with a lower risk of cirrhosis compared with beer and spirits due to the same alcohol dosage (Mitchell et al., 2018). However, the topic of many studies has been whether the pattern of how a person consumes alcohol has any effect on the risk of cirrhosis but gaps has been identified in terms of lifestyle factors and alcohol consumption. Here researchers examined if either lifestyle factors linked to early-life alcohol consumption could anticipate the risk of later-life creating clinically significant liver disease, regardless of the complete amount consumed. They also examined whether wine intake was associated with a lower risk for much the same outcome compared to other drinks.

Research design

Researchers used data from a national population-based survey of all Swedish men who were obligatorily recruited for military service from 1969–1970. In Sweden, conscription was compulsory at that period, with just 2–3 percent of men being exempted from military service, often due to serious disabilities or illnesses. This research was focused on the conscription of 49,321 Swedish men, aged 18–20, during that time. The sample selection as soldiers was not a wise idea as they live in external tough situation which can bring biasness in the results.

Research method

All troops underwent an effective health evaluation and an interview and at the time of conscription filled out a survey question. The number of alcoholic drinks consumed (number of cans or bottles or centiliters of beer, wine, and spirits) and the frequency of consumption recorded in the questionnaire (a couple of times a week, 1–2 times a month, less regularly, and never before). Data on the average alcohol content for the different types of drinks were collected from the Swedish alcohol retailing monopoly during the time the exams were administered. Grams of 100 percent alcoholic beverages each day were projected for each person, and averages of each type of drink (beer, wine, or spirits) were measured of the amount noted each day. Since the questionaires were used for data collection the person cannot sometimes give correct answer fearing the stigmatization with drinking.

Results and limitations of the study

392 people experienced serious hepatic disease during follow-up. In multivariable study, after correction for BMI, cigarettes, use of drugs, physical health, cognitive capacity, and overall volume of alcohol, there was an elevated risk of serious liver problems in individuals who mentioned consuming alcohol to relieve a hangover and individuals who mentioned being apprehended for consuming but not for any other risky behavior. Wine intake has not been linked to a lower risk of serious liver disease relative to beer and spirits. Certain risk habits may classify young people with an increased risk of getting serious liver disease. Wine consumption was not associated with a reduced risk for severe liver disease compared to beer and spirits. The limitations of the study were the group considered for the study as they were soldiers. Their environmental factors play a very important role in such findings and the external factors involved in the group are too harsh. Secondly, the age group used in the study is very narrow and the people considered are too young. At a young age, the liver has more regeneration capacity which goes down with increasing age. So, the group could have considered the broader age range. The implications of the study was either lifestyle factors linked to early-life alcohol consumption could anticipate the risk of later-life creating clinically significant liver disease.

Article 2: Comparing the Effects of Acute Alcohol Consumption in Germ-Free and Conventional Mice: The Role of Gut Microbiota (Canesso et al., 2014)


The corresponding author's Ana Lúcia Brunialti Godard and Angelica Thomaz Vieira do not have a hard-core experience in the hepatology and addiction field. The first author Canesso is also new in the field and is a post doctorate. Ana Godard has experience in human genetics, with an emphasis in animal models of human disease, acting on the following topics: Functional genomics, genetic of the alcoholism, molecular mechanisms of addiction and compulsion. There is no conflict of interest described by the authors in the studies.

Aim of the article

There are various studies which indicate that the gut microbiota after an acute alcohol intake plays a significant role in liver pathology (Tolefree et al., 2019). There is a correlation exist between alcohol consumption and the changes that take place in the gut microbiome after consumption. But the previous studies did not explained the functional aspects of the microbiome in liver disease. The research aimed to examine the functions of commensal bacteria in liver injury caused by alcohol and in the dysbiosis caused by alcohol consumption in germ-free mice, as well as the possibility of defending against alcohol-induced injury in animals fed a high-fiber diet. Of these purposes, germ-free and traditional mice were exposed to an acute ingestion of alcohol consisting of 7-day administration of ethanol in their drinking water, with a higher alcohol dose being provided on day 7.

Research design

The study utilized mice as a model system in vivo to show the effects of alcohol on the gut microbiota. Studies were carried out with eight- to ten-week-old female germ-free NIH Swiss mice. Animals were kept in micro-isolators in a shielded animal caging environment with regulated illumination (12 h sun, 12 h dark), humidity (60-80 percent), and temperatures (22 ± 1 ° C) for studies. Experiments utilizing germ-free mice were performed under aseptically to prevent the animals from being contaminated. Groups of 5–7 animals have been used individually to determine microbiota effects, conventionalization, and high-fiber procedure. The design used was appropriate for the study.

Research method

 The study was performed to assess the role of microbiota in the different mice conditions and the research group has been developed accordingly. The four classes of mice were held as Control on each group: bacteria-free control, ethanol: alcohol-free; control: traditional control; and ethanol: traditional alcohol-treated control. The drug treatment regimen involved delivering ethanol to mice (10 percent vol/vol) in the water supply for 7 days, with an increasing alcohol dose (5 mg/kg) on day 7. Following the oral gavage, the animals then were killed at various points of time. The invivo model system has some limitations as the behavioural aspects cannot be noticed in case of the mice.

Result and limitation of the study

The study findings showed no liver damage after alcohol ingestion, and in germ-free mice, there was less recruitment of neutrophils and decreased rates of pro-inflammatory cytokines in the liver compared to conventional alcohol-fed mice. Besides, the conventionalization of germ-free mice with intestinal contents from normal alcohol-fed mice caused inflammation and injury both in the liver and intestine, indicating that alcohol consumption triggered a subsequent disruption of the intestinal microbiota (dysbiosis) and hepatic damage. Finally, in traditional mice fed of liquor, prior care with a high-fiber diet reduced liver damage and gut permeability. The findings of this study indicate that gut microbiota plays a significant role in liver damage associated with alcohol, possibly by dysbiosis of the gut microbiota environment related to alcohol consumption. Alternatively, high-fiber diet therapy can mitigate hepatocyte pathology and intestinal leak, and thus may be an efficient treatment alternative. The limitation of the study was the use of the mice model. Although the in vivo systems are used in studies and the result makes them more transitional at the human level. But the effect of the alcohol results in mice cannot be correlated with that of the human. The research design can be used to make drug discovery for the treatment of liver disease in the alcohol affected disorders. The implications of the study is find a correlation between the role of microbiome in alcohol consuming individuals in liver disease.

Article 3:Effects of Age, Sex, Body Weight, and Quantity of Alcohol Consumption on Occurrence and Severity of Alcoholic Hepatitis (Liangpunsakul et al., 2016)


The first author of the research study is Suthat Liangpunsakul and his co-authors Puri, P., Shah, V. H., Kamath, P., Sanyal and other helped him in studies. His studies focus on discovering non - intrusive biomarkers to monitor for inappropriate use of alcohol and the underlying mechanisms, lifestyle factors, and treatments for liver damage caused by alcohol. He wrote/co-wrote over 150 peer-reviewed articles and 6 chapters of the book. He is also a participating member of the research group of the NIH HBPP. There was no biasness and the conflict of interest involved in the studies.

Aim of the research

Alcoholic liver disease (ALD) describes a continuum of psychiatric disorder and physiological alteration in people who drink acute and chronic alcohol (Parker et al., 2018). The consumption of alcohol is a significant factor which puts one at risk for ALD. However, studies have also shown that such risk can also depend on the alcohol intake habits, regardless of alcohol consumption levels (Goel et al., 2018). Women's greater susceptibility and reduced safe alcohol consumption restrictions have long been recognized. Females had a considerably higher estimated danger of experiencing ALD than males, at any defined level of alcohol intake (Stickel et al., 2017). It is important to recognize that a detailed study on the relationship between the progression of ALD and the alcohol content consumption is almost impossible because data collection often requires different interpretations and arbitrary alcohol consumption assessments. Bodyweight is another modifiable risk factor for developing ALD. In an experimental study from the US, the risk of alcohol-related abnormal alanine aminotransferase activity increased with overweight and obesity (Niemelä, 2016). The link between the age, sex and the BMI were not discussed in the previous studies so the authors have treid to find the link with the current study. This study has highlighted the causes and consequences of alcoholic hepatitis including age, sex, BMI, drinking habits, and drinking number. This article describes clearly the relationship between alcohol use and liver disease, severe alcohol-related death rates, and ALD occurring only in a small number of heavy drinkers. Several factors associated with alcoholic hepatitis emerge from drug use.

Research design

Based on BMI as they entered the study, the researcher used data from 145 patients with AH cases and 124 controls; groups were balanced for age and race. Drinking styles were evaluated using the timeline following the back method, Alcohol Use Disorders Identification Test, a 6-question survey of the National Institute of Alcohol Abuse and Alcoholism. They conducted univariate analysis and multivariate analysis to determine the impact of various factors and their role in that AH risk.

Research method

The assessment of AH was focused on the daily average intake of > 40 grams of ethanol per day for females and > 60 grams per day for males for six months within 6 weeks of study enrolment, and clinical assessment and sufficient laboratory testing as specified by bilirubin > 2 mg / dL and AST > 50 U / L. A Liver Biopsy (if medically possible without any side effects) was needed when the evaluation of AH appeared in doubt. The method involved the self-reported alcohol intake which was the drawback of the study as the participant can chance their responses giving a biasness in the results.

Results and limitations

Between AH participants, most subjects were males (60%) and White (88%), respectively. There were almost no variations in the mean BMI between groups; and there was no substantially different proportion of participants with a BMI>25. There were no variations in the alcohol consumption interventions between males or females inside the treatment or control groups. In both controls and cases, males recorded higher maximum drinks on a single occasion than females. There has been no connection between total alcohol intake, BMI, and gender and higher likelihood for AH, nor any communication between such variables. The key results in the research are the overall amount of alcohol intake in the last 30 days, and alcohol consumption levels have been slightly lower in AH cases compared with controls. The age was inversely correlated with AH frequency, and subjects with higher BMI were at greater risk for extreme AH. There is no clear connection between the drinking amount and incidence of AH, as per data. The key strength of this analysis is the compilation of context data, collection of various drinking classes and comparisons, assessment of drinking behavior, and methods of gathering data such as surveys, questionnaires, etc. The study's key drawbacks include unattainable data on self-reported drinks that cannot be taken on all patients with liver biopsy. The studies showed no link between the drinking habits and increasing risk for AH.

Summary of Alcoholism and Liver Disease

One of the main forms of chronic liver disease in western nations is alcohol intake, which is associated with significant hepatic damage (e.g., fibrosis and cirrhosis). Amongst many contributing factors to alcohol-induced liver injury pathogenesis, gut-derived microbial products, drinking behavior habits, age, and other factors tend to play a key role in steatosis and inflammatory induction. Canesso et al found that in the blood of individuals with persistent alcohol intake, a high level of lipopolysaccharide (LPS) is observed and this finding is attributed to several causes, including a prevalent alteration in the distribution of the gut microbiome. Hagström et al., 2019 proved that the alcohol intake is linked with an increased incidence of acquiring serious liver disease in the future in a dose-response pattern.

Danger habits associated with early-life excessive drinking may predict the likelihood of later-life experiencing clinically significant liver disease, regardless of the overall amount consumed. Besides, wine intake was studied, as it was linked with a decreased risk for almost the same consequence relative to other drinks. Liangpunsakul et al., 2016 found that the influence of age, gender, body mass, and the total amount and intensity of alcohol intake and increase of AH is restricted, because several earlier studies concentrated on alcoholic cirrhosis in particular. Generally, the incidence of alcoholic cirrhosis is related to the amount of binge drinking. The other three main risk factors repeatedly stated to lead to risk of AH, age, gender, and BMI, and pursued associations with alcohol intake measurements. It was clear that age at presentation is inversely associated with the severity of AH.

Conclusion on Alcoholism and Liver Disease

Heavy alcohol intake is a major health-care epidemic with significant social, economic, and clinical implications. Throughout decades binge alcohol destroys almost every part of the human body. Nonetheless, since it is the main site of ethanol production, the liver sustains the first and highest level of tissue damage from binge consumption. there are several other health implications of persistent alcohol misuse, ranging from elevated blood pressure to strokes. Processing one alcoholic beverage takes the body about an hour. For rising intake, this period rises. The greater the alcohol content in someone's body fluids, the longer it will take to metabolize alcohol. The liver can absorb just any quantity of alcohol at a period. The alcohol remaining unprocessed by the liver rotates through the blood system whenever anyone has more to be drunk.

Alcohol level begins to impact the brain and heart and that's how individuals get impaired. Chronic alcohol abuse induces liver cell death, leading to liver scarring (cirrhosis), alcohol hepatitis, and genetic alteration which can lead to hepatic cancer. Typically these disorders go from liver damage to alcoholic hepatitis to cirrhosis, but heavy drinkers may develop alcoholic cirrhosis without first developing hepatitis. By comparison to moderate drinkers, binge drinkers face a greater risk of developing a variety of liver injury. While the fatty liver disease is usually reversible with abstinence, as many as 20 percent of heavy drinkers develop fatty liver disease. Alcoholic hepatitis, an infection that causes dysfunction of the liver, can evolve into further cirrhosis, which may be fatal. Yet with prohibition, it too is reversed. Countrywide treatment centers create practical liquor cleanse and encourage individuals to share back control over the situation.

References for Alcoholism and Liver Disease

Goel, S., Sharma, A., & Garg, A. (2018). Effect of alcohol consumption on cardiovascular health. Current cardiology reports20(4), 19.

Hagström, H., Hemmingsson, T., Discacciati, A., & Andreasson, A. (2019). Risk behaviors associated with alcohol consumption predict future severe liver disease. Digestive Diseases and Sciences64(7), 2014-2023.

Liangpunsakul, S., Puri, P., Shah, V. H., Kamath, P., Sanyal, A., Urban, T., ... & Crabb, D. W. (2016). Effects of age, sex, body weight, and quantity of alcohol consumption on occurrence and severity of alcoholic hepatitis. Clinical Gastroenterology and Hepatology14(12), 1831-1838.

M C C, Canesso., N L, Lacerda., C M, Ferreira., J L, Goncalves., D, Almeida., C, Gamba., G, Cassali., S H, Pedrosa., C, Moreira., F S, Martins., J R, Nicoli., M M, Teixeira., A L B, Godard., & A T, Vierira. (2014). Comparing the effects of acute alcohol consumption in germ-free and conventional mice: The role of the gut microbiota. BMC Microbiology14, 240.

Mitchell, T., Jeffrey, G. P., de Boer, B., MacQuillan, G., Garas, G., Ching, H., ... & Adams, L. A. (2018). Type and pattern of alcohol consumption is associated with liver fibrosis in patients with non-alcoholic fatty liver disease. American Journal of Gastroenterology113(10), 1484-1493.

Niemelä, O. (2016). Biomarker-based approaches for assessing alcohol use disorders. International Journal of Environmental Research and Public Health13(2), 166.

Osna, N. A., Donohue Jr, T. M., & Kharbanda, K. K. (2017). Alcoholic liver disease: Pathogenesis and current management. Alcohol Research: Current Reviews38(2), 147.

Parker, R., Kim, S. J., & Gao, B. (2018). Alcohol, adipose tissue and liver disease: Mechanistic links and clinical considerations. Nature Reviews Gastroenterology & Hepatology15(1), 50.

Salarian, M., Turaga, R. C., Xue, S., Nezafati, M., Hekmatyar, K., Qiao, J., ... & Li, J. (2019). Early detection and staging of chronic liver diseases with a protein MRI contrast agent. Nature Communications10(1), 1-14.

Seitz, H. K., Bataller, R., Cortez-Pinto, H., Gao, B., Gual, A., Lackner, C., ... & Tsukamoto, H. (2018). Alcoholic liver disease. Nature Reviews Disease Primers4(1), 1-22.

Simpson, R. F., Hermon, C., Liu, B., Green, J., Reeves, G. K., Beral, V., ... & Million Women Study Collaborators. (2019). Alcohol drinking patterns and liver cirrhosis risk: analysis of the prospective UK Million Women Study. The Lancet Public Health4(1), e41-e48.

Stickel, F., Datz, C., Hampe, J., & Bataller, R. (2017). Pathophysiology and management of alcoholic liver disease: Update 2016. Gut and liver11(2), 173.

Tolefree, J. A., Garcia, A. J., Farrell, J., Meadows, V., Kennedy, L., Hargrove, L., ... & Francis, H. (2019). Alcoholic liver disease and mast cells: What's your gut got to do with it?. Liver Research3(1), 46-54.

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