Alcoholic liver disease (ALD) has different stages as it develops, and the severity of ALD is correlated with malnutrition. The consumption of calories from alcohol instead of calories from food results in poor nutrition, as does the malabsorption and maldigestion of numerous nutrients linked to ALD. Alcohol abstinence is the only treatment for ALD that has been proven effective. Infection-related problems linked with ALD may be effectively decreased with enough nutritional replenishment and the right supportive treatment techniques. In some malnourished patients, particularly, nutrition plays a substantial beneficial role in the therapy of ALD [9], and given the frequency of malnutrition, especially of the protein–calorie variety, it seems evident that diet contributes in some way to ALD. Malnutrition typically correlates with the severity of ALD and is linked to the illnesses that hospitalized patients experience. Abstinence from alcohol is the primary, validated treatment for ALD. However, in general, good nutrition does not increase longevity. It does, however, improve nitrogen balance, and it may boost liver tests and reduce hepatic fat buildup. This implies that while appropriate diet is helpful when used in conjunction with other forms of therapy, it is an insufficient therapy on its own. It has been hypothesized that adequate nutritional replenishment along with other forms of therapy may be useful in lowering ALD-related problems, notably infection [10,11]. Appropriate protein, calories, and vitamins are necessary for optimal nutrition. The patient should, ideally, be given enough food to eat orally or through a feeding tube. If this is the case, a nasogastric feeding tube (also known as a nasogastric tube) or, if that is not possible, intravenous nutrition may be needed [12]. In patients with severe AAH, morbidity and mortality rates are substantial. Regrettably, there are still not many therapeutic approaches readily available. As malnutrition has been linked to worse results, nutritional supplementation is a crucial part of AAH treatment. In order to change clinical outcomes, the function of supplemental nutritional assistance, such as enteral feeding and particular supplemental micronutrients, needs to be more clearly defined [13].

The purpose of treatment is to decrease short-term morbidity and mortality through the use of adjuvant pharmaceutical medicines and intensive supportive care. The cornerstone of therapy, which is essential to long-term survival, is abstinence from alcohol. Glucocorticoid therapy is currently the established pharmacological standard of care in the treatment of severe AH, while the ideal length of therapy is still an unknown period [14] Numerous randomised control trials (RCTs) have shown contradictory findings in regards to the survival advantage. Short-term mortality at 28 days has been shown to improve with the use of glucocorticoids, while long-term mortality advantages have not been demonstrated [15,16]. There is no evidence to support pentoxifylline’s effectiveness in reducing mortality [15]. The importance of getting enough calories and nutrients while receiving extensive supportive care has caused this to be a priority area. Poor overall nutritional status, which is frequently seen in individuals with AAH, is caused by a variety of reasons. The fact that nutritional assistance is regarded as a crucial component of the standard treatment for AH is largely due to these long-standing observations. Patients with malnutrition are more likely to experience a slower recovery from AAH, which is not surprising [17] as numerous studies have shown a link between severe AH patients who are protein-calorie malnourished and increased rates of short- and long-term death [18,19]. The degree of protein–calorie malnutrition is closely related to mortality, with a rate that reaches 80% in those patients who are classified as severely malnourished [19]. Numerous investigations have demonstrated that low daily caloric intake is associated with higher mortality in severe AH [20]. Reduced hepatic glycogen levels in patients with severe ALD may cause hypoglycemia and rapid muscle catabolism to promote gluconeogenesis [21], and this can tackled by reducing the amount of time spent without eating, with a focus on having breakfast and a snack before bed as well as avoiding lengthy fasting while in the hospital [21].

For a variety of causes, including delayed stomach emptying and longer small intestinal transit durations that lead to early satiety, standard per oral food intake is frequently impaired in these patients [22]. Additionally, ascites can affect stomach accommodation, which might cause pain after meals [23]. Hepatic encephalopathy (HE), in addition to the mental state changes that can be observed, limits the ability to eat. HE also contributes to reduced appetite, and in certain more covert forms, results in an overall malnourished state [24]. Last but not least, the use of lactulose (a non-absorbable but highly fermentable synthetic sugar) in the treatment of encephalopathy might exacerbate bloating and discomfort feelings, further impairing oral intake [25]. Undernutrition is a danger for patients who develop HE, and enteral access may be necessary [26,27]. Diets with a range of normal to high protein content are secure and do not raise the danger of encephalopathy in alcoholic hepatitis. Enteral nutritional support should be started as soon as it is determined that oral intake is impaired and should consist of 1.5 g of protein per kg of body weight and 30 to 40 kcal per kg of body weight per day [28]. Given that complications such as hypoalbuminemia, edoema, intravascular depletion, and ascites are frequently present in this patient population and can conceal the patient’s true weight, the American Society for Parenteral and Enteral Nutrition (ASPEN) recommends using an estimated euvolemic weight or usual weight rather than the patient’s actual weight for these calculations in patients with cirrhosis and hepatic failure. According to the American Gastroenterological Association and ASPEN, EN is the preferred method for supplying nourishment to individuals who are unable to tolerate oral ingestion [28,29]. The delivery of nutrition to the gut enhances gut mucosal immunity and therefore reduces endotoxemia, which may contribute to the pathophysiology of alcoholic hepatitis. In general, EN is also a less expensive choice with far less consequences [30]. Nonabsorbable disaccharides, including lactulose, should be used to treat patients with hepatic encephalopathy; rifaximin can be given if this treatment is ineffective after 24–48 h [31]. Numerous micronutrient deficiencies, including zinc, folate, thiamine, pyridoxine, vitamins A, B12, D, and E, have all been found in patients with excessive alcohol consumption and ALD in addition to the high prevalence of severe protein-calorie malnutrition [32,33]. These nutritional deficiencies are not just a result of inadequate consumption; they are also a result of decreased absorption, which increases the likelihood of developing alcohol-induced liver damage as well as osteoporosis, myopathy, insulin resistance, and dyslipidemia in these patients. The inability of the liver to produce carrier proteins, as well as the cholestasis that results in fat malabsorption, reduces bile acid synthesis and small bowel delivery, which are all factors that contribute to these deficiencies [34]. Through a number of mechanisms, including the enhancement of intestinal barrier function, the reduction of proinflammatory cytokines, oxidative stress, endotoxinemia, and the counterbalancing of hepatocyte apoptosis, zinc supplementation may attenuate alcohol-induced liver injury and prevent hepatic encephalopathy [35,36]. Usually 50 mg of elemental zinc (220 mg of zinc sulphate) administered once daily with a meal (to reduce potential nausea) is the suggested amount of zinc for treating liver disease. Due to competition for absorption at the brush boundary, long-term zinc supplementation has been linked to copper insufficiency. Further research is necessary to determine the supplementation duration.