August 2025
INTRODUCTION —
Excessive alcohol use is highly prevalent and a major cause of nutrition deficiency in resource-abundant countries [1]. Alcohol causes nutrition complications from both its primary effects on the intake and metabolism of nutrients and secondary effects of end-organ damage (eg, alcohol-induced liver disease, pancreatitis) [1-8].
This topic addresses the epidemiology, pathogenesis, assessment, and treatment of malnutrition in individuals with sustained heavy alcohol use. Malnutrition in patients with chronic liver disease is discussed separately:
●(See "Nutritional issues in adult patients with cirrhosis".)
●(See "Clinical features and diagnosis of alcohol-associated hepatitis".)
●(See "Management of alcohol-associated hepatitis".)
Other medical consequences of excessive alcohol use and the clinical presentation of risky drinking and alcohol use disorder are also discussed separately:
●(See "Overview of the risks and benefits of alcohol consumption".)
TERMINOLOGY —
Terms that describe alcohol use and alcohol-related problems and disorders include the following [9,10]:
●Unhealthy alcohol use – Unhealthy alcohol use encompasses the spectrum of alcohol use that can result in health consequences. It includes risky alcohol use and alcohol use disorders. (See "Risky drinking and alcohol use disorder: Epidemiology, clinical features, adverse consequences, screening, and assessment", section on 'Terminology'.)
●Risky alcohol use – Risky alcohol use refers to the consumption of an amount of alcohol that puts the individual at risk for health consequences, but the pattern of alcohol use is not so severe as to meet diagnostic criteria for alcohol use disorder. Thresholds for risky alcohol use vary:
•The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines risky alcohol use for males aged 65 or younger as having more than four drinks on any day or more than 14 standard drinks per week.
•The NIAAA defines risky alcohol use for females and males over 65 as having more than three drinks on any day or more than seven standard drinks per week. (See "Risky drinking and alcohol use disorder: Epidemiology, clinical features, adverse consequences, screening, and assessment", section on 'Terminology'.)
•Guidelines from the Canadian Centre on Substance Use and Addiction identify the risk of harm from alcohol as "low" in individuals consuming two standard drinks or less per week, "moderate" in those consuming between three and six standard drinks per week, and "increasingly high" for those consuming seven standard drinks or more per week [11].
●Heavy alcohol use – The NIAAA defines heavy alcohol use as more than five drinks per day or more than 15 drinks per week for males and more than four drinks per day or more than eight drinks per week for females [12].
Amounts are based on a standard drink, which is defined in the United States as 12 grams of ethanol, 5 ounces of wine, 12 ounces of beer, or 1.5 ounces of 80 proof spirits. The number and size of drinks used in these estimates vary internationally.
●Alcohol use disorder – Alcohol use disorder is defined by the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision, as a problematic pattern of alcohol use leading to clinically significant impairment or distress, as manifested by 11 specific psychosocial, behavioral, or physiologic criteria (table 1) [13]. (See "Risky drinking and alcohol use disorder: Epidemiology, clinical features, adverse consequences, screening, and assessment", section on 'Terminology'.)
The epidemiology, assessment, clinical features, and consequences of alcohol use disorder and risky alcohol use are discussed elsewhere. (See "Risky drinking and alcohol use disorder: Epidemiology, clinical features, adverse consequences, screening, and assessment" and "Alcohol use disorder: Treatment overview".)
EPIDEMIOLOGY OF ALCOHOL-RELATED MALNUTRITION —
The prevalence and degree of malnutrition vary in those with alcohol use disorder. The prevalence of protein-calorie malnutrition increases with increasingly severe stages of cirrhosis and ranges from 20 to 60 percent in those with Child-Pugh stages A to C, respectively [14].
There are no reliable predictors of who will develop malnutrition as a result of moderate to heavy alcohol use. Individuals with heavy alcohol use who do not have liver disease may be nutritionally normal or have nutrient deficiency and/or malnutrition. As alcohol-associated liver disease progresses to cirrhosis, it is frequently complicated by protein-energy malnutrition and sarcopenia [15].
PATHOGENESIS AND MANIFESTATIONS OF ALCOHOL-RELATED MALNUTRITION
Mechanisms — Acute and chronic alcohol consumption decrease dietary macro- and micronutrient intake, impair nutrient digestion and absorption, decrease protein synthesis and secretion, increase catabolism of gut proteins, and increase breakdown and excretion of nutrients [16,17]. All these processes can cause malnutrition. The degree of malnutrition depends on the amount of alcohol consumed, the quality of food intake, patient genetics, and the presence and severity of comorbid illnesses. The risk of developing micro- and macronutrient deficiencies increases significantly when alcohol makes up more than 30 percent of total caloric intake [16].
●Dietary intake – With chronic, heavy alcohol use, malnutrition can occur in both underweight individuals and those with overweight or obesity. The caloric content of an alcoholic beverage is composed of calories from alcohol (7.1 kcal/gram alcohol) and nonalcohol components (alcohol calorie calculator) [18].
Individuals who drink modest amounts of alcohol (up to 20 grams per day) typically do not reduce their intake of food calories [19,20]. However, with increasing levels of sustained alcohol intake, the proportion of food calories consumed decreases [18,21]. When alcohol accounts for more than 30 percent of total calories, the individual's alcohol consumption typically replaces caloric intake from carbohydrates, fats, and proteins [18,22]. Anorexia, nausea, vomiting, and abdominal pain related to gastritis or hepatitis can further reduce food intake. Alcohol increases serum leptin and cytokines (eg, serum tumor necrosis factor-alpha), which may contribute to anorexia [23,24].
●Absorption and digestion – Chronic alcohol ingestion reduces nutrient absorption [25,26] and combines with enteric dysbiosis [27], bacterial overgrowth, increased intestinal permeability, and altered intestinal motility to cause malnutrition [28-31]. Exocrine pancreatic insufficiency from alcohol-induced pancreatitis can further contribute to malabsorption.
Alcohol is absorbed by simple diffusion in the stomach and, to a lesser degree, in the duodenum and jejunum [27,32]. Acute alcohol ingestion causes mucosal erosions and villous-predominant epithelial loss [25,32]. The effects of chronic alcohol ingestion on intestinal mucosa are not well understood but may include fibrous tissue accumulation [25].
●Energy metabolism – Individuals with modest alcohol consumption do not eat less to compensate for the calories provided by alcohol. However, individuals with high alcohol intake paradoxically lose weight [33].
Chronic consumption of alcohol and a standard-calorie diet reduces adipose accumulation and causes an energy deficit. The energy deficit results from alcohol-induced mitochondrial damage, increased thermogenesis, sympathetic nervous system activation, and oxidation of alcohol [34,35]. Additionally, if present, acute pancreatitis and alcohol-associated liver disease induce a hypermetabolic state [6,36]. (See "Nutritional issues in adult patients with cirrhosis", section on 'Epidemiology and risk factors'.)
●Protein metabolism – Protein-calorie malnutrition (PCM) occurs primarily in patients with advanced alcohol-associated liver disease. Up to 30 percent of individuals hospitalized for alcohol-related liver damage suffer from PCM [4,37,38]. PCM is caused by inadequate calorie and protein intake and is a marker of advanced disease and poor prognosis. (See "Nutritional issues in adult patients with cirrhosis", section on 'Epidemiology and risk factors'.)
Micronutrients — Both water- and fat-soluble vitamin deficiencies occur with moderate to heavy chronic alcohol consumption [39]. The risk of deficiency increases with higher levels of alcohol intake.
Water-soluble vitamins
●Vitamin B1 (thiamine) – Thiamine deficiency is found in up to 80 percent of adults with chronic alcohol use [40-42] and is more common in those with advanced liver disease. Deficiency may be caused by insufficient intake, reduced gastrointestinal absorption, or reduced storage [43]. Thiamine deficiency can cause peripheral neuropathy, cardiomyopathy, and Wernicke-Korsakoff syndrome. Wernicke's encephalopathy is characterized by the triad of delirium, oculomotor abnormalities, and ataxia. Untreated, Wernicke's encephalopathy can progress to Korsakoff's syndrome, which is characterized by anterograde and retrograde amnesia and confabulation. (See "Wernicke encephalopathy" and "Overview of the chronic neurologic complications of alcohol" and "Overview of water-soluble vitamins", section on 'Vitamin B1 (thiamine)'.)
●Vitamin B2 (riboflavin) – Riboflavin deficiency is less common than other vitamin deficiencies in patients with an alcohol use disorder and is primarily caused by reduced dietary intake. Symptomatic riboflavin deficiency is rare but can include oropharyngeal inflammation, behavioral change, neuropathy, anemia, or dermatitis. (See "Overview of water-soluble vitamins", section on 'Vitamin B2 (riboflavin)'.)
●Vitamin B6 (pyridoxine) – Pyridoxine deficiency occurs in over 50 percent of patients with alcohol use disorder and is caused by reduced intake and increased breakdown of pyridoxine during ethanol metabolism [42,44,45]. Clinical manifestations are uncommon but include peripheral neuropathy, stomatitis, confusion, or depression [46]. (See "Overview of water-soluble vitamins", section on 'Vitamin B6 (pyridoxine)'.)
●Vitamin B9 (folate) – Two-thirds of binge drinkers will have folate deficiency caused by malabsorption, reduced intake, and increased urinary excretion [25,42,44,47]. Folate deficiency can cause macrocytic anemia, anorexia, glossitis, angular stomatitis, and mouth ulcers. (See "Clinical manifestations and diagnosis of vitamin B12 and folate deficiency".)
●Vitamin B12 (cobalamin) – In the absence of chronic pancreatitis, cobalamin deficiency is rarely present in adults with an alcohol use disorder [7,25,42]. Clinical manifestations of cobalamin deficiency include macrocytic anemia and neuropsychiatric symptoms such as cognitive impairment, irritability, gait abnormalities, and peripheral neuropathy. (See "Clinical manifestations and diagnosis of vitamin B12 and folate deficiency".)
●Vitamin C – Vitamin C deficiency can be caused by intestinal malabsorption or inhibition of an active metabolite and can present as scurvy, characterized by bleeding gums, ecchymoses, fatigue, and depression [48]. A nutrition-focused finding includes corkscrew hairs. (See "Overview of water-soluble vitamins", section on 'Vitamin C (ascorbic acid)'.)
Fat-soluble vitamins — Vitamin A, D, E, and K levels are often deficient in patients with chronic pancreatitis or alcohol-associated liver disease due primarily to inadequate dietary intake and intestinal malabsorption [7,42]. By contrast, vitamin A and K deficiencies are rare in the absence of liver disease or chronic pancreatitis.
Manifestations of specific vitamin deficiencies include (see "Overview of vitamin A" and "Overview of vitamin D" and "Overview of vitamin E" and "Overview of vitamin K"):
●Vitamin A – Night blindness, Bitot's spots, sexual dysfunction, or immune deficiency [42,49].
●Vitamin D – Can predispose patients to osteomalacia, osteopenia, and fractures [49].
●Vitamin E – Hemolysis, myopathy, and retinopathy [42,50,51].
●Vitamin K – Hemostatic disturbance.
Minerals and trace elements
●Calcium, magnesium, and phosphorus – Deficiency of calcium, magnesium, or phosphorus may be related to decreased intake, malabsorption, or renal losses. Calcium deficiency may also be secondary to magnesium or vitamin D deficiency [7,52].
●Iron – Iron stores are often increased with chronic alcohol consumption, even in the absence of liver disease. This is partly due to increased paracellular absorption of iron in the liver [53-55]. (See "Treatment of iron deficiency and iron deficiency anemia in adults".)
●Zinc – Zinc deficiency can be caused by increased urinary excretion as well as reduced dietary intake and absorption.
ASSESSMENT OF NUTRITION —
Evaluation for the presence of malnutrition should include a focused history and nutrition-focused physical examination to address muscle, fat stores, and micronutrient status. We also perform laboratory testing to assess for liver disease and micronutrient deficiencies.
Role of the primary care clinician — The primary clinician should perform nutrition screening using a validated tool such as the Mini Nutritional Assessment or Patient-Generated Subjective Global Assessment. For individuals at risk of malnutrition, we typically refer to a registered dietitian for an in-depth evaluation. This typically includes individuals with chronic liver disease or other medical comorbidities or symptoms that compromise food intake or absorption (eg, exocrine pancreatic insufficiency) and those with high levels of alcohol use (eg, intake that exceeds 30 percent of total calories).
Multiple validated measures exist for nutrition assessment [56]. One measure, the subjective global assessment, combines historical cues (eg, gastrointestinal symptoms, weakness, amount of oral intake) with signs on physical examination (eg, weight loss, muscle wasting, fat redistribution, edema) [57]. The assessment of nutrition status in patients with chronic liver disease is discussed separately. (See "Dietary assessment in adults" and "Nutritional issues in adult patients with cirrhosis".)
History — We ask individuals with heavy alcohol use or an alcohol use disorder about symptoms that support the presence of malnutrition. These include weight loss, inadequate food intake or diet, dysgeusia, difficulty chewing or swallowing, decreased muscle strength, nausea, vomiting, early satiety, abdominal pain, hematemesis, diarrhea, and constipation. We additionally assess for symptoms of liver disease, such as fatigue, fever, pruritus, easy bruising, increased abdominal girth, lower extremity edema, confusion, or sleep disturbances. Comorbid conditions (eg, diabetes mellitus) and prior surgeries (eg, bariatric surgery) that can affect nutritional status are also important to identify.
Physical examination
●Malnutrition – As part of a nutrition-focused examination, we look for findings that indicate malnutrition. These include weight loss or a low body mass index (calculator 1), muscle wasting, loss of subcutaneous fat, edema, and hair/skin/nail changes. Functional tests, such as using a dynamometer to evaluate handgrip strength, can quantify muscle loss and weakness.
●Signs of cirrhosis – The examination also includes assessment for signs of cirrhosis, such as hepatomegaly, splenomegaly, spider angiomata, ascites, nail changes, gynecomastia, testicular atrophy, and jaundice. (See "Cirrhosis in adults: Etiologies, clinical manifestations, and diagnosis", section on 'Physical examination'.)
●Micronutrient deficiency – We assess for signs of vitamin deficiency. Features suggestive of micronutrient deficiencies include pallor (iron deficiency), hyperkeratosis and dermatitis (vitamin A), bruising (vitamin C and K), and glossitis (folate, vitamin B12) (table 2). Signs of vitamin deficiency may not manifest clinically until late-stage disease (eg, Wernicke's encephalopathy due to thiamine deficiency). (See "Overview of vitamin D" and "Overview of vitamin K" and "Overview of vitamin A" and "Overview of vitamin E" and "Treatment of vitamin B12 and folate deficiencies" and "Overview of water-soluble vitamins".)
●Frailty – Frailty is defined as a syndrome in which physiologic reserves are decreased, leading to heightened susceptibility to health stressors and adverse health outcomes. We screen individuals with heavy alcohol use and cirrhosis for frailty because frailty is independently associated with increased disease progression, hospitalization, and mortality in these patients [58]. We also typically screen those aged 65 years and older with alcohol use disorder for frailty. (See "Frailty".)
Clinical tools for assessing frailty include the clinical frailty scale (figure 1), the liver frailty index, or the short physical performance battery. (See "Nutritional issues in adult patients with cirrhosis", section on 'Assessment questionnaires' and "Frailty", section on 'Rapid screening tools'.)
Laboratory evaluation
●For all patients – We check the following laboratory studies in all individuals with heavy alcohol use or alcohol use disorder:
•Complete blood count
•Aspartate aminotransferase and alanine aminotransferase
•Bilirubin and alkaline phosphatase
•International normalized ratio
•Albumin
•Creatinine
•Electrolytes, including calcium, magnesium, and phosphorus
Although abnormal findings are not required for a diagnosis of malnutrition, they can support the diagnosis and/or help to identify the presence of liver disease.
●For selected patients – Because patients with chronic, heavy alcohol use have a high risk of micronutrient deficiencies that may warrant testing [59-61], we perform additional testing in selected individuals. In those with evidence of malnutrition, we typically check for selected vitamins (B12, folate, thiamine, vitamin D), minerals (phosphorus, magnesium, iron), and trace elements (zinc, copper).
In patients with chronic pancreatitis or in whom the clinical presentation suggests exocrine pancreas insufficiency, we check levels of fat-soluble vitamins (ie, "ADEK").
Assessing inflammation is a cornerstone of malnutrition assessment. When uncertainty exists regarding malnutrition risk, we check levels of C-reactive protein [62-64].
DIAGNOSIS OF MALNUTRITION —
Based on the results of the nutrition assessment, we use standard diagnostic criteria to make a diagnosis of malnutrition. Malnutrition occurs when inadequate nutrition intake results in deficiencies of energy, macronutrients (eg, protein), and/or micronutrients. Several expert consensus groups have developed diagnostic criteria for malnutrition.
Criteria from the Academy of Nutrition and Dietetics/American Society for Parenteral and Enteral Nutrition require two or more of the following six characteristics [65]:
●Insufficient energy intake
●Weight loss
●Decrease in muscle mass
●Loss of subcutaneous fat
●Edema (localized or generalized) that can mask weight loss
●Diminished handgrip strength (measured by a dynamometer) [66,67]
Criteria from the Global Leadership Initiative on Malnutrition require at least one phenotypic and one etiologic criterion for the diagnosis of malnutrition [68]:
●Phenotypic criteria – Unintentional weight loss, low body mass index, and reduced muscle mass
●Etiologic criteria – Reduced food intake or assimilation and disease burden/inflammation
MANAGEMENT OF NUTRITIONAL DEFICIENCIES
Goals of management — The goals of nutrition supplementation are to restore adequate energy and protein intake and to prevent or treat symptoms of micronutrient deficiencies [69]. Clinicians should develop a nutrition treatment plan that includes appropriate macro- and micronutrient supplementation. A registered dietitian can assist with developing the treatment plan.
Macronutrients — Macronutrient replacement should ensure an adequate intake of energy and protein. Patients should eat small, frequent meals that include breakfast and nighttime snacks. Energy needs are based on nutrition status and body weight and can range from 25 to 35 kcal/kg per day with protein intake of 1.2 to 1.5 g/kg of body weight/day for repletion [15,70,71]. Patients who struggle to meet nutritional requirements may benefit from oral nutrition supplements.
Nutrition therapy for patients with alcohol-associated cirrhosis and malnutrition is discussed separately. (See "Management of alcohol-associated steatosis and alcohol-associated cirrhosis", section on 'Nutrition'.)
Micronutrients
Thiamine, pyridoxine, and folate — In all adults with sustained, heavy alcohol use, we suggest empiric administration of an oral multivitamin that includes thiamine, folic acid, and vitamin B6 (pyridoxine) [40,42]. Since multivitamin formulations contain variable doses of component vitamins, the selected multivitamin should contain thiamine 100 mg, pyridoxine 2 mg, and folic acid 400 mcg to 1 mg. They should not exceed the tolerable upper intake levels (table 3). (See "Vitamin intake and disease prevention" and "Overview of water-soluble vitamins".)
Data from randomized trials of vitamin supplementation in adults with heavy alcohol use are lacking; however, the benefits of supplementation typically exceed its risks. Deficiencies of thiamine, folate, and pyridoxine commonly occur in individuals with chronic alcohol use, and the clinical sequelae of deficiency are significant, particularly for thiamine deficiency. In addition, supplementation is relatively safe and inexpensive.
●Vitamin B1 (thiamine) – We empirically give oral thiamine 100 mg daily to all adults with sustained heavy drinking. In hospitalized patients with chronic alcohol use, it is especially important to give thiamine supplementation prior to or along with glucose intravenous infusion to prevent precipitating Wernicke's encephalopathy. Patients admitted for alcohol withdrawal typically receive thiamine 100 mg daily. (See "Overview of water-soluble vitamins", section on 'Vitamin B1 (thiamine)' and "Wernicke encephalopathy", section on 'Prevention'.)
●Vitamin B6 (pyridoxine) – We supplement with 2 mg of oral pyridoxine daily [40,42]. Some multivitamin preparations contain more than the recommended daily dose. (See "Vitamin intake and disease prevention".)
●Vitamin B9 (folate) – We typically provide folic acid supplementation at a dose of 400 mcg to 1 mg per day. Multivitamin preparations often contain this dose [40]. (See "Vitamin intake and disease prevention" and "Clinical manifestations and diagnosis of vitamin B12 and folate deficiency".)
Other water-soluble vitamins
●Vitamin B2 (riboflavin) – We do not empirically supplement riboflavin. In patients with documented riboflavin deficiency, the recommended replacement dose is 1.7 mg per day, which is included in most multivitamin preparations. (See "Vitamin intake and disease prevention".)
●Vitamin B12 (cobalamin) – We do not routinely supplement vitamin B12. Oral doses of more than 50 mcg/day may be needed for replacement in patients with B12 deficiency; multivitamin preparations usually do not contain enough for replacement of cobalamin deficiency [40]. (See "Vitamin intake and disease prevention" and "Clinical manifestations and diagnosis of vitamin B12 and folate deficiency".)
●Vitamin C – The recommended daily dose of vitamin C to prevent scurvy is 60 mg/day, which is found in most multivitamin preparations. (See "Vitamin intake and disease prevention" and "Overview of water-soluble vitamins".)
Fat-soluble vitamins — We do not routinely supplement vitamins A, D, E, or K, except in individuals with chronic pancreatitis or alcohol-associated liver disease who have documented deficiencies.
Minerals and trace elements
●Calcium, magnesium, and phosphorus – Low levels of calcium, magnesium, and phosphorus should be replaced based on blood levels [72].
•Calcium – We adjust total calcium for low albumin levels, which can occur in those with chronic liver disease and protein-calorie malnutrition.
•Magnesium – Magnesium replacement doses range from 200 to 400 mg daily. Intravenous replacement may be needed with symptomatic deficiency (weakness, lethargy, nausea) [40,42].
•Phosphate – In the absence of significant kidney function impairment, oral phosphate is replaced at 15 to 20 mg/kg body weight per day. If patients cannot tolerate oral phosphate supplementation or if the serum level is below 1 mg/dL (0.32 mmol/L) and patients are symptomatic, then intravenous phosphate should be administered.
The approach to the evaluation and treatment of calcium, magnesium, and phosphate is discussed separately. (See "Hypophosphatemia: Evaluation and treatment", section on 'Patients with alcohol use disorder' and "Treatment of hypocalcemia", section on 'Therapeutic approach' and "Hypomagnesemia: Evaluation and treatment".)
●Iron – Patients with iron deficiency should undergo evaluation for potential sources of blood loss and receive iron replacement. (See "Treatment of iron deficiency and iron deficiency anemia in adults".)
●Zinc – Zinc supplementation is usually given at a dose of 50 mg elemental zinc daily [73].
Water and electrolytes — Water and electrolyte levels should be monitored, especially in individuals with chronic anorexia, vomiting, or diarrhea or cirrhosis. Reduced sodium and water absorption in the small intestine with chronic alcohol use predisposes to diarrhea [25,74]. In combination with inebriation, nausea, vomiting, and poor intake of water, reduced sodium and water absorption can predispose to dehydration and hyponatremia. In people with cirrhosis, guidance for salt and water intake needs to take into consideration their cirrhosis and ascites status [75]. (See "Hyponatremia in patients with cirrhosis".)
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Alcohol use disorders and withdrawal" and "Society guideline links: Healthy diet in adults".)
SUMMARY AND RECOMMENDATIONS
●Introduction – Excessive alcohol use is a major cause of nutritional deficiency in resource-abundant countries. (See 'Introduction' above.)
●Terminology – Terms used to describe alcohol use and disorders and alcohol-related problems include (see 'Terminology' above):
•Unhealthy alcohol use – Unhealthy alcohol use encompasses the spectrum of alcohol use that can result in health consequences. It includes risky alcohol use and alcohol use disorders.
•Risky alcohol use – Risky alcohol use refers to the consumption of an amount of alcohol that puts the individual at risk for health consequences, but the pattern of alcohol use is not so severe as to meet diagnostic criteria for alcohol use disorder.
•Heavy alcohol use – The National Institute on Alcohol Abuse and Alcoholism defines heavy alcohol use as more than five drinks per day or more than 15 drinks per week for males and more than four drinks per day or more than eight drinks per week for females.
•Alcohol use disorder – Alcohol use disorder is defined as a problematic pattern of alcohol use leading to clinically significant impairment or distress, as manifested by 11 specific psychosocial, behavioral, or physiologic criteria (table 1). (See "Risky drinking and alcohol use disorder: Epidemiology, clinical features, adverse consequences, screening, and assessment", section on 'Terminology'.)
●Pathogenesis and manifestations of malnutrition – Acute and chronic alcohol consumption can cause malnutrition by decreasing dietary macro- and micronutrient intake, impairing nutrient absorption and digestion, decreasing protein synthesis, and increasing the breakdown and excretion of nutrients. The degree of malnutrition depends on the amount of alcohol consumed, the quality of food intake, patient genetics, and the presence and severity of comorbid illnesses. (See 'Pathogenesis and manifestations of alcohol-related malnutrition' above.)
●Assessment of nutrition – Evaluation for the presence of malnutrition includes a focused history, physical examination, and laboratory evaluation to evaluate for liver and kidney dysfunction. We perform additional micronutrient testing in individuals whose initial evaluation suggests malnutrition or exocrine pancreas insufficiency. (See 'Assessment of nutrition' above.)
●Nutrition supplementation – The goal of nutrition supplementation is to restore adequate energy and protein intake and to prevent or treat symptoms of nutrient deficiencies. This can include supplementation of macronutrients, water- and fat-soluble vitamins, minerals and trace elements, and water and electrolytes. (See 'Management of nutritional deficiencies' above.)
•For adults with an alcohol use disorder or heavy alcohol use, we suggest supplementation with a multivitamin that contains a minimum of thiamine 100 mg daily, vitamin B6 2 mg daily, and folic acid 400 mcg to 1 mg daily rather than no supplementation (Grade 2C). (See 'Management of nutritional deficiencies' above.)
•In the absence of an identified deficiency, we do not routinely supplement vitamins B2, B12, or C.
•We do not routinely supplement vitamins A, D, E, or K, except in individuals with chronic pancreatitis or alcohol-associated liver disease who have fat malabsorption or previously documented deficiencies.
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