Introduction
Alcohol and micronutrient absorption and status
Effects of alcohol on metabolic pathways
AUD and diet quality
Clinical and public health implications
Research gaps and future directions
Conclusions
References
Further reading
Chronic alcohol consumption disrupts nutrient absorption, metabolism, and dietary quality, contributing to widespread micronutrient deficiencies and metabolic dysfunction. These nutritional disturbances exacerbate liver disease, neurological damage, and recovery challenges in individuals with alcohol use disorder.
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Introduction
This article explores the intersection between drinking and nutrition to reveal how alcohol-induced malnutrition can perpetuate a cycle of craving and relapse.
Alcohol use disorder (AUD) is strongly associated with disturbances in nutritional status arising from both reduced dietary intake and alcohol-mediated disruptions in nutrient absorption, metabolism, storage, and utilization. These disturbances contribute to systemic complications, including liver disease, neurological dysfunction, immune impairment, and metabolic dysregulation. Alcohol-derived calories frequently displace nutrient-dense foods, while chronic exposure alters gastrointestinal, hepatic, and endocrine processes required for maintaining nutritional homeostasis.1,3,4
Alcohol and micronutrient absorption and status
The most severe nutritional consequence of chronic alcohol consumption is the depletion of micronutrients that occurs due to impaired intestinal absorption and increased renal excretion.1 Specifically, ethanol acts as a molecular disruptor of the brush border membrane (BBM) by targeting specific transporters required for the uptake of water-soluble vitamins.
Chronic ethanol consumption has been directly implicated in vitamin B1 deficiency by inhibiting the activity of SLC19A2, a transporter protein for thiamine. Similar inhibitory effects on the absorption of vitamins C and B12, riboflavin, biotin, and folate have been clinically observed.
Alcohol can also impair sodium-dependent and carrier-mediated nutrient transport systems located on intestinal epithelial cells, including transporters involved in glucose, amino acid, and micronutrient uptake. Disruption of these brush-border transport processes alters the function of intestinal enterocytes and contributes to malabsorption of essential nutrients in the small intestine.2
Alcohol consumption also alters the absorption and systemic concentrations of several macroelements and trace elements, including magnesium, potassium, sodium, calcium, selenium, zinc, chromium, and phosphorus. These disturbances may result from gastrointestinal malabsorption, increased urinary losses caused by alcohol’s diuretic effects, and impaired hepatic storage or metabolic regulation.7
Ethanol intake also reduces intestinal absorption of calcium, zinc, iron, and magnesium, in addition to interfering with dietary fat absorption in a dose-dependent manner. Drinking alcohol, even in moderate amounts, also reduces glucose absorption by reducing its maximal rate of uptake to limit its active transport into the bloodstream, rather than through its interactions with a specific transporter.
In addition to water-soluble vitamins, chronic alcohol use may also contribute to deficiencies in fat-soluble vitamins (A, D, E, and K), particularly in individuals with liver disease, steatorrhea, or impaired lipid digestion. These vitamins play essential roles in immune function, bone metabolism, antioxidant defense, and blood coagulation, and their depletion may exacerbate complications associated with chronic alcohol use.6
Ethanol possesses a high caloric density despite being entirely devoid of essential vitamins, minerals, and macronutrients.1 Thus, in addition to the direct effects of ethanol intake on nutrient absorption, primary malnutrition also arises due to the substitution of dietary carbohydrate, protein, and fat intake with alcoholic calories.
Furthermore, alcohol consumption can disrupt iron homeostasis through alterations in the hepatic hormone hepcidin, which regulates intestinal iron absorption and systemic iron distribution. Experimental evidence suggests that alcohol exposure can suppress hepatic hepcidin expression while modifying ferroportin activity and other iron-regulatory proteins. These alterations may lead to abnormal iron distribution and contribute to oxidative stress and liver injury in alcohol-related liver disease.8
The nutritional deficiencies observed in individuals with alcohol use disorder (AUD) contribute not only to physiological impairments such as alcohol-related liver disease but also to the core symptoms of alcoholism, such as cognitive dysfunction and increased negative affect, thereby contributing to the vicious cycle of alcoholism and comorbidity.1”
Hepatic ethanol metabolism primarily occurs through the alcohol dehydrogenase (ADH) pathway, which generates acetaldehyde, a highly reactive toxin that forms DNA and protein adducts.1 This process further reduces nicotinamide adenine dinucleotide (NAD+) to NADH, which significantly increases the NADH/NAD+ ratio. The subsequent inhibition of fatty acid oxidation while promoting triglyceride synthesis directly leads to hepatic steatosis.2
Additional metabolic pathways involved in ethanol metabolism include the microsomal ethanol-oxidizing system (MEOS), largely mediated by cytochrome P450 2E1 (CYP2E1), and catalase-mediated oxidation in peroxisomes. Activation of these pathways promotes the generation of reactive oxygen species (ROS), contributing to oxidative stress, lipid peroxidation, mitochondrial dysfunction, and inflammatory signaling.7
Ethanol also acts as a metabolic toxin by inhibiting the mammalian target of rapamycin (mTOR) pathway, a central regulator of muscle protein synthesis. Furthermore, alcohol reduces the phosphorylation of downstream targets such as ribosomal protein S6 kinase beta-1 (S6K1) and eukaryotic translation initiation factor 4E-binding protein 4EBP1, thereby preventing protein synthesis.4
These alterations contribute to skeletal muscle wasting, metabolic dysfunction, and impaired energy homeostasis.9 Chronic inflammation and oxidative stress further suppress anabolic signaling pathways involved in tissue repair and metabolic regulation.7,9
Can Alcohol Abuse Cause Malnutrition?
AUD and diet quality
Diet quality in individuals with AUD can vary greatly during periods of active use and post-cessation recovery. During active drinking, diet quality is generally poor, with patients scoring an average of 42.9 on the Healthy Eating Index-2015 (HEI-2015), compared with 54.3 in healthy controls.4 Using the Nova classification system, ultra-processed foods accounted for approximately 51.8% of total energy intake among individuals with active AUD.4
Despite apparently adequate caloric intake in some individuals with AUD, micronutrient deficiencies remain common because alcohol interferes with nutrient absorption, metabolism, and biological utilization.4
Upon cessation of alcohol use, many individuals report a sweet preference, during which they increase their intake of highly palatable and sweet foods to alleviate withdrawal symptoms. Although diet quality typically improves during abstinence, with HEI scores rising to 52.2 after three weeks of detoxification, these individuals often fail to meet national recommendations for fiber and micronutrient intake.4
Clinical and public health implications
Clinical guidelines from the European Society for Clinical Nutrition and Metabolism (ESPEN) emphasize that nutritional status is a powerful predictor of mortality and morbidity in patients with alcohol-related liver disease.9 Thus, standard AUD assessments and monitoring should extend beyond body mass index (BMI) values to include tools such as the Naples Score, which incorporates serum albumin and inflammatory markers as prognostic indicators of rehospitalization.1
Protein-energy malnutrition and sarcopenia are frequently observed in patients with advanced liver disease, particularly cirrhosis, and may significantly influence clinical outcomes. Deficiencies in trace elements and water-soluble vitamins are also common in alcohol-related liver disease and contribute to metabolic, neurological, and immune complications.9
Bioelectrical impedance analysis (BIA), which is increasingly being incorporated into AUD patient management, can be used to calculate the phase angle, a measurement of cell mass that predicts survival in cirrhotic patients.9
Nutritional interventions, including high-protein diets and targeted micronutrient supplementation, are recommended as essential components of post-cessation recovery.1,3 Integrating these strategies into addiction medicine is hypothesized to potentially stabilize metabolic health needed to maintain neurological health and successful long-term recovery; however, long-term studies are needed to confirm these hypotheses.4
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Research gaps and future directions
Despite significant recent progress, sex-specific vulnerabilities to alcohol-induced damage remain unclear. For example, although men are significantly more likely to develop AUD, females are at a greater risk of experiencing alcohol-related complications like alcoholic liver disease, breast cancer, and cardiovascular disease. These differences may be attributed to females absorbing alcohol differently than their male counterparts, potentially due to lower basal body water content.1
Additionally, current evidence indicates that dietary assessment methods used in AUD research vary widely, underscoring the need for standardized, validated tools to assess diet quality and nutritional status in this population.4
Data on the nutritional impact of moderate alcohol consumption remain inconsistent, with low certainty regarding its effects on body weight and adiposity relative to age and genetics.3 Thus, recent reviews encourage future researchers to prioritize longitudinal studies and the development of validated and AUD-specific dietary assessment tools to better inform clinical care.4
Conclusions
Ethanol functions as a multitarget toxin that displaces essential nutrients, disrupts gut function, and paralyzes anabolic pathways, leading to thiamine, vitamin D, and zinc deficiencies. For healthcare professionals, these findings emphasize the importance of integrating nutritional screening and rehabilitation into AUD treatment.
A comprehensive clinical approach that includes dietary assessment, micronutrient monitoring, and targeted nutritional interventions may improve treatment outcomes and reduce complications associated with chronic alcohol use.1,4,9
References
- White, B., & Sirohi, S. (2024). A Complex Interplay between Nutrition and Alcohol use Disorder: Implications for Breaking the Vicious Cycle. Current Pharmaceutical Design 30(23); 1822-1837. DOI: 10.2174/0113816128292367240510111746. https://pmc.ncbi.nlm.nih.gov/articles/PMC12085226/
- Butts, M., Sundaram, V. L., Murughiyan, U., et al. (2023). The Influence of Alcohol Consumption on Intestinal Nutrient Absorption: A Comprehensive Review. Nutrients 15(7); 1571. DOI: 10.3390/nu15071571. https://www.mdpi.com/2072-6643/15/7/1571
- Review of Evidence on Alcohol and Health (2025). (B. N. Calonge & K. B. Stone, Eds.). National Academies Press. DOI: 10.17226/28582. https://www.nationalacademies.org/read/28582/chapter/1#xxiii
- Barb, J. J., King, L. C., Nanda, S., et al. (2026). Dietary intake, quality, and assessment tools in individuals with problematic alcohol use: a scoping review and meta-analysis. Translational Psychiatry 16(1). DOI: 10.1038/s41398-026-03842-9. https://www.nature.com/articles/s41398-026-03842-9
- Zemp, J., Erol, C., Kaiser, E., et al. (2025). A systematic review of evidence-based clinical guidelines for vitamin D screening and supplementation over the last decade. Archives of Public Health 83(1). DOI: 10.1186/s13690-025-01709-x. https://link.springer.com/article/10.1186/s13690-025-01709-x
- Andrès, E., Lorenzo-Villalba, N., Terrade, J., & Méndez-Bailon, M. (2024). Fat-Soluble Vitamins A, D, E, and K: Review of the Literature and Points of Interest for the Clinician. Journal of Clinical Medicine 13(13); 3641. DOI: 10.3390/jcm13133641. https://www.mdpi.com/2077-0383/13/13/3641
- Baj, J., Flieger, W., Teresinski, G., et al. (2020). Magnesium, Calcium, Potassium, Sodium, Phosphorus, Selenium, Zinc, and Chromium Levels in Alcohol Use Disorder: A Review. Journal of Clinical Medicine 9(6); 1901. DOI: 10.3390/jcm9061901. https://www.mdpi.com/2077-0383/9/6/1901
- Varghese, J., James, J. V., Sagi, S., et al. (2016). Decreased hepatic iron in response to alcohol may contribute to alcohol-induced suppression of hepcidin. British Journal of Nutrition 115(11); 1978-1986. DOI: 10.1017/s0007114516001197. https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/decreased-hepatic-iron-in-response-to-alcohol-may-contribute-to-alcoholinduced-suppression-of-hepcidin/5811E83141229B5DBDD5A2067C58E301
- Plauth, M., Bernal, W., Dasarathy, S., et al. (2019). ESPEN guideline on clinical nutrition in liver disease. Clinical Nutrition 38(2); 485-521. DOI: 10.1016/j.clnu.2018.12.022. https://www.espen.org/files/ESPEN-Guidelines/ESPEN_guideline_on_clinical_nutrition_in_liver_disease.pdf
Further Reading
Last Updated: Mar 4, 2026