Introduction
Alcoholism, also known as alcohol use disorder (AUD), is a common medical condition where people have problems controlling their alcohol consumption despite the risk to their health, safety and personal relationships. Someone suffering from alcoholism physically craves alcohol, needing to drink daily to avoid withdrawal symptoms. Alcoholism has both short-term and long-term effects on your health and safety. Brain damage, heart disease, liver cirrhosis and some forms of cancer are possible health consequences of heavy alcohol use.
The liver breaks down and removes the alcohol you consume from your blood in a process called oxidation.1 Excessive alcohol consumption causes the accumulation of toxic substances in the liver.2 This overwhelms the liver’s ability to process alcohol and ultimately leads to liver damage. While under normal circumstances the liver can regenerate itself, alcoholism can impair this ability and cause permanent liver damage.3
Red blood cells (RBCs), also known as erythrocytes, transport oxygen from the lungs to the rest of the body.5 Oxygen is essential for human life because it is required for converting food into energy, which fuels all bodily functions. RBCs account for 40-45% of the blood’s volume and are responsible for the distinct colour of blood.4
Anaemia is a condition where the body has low levels of healthy red blood cells or the red blood cells don’t function properly. Anaemia prevents your body from getting enough oxygen and can lead to fatigue (tiredness). Normocytic anaemia is a form of anaemia in which the number of red blood cells is reduced, but each cell remains of normal size. Most often, it is caused by other chronic diseases, including inflammatory conditions.5
In normocytic anaemia, the haemoglobin, the protein that helps RBCs carry oxygen, content decreases in RBCs. Haemoglobin is a kind of.4-7 Alcoholism can impair RBC production and can contribute to normocytic anaemia and its underlying causes.
Basics of red blood cell production (erythropoiesis)
RBCs are made in the bone marrow
Erythropoiesis is the production of red blood cells. RBCs are produced in the bone marrow, which is the soft, spongy tissue inside your bones and is responsible for generating billions of new blood cells each day.
The bone marrow also makes the other two types of blood cells: white blood cells and platelets.5 The general term used to describe the production of blood cells is hematopoiesis, with the term erythropoiesis referring specifically to the generation of RBCs.
Fetal erythropoiesis refers to RBC production that occurs before birth. The location of fetal erythropoiesis varies depending on the stage of development of the fetus during pregnancy. Erythropoiesis in children and adults predominantly happens in the bone marrow.
How RBCs are made
The hormone erythropoietin (EPO) is responsible for RBC production. The kidneys secrete EPO, which then signals to the bone marrow to produce more RBCs when levels are low. The kidneys release low levels of EPO to maintain regular RBC production. When there is a sufficient amount of RBCs in the blood, the kidneys sense this through heightened haemoglobin levels and release less EPO to maintain the right amount of RBCs.
Erythropoiesis takes around a week to produce a fully mature RBC, with the average lifespan of 120 days. Erythropoiesis replenishes RBCs that have reached the end of their lifespan. Iron, vitamin B12, and vitamin B9 (also known as folate or folic acid) are key nutrients in erythropoiesis.8
Alcohol’s impact on red blood cell production
Bone marrow suppression
Chronic excessive alcohol consumption decreases RBC production. Alcohol is directly toxic to bone marrow stem cells, the precursors of blood cells, and suppresses the production of blood cells, including RBCs. The toxicity of alcohol to the bone marrow depends on the amount consumed. Serious impairment of blood cell production usually occurs in people with severe alcoholism. Those with severe alcoholism may also have a poor diet, resulting in deficiencies in the nutrients that are important for erythropoiesis. In addition to reducing RBC count, alcoholism may also cause abnormalities in the structure and function of RBCs.5
Nutritional deficiencies caused by alcohol
Malnutrition is common in people with alcoholism.9 Nutritional deficiencies are an indirect result of frequent alcohol consumption. Alcohol use interferes with the absorption of the nutrient iron in haemoglobin. Iron is vital for red blood cells because it allows the protein haemoglobin to carry oxygen within RBCs.
Alcoholism can also cause iron deficiency or excessive amounts of iron in the body. Excessive gastrointestinal bleeding can also cause iron deficiency in alcoholics. Iron deficiency can be hard to diagnose in alcoholics because of symptoms caused by other nutritional deficits, such as liver disease or inflammation.5
Frequent alcohol ingestion can damage the digestive system and negatively impact the absorption of vitamin B12 and B9 from food. Deficiency in vitamin B12 and/or B9 lead to abnormally enlarged red blood cells that do not function normally.
Liver damage
One of the many functions of the liver is to get rid of old RBCs. Alcoholism significantly impacts the liver and can lead to three types of liver disease:
- Fatty liver – accumulation of excess fat in the liver
- Alcoholic hepatitis – inflammation of the liver
- Alcohol-related cirrhosis – normal liver tissue is replaced by scarred tissue
Alcohol-related cirrhosis can lead to decreased RBC production and subsequently normocytic anaemia or other types of anaemia.5
Normocytic anaemia in chronic alcoholism
Alcohol use is toxic to bone marrow, suppressing RBC production without necessarily affecting RBC size. This is known as normocytic anaemia. Nutritional deficiencies in people with alcoholism can arise from poor diets. Certain vitamin deficiencies, such as folate (vitamin B9) can lead to anaemia where RBCs are larger than normal, known as macrocytic anaemia. However, in the early stages of anaemia in malnourished chronic alcoholic patients, the size of red blood cells can remain normal.
Normocytic anaemia commonly arises from complications of chronic diseases or infections.7 Alcoholism can cause gastritis or liver disease, which can lead to gastrointestinal bleeding. This can appear as normocytic anaemia before iron deficiency occurs. Liver disease or chronic inflammation from AUD can lead to anaemia of chronic disease, which is usually normocytic and normochromic anaemia.7,10
Symptoms of normocytic anaemia
Common symptoms of normocytic anaemia are:7
- Fatigue or feeling weak
- Dizziness
- Shortness of breath
- Fast heartbeat
- Headaches
- Pallor (pale)
- Dry skin or easily bruised skin
Diagnosis of normocytic anaemia
Healthcare providers use blood tests and other assessments to diagnose normocytic anaemia. Anaemia can be identified with a Complete Blood Count (CBC) evaluation. This blood test examines the levels of red blood cells, white blood cells, platelets and other markers in the blood. The mean corpuscular volume (MCV) tests for the size of red blood cells.5 The key feature of normocytic anaemia is RBCs that appear normal in size but are low in number.7
Additional tests may be conducted to help diagnose normocytic anaemia, such as:7
- Reticulocyte count
- Peripheral blood smear
- Nutritional assessments
- Liver function tests
Diagnosis of normocytic anaemia requires a professionally branched healthcare team. Determining the underlying disease that leads to normocytic anaemia is a key aspect in the diagnosis of normocytic anaemia.7 It is important to consult your doctor or primary care provider if you experience symptoms of normocytic anaemia or need support regarding alcohol consumption.
Treatment and management
Addressing underlying causes
Treatment and management of normocytic anaemia depend on treating the underlying cause of the anaemia to restore RBC levels to normal.4,7 Addressing excessive alcohol consumption that leads to liver disease and subsequent anaemia is one aspect of managing normocytic anaemia from alcoholism.
Alcohol cessation programs can provide support on how to manage alcohol use. Seeking local alcohol addiction support services to help cut down or stop drinking is one of the first steps in managing your health when you have normocytic anaemia associated with alcohol usage. Treating underlying liver disease from excessive alcohol use is also another important consideration.
Nutritional support
Nutritional deficiencies arise from and accompany chronic alcohol use and normocytic anaemia. Dietary supplement intervention can address deficiencies in iron, vitamin B12 and folate. Eating foods rich in iron, vitamin B12, and folate can also help with nutritional deficiencies related to normocytic anaemia.4
Monitoring and supporting bone marrow recovery
Alcohol use damages the stem cells in the bone marrow that are responsible for RBC production, resulting in aplastic anaemia. A bone marrow transplant is a procedure that replaces damaged bone marrow, which may be necessary to treat aplastic anaemia.7
Summary
Alcoholism is when someone has trouble managing their alcohol consumption. Normocytic anaemia is the condition where someone has fewer RBCs than normal, albeit those are still of normal size. Alcoholism can damage the liver and reduce the production of RBCs, which are essential in transporting oxygen from your lungs to the rest of your body. Alcoholism can lead to nutritional deficiencies in iron, vitamin B12 and folate as well as liver damage, which can cause subsequent anaemia that is normocytic. Diagnosis of normocytic anaemia by healthcare professionals can include blood tests to examine the health and size of your RBCs. Chronic diseases are the most common underlying cause of normocytic anaemia. Therefore, it is crucial to treat the underlying chronic diseases and conditions to address normocytic anaemia. Management of normocytic anaemia due to alcoholism includes managing alcohol use, nutritional support, and monitoring bone marrow health.
References
- Fernández-Checa JC, Kaplowitz N, Colell A, García-Ruiz C. Oxidative Stress and Alcoholic Liver Disease. Alcohol Health Res World [Internet]. 1997 [cited 2025 Apr 17]; 21(4):321–4. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6827680/.
- Lieber CS. Mechanism of ethanol induced hepatic injury. Pharmacol Ther. 1990; 46(1):1–41. Available from: https://pubmed.ncbi.nlm.nih.gov/2181486/.
- Alcohol-related liver disease. nhs.uk [Internet]. 2017 [cited 2025 Apr 17]. Available from: https://www.nhs.uk/conditions/alcohol-related-liver-disease-arld/.
- Ballard HS. The Hematological Complications of Alcoholism. Alcohol Health Res World [Internet]. 1997 [cited 2025 Apr 17]; 21(1):42–52. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826798/.
- Brill JR, Baumgardner DJ. Normocytic Anemia. afp [Internet]. 2000 [cited 2025 Apr 17]; 62(10):2255–63. Available from: https://www.aafp.org/pubs/afp/issues/2000/1115/p2255.html.
- Normocytic Anemia: What It Is, Causes & Symptoms. Cleveland Clinic [Internet]. [cited 2025 Apr 17]. Available from: https://my.clevelandclinic.org/health/diseases/22977-normocytic-anemia.
- Yilmaz G, Shaikh H. Normochromic Normocytic Anemia. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 [cited 2025 Apr 17]. Available from: http://www.ncbi.nlm.nih.gov/books/NBK565880/.
- Koury MJ, Ponka P. NEW INSIGHTS INTO ERYTHROPOIESIS: The Roles of Folate, Vitamin B12 , and Iron. Annu Rev Nutr [Internet]. 2004 [cited 2025 Apr 17]; 24(1):105–31. Available from: https://www.annualreviews.org/doi/10.1146/annurev.nutr.24.012003.132306.
- Barve S, Chen S-Y, Kirpich I, Watson WH, McClain C. Development, Prevention, and Treatment of Alcohol-Induced Organ Injury: The Role of Nutrition. Alcohol Res [Internet]. 2017 [cited 2025 Apr 17]; 38(2):289–302. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5513692/.
- Gonzalez-Casas R, Jones EA, Moreno-Otero R. Spectrum of anemia associated with chronic liver disease. World J Gastroenterol [Internet]. 2009 [cited 2025 Apr 18]; 15(37):4653–8. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754513/.

