Why Does Vitamin B6 Deficiency Lead to Anemia?

January 3, 2026 •

3 min read

According to the Centers for Disease Control (CDC), over 10% of the U.S. population may have a vitamin B6 deficiency, a condition that can have wide-ranging health effects, including the development of anemia. So, why does vitamin B6 deficiency lead to anemia and how does it impact the body's red blood cell production?

Quick Summary

This article explains the biological pathway connecting low vitamin B6 to anemia. It details the role of pyridoxal phosphate in heme synthesis and the resulting impact on hemoglobin and red blood cells.

Key Points

Essential Coenzyme: Vitamin B6 (as pyridoxal 5'-phosphate) is a coenzyme for delta-aminolevulinate synthase (ALAS), the rate-limiting enzyme in heme synthesis.
Impaired Heme Synthesis: Without adequate B6, the production of heme is disrupted, which in turn leads to insufficient hemoglobin formation.
Microcytic Hypochromic Anemia: The resulting anemia is characterized by red blood cells that are smaller (microcytic) and paler (hypochromic) than normal.
Sideroblastic Anemia: Severe B6 deficiency can cause sideroblastic anemia, where iron accumulates in developing red blood cells rather than being incorporated into heme.
Secondary Deficiency: B6 deficiency is often secondary to medical conditions like kidney disease, alcoholism, malabsorption disorders, or medications rather than just poor diet.
Neurological and Other Symptoms: Anemia is often accompanied by other symptoms, including fatigue, peripheral neuropathy, and mood changes.

The Crucial Role of Vitamin B6 in Red Blood Cell Production

Vitamin B6, also known as pyridoxine, is vital for over 100 enzymatic reactions in the body, with its active form, pyridoxal 5'-phosphate (PLP), essential for metabolic processes. Its most significant connection to anemia is its role in heme synthesis. Heme is a fundamental component of hemoglobin, which transports oxygen via red blood cells. A lack of B6 impairs this process, leading to reduced oxygen-carrying capacity and anemia.

The Heme Synthesis Pathway and B6's Role

Heme production primarily occurs in red blood cell precursors' mitochondria and involves multiple steps. The initial, rate-limiting step relies on the enzyme delta-aminolevulinate synthase (ALAS), which requires PLP as a coenzyme.

When vitamin B6 is deficient:

ALAS activity is reduced due to insufficient PLP, hindering the start of heme synthesis.
Heme production significantly decreases as the pathway's initial product is lacking.
Insufficient heme leads to inadequate hemoglobin formation.
Anemia develops, characterized by the release of small, pale red blood cells, potentially leading to microcytic, hypochromic, or sideroblastic anemia.

Sideroblastic Anemia: A Specific Outcome

Sideroblastic anemia is a specific type of anemia linked to vitamin B6 deficiency. In this condition, iron is not properly incorporated into heme, causing iron accumulation in red blood cell precursors' mitochondria, visible as 'ringed sideroblasts'. B6 deficiency is a key cause, and supplementation can often reverse it.

Symptoms and Risk Factors for Deficiency

Vitamin B6 deficiency often co-occurs with other B vitamin deficiencies and is linked to various health conditions. Symptoms vary from mild to severe, especially with developing anemia.

Common Symptoms of B6 Deficiency

Fatigue and weakness due to reduced oxygen transport.
Peripheral neuropathy, causing numbness and tingling.
Skin issues like eczema and a swollen tongue.
Mood changes, including depression and confusion.
Weakened immunity due to impaired immune cell production.

Key Risk Factors for B6 Deficiency

While poor diet can contribute, B6 deficiency is frequently secondary to other medical conditions.

Risk factors include:

Alcohol use disorder, which reduces active B6.
Chronic kidney disease and dialysis, leading to reduced B6 levels.
Malabsorption syndromes such as celiac disease.
Certain medications like isoniazid, which interfere with B6.
Autoimmune disorders causing increased B6 breakdown.

B6 Deficiency Anemia vs. Iron Deficiency Anemia

Both B6 and iron deficiency can cause microcytic, hypochromic anemia, but their underlying mechanisms differ. Iron studies are key to distinction.


Feature	Vitamin B6 Deficiency Anemia (Sideroblastic)	Iron Deficiency Anemia
Mechanism	Impaired iron utilization for heme synthesis due to low B6.	Insufficient iron for heme and hemoglobin production.
Iron Studies	High or normal serum iron and ferritin.	Low serum iron and ferritin.
Bone Marrow	Presence of 'ringed sideroblasts'.	Absent ringed sideroblasts, depleted iron.
Red Blood Cells	Microcytic and hypochromic.	Microcytic and hypochromic.
Treatment	Vitamin B6 supplementation.	Iron supplementation.

Diagnosis and Treatment

Diagnosis of B6 deficiency involves symptoms and lab tests, primarily measuring plasma PLP levels (below 20 nmol/L is deficient). Assessing other B vitamins and iron levels is also common.

Treatment is typically oral B6 supplementation, with dosage adjusted based on severity and cause. Prophylactic B6 may be given with certain medications. Addressing underlying conditions is crucial for long-term recovery. Caution is needed with high doses due to potential neurological toxicity, requiring medical supervision. Further information is available from the NIH Office of Dietary Supplements fact sheet.

Conclusion

Vitamin B6 deficiency leads to anemia by disrupting the synthesis of heme, a critical component of hemoglobin necessary for oxygen transport. As a coenzyme for the key enzyme in heme production, a lack of B6 halts this process, resulting in microcytic, hypochromic, and potentially sideroblastic anemia. While diet contributes, underlying medical conditions and medications are often the primary cause. Diagnosis through blood tests and appropriate B6 supplementation are essential for treatment and recovery.

Frequently Asked Questions

The primary function of vitamin B6 related to blood is its role as a coenzyme in the synthesis of heme, which is a key component of hemoglobin. Hemoglobin is the protein in red blood cells that carries oxygen.

A vitamin B6 deficiency typically causes a microcytic, hypochromic anemia, where red blood cells are smaller and paler than normal. It can also lead to a specific form called sideroblastic anemia.

Medical conditions can cause B6 deficiency through several mechanisms, including malabsorption (e.g., celiac disease), increased metabolic clearance (e.g., kidney disease), or interference by drugs (e.g., isoniazid).

Symptoms of vitamin B6 deficiency include fatigue, skin rashes, swollen tongue, confusion, depression, and peripheral neuropathy, in addition to anemia.

Diagnosis involves a clinical evaluation of symptoms and laboratory tests. A blood test measuring plasma pyridoxal 5'-phosphate (PLP) is the most common and accurate method.

The treatment for vitamin B6 deficiency anemia is oral supplementation with pyridoxine. Dosage and duration depend on the severity and underlying cause of the deficiency.

Yes, while deficiency is problematic, excessive, long-term intake of vitamin B6 can cause neurological toxicity. It is important to only take high doses under medical supervision.

Good sources of vitamin B6 include fish, beef liver, poultry, potatoes, starchy vegetables, and fortified cereals. The vitamin from animal sources is generally more bioavailable.