Hypothyroidism occurs when the thyroid gland does not produce enough thyroid hormone, slowing down various metabolic processes. Anemia is characterized by a lower-than-normal amount of healthy red blood cells, which carry oxygen throughout the body. The connection between low thyroid hormone levels and developing anemia is well-established. Since anemia symptoms, such as fatigue and weakness, often overlap with those of hypothyroidism, the anemia can sometimes be overlooked until thyroid function is evaluated.
Specific Anemia Types Linked to Hypothyroidism
Hypothyroidism predisposes individuals to three distinct classifications of anemia, determined by the size and appearance of the red blood cells. The most frequently observed type is normocytic anemia, often called anemia of chronic disease. In this condition, red blood cells appear normal in size, but their overall number is reduced due to the systemic effects of the underlying chronic thyroid condition.
Microcytic anemia is another common presentation, where red blood cells are visibly smaller and paler than usual. This morphology is a classic sign of iron deficiency anemia. Low thyroid function disrupts nutrient processing, often leading to inadequate iron availability for red blood cell production.
The third type is macrocytic anemia, which involves the production of abnormally large red blood cells. This classification usually indicates a deficiency in vitamin B12 or folate. Macrocytic anemia is strongly associated with the autoimmune nature of many hypothyroidism cases.
How Low Thyroid Function Causes Anemia
The link between low thyroid function and anemia involves several interconnected physiological pathways impacting red blood cell health. Thyroid hormone (T3) is necessary for stimulating the bone marrow, which produces red blood cells (erythropoiesis). When thyroid hormone levels are low, bone marrow activity is suppressed, directly decreasing the rate of red blood cell creation.
The thyroid also influences the production of erythropoietin, a hormone primarily made by the kidneys that signals the bone marrow to accelerate red blood cell production. Reduced thyroid hormone levels result in lower erythropoietin production, further limiting the body’s ability to generate new blood cells. This dual effect contributes significantly to the development of normocytic anemia.
Hypothyroidism also compromises the gastrointestinal tract, leading to nutrient deficiencies that cause microcytic and macrocytic anemias. Low thyroid hormone levels can reduce the secretion of gastric acid in the stomach, known as hypochlorhydria. Gastric acid is necessary to convert dietary non-heme iron into its absorbable form. This means the body cannot absorb enough iron, even with adequate intake.
When hypothyroidism is caused by Hashimoto’s thyroiditis, there is a higher chance of developing autoimmune gastritis. This disorder causes the immune system to attack the stomach lining, impairing the production of intrinsic factor. Intrinsic factor is required for the absorption of vitamin B12 in the small intestine, and its deficiency leads directly to pernicious anemia, a form of macrocytic anemia.
The systemic inflammation associated with autoimmune hypothyroidism also plays a role in anemia of chronic disease through the action of hepcidin. Chronic inflammatory states elevate hepcidin levels, which block the release of stored iron from macrophages and liver cells. This mechanism traps the iron in storage, making it unavailable for the bone marrow to synthesize hemoglobin. This functional iron deficiency prevents the normal production of healthy cells, contributing to the overall anemia.
Diagnosing and Resolving the Anemia
Diagnosing anemia in a patient with hypothyroidism requires a specific panel of blood tests to pinpoint the type and underlying cause. A Comprehensive Blood Count (CBC) is the first step; it confirms anemia by measuring hemoglobin and hematocrit levels. The CBC also provides the Mean Corpuscular Volume (MCV) to classify red blood cell size as microcytic, normocytic, or macrocytic, which directs further investigation.
Thyroid function tests, including TSH and Free T4, confirm the diagnosis of hypothyroidism. To determine if the anemia is due to nutrient deficiencies, blood work must also include testing for serum ferritin, which indicates iron stores, and levels of vitamin B12 and folate. These results help distinguish between a production problem and an absorption problem.
The primary strategy for resolving anemia caused by hypothyroidism is to treat the underlying thyroid condition with hormone replacement therapy, typically using Levothyroxine. Normalizing thyroid hormone levels often reverses bone marrow suppression and the chronic inflammatory state, allowing the body to correct the anemia over several months. This resolution occurs because the therapeutic dose restores erythropoietin production and normalizes metabolism.
However, thyroid treatment alone may not be sufficient in cases of severe or long-standing nutrient deficiencies. Targeted supplementation is necessary, such as oral or intravenous iron for iron deficiency anemia, or vitamin B12 injections for pernicious anemia. Iron and calcium supplements can interfere with Levothyroxine absorption, requiring a separation of at least four hours between taking the medication and the supplements.