Hypothyroidism, or an underactive thyroid gland, is a condition where the thyroid does not produce enough hormones. These hormones regulate metabolism, affecting nearly every organ and process in the body. Iron deficiency anemia (IDA) occurs when the body lacks sufficient iron to produce healthy red blood cells, leading to symptoms like fatigue and weakness. Research confirms a strong relationship between hypothyroidism and low iron levels. Patients frequently experience both conditions simultaneously, and the presence of one can worsen the other. Understanding this connection is important for achieving the best health outcomes.
How Hypothyroidism Affects Iron Absorption and Utilization
Hypothyroidism commonly leads to hypochlorhydria, a reduction in the production of stomach acid. Thyroid hormones stimulate the stomach lining to secrete this acid. When thyroid hormone levels are low, this stimulation is diminished, resulting in less stomach acid being produced.
Adequate stomach acid is required to convert dietary non-heme iron (found in plant sources) into its absorbable form, ferrous iron (\(\text{Fe}^{2+}\)). Without sufficient acid, iron remains in the less absorbable ferric form (\(\text{Fe}^{3+}\)), meaning the small intestine cannot efficiently absorb it. This failure directly impedes the body’s ability to acquire healthy iron stores.
The resulting chronic malabsorption sets the stage for iron deficiency, even in individuals consuming an iron-rich diet. This creates a cycle where poor thyroid function hinders iron absorption, which in turn can complicate thyroid hormone production.
Specific Biological Mechanisms of the Connection
Low thyroid hormone levels also impair the body’s ability to use iron for making red blood cells (erythropoiesis). Thyroid hormones, specifically triiodothyronine (\(\text{T}_3\)), stimulate the bone marrow to produce red blood cells. When these hormones are deficient, this stimulation is reduced, resulting in fewer red blood cells being produced.
A major pathway linking the two conditions involves chronic inflammation, often present in autoimmune hypothyroidism (Hashimoto’s thyroiditis). Inflammation triggers the production of the liver hormone hepcidin, the master regulator of iron metabolism. Hepcidin blocks ferroportin, the protein that exports iron from storage cells and intestinal cells, effectively locking iron away.
Elevated hepcidin prevents iron from being released into the bloodstream from internal stores and inhibits its absorption from the gut. This leads to anemia of chronic disease, where iron stores may appear normal but the iron cannot be utilized for red blood cell production. This mechanism explains why low iron is common in autoimmune thyroid disease.
Low thyroid hormones also affect the expression of transferrin receptors (\(\text{TfR}\)). Transferrin carries iron in the blood, and these receptors are needed for cells to take up the iron. Reduced \(\text{T}_3\) and \(\text{T}_4\) levels interfere with the signaling pathways that regulate these receptors, limiting the amount of iron delivered to the bone marrow and other tissues.
Comprehensive Testing for Low Iron in Thyroid Patients
Diagnosing iron deficiency requires more than a Complete Blood Count (CBC), which measures the number and size of red blood cells and hemoglobin. A patient can be significantly iron deficient without yet showing clinical anemia on a CBC. Therefore, a comprehensive iron panel is required to accurately assess iron status.
The most important marker is Ferritin, the primary protein used to store iron in the body. A low ferritin level is the most reliable indicator of true iron deficiency, reflecting depleted iron stores. However, ferritin is an acute phase reactant, meaning its levels can rise significantly in the presence of inflammation, which is common in autoimmune thyroid disease.
Because inflammation can artificially inflate ferritin levels, other markers must be used for a complete picture. These include Serum Iron (measuring iron currently in the blood) and Total Iron Binding Capacity (TIBC), which measures the total amount of protein available to carry iron. These values calculate Transferrin Saturation, indicating the percentage of iron-carrying proteins bound to iron. A low transferrin saturation (typically below 20%) is a strong indicator of iron deficiency, even if ferritin levels are misleadingly normal.
It is also essential to test for the underlying thyroid condition by measuring Thyroid-Stimulating Hormone (TSH) and Free Thyroxine (\(\text{FT}_4\)), as optimizing thyroid function is part of resolving the iron deficiency.
Integrated Treatment Approaches for Both Conditions
The management of coexisting hypothyroidism and iron deficiency requires a coordinated approach targeting both the hormone deficiency and the nutrient deficit. Optimizing thyroid hormone replacement, typically with Levothyroxine, is the first step. Restoring thyroid hormone levels can improve iron absorption and utilization naturally by resuming normal stomach acid production and improving erythropoiesis.
However, iron supplementation is often necessary, and the timing of medications is a practical consideration. Iron supplements, particularly those containing calcium, interfere with the absorption of Levothyroxine. This interaction involves the physical binding of the thyroid drug to the iron, preventing absorption in the gut.
To prevent this drug interaction, iron supplements should be taken at least four hours apart from the thyroid medication. Treating both conditions simultaneously with Levothyroxine and iron results in better improvements in hemoglobin and ferritin levels than treating either condition alone. Dietary considerations, such as increasing consumption of heme iron (found in meat) and non-heme iron sources with vitamin C, also support the treatment.