Iron deficiency anemia (IDA) occurs when the body lacks sufficient iron to produce healthy red blood cells, impairing oxygen transport. After menopause, the causes of low iron shift profoundly because monthly iron loss through menstruation ceases. Pre-menopausal iron requirements (around 18 milligrams per day) drop significantly to about 8 milligrams daily. Since iron stores are no longer routinely depleted by menstrual blood loss, new iron deficiency in this life stage signals the need for thorough medical investigation.
Chronic Blood Loss in the Gastrointestinal Tract
The most common reason for iron deficiency anemia in post-menopausal women is slow, chronic blood loss from the gastrointestinal (GI) tract. This loss is often occult, meaning the blood is not visible in the stool, allowing iron stores to be gradually depleted. The body cannot absorb enough new iron from the diet to keep pace with this ongoing, small hemorrhage.
A primary source of chronic bleeding is damage to the mucosal lining of the stomach or small intestine, often caused by prolonged use of nonsteroidal anti-inflammatory drugs (NSAIDs). These medications can lead to gastritis and peptic ulcers, which bleed slowly without acute symptoms. Other common benign causes include internal hemorrhoids, diverticular disease, or vascular lesions known as angiodysplasias.
However, iron deficiency anemia in this demographic can also indicate more serious pathology, such as polyps or colorectal cancer. Due to this risk, every case of unexplained iron deficiency in a post-menopausal woman necessitates a comprehensive evaluation of the entire GI tract. A serious underlying cause must be assumed until a benign source is definitively identified and treated.
Dietary Insufficiency and Impaired Iron Absorption
Low iron can result from a failure to get enough iron into the bloodstream, either through insufficient intake or impaired absorption. Dietary choices play a role, especially in older adults who may have lower overall food consumption or follow restricted diets. Iron from animal sources (heme iron) is absorbed much more efficiently than non-heme iron found in plant-based foods. Individuals limiting red meat or following vegetarian/vegan diets may struggle to maintain adequate iron levels without careful planning or supplementation.
Even with sufficient dietary iron, the body may be unable to absorb it effectively due to changes in the GI environment. Iron absorption relies heavily on stomach acid (hydrochloric acid) to convert dietary iron into an absorbable form. Reduced stomach acid production (hypochlorhydria) can occur naturally with age or be induced by common medications.
Medications and Conditions Affecting Absorption
Medications like proton pump inhibitors (PPIs) and antacids are often prescribed for acid reflux or ulcers, but their long-term use significantly hinders iron uptake. Additionally, conditions that damage the intestinal lining directly impair the small intestine’s ability to process and absorb the mineral. These include Celiac disease or infection with the bacterium Helicobacter pylori.
Anemia of Chronic Inflammation
A third distinct cause of low iron is Anemia of Chronic Disease (ACD) or Anemia of Inflammation (AI), which is a functional iron deficiency. This condition differs from absolute iron deficiency because the body has iron stores available, but chronic inflammation prevents their utilization. This state is driven by the immune response to conditions like autoimmune disorders, chronic kidney disease, or obesity.
Inflammation triggers the production of signaling molecules, which upregulate the liver’s synthesis of the hormone hepcidin. Hepcidin is the master regulator of iron metabolism, and its increased concentration is the core mechanism of this anemia. The hormone works by binding to and causing the degradation of ferroportin, the protein responsible for exporting iron out of cells. By disabling ferroportin, hepcidin effectively traps iron within the body’s storage cells, particularly macrophages, preventing its release into the bloodstream. It also blocks the absorption of new iron from the gut. The result is a functional iron deficiency where serum iron levels are low, but the body’s iron stores (ferritin) can appear normal or elevated due to this sequestration.
Medical Investigation and Next Steps
The investigation of low iron after menopause begins with a panel of blood tests to determine the type and severity of the deficiency. Initial laboratory work includes measuring hemoglobin levels and assessing iron status through serum ferritin, transferrin saturation, and serum iron. Ferritin is the primary marker of iron stores, but a C-reactive protein (CRP) test is often run concurrently to check for underlying inflammation.
Inflammation can artificially elevate ferritin. A ferritin level below 45 micrograms per liter indicates absolute iron deficiency, but a level up to 100 micrograms per liter may signify a functional deficiency if chronic inflammation is present. If tests confirm iron deficiency, a physician will not immediately begin iron supplementation alone.
The next step involves a strong recommendation for a bidirectional endoscopic evaluation. This comprehensive procedure includes both an upper endoscopy (gastroscopy) and a colonoscopy to physically inspect the upper and lower GI tract for sources of bleeding or malabsorption. Identifying and treating the underlying cause—whether a bleeding ulcer, a polyp, or Celiac disease—is paramount before starting iron therapy. Delaying this investigation while only treating the anemia with supplements could mask a serious condition and postpone a necessary diagnosis.