Multiple Sclerosis (MS) is a chronic autoimmune disease that targets the central nervous system, leading to inflammation and damage to the protective myelin sheath surrounding nerve fibers. For many patients, a major challenge is managing the profound fatigue, cognitive fog, and weakness that significantly impair daily life. Ferritin, a protein that stores iron, is often checked as a measure of the body’s iron reserves. Low levels can mirror or intensify many of the neurological symptoms experienced by those with MS. The relationship between MS and low ferritin is complex, involving both the disease’s underlying inflammatory processes and other co-occurring factors.
What Ferritin Measures
Ferritin is the body’s primary iron storage protein, acting as a reservoir for iron inside cells, especially in the liver, spleen, and bone marrow. A simple blood test measures serum ferritin, which directly reflects the total amount of iron stored in the body for future use. Serum ferritin levels are a more reliable indicator of iron stores than a general iron blood test, which only shows the iron currently circulating in the bloodstream.
When ferritin levels drop below the optimal range, it signifies iron deficiency, even if the red blood cell count and hemoglobin are still within normal limits. This condition is known as non-anemic iron deficiency, and it can cause symptoms because iron is necessary for numerous cellular functions, including energy production and neurotransmitter synthesis. Low ferritin can manifest as severe fatigue, difficulty concentrating, and dizziness, symptoms that often exacerbate the effects of MS itself.
The Inflammatory Link Between MS and Iron
Multiple Sclerosis is fundamentally an inflammatory condition, and this chronic systemic inflammation directly impacts how the body manages iron. Inflammation triggers the release of pro-inflammatory messengers, known as cytokines, such as interleukin-6 (IL-6). These cytokines increase the production of hepcidin, a hormone produced primarily by the liver that acts as the body’s main regulator of iron.
Elevated hepcidin levels work to lock iron away, which is a defense mechanism the body uses during inflammation. Hepcidin achieves this by binding to ferroportin, the only known iron export protein, causing it to be degraded. This action blocks the release of stored iron from cells and also inhibits the absorption of new iron from the gut.
This mechanism often leads to “anemia of chronic disease,” where ferritin levels are paradoxically high or normal, masking a functional iron deficiency. However, in MS patients, particularly those with progressive forms of the disease, studies have noted lower serum iron levels compared to healthy individuals. If underlying iron stores are already low, the chronic inflammatory state caused by MS can combine with insufficient iron intake, resulting in a measurable decline in ferritin and a true systemic iron deficiency.
Other Reasons MS Patients Experience Low Ferritin
Beyond the core inflammatory processes of the disease, several co-occurring factors common in the MS population contribute to low ferritin levels. Dietary restrictions are a frequent cause, as some individuals adopt specific exclusion diets to manage their MS symptoms, which can unintentionally reduce their intake of iron-rich foods. Strict vegetarian or vegan diets require careful planning to ensure adequate iron from non-heme sources, which are less easily absorbed than meat-based heme iron.
Certain medications used to manage MS or its symptoms can also interfere with iron absorption. For instance, common medications for heartburn or acid reflux, such as proton pump inhibitors, impair the stomach’s ability to create the acidic environment necessary for iron absorption. Furthermore, some MS patients experience undiagnosed gastrointestinal issues or general malabsorption, preventing the body from effectively drawing iron from the food they consume.
A significant factor contributing to iron deficiency, especially in the female MS population, is blood loss, particularly heavy menstrual bleeding. Ruling out these external sources of blood loss is a fundamental step in diagnosing the cause of low ferritin in any patient, including those with MS.
Addressing and Treating Low Ferritin
The first step in addressing low ferritin is accurate diagnosis, which requires a comprehensive blood panel to look beyond just the ferritin number. This panel should include:
- Serum iron
- Total iron-binding capacity (TIBC)
- Transferrin saturation (TSAT)
- A marker of inflammation like C-reactive protein (CRP)
In a person with inflammation, iron deficiency is often suspected if the ferritin level is below 50 nanograms per milliliter, or if the TSAT is below 20%.
Treatment for confirmed iron deficiency typically begins with oral iron supplementation, often prescribed at a dose of 120 milligrams of elemental iron per day. To maximize absorption, the supplement should be taken on an empty stomach with a source of Vitamin C, while avoiding coffee, tea, and large amounts of dairy around the time of dosing. Side effects like constipation or stomach upset are common; managing them may involve reducing the dose or trying an alternate-day regimen.
For individuals who cannot tolerate oral supplements, have severe malabsorption, or whose levels do not improve, intravenous (IV) iron infusion is a highly effective option to rapidly replenish iron stores. The goal of treatment is to replenish stores until the ferritin level is at least 50 micrograms per liter. Due to the complex nature of iron dysregulation in MS, coordinating management between the neurologist and a hematologist or primary care physician is necessary to ensure a safe and effective treatment plan.