Why Ferritin Levels Can Be High in Hypothalamic Amenorrhea (Even When Iron Is Low)
Before we dive in, we want to give credit to the author. This was written by Cat, a graduate of our Holistic HA Practitioner (HHAP) Certification Program. Cat brings a deep understanding of the root causes of HA and is passionate about supporting women on the path to recovery through education, empowerment, and holistic strategies.
Why Ferritin Can Be Elevated Even When Iron Is Low
Ferritin is widely recognized as the main protein that stores iron, and in most cases, blood. Ferritin, levels are used to estimate how much iron the body has in reserve. Under normal circumstances, a high ferritin level is taken to mean that iron stores are high.(1) But in the context of HA, this is not always the case. Ferritin may appear elevated even when iron stores are normal or low. (2) Understanding why this happens requires looking beyond iron storage alone and recognizing ferritin’s broader role in the body’s stress and immune responses.
Ferritin: More Than Just an Iron Storage Marker
Ferritins primary biological role is to safely store iron within cells and release it when needed. This helps maintain iron balance and protects the body from the damaging effects of free iron, which can generate harmful oxidative stress. Small amounts of ferritin circulate in the bloodstream, and this is what is measured in blood tests. (1)
In most medical settings, serum ferritin is used as a proxy for total body iron stores. This works well when the body is in a state of equilibrium (1,3) —but HA is not a state of equilibrium. It is a state of physiological adaptation to chronic energy deficit, psychological stress, and often excessive physical activity. 4 In this altered metabolic state, ferritin can behave differently.
Importantly, ferritin is also an acute-phase reactant. 5 This means that it is a protein that increases in number during inflammation, infection, or systemic stress. When the body experiences any type of physiological stress, including low energy availability or hormonal imbalance, it activates the immune system in subtle ways. This immune activation stimulates the liver to increase ferritin production, regardless of iron status. (6)
Inflammation and Stress Responses in HA
HA is not simply a reproductive condition; it reflects a broader shift in how the body allocates resources under perceived threat. When energy intake is insufficient to support basic metabolic needs in addition to physical activity, the hypothalamus downregulates non- essential systems with reproduction being one of the first to go. (4)
In HA we know that this energy deficit activates the hypothalamic-pituitary-adrenal (HPA) axis, increasing the production of cortisol, the body’s main stress hormone. Cortisol is well known for its role in mobilizing glucose and suppressing reproductive hormones, but it also contributes to a low-grade pro-inflammatory state. (7) Alongside cortisol, the body increases production of cytokines which are small signaling proteins involved in the immune response. Cytokines signal the liver to increase ferritin production. This response is part of the body’s innate immune defense: by increasing ferritin, the body can limit the availability of circulating iron, which many pathogens (infection causing microorganisms) need to grow. (8) This mechanism, while protective in the context of infection, also gets activated in non-infectious chronic stress states like HA. As a result, ferritin levels rise even though iron availability may be low. (9)
The Role of Exercise and Muscle Inflammation
In many individuals with HA, excessive or intense exercise is part of the underlying stress load. (9) Exercise, particularly endurance or high-volume training, causes microtears and damage to muscle tissue. This triggers a localized inflammatory response that helps the muscle repair and adapt, but it also contributes to systemic inflammation. During and after strenuous exercise, reactive oxygen species (ROS) and cytokines are released into the bloodstream. These inflammatory signals further stimulate ferritin synthesis as part of the acute-phase response. (10) So in athletic individuals with HA, ferritin may be elevated not because iron stores are high, but because the body is in a constant state of low-grade inflammation and tissue repair.
Estrogen’s Influence on Ferritin and Inflammation
Estrogen plays a key anti-inflammatory role in the body. It helps regulate the immune response, suppresses excessive cytokine production, and supports overall immune balance. (11) Hypothalamic suppression of the reproductive axis in HA means that estrogen levels are significantly reduced. This hormonal environment allows for a heightened inflammatory state, further contributing to elevated ferritin.
Low estrogen also affects iron regulation indirectly through its relationship with hepcidin, a hormone that controls iron absorption and release from stores. (12) Estrogen has been shown to suppress hepcidin, enhancing iron availability. When estrogen is low, as in HA, hepcidin levels may rise, blocking iron release from ferritin and reducing intestinal absorption—even when the body needs it. This results in what is known as iron ‘sequestration’: ferritin levels appear elevated, but the iron is essentially “locked away” and unavailable for use. (12,13)
This creates a paradox: the iron is technically present, stored within cells, but it’s inaccessible to the tissues that need it. This is known as functional iron deficiency.
Functional Iron Deficiency: What It Means
Functional iron deficiency occurs when ferritin levels are normal or elevated, but serum iron and transferrin saturation are low. Red blood cells, muscles, and other tissues lack sufficient iron for optimal function, even though total body iron appears adequate. This can result in fatigue, poor exercise recovery, dizziness, shortness of breath, or even anemia over time. (14)
In the context of HA, functional iron deficiency can potentially be missed because elevated ferritin masks the underlying issue. Without looking at the full iron panel—including serum iron, transferrin saturation, total iron-binding capacity (TIBC), and markers of inflammation like C-reactive protein (CRP)—it’s possible to misinterpret the picture.
What This Means In HA Recovery
If you’ re recovering from HA and notice high ferritin levels, it’s important to understand that this result may not reflect true iron overload. Instead, it could be a signal of chronic physiological stress, inflammation related to underfueling, overtraining, or low estrogen, and reduced iron absorption and release due to hormonal disruption
Work with your healthcare provider to evaluate a full iron panel, assess inflammation markers, and interpret your results in the context of your overall health and recovery stage in HA. As your body returns to balance, it is likely that inflammation will decrease, cortisol and estrogen levels will stabilize, and ferritin will become a more accurate reflection of your true iron status.
Struggling to make sense of your labs or feeling stuck in recovery?
If you’ve been told your ferritin is “high” but you still feel exhausted, dizzy, or run down, you’re not alone. For women with hypothalamic amenorrhea, labs can be confusing, especially when results like ferritin don’t tell the full story. What’s often missed is how stress, underfueling, and low estrogen can all affect iron metabolism and inflammation.
Through our 1:1 coaching and group coaching programs at The HA Society, we help you understand what your labs are really saying, restore balance to your hormones, and rebuild the energy your body needs to cycle naturally and thrive.
Recovery isn’t just about getting your period back—it’s about feeling strong, clear-headed, and confident again.
Keep Reading:
What is Hypothalamic Amenorrhea?
What Labs to Request if You Suspect Functional Hypothalamic Amenorrhea (HA)
References:
1. Knovich, M. A., Storey, J. A., Coffman, L. G., Torti, S. V., & Torti, F. M. (2009). Ferritin for the clinician. Blood Reviews, 23(3), 95–104. https://doi.org/10.1016/j.blre.2008.08.001
2. Cullis, J. O., Fitzsimons, E. J., Griffiths, W. J., Tsochatzis, E., Thomas, D. W., & British Society for Haematology. (2018). Investigation and management of a raised serum ferritin. British Journal of Haematology, 181(3), 331–340. https://doi.org/10.1111/bjh.15166
3. Garcia-Casal, M. N., Pasricha, S. R., Martinez, R. X., Lopez-Perez, L., & Peña-Rosas, J. P. (2021). Serum or plasma ferritin concentration as an index of iron deficiency and overload. The Cochrane Database of Systematic Reviews, 2021(5), CD011817. https://doi.org/10.1002/14651858.CD011817.pub2
4. Dobranowska, K., Plińska, S., & Dobosz, A. (2024). Dietary and lifestyle management of functional hypothalamic amenorrhea: A comprehensive review. Nutrients, 16(17), 2967. https://doi.org/10.3390/nu16172967
5. Kernan, K. F., & Carcillo, J. A. (2017). Hyperferritinemia and inflammation. International Immunology, 29(9), 401–409. https://doi.org/10.1093/intimm/dxx031
6. Mahroum, N., Alghory, A., Kiyak, Z., Alwani, A., Seida, R., Alrais, M., & Shoenfeld, Y. (2022). Ferritin – From iron, through inflammation and autoimmunity, to COVID-19. Journal of Autoimmunity, 126, 102778. https://doi.org/10.1016/j.jaut.2021.102778
7. Sic, A., Cvetkovic, K., Manchanda, E., & Knezevic, N. N. (2024). Neurobiological implications of chronic stress and metabolic dysregulation in inflammatory bowel diseases. Diseases, 12(9), 220. https://doi.org/10.3390/diseases12090220
8. Liao, Y., Zeng, T., Guo, X., & Li, X. (2025). Ferritin’s role in infectious diseases: Exploring pathogenic mechanisms and clinical implications. New Microbes and New Infections, 65, 101582. https://doi.org/10.1016/j.nmni.2025.101582
9. Reid, B. M., & Georgieff, M. K. (2023). The interaction between psychological stress and iron status on early-life neurodevelopmental outcomes. Nutrients, 15(17), 3798. https://doi.org/10.3390/nu15173798
10. Cheng, A. J., Jude, B., & Lanner, J. T. (2020). Intramuscular mechanisms of overtraining. Redox Biology, 35, 101480. https://doi.org/10.1016/j.redox.2020.101480
11. Yang, Q., Jian, J., Katz, S., Abramson, S. B., & Huang, X. (2012). 17β-Estradiol inhibits iron hormone hepcidin through an estrogen responsive element half-site. Endocrinology, 153(7), 3170–3178. https://doi.org/10.1210/en.2011-2045
12. Martín-Millán, M., & Castañeda, S. (2013). Estrogens, osteoarthritis and inflammation. Joint Bone Spine, 80(4), 368–373. https://doi.org/10.1016/j.jbspin.2012.11.008
13. Ganz, T., & Nemeth, E. (2009). Iron sequestration and anemia of inflammation. Seminars in Hematology, 46(4), 387–393. https://doi.org/10.1053/j.seminhematol.2009.06.001
14. Jung, H. L. (2025). Absolute versus functional iron deficiency. Clinical and Experimental Pediatrics, 68(2), 138–140. https://doi.org/10.3345/cep.2023.01732
