One of my most compelling client studies involved a 28-year-old woman with iron deficiency anaemia. As a nutritional therapist, I don’t focus solely on one symptom; instead, I consider the person as a whole, examining all symptoms and exploring the client’s timeline to uncover the potential root cause of the complaint. Ultimately, this case was much more than just an anaemia case—I learned a great deal about the treatment of anaemia and the mechanisms of iron within the body. I also had a question mark over the standardised methods that are used to treat iron deficiency anaemia.
A case study on Iron Deficiency Anaemia
For confidentiality, I’ve changed the case study name. Here is a little background information for you to better understand the case. Sarah came to me with the main goal of nutritional support for her ongoing iron deficiency anaemia. She wants to improve her energy levels as one of her presenting symptoms is fatigue. Her lack of energy has forced her to slow down and decrease sporting activities which she loves doing. Sarah has an office based job, but she exercises daily, taking up a broad range of activities, outdoor sports, running, yoga, and weight lifting. Her accompanying symptoms are fatigue, lethargy, heavy eyes, afternoon yawner, drowsy, heavy limbs, and breathlessness, which are all typical symptoms of anaemia.
Sarah's Medications and Supplements
| Supplement/ Medication | Dosage | Period |
| Ferrous Fumarate 210 mg | Twice Daily | 2 Years |
| Lindens Vitamin D3 2000 IU | Once Daily | Several months |
| Copper IUD | Intrauterine device | 3 Years |
Sarah has followed a vegetarian diet for several years. While her diet is rich in fresh vegetables, she also consumes large amounts of highly processed foods containing myco-proteins (such as “Quorn” meat replacement products). Clinical studies have shown that myco-proteins can potentially damage the gut, leading to inflammation or impaired digestion and nutrient absorption. As a vegetarian, she doesn’t consume foods that are naturally high in iron. This lack of iron-rich foods in her diet could be a contributing factor to her iron deficiency anaemia. While plant-based sources of iron exist, they are often less bioavailable than heme iron found in animal products. Additionally, the consumption of myco-proteins and processed foods may further compromise her gut health and nutrient absorption capabilities, exacerbating the issue of iron deficiency.
Sarah was diagnosed with iron deficiency anaemia two years ago. Her latest blood tests show low serum ferritin levels, recorded at 11 ng/ml, which is considered abnormal since the ideal range is between 20 and 204 ng/ml. Her GP prescribed an iron supplement, ferrous fumarate, two years ago when her low serum ferritin levels were first discovered. She has been taking the iron supplement intermittently for the past two years. Taking this into consideration, this begs the question, why is the serum ferritin level still low after supplementing with iron for two years?
Labs:
| Name | Result | Normal Range | Level |
| Serum iron levels | 15.1 umol/L | 4.4-27.9 | Normal |
| Serum transferrin | 2.70 g/L | 2.0-3.2 | Normal |
| Transferrin saturation index | 22% | 0-55 | Normal |
| Low serum ferrtin | 11 ng.mL | 20-204 | Abnormal |
Serum ferritin serves as the storage form of iron and is the component that the test measures to determine the level of serum ferritin present in the bloodstream. Medical professionals rely on this test to assess how much iron is stored within the body. Nonetheless, it is important to note that this test is not always considered a reliable indicator. This is because the blood works tirelessly to maintain homeostasis and equilibrium within itself. The primary role of the blood is to serve as a means of transportation, carrying various elements throughout the body. It is not intended to act as a storage space. Consequently, everything within the bloodstream must be regulated and kept within a safe and balanced range.
So what happens to all the minerals? All the minerals in the bloodstream are carefully managed by the body’s regulatory systems. They either get absorbed into tissues where they are needed, or excreted if they are in excess, ensuring that there is no imbalance that might disrupt bodily functions. This regulation is crucial to maintaining overall health and preventing conditions that might arise from mineral deficiencies or toxicities.
| Term | Definition |
| Iron deficiency anaemia | Anaemia is simply defined as having fewer red blood cells or having a low amount of haemoglobin. Blood carries oxygen, when there is low count of haemoglobin or red blood cell count the concentration of oxygen in the blood is lower, leading to reduced amounts of oxygen to the entire body. There are a number of considerations which may cause anaemia which are blood loss; heavy periods, internal bleeding, gastric intestinal blood loss for instance leaky gut, compromised gut health, hypothyroidism; which can slow down the production of red blood cells, deficiencies in vitamins & minerals and infections [1] |
| Low serum ferritin | Ferritin is a blood protein that contains iron. A ferritin test helps GP’s determine how much iron your body stores. If blood ferritin level is lower than normal, it indicates the iron stores in the body are low and possible iron deficiency |
The recommended daily intake of dietary iron for women aged 19 to 50 is about 18 mg per day. This requirement increases to 27 mg per day during pregnancy to support increased blood volume and fetal development. Sarah was prescribed 210 mg of ferrous fumarate, taken twice daily. Ferrous fumarate is an iron supplement that is used to treat or prevent low blood levels of iron. It is a form of iron that is absorbed by the body to help produce red blood cells and maintain good health. Although it is often prescribed to boost iron levels rapidly, it can also cause side effects and may not work effectively if other underlying factors, such as absorption issues, are present… and that was just my thinking.
If you haven’t done the math already, Sarah was consuming 420 mg of ferrous fumarate daily—far exceeding the national guidelines that recommend an ideal level of 18 mg per day for women. Yet her serum ferritin levels remained abnormally low. Where was all that iron going? Was she absorbing it efficiently? If it did get absorbed, was her body even able to access it? It’s time to dive deeper into this mystery.
History and aetiology of Sarah
Before being diagnosed with anaemia, Sarah experienced several traumatic events that brought significant grief: the death of her beloved nan at 23, a difficult break-up at 25, followed by glandular fever and tonsillitis at 26. Shortly after, she developed sepsis, and anaemia was diagnosed soon afterward. Sepsis affects the blood by causing systemic inflammation, disrupting normal blood cell production and function. This inflammatory response can decrease production of red blood cell production and increase their destruction, leading to anaemia. Additionally, sepsis can alter iron regulation, further complicating anaemia.
Case 02 had the Copper coil fitted at age 25, a year before the anaemia was discovered. This suggests that the Copper Coil could have negatively affected her body, potentially impacting iron stores. Copper and iron compete for binding sites in the body, which may result in decreased re-uptake of iron stores and possible nutritional depletion of iron. This interplay between copper and iron could potentially worsen symptoms of anaemia, as the body struggles to maintain adequate iron levels. Addressing the balance of these minerals through dietary changes or lifestyle methods is necessary to improve iron absorption and overall health, but more about Copper later.
What next? How can a HTMA test help?
Since the blood labs may not be giving a true picture of the stored iron levels and to investigate the case further, I suggest carrying out a Hair Tissue Mineral Analysis (HTMA). Why? Because a HTMA test can reveal imbalances or deficiencies that might not be apparent in blood tests, as it reflects the mineral content stored over a longer period (3-4 months). This can be crucial for understanding the underlying causes of anaemia and tailoring treatment plans effectively.
What might the HTMA results reveal?
Given the low serum ferritin levels in the blood tests, I would expect to see similarly low iron levels in the tissues in the HTMA results. However, if iron levels are high or within range, further investigation would be necessary. We’d need to determine if the iron is accessible and being utilized by the body. If not, we must ask why. I’ll also be examining copper levels due to Sarah’s copper IUD. Copper and iron compete for binding sites in the body, which could potentially lead to decreased re-uptake of iron stores and possible iron depletion. But let’s not get ahead of ourselves—we’ll delve deeper into copper’s role in Part Two.
Sarah's HTMA Results
So what’s happening here?
In the results above you can see three areas of interest highlighted; Iron, Calcium, Copper, and Magnesium
- Iron level is 1.2 mg – The HTMA results show iron levels in tissue within the ideal range of 0.5 – 2.0 mg, suggesting sufficient iron stores. However, the blood test reveals low serum ferritin, typically an indicator of iron stores in the body. This raises a puzzling question: If iron stores in the tissues are adequate, why is serum ferritin low, and why does Sarah experience exhaustion and other anaemia symptoms? Research indicates that ferrous fumarate can be antagonistic to iron circulation. Hepcidin, triggered when iron levels are high, halts iron circulation. This mechanism could explain the low serum ferritin despite normal tissue levels.
- Copper – 4.0 mg – Copper is elevated, indicating copper toxicity. Copper plays several critical roles in the body, including aiding in the formation of red blood cells, maintaining healthy bones, blood vessels, nerves, and immune function. It also assists in iron absorption, which is essential for preventing anaemia. However, when copper levels are elevated, as in this case, it can interfere with iron metabolism, exacerbating symptoms of iron deficiency anaemia.
- Magnesium – At 2.2 mg, it’s critically low. Magnesium is essential for energy production through ATP, bone health, carbohydrate metabolism, muscle function, and blood pressure regulation. It’s also vital for DNA and RNA synthesis, protein production, and cellular communication. Sarah’s symptoms align with magnesium deficiency, suggesting that her condition may not be solely due to low iron levels.
Before we get completely sidetracked, let's get back to iron. How do we use iron in the body?
- Haemoglobin production: Iron is a vital component of haemoglobin in red blood cells, essential for transporting oxygen throughout the body.
- Myoglobin formation: Iron helps create myoglobin in muscles, aiding in the storage and transport of oxygen within muscle tissues.
- Enzyme production: Iron plays a role in producing various enzymes necessary for different bodily functions.
Hepcidin, a hormone produced by the liver, regulates the body’s use of iron. It controls iron levels by managing absorption from the gut and release from storage sites. When iron is deficient, hepcidin levels drop, promoting increased iron absorption and mobilization from stores to meet the body’s needs. Here are key points about hepcidin:
- Function: Hepcidin regulates iron levels by controlling absorption from the gut and release from body storage sites.
- Production: The liver primarily produces hepcidin in response to iron levels, inflammation, and other factors.
- Mechanism: Hepcidin binds to and degrades ferroportin, a protein that allows iron to exit cells. This traps iron inside cells, reducing its availability in the bloodstream.
- Role in iron deficiency anaemia: Hepcidin levels decrease in iron deficiency, boosting iron absorption and mobilization. However, in conditions like inflammation-induced anaemia, inappropriately high hepcidin levels can contribute to iron deficiency.
- Regulation: Iron status, inflammation, erythropoietic activity, and hypoxia influence hepcidin levels.
What about supplements?
If tissue iron levels are within the ideal range, are they being accessed? If not, why? Could it be because hepcidin is decreasing iron circulation?
When a substantial amount of iron circulates in the body, hepcidin is released as an automatic reaction to maintain homeostasis. Hepcidin reduces iron re-uptake, decreasing absorption and circulation of stored iron [2].
Consistently supplementing with large doses of iron (ferrous fumarate) may counterintuitively trigger hepcidin release. This influx of iron prompts hepcidin production, which then signals the body to reduce iron absorption and hinders its circulation in the blood. “There are two possible fates for the absorbed dietary Fe. If the body stores are adequate, Fe can be re-oxidised to Fe3+ and stored in the enterocytes as ferritin. Fe stored as ferritin is lost into the intestinal lumen when the enterocytes are sloughed off at the villus tip and may exit the body in the faeces.” [3]
Consequently, the iron supplement may simply leave the body during bowel movements. This process highlights the complexity of iron supplementation and absorption in the body. When iron stores are adequate, the body has mechanisms to prevent excessive iron accumulation, which can be harmful. In Sarah’s situation, this could explain why despite taking high doses of ferrous fumarate, her serum ferritin levels remain low. The body may be actively preventing the absorption of excess iron, leading to its excretion rather than storage or utilisation.
What about the Vitamin D supplement?
Sarah has been taking a vitamin D supplement, which complicates the iron absorption process further. Vitamin D interferes with hepcidin, the hormone responsible for iron circulation, by reducing its activity in the body.
This effect can be beneficial for someone with anaemia because it promotes iron absorption. By down-regulating hepcidin activity, vitamin D allows iron to be absorbed and recycled in the body more freely. However, vitamin D’s impact on iron metabolism is complex and potentially contradictory. While it may enhance iron absorption through its effect on hepcidin, vitamin D also increases calcium absorption, which can hinder iron uptake: “As an example, vitamin D, by enhancing the absorption of calcium, can lead to poor iron absorption.” [1]
Sarah is taking ferrous fumarate. The increased calcium absorption caused by vitamin D may be reducing the uptake and absorption of ferrous fumarate in the gut. Consequently, this could prevent the replenishment of iron stores needed to alleviate anaemia.
Vitamin D has recently been shown to act directly on the antimicrobial peptide hepcidin, which is responsible for the regulation of systemic iron concentrations. Hepcidin, which prevents further iron absorption and iron release from cells during times of iron sufficiency by binding to and inducing the degradation of the cellular iron exporter, ferroportin, is also up-regulated by pro-inflammatory cytokines, interleukin-6 (IL-6) and interleukin-1β (IL-1β)
So what does this all mean?
The case study of Sarah highlights several important factors that can influence the effectiveness of iron supplements in treating anaemia:
- Hepcidin regulation: High doses of iron supplements like ferrous fumarate can trigger increased hepcidin production, which paradoxically reduces iron absorption and circulation in the body.
- Supplement interactions: Vitamin D supplements, while potentially beneficial for iron absorption through hepcidin regulation, can also increase calcium absorption, which may interfere with iron uptake.
- Complex mineral interactions: The interplay between iron, calcium, copper, and vitamin D levels in the body can affect overall iron absorption and utilisation.
- Underlying health conditions: Factors such as compromised immune system, gut health issues, and a history of infections (like sepsis) can impact iron absorption and metabolism.
- Insufficient dietary intake of heme iron: Heme iron, found mainly in animal-based foods like red meat, poultry, and fish, is more easily absorbed by the body than non-heme iron from plant sources. Ensuring adequate intake of heme iron-rich foods, coupled with proper food combining to boost iron absorption, can be crucial in preventing and managing iron deficiency anaemia.
- Gut dysfunction: Impaired mineral absorption in the digestive system leading to poor uptake and replenishment of minerals, including iron.
- Copper imbalance: Elevated copper levels, possibly due to the Copper IUD, can interfere with iron metabolism and exacerbate anaemia symptoms.
These factors demonstrate that simply taking an iron supplement may not be sufficient to address anaemia. A more holistic approach, considering the body’s overall mineral balance, underlying health conditions, and the complex interactions between different nutrients and supplements, is necessary for effective treatment. Additionally, focusing on whole food sources of iron and addressing any gut health issues may be more beneficial than relying solely on isolated iron supplements.
This case underscores the importance of personalised treatment plans and comprehensive testing, such as HTMA, to uncover the root causes of anaemia and develop more effective strategies for managing iron deficiency.
Appendix
- The Nutritional Relationships of Iron – https://isom.ca/wp-content/uploads/2020/01/JOM_1988_03_3_03_The_Nutritional_Relationships_of_Iron.pdf
- Vitamin D and Anaemia: Insights into an Emerging Association – Current Opinion in Endocrinology, Diabetes and Obesity – US National Library of Medicine – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4659411/
- The molecular basis of copper and iron interactions – Nutritional Society – https://www.cambridge.org/core/journals/proceedings-of-the-nutrition-society/article/molecular-basis-of-copper-and-iron-interactions/146B23777CB8304406BF7B-04BAC7FF68
