Nutritional Management of Iron Deficiency

Catherine Wall, D-ECCO Member

Catherine Wall

Iron deficiency and iron-deficiency anaemia (IDA) are characterised by fatigue and reduced capacity for normal activities of daily living and consequently poorer quality of life. Iron deficiency is estimated to affect 60%–80% of people with IBD at some point [1]. Recurrent iron deficiency is also common and is estimated to occur in 30% of patients [1]. Given the prevalence of iron deficiency, some patients and practitioners have learned to accept this impaired quality of life as an unavoidable consequence of IBD [2]. However, correction of iron deficiency in patients without anaemia can result in improved quality of life and less fatigue and should, therefore, be an important treatment goal.

Diagnosis of iron deficiency and iron-deficiency anaemia

The diagnosis of iron deficiency and IDA can be challenging, especially in the presence in inflammation.
The 2015 ECCO Guidelines on the diagnosis and management of iron deficiency and IDA provide comprehensive guidance for clinicians [3]. One of the ECCO Guideline recommendations is that all patients with IBD are screened annually for iron deficiency. The recommended screening tests are a complete blood count, serum ferritin and serum c-reactive protein. Literature suggests, however, that full screening is inadequately completed [4]. Screening is an important part of IBD management as it is well documented that patients adapt to low blood iron and learn to accept its consequences.

Why is iron deficiency common during active and quiescent IBD?

The pathogenesis of iron deficiency in IBD is multifactorial. During periods of inflammation iron deficiency may occur due to:

  1. Increased excretion of iron from epithelial desquamation and active bleeding
  2. Decreased intake of dietary iron due to changes in diet in response to active disease symptoms
  3. Reduced transport of iron to the blood due to an inflammation-induced high hepcidin concentration (see below) [5]
  4. Impaired erythropoiesis as a result of inflammation

Hepcidin is a peptide hormone released by the liver. In the last decade, hepcidin has been shown to play a pivotal role in the regulation of iron status. The intestinal pro-inflammatory cytokines IL-1 and IL-6 stimulate increased secretion of hepatic hepcidin. Hepcidin interacts with the iron transporter ferroportin to ultimately limit the movement of iron from cells into the circulation. In this instance, limited luminal iron is absorbed from oral diet or supplements because epithelium iron stores are saturated. With this in mind, many studies have shown that oral iron supplements are unlikely to improve blood iron status in the presence of inflammation and high serum hepcidin.

During quiescent disease, iron deficiency may continue or occur due to:

  1. Inadequate iron repletion after active disease
  2. Ongoing low-grade inflammation that inhibits optimal blood iron concentrations (as described above), which contributes to development of anaemia of chronic disease
  3. Persistent poor intake of iron-rich foods
  4. Low intake of iron absorption promoting foods (e.g. fruit and vegetables high in vitamin C)
  5. High dietary intake of inhibitors of iron absorption (e.g. tannins, phytic acid, high protein intake, calcium)
  6. Concurrent micronutrient deficiency

Emerging research suggests that iron deficiency may coexist with deficiency or suboptimal vitamin D concentration. Vitamin D binds to the promoter region of hepcidin and thus may reduce hepcidin concentration. Clinical research in non-IBD cohorts suggests that short-term high-dose supplementation with vitamin D improves haemoglobin concentration [6]. These findings need further investigation in IBD patient cohorts.

Dietary treatment to improve intestinal iron absorbtion

Dietary manipulation is an often-overlooked treatment to optimise iron status during quiescent IBD. The food and nutrition knowledge and counselling skills of a dietitian are essential to help patients alter their dietary habits in order to improve dietary iron intake and absorption.


Dietary education topics may include:

  1. Iron-fortified foods. Fortified foods effectively improve haemogloblin concentrations in people with mild IDA [7] and are a source of well-tolerated iron supplementation for patients who are intolerant of oral iron supplements.
  2. Non-haem iron-rich foods (plant sources of iron). Non-haem iron is the main source of dietary iron for most people.
  3. Haem iron foods. Animal protein (e.g. red meat and offal) provides an easily absorbable form of iron. Soft textures (e.g. minced, pate), finer grain animal proteins (e.g. premium cuts) and cooking methods (e.g. slow-cooked, casserole) can improve the tolerance of haem iron foods for some people with IBD.
  4. Promoters and inhibitors of iron absorption. The combination of foods that are high in promoters (e.g. vitamin C-rich fruit and vegetables) or inhibitors (e.g. phytate, tannins, caffeine, polyphenols, calcium) of iron absorption with foods high in iron within a meal or snack influences the epithelial absorption of iron.

Multidisciplinary treatment of iron deficiency

The optimal treatment of patients with iron deficiency, including the choice to use oral iron supplements, IV iron preparations and/or dietary education, can be achieved with a multidisciplinary team approach. An IBD dietitian is an essential member of the multidisciplinary team who can counsel patients on the relative absorption and side effects of different types of oral iron supplement as well as provide patients with individualised dietary and nutritional strategies to help improve their short- and longer-term intake and absorption of dietary iron and manage the risk of iron deficiency.


  1. Stein J, Dignass A. Management of iron deficiency anaemia in inflammatory bowel disease – a practical approach. Ann Gastroenterol. 2013;26:104–13.
  2. Danese S, Hoffman C, Vel S, et al. Anaemia from a patient perspective in inflammatory bowel disease: results from the European Federation of Crohn’s and Ulcerative Colitis Associations’s online survey. Euro J Gastroenterol Hepatol 2014;26:1385–91.
  3. Dignass AU, Gasche C, Bettenworth D, et al. European consensus of the diagnosis and management of iron deficiency and anaemia in inflammatory bowel disease.  J  Crohns Colitis. 2015;9:211–22.
  4. Akhuemonkhan E, Parian A, Miller K, Hanauer S, Hutfless S. Prevalence and screening for anaemia in mild to moderate Crohn’s disease and ulcerative colitis in the United States, 2010–2014. BMJ Open Gastroenterol. 2017;4:e000155.
  5. Nielsen OH, Soendergaard C, Vikner ME, Weiss H. Rational management of iron deficiency anaemia in inflammatory bowel disease. Nutrients. 2018;10:82.
  6. Smith EM, Jones JL, Han JE, et al. High-dose vitamin D3 administration is association with increases in hemoglobin concentrations in mechanically ventilated critically ill adults: a pilot double-blind randomized, placebo-controlled trial. JPEN 2018;42:87–94.
  7. Karl JP, Lieberman HR, Cable SJ, Williams KW, Young AJ, McClung JP. Randomized, double-blind, placebo-controlled trial of an iron-fortified food product in female soldiers during military training: relations between iron status, serum hepcidin and inflammation. Am J Clin Nutr. 2010;92:93–100.

Posted in ECCO News, Committee News, D-ECCO, Volume 15, Issue 4