Both haem and non-haem iron are either used immediately after entry into the enterocytes or exported via the carrierprotein ferroportin (FPN-1) and stored subsequently by storage proteins (Anderson & Frazer, 2017). In the body, iron is bound to proteins or other molecules to keep it soluble, limit its redox potential (likelihood of interaction with other molecules) and its availability to intestinal microorganisms. Approximately 60% of the body's iron is bound to haemoglobin, a reaction that takes place within the bone marrow, and subsequently circulates through the system. Another 30% is bound to storage proteins (ferritin and hemosiderin) and the remaining iron is bound to myoglobin, enzymes and transferrin (Friel et al., 2018, Yiannikourides & Latunde-Dada, 2019). Together, these form the iron pool.

The body's iron status must be strictly regulated as the human body has no controlled mechanism for excreting excess iron. Iron can only be discarded by blood loss, via sloughing of intestinal cells over the faeces and skin desquamation. Iron homeostasis is largely regulated by the liver via hepcidin. This hormone negatively regulates iron absorption by binding to ferroportin, the membrane export protein, thus blocking iron export from the endocytes into the blood stream (Wallace, 2016). The lack of a controlled excretion mechanism is the reason why iron toxicity can arise by over-fortification or over-supplementation. It has detrimental effects, like increased risk of infections, microbiome dysbiosis and increased oxidative stress (Domellöf, 2017, Friel et al., 2018). The risk of systemic iron overload is usually negligible with normal intestinal function and when iron is not supplemented. However, large intakes of iron could have a corrosive effect on the intestinal mucosa due to the production of free radicals, leading to bleading and loose stools or even organ damage (EFSA NDA, 2015, Milman, 2012).