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What do we know about iron?

Iron is familiar to us as a vital component of the haemoglobin which gives red blood cells their colour, and iron supplements are often taken by people at risk of anaemia. Iron is found naturally in animal products, particularly red meat; liver is a good source. Vegetarians can obtain iron from lentils, chickpeas and leafy vegetables, and it is also sometimes added to breads and cereals.

Once absorbed by cells in the gut, iron is tightly regulated in the body, which does not have specialised pathways for excreting it. On average, an adult human contains 3-4 g of iron. Little of this is normally lost; for example, iron is recycled from elderly red blood cells. It is estimated that natural iron absorption from the diet needs to average 1-2 mg daily, to balance the amount lost by cell sloughing (from the skin and gut) and blood loss.

What happens if I consume too much?

Too much iron intake can lead to lethal poisoning, especially in young children who mistake supplement tablets for sweets. A US study reported that from 1983-1990, this was “the single most frequent cause of unintentional pharmaceutical ingestion fatality in children younger than 6 years”, causing 30% of such events.1 Since then, changes in packaging have greatly reduced the number of poisonings and fatalities.

What is iron dificiency? 

Iron deficiency, which can be aggravated by poor diet, intestinal parasites, menorrhagia, copper deficiency or by infectious disease, is a much more common problem. The World Health Organisation (2003) described it as “the most common and widespread nutritional disorder in the world”, with about 2 billion people suffering from anaemia.2 Fatigue is a common symptom, reducing productivity. Iron deficiency can also increase the body’s susceptibility to lead poisoning, which can have severe effects on brain development. Iron deficiency, common in pregnant women, has also been found to have a lasting negative impact on their offspring’s brain function, reducing language and fine motor skills, social and emotional processing, and measures of cognitive function.3

Iron’s atomic structure enables it to both give and take electrons, making it a versatile and necessary component of many enzymes. However, it tends not to dissolve well in cellular fluids, and can combine with other molecules to form highly damaging free radicals. To prevent this, blood plasma contains an enzyme, transferrin, which binds the iron as it is absorbed in the gut.

Iron is used by the muscles to make myoglobin, and by the bone marrow for making haemoglobin in red blood cells. It is also stored by the liver and by immune cells (macrophages, including microglia in the brain). Its availability is regulated by the hormone hepcidin, which is stimulated by rising levels of iron storage to reduce the uptake of iron from the gut. Hepcidin is also stimulated by pro-inflammatory cytokines, which is why some inflammatory diseases can produce symptoms of anaemia.

Iron is also important for brain function, although its metabolism is complex and not yet fully understood. Microglia, the brain’s immune cells, are thought to play a key role by storing iron and releasing it when required – for example, in response to stimulation by pro-inflammatory cytokines. Iron is also needed for myelination, and for the control of oxidative processes (such as the formation of free radicals).

Iron and brain function

Imbalances in iron metabolism have been linked to a number of brain disorders, from restless legs syndrome to Alzheimer’s disease.4 Brain iron levels are thought to rise during neurodegenerative disorders, although this finding is debated; iron is found in the amyloid plaques characteristic of Alzheimer’s, and is thought to make the amyloid protein itself more toxic.5 However, it is not clear whether any rise in brain iron is a cause of brain damage, a consequence of the brain’s attempts at self-repair following earlier damage, or both. Nonetheless, attempts to develop drugs for neurodegenerative disorders which act by rebalancing iron metabolism, or removing excess iron, are ongoing.


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  3. Gambling, L., C. Kennedy, et al. (2011). “Iron and copper in fetal development”, Seminars in Cell & Developmental Biology, 22(6), 637-644.
  4. Singh, N., S. Haldar, et al. (2014), “Brain Iron Homeostasis: From molecular mechanisms to clinical significance and therapeutic opportunities”, Antioxidants and Redox Signaling, 20(8),  1324-1363.
  5. Bandyopadhyay, S. and J. T. Rogers (2014), “Alzheimer’s disease therapeutics targeted to the control of amyloid precursor protein translation: Maintenance of brain iron homeostasis”, Biochemical Pharmacology, 88(4), 486-494.

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