As a company, we have been recommending the use of cast iron pans and griddles for healthier cooking. Indeed, this type of cooking requires no addition of oils or even water. The reason being is that placing food on a hot pan will lift itself when cooked (juices released generate steam, and so, it is ready to flip and remove from the pan without any effort or scrapping the bottom of the pan. Food will stick if cold (taken straight from the fridge) or the cast iron pan/griddle was not hot enough). Cast iron is not suitable for boiling vegetables or other foods. Use a stainless steel pan/stockpot or enamel cookware.

Now that you know how to use it, you may feel more confident and tempted to use it more often.

Would the iron from the pan leach into the food?

Why some people share on social media adding a piece of iron shaped into a fish or other cute little things, claiming that these boost their iron levels?

Iron deficiency/overdose.

The cause of iron deficiency is very similar to other mineral deficiencies. The usual main suspect is low stomach acid. Without sufficient hydrochloric acid, the body may not be able to fully break down and assimilate minerals (magnesium, iron, and zinc).

Low stomach acid can result from chronic stress, anxiety and depression, as well as some drugs (antacids and proton-pump inhibitors, the main one being Omeprazole, and similar medicines ending in -zole), and H. pilori infection.

A diet poor in dietary iron will lead to deficiency. Some vegetarians and vegans who rarely cook from scratch may be more prone to iron deficiency, especially if their main staple protein is soy. Losses of iron can also lead to deficiency as it is the case in heavy bleeding (women have greater requirements for iron, and more so during pregnancy), chronic blood loss, or consuming too many foods that restrict absorption. Stress, intense training and overtraining can lead to iron deficiency due to greater losses via the sweat.

Some foods may also reduce the availability of dietary iron (e.g., teas and coffee (tannins bind to iron and increase elimination via the bowel), soy proteins, phytic acid and dietary fibres.

Vitamin A is needed for the release of stored iron, therefore, vitamin A deficiency can lead to symptoms of iron deficiency.

Iron deficiency anaemia occurs when there is not enough iron to carry oxygen to the cells (symptoms include breathlessness, dizziness, fatigue and poor immune function — repeated infections, including colds and flu, and longer recovery). Iron deficiency anaemia in children can affect growth and brain development.

Inversely, too much iron is also bad for the body. The body cannot excrete excess iron. It simply divert stores to certain organs, typically the liver, heart, and pancreas, which can lead to organ damage on the long-term. Deposits of iron in the liver can cause cirrhosis, while in the pancreas, it may lead to diabetes. Iron toxicity can affect the pituitary, leading to decreased levels of several hormones including androgens.[1] The body, therefore, has some systems in place to reduce uptake from food, and so less is assimilated via the intestinal wall (the liver secretes hepcidin to signal gastrointestinal cells to decrease their absorption of iron, and for other cells around the body to sequester their iron into ferritin, an iron-storage protein).

Iron overdose (usually achieved via the use of supplements and exceeding dosage for long periods of time) can lead to cell death. Typical symptoms of iron toxicity include stomach pain, nausea, vomiting, and diarrhoea. It can also lead to colon cancer on the long-term.

Haemochromatosis is a condition that lead to dangerously high concentration of iron in some people with genetic predisposition.[2] Vitamin c promotes the uptake of dietary iron and so supplementation with vitamin C is contra-indicated in this case. Cooking vegetables also increased their iron content. Alcohol should also be avoided at al times. Haemochromatosis increases the risk of arthritis, cancer, liver problems, diabetes and heart failure, and so it must be monitored very closely.[1,

Medical attention is required at doses greater than 40 mg/kg, and more than 60 mg/kg can be lethal.

Why is iron important?

Iron is mineral that is involved in various bodily functions, including the transport of oxygen in the blood. Oxygen is vital for our survival, cellular function, brain function and just about every organ and system in the body rely on oxygen to support our health.

Iron deficiency is often characterised by fatigue, difficulty in concentrating, and poor work productivity. This why some iron-containing products are advertised just about everywhere on public transport and stations deserving the office quarters of busy cities. But fatigue itself is not only the result of low iron in the body. Often sleep and many other lifestyle and dietary habits lead to fatigue. In this case, taking more iron will not resolve fatigue.

Iron is also stored in myoglobin, which gives muscle tissue its red colour. And so, allows for the storage of iron and quicker delivery of oxygen to muscle cells.

Many enzymes contain iron and so iron is essential to their function. These enzymes catalyse many processes including the biosynthesis of hormones, energy production in mitochondria, the metabolism of drugs, and DNA and RNA base repair. Thus, iron is a key enzyme in DNA synthesis.

Iron is also required in immune function, and so deficiency can lead to immune dysfunction (iron alters proportion and function of various T lymphocyte subsets, and in free-radical controlled process for microbe killing).

Iron is also involved in the delicate role of formation of the connective tissue of several neurotransmitters in the brain.

Recommended intake

• 9 mg a day for men over 18

• 15 mg a day for women aged 19 to 50

• 8 mg a day for women over 50

• 27 mg pregnant women

• 8 mg breastfeeding women

• 9-11 mg children 1-18 years old (boys)

• 8-15 mg children 1-18 years old (girls)

When too much is too much

Breakfast cereals and many fortified processed foods contain high level of (synthetic) iron. Some products like breakfast cereals advertise iron levels up to 18 mg per serving. However, a study found that some contain up to 200% that. 21 out of 29 samples 21 contained 120 percent of the label value.[3]

Since most people and even children consume more than one serving for breakfast, they are dangerously at risk of toxicity. Even more so, if their breakfast is always/mostly breakfast cereals.

It is thus very likely that many people exceed the upper limit of dietary iron on a daily basis, and yet not many are aware of the danger. Dr Christina Ellervik, Associate Professor at the University of Copenhagen in Denmark, who studies the connection between iron and diabetes, explains: “Where we are with iron now is like where we were with cholesterol 40 years ago.” [4]

During the processes of metabolism, mitochondria use oxygen to produce ATP (electron transport chain). As a result of energy production, this create oxygen reactive species, also known as free radicals. One of the main byproducts is superoxide. Superoxide dismutase (SOD), an antioxidant enzyme, converts the superoxide radical to hydrogen peroxide (H2O2). H2O2 can then be converted to •OH by ferrous iron (Fe2+) or copper ion (Cu+) when levels of oxygen are low,[5] or it can be catalysed to H2O by catalase, glutathione peroxidase (GPx) and peroxiredoxin III (PrxIII).[6]

When hydrogen peroxide meets iron it produces hydroxyl radical, a very damaging free radical. In fact, it is the most reactive species of oxygen, which can damage the cell membrane and DNA sequences, inducing the disintegration of the double-helix structure. Damage to DNA can lead to mutation (cancer), and cell death.[7]

The brain burns 20% of the body’s total oxygen requirement, and so generates a myriad of free radicals as a result. Interestingly, the brain does not appear to have much antioxidant defences compared to the rest of the body. For many decades, it is also recognised that neurodegenerative diseases (e.g., Parkinson’s, Alzheimer’s) have a common problem: iron deposits in the brain [8,9,10] which promote aggregation of amyloid-b, the major constituent of Alzheimer’s plaques.[11] Interestingly the greater the concentration of iron the more plaques are found in the brain.[12]

Oxidative damage is one of the earliest detectable changes associated with Alzheimer’s.[13,14,15] However, it was not clear if iron in neurodegeneration was the cause or part of the disease process. These findings suggest that abnormal iron metabolism in the brain could be a causative factor in Alzheimer’s and other neurodegenerative diseases, and those with iron disorders may be at a higher risk of cognitive decline, Alzheimer’s dementia and Parkinson’s.[16,17,18,19]

We may thus hypothesise that amyloid plaques might actually represent an adaptive response rather than a cause, an idea that has been indirectly supported by the spectacular failure of essentially all efforts to directly target amyloid protein as treatment for the disease.

Well, a two-year treatment with chelators — a class of molecules that bind metal cations like iron and facilitate their excretion — has shown a reduction in cognitive decline by half.[20]

The results were published in the highly-respected Lancet journal many decades ago and yet have been completely ignored in the chase for the magic multi-billion-dollar pill that would make Alzheimer’s a ‘thing’ of the past.

Is it possible to also increase the risk of cognitive decline with excessive supplementation on the long-term?

Potentially yes.

Is supplementing with iron necessary.

Probably not.

When to supplement?

if your latest blood tests reveal low levels of iron or Iron deficiency anaemia, then you may supplement with iron following the guidelines of your doctor. Do not supplement unsupervised and without blood test evidences.

Also note that iron supplementation inhibits zinc uptake.[21] Therefore, never supplement iron and zinc at the same time (zinc absorption is significantly higher in the absence of iron). Always space your intake. There seems to be no competition between iron and copper for absorption.[21] In fact, copper is essential for the uptake of iron.[22]

Additionally copper is required to produce ATP. Copper deficiency may thus cause iron deficiency anaemia or compromise ATP production, leading to fatigue and weakness.[23,24]

Dietary sources of iron

• Offal (liver), red meat, pork and poultry.

• Seafood, fish (muscles, oysters, sardines)

• Beans and Soy

• Dark green leafy vegetables (spinach)

• Dried fruits (raisins and apricots)

• Iron-fortified ultra-processed foods (cereals, breads and pastas)

• Peas

• Wheatgerm, nuts and seeds

Looking at the list above, it is easy to incorporate iron-containing foods in the diet and prevent deficiency. Again, consuming vitamin C-rich foods will also increase the rate of absorption.

References

1. Ellervik, C. et al. (2012). Response to Comment on: Ellervik et al. (2011). Elevated Transferrin Saturation and Risk of Diabetes: Three Population-Based Studies. Diabetes Care. 34, pp. 2256–2258. Diabetes Care. 35(6), e48. https://doi.org/10.2337/dc12-0382

2. https://www.nhs.uk/conditions/haemochromatosis

3. Whittaker, P. Tufaro, PR. Rader, JI. (2001). Iron and folate in fortified cereals. The Journal of the American College of Nutrition. 20, pp. 247-254.

4. llervik, C. et al. (2014). Total and Cause-Specific Mortality by Moderately and Markedly Increased Ferritin Concentrations: General Population Study and Metaanalysis. Clinical Chemistry. 60, pp. 1419-1428. Transcript available at: https://www.aacc.org/science-and-research/clinical-chemistry/clinical-chemistry-podcasts/2015/total-and-cause-specific-mortality-by-moderately-and-markedly-increased-ferritin-concentrations.

5. C. Michiels, C. (2004). Physiological and pathological responses to hypoxia. American Journal of Pathology. 164(6), pp. 1875–1882

6. Chen, Y. Azad, M. Gibson, S. (2009). Superoxide is the major reactive oxygen species regulating autophagy. Cell Death Differentiation. 16, pp. 1040–1052. doi.:10.1038/cdd.2009.49

7. Lipinski, B. (2011). Hydroxyl Radical and Its Scavengers in Health and Disease. Oxidative Medicine and Cellular Longevity. 2011, Article 809696. doi.:10.1155/2011/809696

8. Lee, HG. et al. (2007). Amyloid-beta in Alzheimer disease: The null versus the alternate hypotheses. Journal of Pharmacology and Experimental Therapeutics. 321, pp. 823-829

9. Lhermitte, J. Kraus, WM. Mcalpine, D. (1924). Original Papers: On the occurrence of abnormal deposits of iron in the brain in Parkinsonism with special reference to its localisation. Journal of Neurology and Psychopathology. 5, pp. 195-208 .

10. Goodman, L. (1953). Alzheimer’s disease; a clinico-pathologic analysis of twenty-three cases with a theory on pathogenesis. The Journal

    of Nervous and Mental Disease. 118, pp. 97-130.

11. Bartzokis, G., et al. (1994). In vivo evaluation of brain iron in Alzheimer’s disease and normal subjects using MRI. Biological Psychiatry. 35, pp. 480-487.

12. Rogers, JT. et al. (1999).Translation of the alzheimer amyloid precursor protein mRNA is up-regulated by interleukin-1 through 5’-untranslated region sequences. Journal of Biological Chemistry. 274, pp. 6421-6431

13. Nunomura, A., et al. (2001). Oxidative damage is the earliest event in Alzheimer disease. Journal of Neuropathology and Experimental Neurology. 60, pp. 759-767.

14. Smith, MA. et al. (2010). Increased iron and free radical generation in preclinical Alzheimer disease and mild cognitive impairment. Journal of Alzheimer’s Disease. 19, pp. 363-372

15. Ayton, S. et al. (2015). Ferritin levels in the cerebrospinal fluid predict Alzheimer’s disease outcomes and are regulated by APOE. Nature Communications. 6, 6760.

16. Moalem, S. et al. (2000). Are hereditary hemochromatosis mutations involved in Alzheimer disease? American Journal of Medical Genetics. 93, pp. 58-66.

17. Combarros, O. et al. (2003). Interaction of the H63D mutation in the hemochromatosis gene with the apolipoprotein E epsilon 4 allele modulates age at onset of Alzheimer’s disease. Dementia and Geriatric Cognitive Disorders. 15, pp. 151-154

18. Robson, KJ. et al. (2004). Synergy between the C2 allele of transferrin and the C282Y allele of the haemochromatosis gene (HFE) as risk factors for developing Alzheimer’s disease. Journal of Medical Genetics. 41, pp. 261-265

19. Pulliam, JF. et al. (2003). Association of HFE mutations with neurodegeneration and oxidative stress in Alzheimer’s disease and correlation with APOE. American Journal of Medical Genetics; Part B. 119B, pp. 48-53.

20. Crapper-McLachlan, DR. et al. (1991). Intramuscular desferrioxamine in patients with Alzheimer’s disease. The Lancet. 337, pp. 1304-1308.

21. Freddy, J. et al. (2003). Iron supplements inhibit zinc but not copper absorption in vivo in ileostomy subjects, The American Journal of Clinical Nutrition, 78(5), pp. 1018–1023, doi.:10.1093/ajcn/78.5.1018

22. Reeves, PG, DeMars, LC. (2004). Copper deficiency reduces iron absorption and biological half-life in male rats. The Journal of Nutrition. 134(8), pp. 1953-1957. doi:10.1093/jn/134.8.1953.

23. Medeiros DM, Jennings D. (2002). Role of copper in mitochondrial biogenesis via interaction with ATP synthase and cytochrome c oxidase. Journal of Bioenergetics and Biomembranes. 34(5), pp. 389-95. doi:10.1023/a:1021206220851. PMID: 12539966

24. Zeng, H. Saari, JT. Johnson, WT. (2007). Copper deficiency decreases complex IV but not complex I, II, III, or V in the mitochondrial respiratory chain in rat heart, The Journal of Nutrition. 137(1), pp, 14–18, doi.:10.1093/jn/137.1.14
    

Resources

American Hemochromatosis Society
http://www.americanhs.org

Iron Disorders Institute
http://www.irondisorders.org