'No evidence' iron levels are linked to hardened arteries

By Nathan Gray contact

- Last updated on GMT

Related tags: Atherosclerosis

'No evidence' iron levels are linked to hardened arteries
Long-held beliefs that the hardening of the arteries involved in atherosclerosis is linked to the body's iron levels may be unfounded, according to new research from UCLA.

Common thinking is that the greater risk of atherosclerosis in men and post-menopausal women compared to pre-menopausal women is related to higher levels of iron in the body in both groups, the study's lead author Professor Elizabeta Nemeth remarked.

Under this 'iron hypothesis' it is believed the iron-regulatory hormone hepcidin causes the build-up of iron in plaque macrophages - which leads to oxidative stress and inflammation and contributes to atherosclerosis.

However, the new study by Nemeth and her team showed little evidence to support the theory, as the progression of atherosclerosis in animals exposed to excessive iron levels in the macrophage cells was no different than in those with normal iron counts.

Writing in Cell Reports​, the team also revealed that there was no increase in the level of hepcidin in the mice at any stage of atherosclerosis progression.

Léon Kautz, first author on the study, branded the lack of evidence for either iron's link with atherosclerosis, or atherosclerosis influence on hepcidin a 'surprise', but conceded the study needs to be replicated in humans to see if the same is true.

Other research groups have started to study hepcidin in atherosclerosis patients, Nemeth noted. A further question raised by her team's study is whether lowering iron beyond normal levels could have a positive effect over atherosclerosis.

"Understanding risk factors for atherosclerosis progression is important for better prevention and treatment of the disease,"​ Nemeth added.

Source: Cell Reports
Published online ahead of print, DOI: 10.1016/j.celrep.2013.11.009
"Testing the Iron Hypothesis in a Mouse Model of Atherosclerosis"
Authors: Leon Kautz, Victoria Gabayan et al.

Related topics: Research, Minerals, Cardiovascular health

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1 comment

Iron Neurosis?!

Posted by Carsten Smidt, Ph.D.,

It’s time for our industry to stop being neurotic about iron. This and other recent studies have debunked the long-held theory (myth) that excess iron may cause diabetes or cardiovascular disease(1). In fact, iron has antioxidant functions as a cofactor for catalase. Iron deficiency anemia is very common in the US and the world, especially in young women, children and vegetarians(2-7). Paleolithic diets have been estimated to provide a whopping 87 mg iron daily(8)! We in the industry need to overcome our unfounded fears about iron, use it more in multivitamin/minerals and reeducate the consumer in the interest of better public health. (Disclaimer: Author has no associations with iron suppliers)
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3. Lim KH, Riddell LJ, Nowson CA, Booth AO, Szymlek-Gay EA. Iron and zinc nutrition in the economically-developed world: a review. Nutrients. 2013;5(8):3184-3211.
4. Thane CW, Bates CJ. Dietary intakes and nutrient status of vegetarian preschool children from a British national survey. Journal of human nutrition and dietetics : the official journal of the British Dietetic Association. Jun 2000;13(3):149-162.
5. Craig WJ. Nutrition concerns and health effects of vegetarian diets. Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition. Dec 2010;25(6):613-620.
6. Waldmann A, Koschizke JW, Leitzmann C, Hahn A. Dietary iron intake and iron status of German female vegans: results of the German vegan study. Annals of nutrition & metabolism. 2004;48(2):103-108.
7. Gorczyca D, Prescha A, Szeremeta K, Jankowski A. Iron status and dietary iron intake of vegetarian children from poland. Annals of nutrition & metabolism. 2013;62(4):291-297.
8. Eaton SB, Eaton SB, 3rd, Konner MJ. Paleolithic nutrition revisited: a twelve-year retrospective on its nature and implications. European journal of clinical nutrition. Apr 1997;51(4):207-216.

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