Evidence has been mounting that excess iron stores may promote the development of insulin resistance, the metabolic syndrome, type 2 diabetes, and liver damage.1 Excess body fat stores can lead to insulin resistance and the development of a fatty liver in some people. Increased iron stores in the liver can also contribute to liver damage. The combination of excess iron stores in the liver, coupled with insulin resistance, is called the insulin resistance-associated hepatic iron overload (IR-HIO) syndrome.2
Up to 25% of those with IR-HIO develop a fatty liver and approximately 10% have either cirrhosis or severe fibrosis of the liver. Growing evidence suggests that excess iron stores may promote the development of insulin resistance and the metabolic syndrome.3 It appears that excess iron stores also damage the beta-cells that make insulin thus contributing to the development of type 2 diabetes. In the muscle cell increased iron interferes with glucose uptake aggravating insulin resistance. To determine if reducing excess iron stores would improve insulin sensitivity, researchers reduced iron stores by removing blood from a group of 40 to 60 year old men who had modestly elevated iron stores. Over 2 years repeated blood removal reduced their ferritin levels 179%. They showed that reducing iron stores improved insulin sensitivity suggesting that even moderately elevated iron stores play a role in the development of insulin resistance and eventually type 2 diabetes.4
Bottom Line: There is now compelling evidence that even moderately elevated iron stores contribute to the development of insulin resistance, the metabolic syndrome, liver damage, and type 2 diabetes. Individuals should have their iron stores evaluated by a check of their serum ferritin level. Those with ferritin levels in excess of 100mcg/L should be counseled to avoid red meats, iron-fortified foods, and food supplements containing iron. Those with iron stores above 200 to 300mcg/L might be encouraged to donate blood especially if they are overweight and have the metabolic syndrome.
By James J Kenney, PhD, RD, FACN
1. Diabetes 2002;51:2348-54
2. Lancet 2000;355:2181-2
3. Diabetes Care 2005;28:2061-63
4. Diabetes Care 2008;31:3-8
Stephanie Ronco has been editing for Food and Health Communications since 2011. She graduated from Colorado College magna cum laude with distinction in Comparative Literature. She was elected a member of Phi Beta Kappa in 2008.