Iron is required for life. It is a chemical element and one of the most common elements on earth. It is the critical element in the metabolism of hundreds of protein and enzymes involved in diverse body functions, such as oxygen transport, cell growth and DNA synthesis. Here Clayton Dalton, Nautil.us, reflects on elevated iron being the center of many diseases from cancer to diabetes:
“Cheerios are the best-selling breakfast cereal in America. The multi-grain version contains 18 milligrams of iron per serving, according to the label. Like almost any refined food made with wheat flour, it is fortified with iron. As it happens, there’s not a ton of oversight in the fortification process. One study measured the actual iron content of 29 breakfast cereals, and found that 21 contained 120 percent or more of the label value, and 8 contained 150 percent or more.1 One contained nearly 200 percent of the label value.
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If your bowl of cereal actually contains 120 percent more iron than advertised, that’s about 22 mg. A safe assumption is that people tend to consume at least two serving sizes at a time.1 That gets us to 44 mg. The recommended daily allowance of iron is 8 mg for men and 18 mg for pre-menopausal women. The tolerable upper intake—which is the maximum daily intake thought to be safe by the National Institutes of Health—is 45 mg for adults.
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It is entirely feasible that an average citizen could get awfully close to exceeding the maximum daily iron intake regarded as safe with a single bowl of what is supposed to be a pretty healthy whole-grain breakfast option.
And that’s just breakfast.
At the same time that our iron consumption has grown to the borders of safety, we are beginning to understand that elevated iron levels are associated with everything from cancer to heart disease. Christina Ellervik, a research scientist at Boston Children’s Hospital who studies the connection between iron and diabetes, puts it this way: “Where we are with iron now is like where we were with cholesterol 40 years ago.”
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The story of energy metabolism—the basic engine of life at the cellular level—is one of electrons flowing much like water flows from mountains to the sea. Our cells can make use of this flow by regulating how these electrons travel, and by harvesting energy from them as they do so. The whole set-up is really not so unlike a hydroelectric dam.
The sea toward which these electrons flow is oxygen, and for most of life on earth, iron is the river. (Octopuses are strange outliers here—they use copper instead of iron, which makes their blood greenish-blue rather than red). Oxygen is hungry for electrons, making it an ideal destination. The proteins that facilitate the delivery contain tiny cores of iron, which manage the handling of the electrons as they are shuttled toward oxygen.
This is why iron and oxygen are both essential for life. There is a dark side to this cellular idyll, though.
Normal energy metabolism in cells produces low levels of toxic byproducts. One of these byproducts is a derivative of oxygen called superoxide. Luckily, cells contain several enzymes that clean up most of this leaked superoxide almost immediately. They do so by converting it into another intermediary called hydrogen peroxide, which you might have in your medicine cabinet for treating nicks and scrapes. The hydrogen peroxide is then detoxified into water and oxygen.
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Things can go awry if either superoxide or hydrogen peroxide happen to meet some iron on the way to detoxification. What then happens is a set of chemical reactions (described by Haber-Weiss chemistry and Fenton chemistry) that produce a potent and reactive oxygen derivative known as the hydroxyl radical. This radical—also called a free radical—wreaks havoc on biological molecules everywhere. As the chemists Barry Halliwell and John Gutteridge—who wrote the book on iron biochemistry—put it, “the reactivity of the hydroxyl radicals is so great that, if they are formed in living systems, they will react immediately with whatever biological molecule is in their vicinity, producing secondary radicals of variable reactivity.”2
Such is the Faustian bargain that has been struck by life on this planet. Oxygen and iron are essential for the production of energy, but may also conspire to destroy the delicate order of our cells. As the neuroscientist J.R. Connor has said, “life was designed to exist at the very interface between iron sufficiency and deficiency.”3
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At the end of the 20th century, the metabolism of iron in the human body was still a bit of a mystery. Scientists knew of only two ways that the body could excrete iron—bleeding, and the routine sloughing of skin and gastrointestinal cells. But these processes amount to only a few milligrams per day. That meant that the body must have some way to tightly regulate iron absorption from the diet. In 2000 a major breakthrough was announced—a protein was found that functioned as the master regulator for iron. The system, as so many biological systems are, is perfectly elegant. When iron levels are sufficient, the protein, called hepcidin, is secreted into the blood by the liver. It then signals to gastrointestinal cells to decrease their absorption of iron, and for other cells around the body to sequester their iron into ferritin, a protein that stores iron. When iron levels are low, blood levels of hepcidin fall, and intestinal cells begin absorbing iron again. Hepcidin has since become recognized as the principal governor of iron homeostasis in the human body.
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But if hepcidin so masterfully regulates absorption of iron from the diet to match the body’s needs, is it possible for anyone to absorb too much iron?
In 1996, a team of scientists announced that they had discovered the gene responsible for hereditary hemochromatosis, a disorder causing the body to absorb too much iron. They called it HFE. Subsequent work revealed that the product of the HFE gene was instrumental in regulating hepcidin. People with a heritable mutation in this gene effectively have a gross handicap in the entire regulatory apparatus that hepcidin coordinates.
This, then, leaves open the possibility that some of us could in fact take in more iron than the body is able to handle. But how common are these mutations? Common enough to matter for even a minority of people reading these words?
Surprisingly, the answer is yes. The prevalence of hereditary hemochromatosis, in which two defective copies of the HFE gene are present and there are clinical signs of iron overload, is actually pretty high—as many as 1 in 200 in the United States. And perhaps 1 in 40 may have two defective HFE genes without overt hemochromatosis.4 That’s more than 8 million Americans who could have a significant short-circuit in their ability to regulate iron absorption and metabolism.
What if you have only one defective HFE gene, and one perfectly normal gene? This is called heterozygosity. We would expect to find more people in this situation than the homozygotes, or those with two bad copies of the gene. And in fact we do. Current estimates suggest that more than 30 percent of the U.S. population could be heterozygotes with one dysfunctional HFE gene.4 That’s pretty close to 100 million people.
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Does this matter? Or is one good gene enough? There isn’t much research, but so far the evidence suggests that some heterozygotes do have impaired iron metabolism. Studies have shown that HFE heterozygotes seem to have modest elevations of ferritin as well as transferrin, a protein which chaperones iron through the blood, which would indicate elevated levels of iron.5,6 And a study published in 2001 concluded that HFE heterozygotes may have up to a fourfold increased risk of developing iron overload.4
Perhaps more concerning is that these heterozygotes have also been shown to be at increased risk for several chronic diseases, like heart disease and stroke. One study found that heterozygotes who smoked had a 3.5 times greater risk of cardiovascular disease than controls, while another found that heterozygosity alone significantly increased the risk of heart attack and stroke.7,8 A third study found that heterozygosity increased nearly sixfold the risk of cardiomyopathy, which can lead to heart failure.9
The connection between excessive iron and cardiovascular disease may extend beyond HFE heterozygotes. A recent meta-analysis identified 55 studies of this connection that were rigorous enough to meet their inclusion criteria. Out of 55 studies, 27 supported a positive relationship between iron and cardiovascular disease (more iron equals more disease), 20 found no significant relationship, and 8 found a negative relationship (more iron equals less disease).10
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A few highlights: a Scandinavian study compared men who suffered a heart attack to men who didn’t, and found that elevated ferritin levels conferred a two- to threefold increase in heart attack risk. Another found that having a high ferritin level made a heart attack five times more likely than having a normal level. A larger study of 2,000 Finnish men found that an elevated ferritin level increased the risk of heart attack twofold, and that every 1 percent increase in ferritin level conferred a further 4 percent increase in that risk. The only other risk factor found to be stronger than ferritin in this study was smoking.
Ferritin isn’t a perfect marker of iron status, though, because it can also be affected by anything that causes inflammation. To address this problem a team of Canadian researchers directly compared blood iron levels to heart attack risk, and found that higher levels conferred a twofold increased risk in men and a fivefold increased risk in women.”
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