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Complex interactions frustrate nutrition researchers.

The more I study, nutrient interactions, the more I realize how little we know about them," Meira Fields says in her delightful way as she throws up her hands in a gesture of surrender.

"People have to be aware that when we talk about nutrients we have to talk about interactions. We don't eat or drink carbohydrates, proteins, tat, alcohol, or supplements alone. We take them together," notes Fields.

And when our intakes are out of balance, it can throw the interactions out of balance.

The trace metals--such as iron, copper, or zinc--are particularly meddlesome. In the body, they are bound to proteins to keep them nontoxic, she says. "It could be that many of our metabolic diseases, including heart disease, are due to adverse interactions between metals and metabolites ."

In her laboratory at the Beltsville Human Nutrition Research Center in the Maryland suburbs of Washington. D.C., Fields and colleagues Charles G. Lewis and Mark D, Lure have been developing a scorecard to rate the various factors that determine whether or not rats suffer organ damage and die young from eating copper-deficient diets.

Fields has established that a copper-deficient diet alone is not enough to damage the heart, liver, and pancreas of her test rats. They also have to be getting excess fructose or sucrose (table sugar) in their feed or have their drinking water spiked with alcohol. Rats, like people and other animals, metabolize fructose and alcohol via a similar biochemical pathway, she explains. And it differs from the pathway used in metabolizing glucose--the basic unit of all starches.

However, not all rats develop organ damage and die from a copper-deficient diet containing high levels of fructose or alcohol. Only the male rats suffer, and only if they get this diet very early.

"The females are somehow protected," Fields says, but she doesn't know how. She tested the theory that female hormones or reproductive organs were giving female rats the edge but found that animals whose reproductive organs are removed come through the dietary challenge quite well. So rats have to be young and male and consume lots of fructose or alcohol along with too little copper before they suffer lethal organ damage. Eliminate any one of these factors and the animals survive normally.

Although Americans eat less than a fourth of the fructose in Fields' experimental diets which is 62 percent of total calories--U.S. consumption has been growing steadily. Fructose constitutes half of the sugar in table sugar and slightly more than half of the sugar in high-fructose corn sweeteners, which are used today in most processed foods and beverages-not just in the sweet ones. So it's virtually impossible for people to avoid fructose. The typical U.S. diet contains no more copper. on a pound-for-pound basis, than the rats got. However, it's dill]cult to compare human intakes with the rats' diet because these were rapidly growing baby rats who need more copper than an adult. And they breathed purified air and drank distilled water so their only source of copper was the feed.

Still, diets resembling U.S. intakes of fructose and copper have caused damage in pigs.

The damage in rats. according to Fields and colleagues. appears to be due to iron. That's right, iron. It's not so surprising, she says, because copper and iron are antagonist elements. Their common physical and chemical properties mean that they compete for the same metabolic sites.

She says one of the first symptoms in the male rats is anemia. 11 occurs even though all rats--males and females-- store a lot more iron in their livers when their food is copper-deficient. And they do so regardless of whether they get excess fructose or not. "So something is wrong with iron metabolism in the males that get fructose. They can't use what they have.

"The amount of iron is not important," she continues. "It's what form the iron is in. For example, if I want to make a call on a pay phone and don't have any change, all the dollar bills in the world won't help me. I need quarters!"

A collaborative study with William E. Antholine at the National Biomedical Electron Spin Resonance Center of the Medical College of Wisconsin in Milwaukee demonstrated that the livers of male rats on a copper-deficient, high-fructose diet did indeed seem to store dollar bills instead of quarters.

What's more, the unusable iron was in the form that prompts docile oxygen molecules to turn into destructive free radicals. These unstable oxygen molecules have a penchant for pulling electrons out of just about any biological molecule in their immediate vicinity and thus can damage cell membranes, proteins, even DNA.

If iron was the instigator, then reducing the amount of iron in the rats' bodies should reduce abnormalities, she reasoned. And that's exactly what happened.

Fields and colleagues tested two different methods to reduce iron levels in male rats. First, they fed the rats an iron-binding agent, deferoxamine, which is used in medical practice to remove excess iron in patients with iron overload. And because deferoxamine binds to iron, it also defuses the form that generates free radicals, preventing oxidation. In a second experiment, they cut the amount of iron in the rats' feed by two-thirds.

In both cases, she says, the anemia and damage to the heart and pancreas were prevented. They did not test the liver. The most dramatic effect: All the rats survived the study.

"All the pathology for copper deficiency can be prevented by making the diet iron deficient or by substituting starch for fructose," she says. The lesson here is that "under certain conditions, iron can be very toxic."

She strongly suspects that this toxic form of iron is responsible for the animals' liver and pancreatic damage but says she hasn't ruled out other causes. The heart damage, however, she attributes to the animals' anemia because Antholine saw no evidence of free radicals in their heart tissue.

Just recently, Fields found that the type of protein in the diet also plays a role in the severity of copper deficiency. In her experimental diets, she used one of three different proteins: lactalbumin or casein, both of which are milk proteins, or egg white. The male rats getting lactalbumin had the most abnormalities.

Fields notes that female rats on copper-deficient diets store even more iron in their livers than males but do not generate the free radicals that males do. She believes that men who consume a lot of sugar or drink alcohol regularly may be putting themselves at risk of iron toxicity if their diets are inadequate in copper. And the amount of copper needed by humans is still uncertain. "It's a cumulative problem," she stresses. "We're talking about long term in people.

"How do we know that other nutrients aren't involved in similar interactions?" she asks. "We don't, because no one has done the research."

"If researchers don't take adverse nutrient interactions seriously, we cannot progress in understanding what's behind metabolic diseases," she warns.

To ensure that interactions stay in balance, she recommends the same dietary habits grandmother urged on us: Eat everything in moderation, for a wide variety of foods ensures getting all the nutrients in the right proportions.- By Judy McBride, ARS.

Meira Fields is at the USDA-ARS Beltsville Human Nutrition Research Center, Bldg. 307, 10300 Baltimore Ave, Beltsville, MD 20705-2350. Phone (301) 504-9412, fax number (301) 504-9456.
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Author:McBride, Judy
Publication:Agricultural Research
Date:Jun 1, 1993
Words:1233
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