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Tracing disease to trace minerals - deficiency diseases

Tracing disease to trace minerals - deficiency diseases
Trace mineral deficiencies in the diet may play a bigger role in human health than most physicians now realize, according to a series of papers presented last week at the AAAS meeting. Many of these reported links between trace minerals and health problems -- such as heart disease and diabetes -- are still only suggestive. However, the deficiency levels discussed at the meeting are common in the typical American diet, the researchers warn, and if such subtle deficiencies are definitively found to jeopardize health, they may be affecting millions of people in the United States alone.
For example, while the safe and adequate amount of copper is generally thought to be 2 to 3 milligrams per day, "probably 75 percent of daily diets in the United States contain less than 2 mg of copper," reports Leslie Klevay, acting director of the Agriculture Department's Human Nutrition Research Center in Grand Forks, N.D. Several papers reported data suggesting that copper-deficient diets may increase one's risk of developing a host of health-threatening conditions, including coronary heart disease.
When fed a diet deficient in copper, animals have developed bone fragility, anemia, defects of the connective tissue, arteries and bone, infertility, heart arrhythmias, high cholesterol levels, heart attacks and an inability to control blood sugar levels. Klevay notes that any condition associated with coronary heart disease in humans can be triggered in laboratory animals merely by putting them on a copper-deficient diet.
And he recently did. Using mice, he attempted to repeat a study performed 20 years ago, which had reported finding a link between dietary fat and coronary heart disease-type effects. But there was a "hidden variable" in that earlier diet, Klevay says, because it had been low in copper. When he compared the disease effects reported with factors linked elsewhere to copper deficiency, he says, it became apparent that nearly all the factors attributed to fat could be accounted for by the copper deficiency alone. To test that, he repeated the study with copper being the only variable. And his results, published in the February ATHEROSCLEROSIS, matched those of the earlier study -- serious heart disease.
In another previous study, 13 of 15 animals on copper-deficient diets had dropped dead in the fifth week of a six-week study. "Limited autopsies showed ruptured hearts and aneurysms," Klevay says. In later, similar tests, he identified major electrocardiogram (EKG) changes as well. While puzzling over the EKG changes, Klevay ran across a reference to EKG changes in human participants in the famous Framingham study (SN: 1/24/81, p. 55) that were deemed predictive of an individual's potential for developing heart disease. Klevay's animals had exhibited two of those predictive EKG changes.
Harold Sandstead, former director of the Agriculture Department's Human Nutrition Research Center on Aging at Tufts University in Boston, described his research showing elevations in one man's blood cholesterol--from 206 mg/deciliter of blood to 235 mg/dl--after the man was put on a diet having only 0.8 mg of copper for 105 days. The man's cholesterol levels dropped back to 200 once he resumed a copper-adequate diet.
Copper is found in such foods as beef liver, nuts and seeds, dark chocolate, breakfast cereals and goose breast. But eating 2 mg worth of copper daily won't ensure a sufficiency of the mineral. Sandstead cites animal studies by Sheldon Reiser at the Agriculture Department's Carbohydrate Nutrition Lab in Beltsville, Md., that suggest that diets high in fructose -- a simple sugar contained in ordinary sucrose, or table sugar -- reduce the body's ability to absorb copper. In fact, Reiser says, copper-deficient animals fed fructose will start dying in five weeks of catastrophic heart disease -- such as ruptured hearts -- while similarly copper-deficient animals whose sugar source was cornstarch survive comfortably. Reiser says that in the fructose group, "every index of unfavorable metabolic effect was magnified."
Fructose appears to be only one of a group of chemicals that raise cholesterol and inhibit copper metabolism, Klevay says. Moreover, there is also a group that lowers cholesterol and enhances the body's uptake of copper; it includes aspirin, calcium and carbonates.
Walter Mertz, director of the Agriculture Department's Beltsville Human Nutrition Research Center, focused on chromium. In humans, he says, this is one of the few trace elements "that consistently declines with age." In the United States and other industrialized countries, he notes, glucose tolerance -- the rate at which the body metabolizes excess sugar -- also declines with age. Since chromium is known to help bring the hormone insulin together with insulin receptors on a cell's surface, there's growing suspicion that some element of mature-onset diabetes may be fostered by a chromium deficiency. Animals with chromium deficiency will metabolize sugar at almost half the normal rate, Mertz says, "which means, at least in animals, that chromium is necessary for maximum effectiveness of insulin." Currently, he is trying to find out "in what cases and under what conditions we can improve the glucose metabolism of middle-aged people." He's also trying to identify what conditions, such as exercise, influence human chromium requirements.

Tracing disease to trace minerals - deficiency diseases

Tracing disease to trace minerals - deficiency diseases
Trace mineral deficiencies in the diet may play a bigger role in human health than most physicians now realize, according to a series of papers presented last week at the AAAS meeting. Many of these reported links between trace minerals and health problems -- such as heart disease and diabetes -- are still only suggestive. However, the deficiency levels discussed at the meeting are common in the typical American diet, the researchers warn, and if such subtle deficiencies are definitively found to jeopardize health, they may be affecting millions of people in the United States alone.
For example, while the safe and adequate amount of copper is generally thought to be 2 to 3 milligrams per day, "probably 75 percent of daily diets in the United States contain less than 2 mg of copper," reports Leslie Klevay, acting director of the Agriculture Department's Human Nutrition Research Center in Grand Forks, N.D. Several papers reported data suggesting that copper-deficient diets may increase one's risk of developing a host of health-threatening conditions, including coronary heart disease.
When fed a diet deficient in copper, animals have developed bone fragility, anemia, defects of the connective tissue, arteries and bone, infertility, heart arrhythmias, high cholesterol levels, heart attacks and an inability to control blood sugar levels. Klevay notes that any condition associated with coronary heart disease in humans can be triggered in laboratory animals merely by putting them on a copper-deficient diet.
And he recently did. Using mice, he attempted to repeat a study performed 20 years ago, which had reported finding a link between dietary fat and coronary heart disease-type effects. But there was a "hidden variable" in that earlier diet, Klevay says, because it had been low in copper. When he compared the disease effects reported with factors linked elsewhere to copper deficiency, he says, it became apparent that nearly all the factors attributed to fat could be accounted for by the copper deficiency alone. To test that, he repeated the study with copper being the only variable. And his results, published in the February ATHEROSCLEROSIS, matched those of the earlier study -- serious heart disease.
In another previous study, 13 of 15 animals on copper-deficient diets had dropped dead in the fifth week of a six-week study. "Limited autopsies showed ruptured hearts and aneurysms," Klevay says. In later, similar tests, he identified major electrocardiogram (EKG) changes as well. While puzzling over the EKG changes, Klevay ran across a reference to EKG changes in human participants in the famous Framingham study (SN: 1/24/81, p. 55) that were deemed predictive of an individual's potential for developing heart disease. Klevay's animals had exhibited two of those predictive EKG changes.
Harold Sandstead, former director of the Agriculture Department's Human Nutrition Research Center on Aging at Tufts University in Boston, described his research showing elevations in one man's blood cholesterol--from 206 mg/deciliter of blood to 235 mg/dl--after the man was put on a diet having only 0.8 mg of copper for 105 days. The man's cholesterol levels dropped back to 200 once he resumed a copper-adequate diet.
Copper is found in such foods as beef liver, nuts and seeds, dark chocolate, breakfast cereals and goose breast. But eating 2 mg worth of copper daily won't ensure a sufficiency of the mineral. Sandstead cites animal studies by Sheldon Reiser at the Agriculture Department's Carbohydrate Nutrition Lab in Beltsville, Md., that suggest that diets high in fructose -- a simple sugar contained in ordinary sucrose, or table sugar -- reduce the body's ability to absorb copper. In fact, Reiser says, copper-deficient animals fed fructose will start dying in five weeks of catastrophic heart disease -- such as ruptured hearts -- while similarly copper-deficient animals whose sugar source was cornstarch survive comfortably. Reiser says that in the fructose group, "every index of unfavorable metabolic effect was magnified."
Fructose appears to be only one of a group of chemicals that raise cholesterol and inhibit copper metabolism, Klevay says. Moreover, there is also a group that lowers cholesterol and enhances the body's uptake of copper; it includes aspirin, calcium and carbonates.
Walter Mertz, director of the Agriculture Department's Beltsville Human Nutrition Research Center, focused on chromium. In humans, he says, this is one of the few trace elements "that consistently declines with age." In the United States and other industrialized countries, he notes, glucose tolerance -- the rate at which the body metabolizes excess sugar -- also declines with age. Since chromium is known to help bring the hormone insulin together with insulin receptors on a cell's surface, there's growing suspicion that some element of mature-onset diabetes may be fostered by a chromium deficiency. Animals with chromium deficiency will metabolize sugar at almost half the normal rate, Mertz says, "which means, at least in animals, that chromium is necessary for maximum effectiveness of insulin." Currently, he is trying to find out "in what cases and under what conditions we can improve the glucose metabolism of middle-aged people." He's also trying to identify what conditions, such as exercise, influence human chromium requirements.