LiveingWell Health News Letter
1.Chromium 2. HEALTH SITES 3.THOUGHT OF THE DAY
Although trivalent chromium is recognized as a nutritionally essential mineral, scientists are not yet certain exactly how it functions in the body. The two most common forms of chromium are trivalent chromium (III) and hexavalent chromium (VI). Chromium (III) is the principal form in foods, as well as the form utilized by the body. Chromium (VI) is derived from chromium (III) by heating at alkaline pH and is used as a source of chromium for industrial purposes. It is a strong irritant and is recognized as a carcinogen when inhaled. At low levels, chromium (VI) is readily reduced to chromium (III) by reducing substances in foods and the acidic environment of the stomach, which serve to prevent the ingestion of chromium (VI).
A biologically active form of chromium participates in glucose metabolism by enhancing the effects of insulin. Insulin is secreted by specialized cells in the pancreas in response to increased blood glucose levels, for example, after a meal. Insulin binds to insulin receptors on the surface of cells, activating those receptors and stimulating glucose uptake by cells. Through its interaction with insulin receptors, insulin provides cells with glucose for energy and prevents blood glucose levels from becoming elevated. In addition to its effects on carbohydrate (glucose) metabolism, insulin also influences the metabolism of fat and protein. A decreased response to insulin or decreased insulin sensitivity may result in impaired glucose tolerance or type 2 diabetes, also known as non-insulin dependent diabetes mellitus (NIDDM). Type 2 diabetes is characterized by elevated blood glucose levels and insulin resistance.
The precise structure of the biologically active form of chromium is not known. Recent research suggests that a low-molecular-weight chromium-binding substance (LMWCr) may enhance the response of the insulin receptor to insulin. The following is a proposed model for the effect of chromium on insulin action (diagram). First, the inactive form of the insulin receptor is converted to the active form by binding insulin. The binding of insulin by the insulin receptor stimulates the movement of chromium into the cell and results in binding of chromium to apoLMWCr, a form of the LMWCr that lacks chromium. Once it binds chromium the LMWCr binds to the insulin receptor and enhances its activity. The ability of the LMWCr to activate the insulin receptor is dependent on its chromium content. When insulin levels drop due to normalization of blood glucose levels, the LMWCr may be released from the cell in order to terminate its effects.
Iron: Chromium competes for one of the binding sites on the iron transport protein, transferrin. However, supplementation of older men with 925 mcg of chromium/day for 12 weeks did not significantly affect measures of iron nutritional status. A study of younger men found an insignificant decrease in transferrin saturation with iron after supplementation of 200 mcg of chromium/day for 8 weeks, but no long-term studies have addressed this issue. Iron overload in hereditary hemochromatosis may interfere with chromium transport by competing for transferrin binding. This has led to the hypothesis that decreased chromium transport might contribute to the diabetes associated with hereditary hemochromatosis.
Vitamin C: Chromium uptake is enhanced in animals when given at the same time as vitamin C (1). In a study of three women, administration of 100 mg of vitamin C together with 1 mg of chromium resulted in higher plasma levels of chromium than 1 mg of chromium without vitamin C.
Carbohydrates: Diets high in simple sugars (e.g., sucrose), compared to diets high in complex carbohydrates (e.g., whole grains), increase urinary chromium excretion in adults. This effect may be related to increased insulin secretion in response to the consumption of simple sugars compared to complex carbohydrates.
Chromium deficiency was reported in three patients on long-term intravenous feeding who did not receive supplemental chromium in their intravenous solutions. These patients developed evidence of abnormal glucose utilization and increased insulin requirements that responded to chromium supplementation. Additionally, impaired glucose tolerance in malnourished infants responded to an oral dose of chromium chloride. Because chromium appears to enhance the action of insulin and chromium deficiency has resulted in impaired glucose tolerance, chromium insufficiency has been hypothesized to be a contributing factor to the development of Type 2 diabetes.
Several studies of male runners indicated that urinary chromium loss was increased by endurance exercise, suggesting that chromium needs may be greater in individuals who exercise regularly. In a more recent study, resistive exercise (weight lifting) was found to increase urinary excretion of chromium in older men. However, chromium absorption was also increased, leading to little or no net loss of chromium as a result of resistive exercise.
At present, research on the effects of inadequate chromium intake and risk factors for chromium insufficiency are limited by the lack of sensitive and accurate tests for determining chromium nutritional status.
By Lillian Waugh
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"Jesus said, surely I am with you always to the very end of the age. "
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