The safety and efficacy of high-dose chromium - High-Dose Chromium

Alternative Medicine Review, June, 2002 by Davis W. Lamson, Steven M. Plaza

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This insulin potentiating or autoamplification action stems from the ability of LMWCr to maintain stimulation of tyrosine kinase activity. (25,57) Once insulin is bound to its receptor, LMWCr binds to the activated receptor on the inner side of the cell membrane and increases the insulin-activated protein kinase activity by eightfold. (75) There is also evidence the autoamplification effect of LMWCr may be enhanced by the inhibition of phosphotyrosine phosphatase, which inactivates tyrosine kinase. (25) Further study is required to understand the inconsistent results of Davis et al (77) who found that LMWCr actually activates membrane-associated phosphotyrosine phosphatase in insulin sensitive cells. As insulin levels drop and receptor activity diminishes, LMWCr is transported from the cell to the blood and excreted in the urine. (78) When chromium is absorbed from the gut, it is carried by transferrin, which transfers chromium to the apo-LMWCr. Excess chromium is carried by albumin. It has been estimated that each millimeter of serum contains 2-3 mg of transferrin, of which only 30 percent is saturated with iron, leaving the remaining unsaturated sites able to bind trivalent chromium. (71)

Chromium Absorption

In the last three decades evidence has been collected demonstrating that both exogenous and endogenous factors significantly alter absorption and ultimately bioavailability of chromium. A considerable variance with respect to absorption is reported in the literature. One study of men over age 60 found absorption of trivalent chromium from dietary consumption was approximately 1.8 percent. (79) Other sources cite absorption between 0.5 and 2.0 percent. (80) Variations in absorption of trivalent chromium can be traced to differences in the type of chromium ingested, competing minerals, and the effect of vitamins, proteins, drugs, and other nutritional factors used in combination (Table 1).

Dietary factors such as starch, ascorbic acid, minerals, oxalate, and amino acid intake can have a significant influence on chromium absorption. Carbohydrate intake has been shown to influence chromium urinary excretion and tissue concentration. Mice fed [sup.51]Cr-labeled chromium III chloride concomitantly with starch were found to have significantly higher concentrations of chromium in blood and tissue compared to those fed with chromium III chloride mixed with sucrose, fructose, or glucose. (86) Diets high in simple sugars have also been shown to increase urinary excretion of chromium by 10-300 percent, with no change in absorption rates. (87) Animals fed ascorbic acid with chromium supplementation demonstrated increased absorption. (88) A study of three women found that the ingestion of ascorbic acid (100 mg) in conjunction with chromium III chloride (1 mg) increased the absorption of chromium as measured in plasma levels. (89)

A number of minerals influence absorption. In rat studies, zinc supplementation reduced chromium absorption, while zinc deficiency had the opposite effect, elevating [sup.51]Cr levels. (90) A later study by Anderson et al (81) found no alteration in tissue levels of copper and zinc when mice were fed a diet with 5000 ng Cr III/g of feed. In in vitro rat studies, iron, manganese, and calcium have all been shown to depress intestinal transport of chromium at levels of only 100-fold that of chromium, while in the case of titanium, concentrations only 10 times that of chromium inhibited absorption. (91) In a study of rats fed 5000 ng/g of feed of a number of organic chromium compounds (chromium picolinate, nicotinate, acetate, glycinate, histidinate, or chloride), results showed that all compounds tested increased the iron content in the liver and spleen while decreasing iron levels in the heart. (81)