Chromium

Discovery of Nutritional Importance

By 1948, chromium had been recognized as a consistent component of plant and animal tissue. The first suggestion that chromium might have biologic activity appeared in 1954 (Curran 1954), when it was found that chromium enhanced the synthesis of cholesterol and fatty acids from acetate by rat liver. In 1959, trivalent chromium was identified as the active component of the “glucose tolerance factor,” which alleviated the impaired glucose tolerance in rats fed certain diets apparently inadequate in chromium (Schwarz and Mertz 1959). Between 1964 and 1968, the first reports appeared indicating that chromium could affect glucose tolerance in humans (Mertz 1993).

Subsequently, it was found that chromium supplementation also decreased serum cholesterol concentrations and normalized exaggerated insulin responses to glucose loads. Despite these suggestive findings, chromium did not receive much attention as a possible essential element for humans until 1977, when apparent chromium deficiency signs were found in a patient receiving total parenteral nutrition (Jeejeebhoy et al. 1977). Shortly thereafter, other patients receiving total parenteral nutrition were found to exhibit abnormalities of glucose metabolism that were responsive to chromium supplementation.

Dietary Importance

In 1959, it was reported that chromium-deficient rats exhibited a glucose intolerance similar to that of clinical diabetes mellitus (Schwarz and Mertz 1959). Since that time, several other deficiency signs have been described for animals, including impaired growth, elevated serum cholesterol and triglyceride concentrations, increased incidence of aortic plaques, corneal lesions, and decreased fertility and sperm count (Anderson 1988). Many of these signs were made more evident by using nutritional, metabolic, physiological, or hormonal stressors.

Signs of apparent chromium deficiency have been found in three women receiving long-term total parenteral nutrition containing low amounts of chromium. One subject, who had received total parenteral nutrition for 3 5 years, exhibited impaired glucose tolerance and glucose use, weight loss, neuropathy, elevated free fatty acid concentrations, depressed respiratory exchange ratio, and abnormalities in nitrogen metabolism (Jeejeebhoy et al. 1977). These abnormalities were alleviated by chromium supplementation. Another subject, who had received total parenteral nutrition for 5 months, developed severe glucose intolerance, weight loss, and a metabolic encephalopathylike confusional state. All of these abnormalities were reversed by chromium supplementation (Freund, Atamian, and Fischer 1979). Chromium supplementation also reversed the development of unexplained high blood and urine glucose in a third patient who had followed a total parenteral nutrition regimen of several months’ duration (Brown et al. 1986).

Although these three descriptions of human chromium deficiency are somewhat dissimilar, in all cases the apparently chromium-deficient subjects exhibited impaired glucose tolerance, or high blood glucose with glucose spilling into the urine, and a refractoriness to insulin. In addition, since 1966, a large number of reports from numerous research groups have described beneficial effects from chromium supplements in subjects with degrees of glucose intolerance ranging from low blood sugar to insulin-dependent diabetes. Most recent are reports that relatively high chromium supplementation (200 to 1000 pg/day of chromium picolinate) decreased blood glucose and glycated hemoglobin in 162 Beijing, China, residents with high blood glucose (Anderson et al. 1997); such supplementation also decreased blood glucose, C-peptide, and insulin concentrations in gestational diabetic women undergoing a glucose tolerance test (Jovanovic-Peterson, Gutierrez, and Peterson 1996). Thus, there is a growing body of evidence suggesting that chromium supplements may be a viable treatment option for some people with diabetes resulting from inadequate synthesis of insulin or insulin resistance. In other words, chromium is potentiating the action of low amounts of insulin or improving its efficiency so that the need for exogenous sources is reduced or eliminated. Beneficial effects of chromium supplementation on blood lipid profiles also have been reported.

Even though a biochemical function has not been defined for chromium, it most likely is an essential element. Even the skeptics of chromium essentiality agree that chromium can be beneficial because of its positive effects on glucose and lipid metabolism in some individuals. This is apparently the reason that in 1980 an Estimated Safe and Adequate Daily Dietary Intake (ESADDI) was established for chromium (National Research Council 1980). For children over age 7 and adults, this amount is 50 to 200 pg/day.

There is some evidence that an intake of chromium of less than 20 pg/day is inadequate, and dietary surveys indicate that a significant number of people consume less than this amount. Thus, it seems possible that inadequate chromium status may be partially responsible for some cases of impaired glucose tolerance, high blood glucose, low blood glucose, refractoriness to insulin, and, ultimately, diabetes. Furthermore, because impaired tissue responsiveness to insulin is a possible risk factor for cardiovascular disease, and because chromium deprivation has unfavorable effects on cholesterol and lipid metabolism, inadequate chromium status may increase susceptibility to ischemic heart disease.