The Nutritional Biochemistry of Chromium(III) - Survival-training.info

Introduction: A history of chromium studies (1955–1995) 19and LDL levels differed significantly between the subjects started on the supplement andthe group started on the placebo, with those on the placebo having lower initial values.Another well-performed study of interest was performed using hypoglycemic subjectsby Anderson, et al. [143] Eight female subjects were given 200 g Cr/day asCrCl 3 for 12 weeks. No change was observed in total cholesterol, HDL, LDL, VLDL,or triglyceride levels. The area of glucose below the fasting glucose level in glucosetolerance tests was lowered after 6 weeks of supplementation but was not significantlychanged after 12 weeks.The consensus of these studies is that Cr supplementation of healthy adults hasno effect on glucose, insulin, or blood lipids, while it is possible that subjects withmarginally abnormal blood glucose levels after a glucose challenge may be affectedbeneficially by supplementation.Perhaps the strongest evidence for an essential role of chromium in humans arisesfrom studies of patients on total parenteral nutrition (TPN) [115, 144]. Patients on TPNhave developed impaired glucose utilization [145] or glucose intolerance and neuropathyor encephalopathy [146–148]. The symptoms were reversed by chromium infusionand not other treatments. While limited to five individual cases, these studies provideevidence of clinical symptoms associated with Cr deficiency that can be reversed by supplementation.Another patient on TPN who developed symptoms of adult-onset diabetesand hyperlipidemia but died had low tissue Cr levels [149]. Curiously, the developmentof symptoms which were reversible by Cr supplementation does not correlate with serumCr levels [115], indicating that serum Cr levels are not an indicator of Cr deficiency.These incidences have recently been reviewed [115, 150]. Additionally, these incidencesof diagnosed potential Cr deficiency have been questioned recently as they lack consistentrelationships between the Cr in the TPN, time on TPN before symptoms, serum Crlevels, and symptoms [151]. Hence, no known indicator of Cr deficiency exists otherthan reversal of symptoms upon Cr supplementation [115]; a marker for Cr status intissues is desperately needed.Additional evidence for a potential role for Cr comes from studies of Cr absorptionas a function of chromium intake. Absorption varies inversely with intake as low intakes(∼15 g/day) lead to high rates of absorption (∼2%) while high intake (∼35 g/day)reduces absorption to ∼0.4% [152]. Work from the same research group indicates thatabsorption of Cr may not be inversely proportional to intake in rats [153].A role for Cr in the body is also suggested by an association between insulinaction and increased urinary loss, although other explanations may be possible. Inhuman euglycemic hyperinsulinemic clamp studies, Morris and coworkers have shownthat increases in blood insulin concentrations following an oral glucose load result insignificant decreases in plasma chromium levels; a subsequent infusion of insulin led tofurther chromium losses [154]. Within one-and-a-half hours after the increases of bloodinsulin concentrations, blood chromium levels started to recover. Patients also showedincreased urinary chromium losses during the course of the experiments, with the amountof chromium lost roughly corresponding to the amount of chromium estimated to be lostfrom the intravascular space [154]. Studies with human and rat tissue have demonstratedthat chromium binding by insulin-dependent tissues is significantly enhanced by glucose,suggesting that chromium may translocate from the blood compartment to insulinsensitivetissues [155]. (However, these studies used CrCl 3 as the chromium source; the