Researchers1 have investigated the effects of chromium chloride supplementation on the excretion of chromium in free-living subjects. At baseline, the urinary excretion of chromium was 0.20µg/d and 0.17µg/d in 15 healthy female and 27 healthy male subjects, respectively. The authors calculated that the absorption rate in the subjects was ≈0.4% of ingested chromium based on an estimated 60 µg/d intake. However, this intake is likely an over estimate based on more recent findings (here). Subjects were then randomly allocated to receive 200 µg/d chromium chloride, or a placebo for 3 months, before crossing-over to the other treatment. During the supplementation period, chromium excretion was significantly higher in the supplemental group (0.98µg/d) compared to the placebo group (0.22 µg/d). The 4-5 fold increase in chromium resulted in a roughly 4-5 fold increase in excretion, suggesting that absorption was still ≈0.4% (assuming loss by no other mechanism).
Earlier studies (in 1960s and 1970s) may have overestimated chromium excretion because of insensitivity with analytical methods. In addition, chromium intakes since the earlier studies in the 1960s, may have fallen. The result is that more recent studies have shown a decline in chromium excretion rates in urine. Generally, it is accepted now that low intakes of around 10 µg/d produce absorption rates of ≈2%, but that as chromium content rises to >40 µg/d, absorption falls to ≈0.5%. In addition, the form of chromium ingested may play a part in determining the absorption rate, with organic forms of chromium generally being less well absorbed. Inorganic chromium may also react with hydroxyl ions (Cr-OH–) in an alkali environment, followed by polymerisation that forms inabsorbable high molecular weight compounds in a process called olation. Further, some amino acids (methionine and histidine) can chelate inorganic chromium in the stomach and increase absorption.
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