Chromium

BACKGROUND

Chromium is involved in potentiating the action of insulin in vivo and in vitro (Mertz 1969, 1993, Mertz et al 1961) and several studies have shown beneficial effects of chromium on circulating glucose, insulin and lipids in humans, although not all studies were positive. These studies have been reviewed by Anderson (1997), Mertz (1993), Offenbacher et al (1997) and Stoecker (1996).

In man, chromium accumulates in liver, spleen, soft tissue and bone (Lim et al 1983). Research on chromium metabolism is limited by the lack of a good measure for establishing deficiency states in man. However, data from metabolic balance and urinary excretion studies suggest that only 0.4–2.5% of chromium is absorbed, the actual amount being determined by the environment of the gastrointestinal tract and ligands provided by foods (Clydesdale 1998).

Chromium is widely distributed through the food supply but the content within a given type of food can vary widely because of geochemical factors (Welch & Carey 1975).

Most ingested chromium is excreted unabsorbed in the faeces (Mertz 1969, Offenbacher et al 1986) whilst absorbed chromium is excreted mainly in the urine (Anderson et al 1983). Vitamin C appears to increase absorption (Davis et al 1995, Offenbacher 1994, Seaborn & Stoecker 1990). Animal experiments have shown that high phytate levels can reduce absorption (Chen et al 1973) although lower levels appear to have no effect (Keim et al 1987). There are no systematic data for humans. Animal experiments have shown that long-term consumption of some medicines can affect chromium absorption through affecting stomach acidity or gastrointestinal prostaglandins (Davis et al 1995, Kamath et al 1997). It has also been suggested that absorption may increase with chronic resistive exercise (Rubin et al 1998).

In man, diets very high in simple sugars (35% energy) have been shown to increase urinary chromium excretion (Kozlovsky et al 1986) which may be related to the insulinogenic actions of carbohydrates (Anderson et al 1990). Urinary excretion also appears to be increased by aerobic exercise (Anderson et al 1982, 1984, 1988).

Chromium deficiency is relatively rare but has been reported in patients on total parenteral nutrition (Brown et al 1986, Freund et al 1979, Jeejeebhoy et al 1977). It has been hypothesised that poor chromium status contributes to the incidence of impaired glucose tolerance and type II diabetes which has led to interest in a potential role for chromium supplements in type II diabetes. One Chinese study involved 180 subjects with type II diabetes being given placebo, 200 µg or 1,000 µg chromium as chromium picolinate for 4 months. The subjects showed decreased fasting and 2-hour insulins at two months at both supplement levels, with glycosylated haemoglobin and fasting and 2-hour glucose concentrations being lower in the higher supplement group only. The reduced glucose and insulin concentrations were maintained to 4 months and glycosylated haemoglobin in both dosage groups was also reduced (Anderson et al 1997).

Approaches to the estimation of chromium requirements have included balance studies (Bunker et al 1984, Offenbacher et al 1986), urinary chromium excretion (Anderson et al 1982, 1983, 1991, Anderson & Kozlovsky 1985, Paschal et al 1998), plasma chromium concentration (Anderson 1987, Veillon 1989) and blood glucose and insulin concentrations (Anderson et al 1991). However, none of these approaches has been found to be satisfactory (FNB:IOM 2001).