The Effect of a High Chromium Yeast on the Blood Glucose Control and Blood Lipids of Normal and Diabetic Human Subjects

نویسنده

  • J. A. Vinson
چکیده

A new high potency organic chromium yeast was investigated for its effect on blood control and serum lipids in a group of 23 normal and diabetic subjects which were sub-divided into normals, hyperglycaemics, insulin-dependent diabetics and noninsulin dependent diabetics. Each volunteer daily took 100 mg of yeast containing 218 μg of chromium for a period of six months. The blood and serum was analysed before supplementation and periodically throughout the study. Transient improvements in the various parameters occurred in all the groups in the early portion of the study. However, after six months of supplementation, the only group to statistically significantly benefit was the hyperglycaemic group. This group had improved blood glucose control, lowered serum lipids and a decreased risk of coronary heart disease. Introduction Chromium has been recognised as an essential trace element for both animal and human nutrition. Recently, the National Academy of Sciences/National Research Council suggested that the daily intake of chromium for adults be between 50 and 200 μg [1]. The chromium levels in the diet of the United States and Western Europe are lower than in the Near and Far East which is at least partly the result of processing [2]. Tissue levels are also lower in the United States than in other countries [3, 4]. Inorganic chromium compounds are poorly absorbed in man, amounting to 1-3% regardless of dose or dietary chromium status [5]. Organic chromium, such as found in brewer's yeast, is much better absorbed than inorganic chromium [6]. Over half of the chromium in brewer's yeast is in a volatile, organic form [7]. This form of trivalent chromium, complexed with nicotinic acid and amino acids, is known as glucose tolerance factor (GTF). Among foods, brewer's yeast is the richest source of GTF. This biologically important form of chromium is hypothesised as a co-factor for the binding of insulin tom membrane receptors in insulin-sensitive tissues [6]. GTF has been shown to be a requirement for normal carbohydrate metabolism [8]. When an animal or human is chromium deficient, the result is an impaired glucose tolerance. To date, there is but indirect evidence to support the view that chromium deficiency occurs in normal human populations. It does appear that older individuals and those consuming large amounts of carbohydrates might be deficient. Tissue chromium levels have been found to dramatically decrease with age in the United States [2]. It has also been shown that chromium is mobilised from body stores as a response to administration of glucose by mouth [9]. High consumption of refined sugars and carbohydrates is thus likely to induce chromium deficiencies by excretion. These refined carbohydrates are themselves low in chromium and contribute to the problem. Diabetics represent the most susceptible group of individuals toward chromium deficiency. Diminished chromium stores have been reported in the hair [10] and liver [11] of diabetic humans. Insulin-requiring diabetics have been shown to have an abnormal rate of chromium absorption. During the first 24 hours after a single oral dose of chromium, these individuals absorb two to four times more chromium than normal subjects [8]. Recently, this effect was also seen in diabetic rats given radiochromium. These rats, when given insulin after chromium, had their chromium levels restored to normal [12]. Diabetics have been found to excrete in their urine almost twice as much chromium per day than do normal individuals [13]. This is due to the fact that when insulin id taken, 20% of the chromium mobilised from the body stores is excreted in the urine. thus, it appears that administration of insulin may result in an increased excretion of chromium and a tendency to chromium deficiency. This hypothesis is supported by the recent work of Thompson [14] who found insulintreated diabetics to have significantly lower levels of plasma chromium than normal subjects. In genetically diabetic mice with hyperglycaemia and hyperinsulinemia, GTF administration, both acutely and chronically, reduced the elevated blood glucose levels to normal, inorganic chromium was completely without effect [7]. It was thus hypothesised that diabetic mice had an impaired ability to convert inorganic chromium into the biologically active GTF. If this impairment exists in humans it may explain the lack of success of chromium supplementation studies such as that by Sherman [15]. This group and other groups used inorganic chromium for their studies. For instance, Levine found that the abnormal glucose tolerance of only 4/10 elderly subjects became normal after 1-4 months of inorganic chromium supplementation [16]. This improvement of glucose tolerance was not due to retarded glucose absorption or to an increased rise in plasma insulin activity after the glucose load. In fat, in a more recent study, Doisy [8] found that the serum insulin concentration reached lower peak values after a glucose load, following an 8 month chromium supplementation, than before supplementation. This effect was seen in both normal subjects and siblings of diabetics. Thus, it appears that less insulin is required to keep glucose controlled when adequate chromium is present. A study with several offspring of an insulin-requiring diabetic [8] showed that inorganic chromium was ineffective in improving glucose tolerance while a six month supplement of brewer's yeast normalised the glucose tolerance as measured by the glucose tolerance test. The present study is an attempt to verify the effect of a long-term supplementation chromium on glucose control and body lipids in humans using a new high potency chromium yeast. Materials and Methods Twenty three subjects (ages 17-63) volunteered for the study and their informed consent obtained. Six normal individuals (ages 38-63) served as controls. Five hyperglycaemic individuals (ages 47-60) had abnormal blood glucose control as determined by % glycosylated haemoglobin (%GHb) and a high normal fasting blood glucose. Seven individuals (ages 19-62) were insulin-dependent diabetics who had had the disease at least five years. Their insulin requirement was stabilised. Five subjects (ages 39-59) were not insulin-dependent diabetics who were taking oral antidiabetic medication. With the subjects in a seated position, after an overnight fast, venous blood was collected into a vacutainer containing EDTA. The blood was frozen at -20°C until analysis. The %GHb in the blood was determined with an isolab kit using the optimum room temperature and a control of known value. This column chromatographic method determines the fast haemoglobin HbA 1 which equals HbA 1a + HbA 1a + HbA 1c , with a reproducibility of approximately 5%. Two other vacutainers of blood were taken. One was used for blood glucose and by a conventional automated enzyme method. The second vacutainer's contents was allowed to clot and the serum frozen until assay. The serum was analysed for cholesterol and triglycerides by conventional automated methods. High density lipoprotein cholesterol (HDL) was determined after Mn2+ precipitation by a conventional automated enzymatic method. Low density lipoprotein cholesterol (LDL) was calculated from the formula LDL = Cholesterol = HDL Triglycerides/5.

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تاریخ انتشار 2001