ABSTRACT
Ubiquinones (coenzyme Qs (CoQ)) are essential for oxidative phosphorylation in yeasts and humans, although the isomers present in each are different. The human coenzyme Q, CoQ10, is administered orally for the treatment of heart disease and other disorders. Some patients, however, require much higher doses than others to attain a therapeutic CoQ10 blood level. We propose that one possible explanation for this variability is Candida colonization of the GI tract. Many common medical treatments including antibiotics and anti-hyperchlorhydric agents increase the risk of GI tract Candida colonization. Subsequent uptake and utilization of supplemental CoQ10 by the yeast could diminish availability for the human subject. Data from one patient and an in vitro pilot study using two pathogenic strains of C. albicans support this hypothesis. If C. albicans in the GI tract can hinder availability and interfere with therapeutic effects of CoQ10, it could be of clinical significance for large numbers of patients.
Subject(s)
Candida albicans/physiology , Digestive System/microbiology , Ubiquinone/analogs & derivatives , Ubiquinone/metabolism , Coenzymes , Humans , Intestinal Absorption , Pilot ProjectsABSTRACT
Seven zinc-containing dietary supplements were analyzed for zinc (Zn) and cadmium (Cd) by inductively coupled plasma/mass spectrometry (ICP/MS). Cadmium was detected in all samples; however, the amount of Cd per 15 mg Zn (the daily US Recommended Dietary Allowance) varied by over 37-fold (0.039 to 1.46 micrograms Cd/15 mg Zn). Supplements with Zn in the form of a gluconate consistently contained the lowest amounts of Cd. Because Cd is a non-essential potentially toxic element for humans, its concentration in nutritional supplements should be minimized and possibly regulated by government-established standards.
Subject(s)
Cadmium/analysis , Dietary Supplements/analysis , Drug Contamination , Zinc/analysis , Humans , Maximum Tolerated DoseSubject(s)
Ascorbic Acid/blood , Glycated Hemoglobin/analysis , Animals , Blood Glucose/analysis , MiceABSTRACT
The frequent association of various reproductive anomalies with maternal diabetes is explained by a theory that predicts such defects will occur even in transient moderate hyperglycemia in non-diabetic gravidae. A first test of this hypothesis produced strongly supportive results in a mouse model. Thirteen C57BL/6J dams on a grain (control) diet produced (in the 4th week after first mating) 64 pups, 62 surviving to maturity. In the same time interval on a high sucrose diet, fourteen isogenic dams produced only 5 pups, none surviving 5 days (p much less than .001). Additional ongoing studies of the underlying glucose-ascorbate antagonism and of early vs. perinatal hyperglycemia are described briefly.
Subject(s)
Hyperglycemia/complications , Reproduction , Animals , Female , Fetal Death/etiology , Infertility, Female/etiology , Litter Size , Mice , Mice, Inbred C57BL , PregnancyABSTRACT
Marked sensitivity of tumor tolerance to blood glucose level is demonstrated in a mouse model of human breast cancer. A theory is cited that explains the high association of hyperglycemia with malignancy, especially breast cancer, via glycemic modulation of cellular immunity. Three groups of BALB/C mice were injected with an aggressive mammary tumor and placed on three dietary regimens designed to produce three different glycemic levels. Mortalities 70 days after injection were 16 of 24 hyperglycemic mice, 8 of 24 normoglycemic, and 1 of 20 hypoglycemic (chi-square p less than .005). Taken together with other experiments and human data discussed briefly, this result suggests that glycemic modulation of tumor tolerance should be evaluated in human trials.
