Candida
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CANDIDA

Selenium deficiency and anemia appear to be the biggest factors in promoting candida growth. Years ago when I had hypoT I also had a severe candida infection. I found a book titled "Candida: Silver (Mercury) Fillings and the Immune System" which eventually led me to getting my mercury fillings removed. Following this and supplementation with zinc and selenium, my candida and hypoT both ended.

Experiments with animals show that candida growth can be increased by selenium deprivation and reduced by selenium supplementation. Since mercury depletes selenium, it makes sense that candida is higher when there are mercury fillings in the teeth.

Other studies show that anemia and iron deficiency increase candida growth. There are some studies suggesting that B12 and folic acid deficiencies may be involved in candida, since deficiencies of these lead to anemia. In anemia and iron deficiency friendly bacteria cannot grow well in the body. A lack of these bacteria probably is a key factor which promotes candida growth, since candida is a fungal growth rather than a bacteria growth. 

Another study showed that women with recurrent vulvovaginal candidiasis are deficient in zinc compared to normals and that only a mild zinc deficiency is necessary for this recurring problem.

Basically it seems that the deficiencies associated with candidiasis correlate very well with the deficiencies associated with hypothyroidism. The key nutrient deficiencies are probably selenium, zinc, iron, B12, and folic acid. 

Probably the best indicator of the level of candida growth in the body is the coating on the tongue. The more white coating there is, the more candida there probably is throughout the body. We want to get to the point where our tongues are clear, pink, and not sore.

The following study shows that candida albicans has a higher resistance to elevated concentrations of copper than baker's yeast. This may mean that in hypothyroidism, when zinc is low and copper is high, candida growth will not be suppressed by copper, which is normally toxic to fungal infections.

Proc Natl Acad Sci U S A 2000 Mar 28;97(7):3520-5

The high copper tolerance of Candida albicans is mediated by a P-type ATPase.

Weissman Z, Berdicevsky I, Cavari BZ, Kornitzer D

Department of Molecular Microbiology, The Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 31096, Israel.

The pathogenic yeast Candida albicans has higher resistance than the baker's yeast Saccharomyces cerevisiae to elevated concentrations of copper. To understand the basis of this differential resistance, we performed a functional screen for C. albicans genes involved in copper detoxification. Here, we report the isolation of two such genes: a metallothionein, CaCUP1, and a copper-transporting P-type ATPase, CaCRP1. Both genes are induced by extracellular copper. Gene disruptions indicated that the copper extrusion pump is responsible for the unusual resistance of C. albicans to copper, whereas the metallothionein is responsible for the residual copper resistance of the Cacrp1Delta mutant. We show further that under acidic and anaerobic conditions, such as prevail in the natural niche of C. albicans, the digestive tract of animals, CaCRP1 function becomes essential for survival in the presence of even very low copper concentrations. These observations suggest that copper in the gastrointestinal tract may present a toxic challenge to which enteric organisms had to adapt.

The following studies show that selenium is a key nutrient in the control of candida albicans.
 
J Nutr 1986 May;116(5):816-22

The response of selenium-deficient mice to Candida albicans infection.

Boyne R, Arthur JR

The effects of selenium deficiency on the responses to Candida albicans infection were examined in mice. When selenium-deficient and selenium-supplemented mice were given i.v. injections of 0.1 ml suspensions of 1 X 10(5) or 5 X 10(4) C. albicans in 0.9% sterile saline, deaths in the selenium-deficient animals started after 2.5-3.5 d compared with 7-8.5 d in the selenium-supplemented animals. Further studies demonstrated that 3 d after an i.v. injection of 1 X 10(5) C. albicans, significantly more of the microorganisms were found in the kidneys (P less than 0.001), livers (P less than 0.025) and spleens (P less than 0.01) of the selenium-deficient mice compared with the same organs of selenium-supplemented animals. Selenium deficiency was also demonstrated to impair the ability of mouse neutrophils to kill C. albicans in in vitro tests. The possible relationships of this defect in function to decreased resistance to C. albicans infection is discussed.
 
J Comp Pathol 1986 Jul;96(4):379-86

An in vivo and in vitro study of selenium deficiency and infection in rats.

Boyne R, Arthur JR, Wilson AB

Selenium deficiency in rats impairs the ability of neutrophils and peritoneal macrophages to kill Candida albicans organisms in vitro. In contrast, killing of Salmonella typhimurium and Staphylococcus aureus organisms is unaffected by the deficiency. Survival of rats after intraperitoneal injection of 8 X 10(7) S. aureus organisms was not affected by Se deficiency, but a 5-fold increase in the dose (4 X 10(8) S. aureus organisms) led to a significantly greater mortality in the Se deficient rats.

Indian J Biochem Biophys 1994 Oct;31(5):427-9

Effect of experimental selenium deficiency and its supplementation on the candidacidal activity of neutrophils in albino rats.

Kukreja R, Khan A

Department of Biochemistry, Nagpur University.

The role of selenium in the diet of rats has been examined with respect to the neutrophil functions. Feeding of Se-deficient diet for 75 days resulted in reduction in candidacidal activity, superoxide production, oxygen consumption, glucose utilisation and glutathione peroxidase activity. Supplementing the diet with Se for 30 days resulted in partial restoration of all the activities.
Biotin deficiency may also be involved in candida albicans.
Semin Dermatol 1991 Dec;10(4):296-302

Skin manifestations of biotin deficiency.

Mock DM

Department of Pediatrics, University of Iowa Hospitals and Clinics, Iowa City 52242.

This article reviews current knowledge concerning the dermatologic manifestations of biotin deficiency. Biotin is a water-soluble vitamin that acts as an essential cofactor for four carboxylases, each of which catalyzes an essential step in intermediary metabolism. For example, acetyl-CoA carboxylase catalyzes the rate-limiting step in fatty acid elongation. In infants, children, and adults, deficiency of biotin causes alopecia and a characteristic scaly, erythematous dermatitis distributed around body orifices. The rash closely resembles that of zinc deficiency. Candida albicans often can be cultured from the skin lesions. Biotinidase deficiency, an inborn error, causes biotin deficiency, probably as a consequence of unpaired intestinal absorption, cellular salvage, and renal reclamation of biotin; biotinidase deficiency causes dermatologic manifestations similar to biotin deficiency. There is evidence that impaired fatty acid metabolism secondary to reduced activities of the biotin-dependent carboxylases (especially acetyl-CoA carboxylase) plays an etiologic role in the dermatologic manifestations of biotin deficiency. Candida infections secondary to impaired immune function might also contribute to the dermatitis of biotin deficiency.
 
Am J Obstet Gynecol 1986 Nov;155(5):1082-5

Zinc status in women with recurrent vulvovaginal candidiasis.

Edman J, Sobel JD, Taylor ML

Zinc status has been shown to influence various cell-mediated immunologic mechanisms. These cell-mediated mechanisms are important in preventing mucocutaneous infections caused by Candida albicans. This study evaluated the relationship between zinc status and recurrent vaginal candidiasis by comparing plasma and erythrocyte zinc in 29 patients with recurrent vaginal candidiasis and 20 control subjects matched for age, race, and parity. The results indicated that there was a significantly lower level of plasma zinc in women with recurrent vaginal candidiasis (81 + 11.6 mg/dl) than in the control subjects (91 +/- 14.2 mg/dl) with a significant value of p = 0.015. These differences in plasma zinc levels were even greater when adjusted for dietary zinc and supplemental zinc with the use of analyses of covariance. No differences in erythrocyte zinc measurements were found between the two groups. These results suggest that mild zinc deficiency is associated with recurrent vaginal candidiasis and may play a role in the susceptibility of women to recurrent vaginal candidiasis.
 
J Med Microbiol 1983 Aug;16(3):363-9

The role of iron deficiency in experimentally-induced oral candidosis in the rat.

Rennie JS, Hutcheon AW, MacFarlane TW, MacDonald DG

In comparison with normal rats, those with iron deficiency anaemia showed no significant difference in susceptibility to experimental infection with Candida albicans although anaemic rats had a significantly greater incidence of persistent infection. These findings support the suggestion that patients with chronic candidosis should be investigated for iron deficiency.
 
Arch Oral Biol 1982;27(6):497-503

Experimental oral infection with the yeast Candida albicans in mice with or without inherited iron-deficiency anaemia (sla).

Sofaer JA, Holbrook WP, Southam JC

The role of iron deficiency in the development of oral candidosis was investigated using the mouse mutant sex-linked anaemia (sla). Susceptibility was assessed in terms of the recovery of organisms, particularly from oral swabs, and histological evidence of infection approximately 10 days after the last exposure to Candida albicans. The influence of three factors was studied in mixed groups of normal and anaemic mice: mode of inoculation, treatment with tetracycline and treatment with hydrocortisone. The most susceptible group had received drinking water containing tetracycline (1 mg/ml), hydrocortisone (0.1 mg/ml) and candida (5 X 10(4) c.f.u./ml for 6 days). Anaemic mice showed a rather higher rate of recovery of organisms and more frequent histological evidence of infection than normal mice in certain groups. Neither of these tendencies was statistically significant alone but, taken together, they suggest that some small difference of susceptibility may exist between normal mice and mice with sla. The mouse model could be of value in studying the influence of several other inherited disorders on susceptibility to candidosis.