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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
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
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
|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
|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.
Department of Pediatrics, University of Iowa Hospitals and Clinics, Iowa
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
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
|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.