Some interesting things about candida

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    Limited effect of refined carbohydrate dietary supplementation on colonization of the gastrointestinal tract of healthy subjects by Candida albicans

    I posted this study somewhere before, but I didn’t read the full text at the time, which is available for free. The discussion section makes for interesting reading and I’ve added it below. I think it tells us a few interesting things, and the bibliography is worth checking out too. If nothing else, it’s suggestive that you should be able to eat what you want when you’ve recovered, assuming that whatever maintains your health and good nutritional status.

    1. Gut flora does play a vital role in infection and recovery, and this is supported by research, such as that by Kinsman et al, 1989 and Kennedy et al, 1985.

    Dosing with some antibacterials promoted an increase in gastrointestinal Candida and invasion to a greater extent than immunosuppression.

    indigenous intestinal microflora suppresses C. albicans colonization and dissemination from the gut by inhibiting Candida-mucosal association and reducing C. albicans population levels in the gut.

    2. Immunity is also vital and improving anything that may be weakening the immune system, such as poor thyroid, stress and nutrient deficiencies, including glucose and protein, is just as important as restoring healthy gut flora.

    3. Treatment and diagnosis isn’t straightforward. Sugar doesn’t feed candida unless it reaches candida. People without colonisation in the small intestine may actually benefit from sensible carbohydrate consumption. Ketones may contribute to virulence (Saeed, 2000), and poorly controlled blood sugar is well documented in candida pathogenisis.

    We observed no significant modulation in the frequency of C. albicans–positive fecal and oral samples and no alteration in the number of subjects positive for C. albicans in the mouth washes during or after the high-sugar diet. Furthermore, no significant change in the C. albicans germ cell concentration in the mouth washes and stool samples for the 28 subjects during or shortly after the diet were detected. These results suggest little modulating effect of dietary carbohydrates on colonization of the human gastrointestinal tract by C. albicans. Therefore, we conclude that healthy individuals do not develop increased Candida counts as a result of consuming high-sugar diets. Although glucose is a substrate for C. albicans, the complex interplay of the yeast germs with the host and the indigenous bacterial microflora might explain these results. In the gastrointestinal ecosystem, various mucosal defense mechanisms control C. albicans germ cell concentrations (26), and numerous bacterial properties and products are known to modulate candidal growth (27, 28).

    Monosaccharides such as glucose and degradable oligo- and polysaccharides are absorbed in the small intestine. Therefore, it might be expected that dietary glucose does not affect yeast growth distal to this region. Hypothesizing that an effect of dietary glucose is restricted to yeasts inhabiting the proximal gastrointestinal tract, we speculated that the modulating effect of glucose is more likely to be observed in persons with an elevated candidal colonization of the upper gastrointestinal tract. Indeed, we did observe a significant, although moderate, increase in fecal C. albicans counts during the high-sugar-diet period in those subjects whose baseline mouth wash counts were >1.0 × 104 CFU/L. Furthermore, we observed an increased number of subjects with C. albicans–positive fecal samples in response to the high-sugar diet. Taken together, these data support the hypothesis that excessive dietary glucose leads to a multiplication of C. albicans proximal to the small intestine and that replicated yeasts reach the large intestine with the feces. However, it should be emphasized that the limited effects observed in our study apply to healthy individuals with intact control mechanisms to keep Candida counts low. The role of refined carbohydrates in patients with compromised defense mechanisms is still speculative.

    Clinical follow-up studies should address the question of whether restriction of refined carbohydrates might decrease the number of C. albicans organisms colonizing the human gastrointestinal tract in specific patient groups, eg, in persons receiving broad-spectrum antibiotics or in heavily colonized, immunosuppressed patients with a high risk of disseminated candidiasis. Because long-term restriction of food groups containing mono- and oligosaccharides seems nutritionally unbalanced, a clear definition of those patients who would benefit from such a diet is necessary.


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    yeah… I was thinking that for any one of us maybe the problem isn’t so much candida per se, rather it’s some other health issue with candida presenting as an opportunistic infection.

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