@sunsunsun said:
any opinion on pH and yeasts?
Which pH where are you thinking of?
I'd confidently say that high stomach pH is a very significant risk factor.
Especially over time.
Not only is there a higher quantity of yeasts passing the stomach but also the less acidic chymus will be met by less alkalic bile (or lesser quantities thereof).
Unless there's some metabolic bicarbonate depletion (on top) which puts the less alkalic bile into first place of such chicken-egg interdependencies.
Any way, there'll be more exogenous microorganisms than there ought to be and along with the incomplete digestion and shifts in microbiome more mucosal disturbances and pathogenic colonization and translocation.
I've come across this publications from 1965 on moniliasis (=candidiasis) Moniliasis, Steatorrhea, Diabetes Mellitus, Cirrhosis, Gallstones, and Hypoparathyroidism in a 10-Year-Old Boy and found it interesting how they (unsuccesfully) discussed the very confusing and complex relations.
They had probably stumbled upon the back then still unestablished "Autoimmune Polyglandular Syndrome Type 1 (APS-1) / Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy (APECED)".
Yet I don't know whether such a term and associated genetic variance has resolved any underlying mechanisms.
They were really confused as to what's causing what.
What they observed were strongly reduced magnesium uptakes (probably because of fungal infection), which is necessary for parathyroid hormone synthesis, followed by accordingly diminshed calcium uptake. D3 was of no assistance. There was also lots of steatorrhea which preceded many of the other symptoms by years and is somehow reciprocally dependent on calcium. And autoimmunity (intracellular fungal vacuoles? antibody or T-cell cross-reactivity? antigenic mimickry?) against the (para)thyroid gland, as well as hepatic changes. A real mess!
-> I'm suspecting that any mess with having both decreased magnesium yet also decreased/intolerable Mg uptake and a chronically fluctuating/insufficent calcium metabolism should point oneself to consider fungal infections! It surely won't be as extreme as in those genetic cases but how would you ever know whether PTH levels are as high as they need to be?
Disturbances of these essential alkaline electrolytes sort of lead back, over a long stretch, to your general pH question.
Pertinent to the discussion may be work presented by Louria and Brayton in Nature (Jan. 18, 1964, p. 309), who found a substance in blood lethal to Candida albicans in normal persons. A moderate to marked reduction to this substance was found among patients with cirrhosis, hepatitis, diabetic azotemia, and in patients with mucocutaneous and systemic moniliasis.
The percentage of persons possessing the factor is slightly reduced among groups of patients with diabetes (without azotaemia) and with disseminated carcinoma.
This is about transferrin again @sunsunsun .
Specifically, back then they had narrowed it down to a molecule between 10-20kDa - which surprisingly doesn't match up with transferrin but suggests an even more potent polypeptide that has been split off the complete transferrin molecule. Unless their filter meshes back then were somehow wrong. Anyway the results of the other studies suggest that transferrin is a direct source of this active polypeptide.
The substance appears to have impressive specificity. It is active against Candida albicans and Candida stellatoidea but not against other Candida species [glabrata, krusei] or other yeasts such as Cryptococcus neoformans or Saccharomyces cerevisae.
! The iron-chelating property of this likely transferrin peptide does not harm C. glabrata or C. krusei or other non-albicans fungi! This is highly relevant.
Puts the approaches directed at iron-chelation also in a highly species-specific context to consider.
Tannic acids are highly anti-fungal. Among other mechanisms, they inhibit hyphal growth of C. albicans and hinder their adhesion to mucosal cells. In animal experiments, sufficient dietary tannic acids directly increased Candida excretion (i.e. fungi which failed to colonize or invade).
This may be an important mechanism behind the acutely anti-diarrheal and anti-microbial activities of oral tannin-albuminate or tannin-gelatinate.
Sort of shifts the dietary focus away from those merry-go-round prebiotic and soluble or insoluble fiber discusstion and puts weight onto dietary tannic acid content. Which also lead to fruit (berries!) and vegetables and rather more traditional, more natural, tarter or more bitter varieties than today's varieties aimed at maximizing sweetness and yield.
One of the most widespread and available tannins which also offers large mucosal absorption is EGCG.
EGCG of course strongly chelates iron. Surprisingly, though, it provides a more complex mechanism of action.
EGCG is indeed most antifungal against C. glabrata! EGCG sort of also targets liver tissues so this is good news.
Have ordered EGCG (decoffeinated) to augment the FCy/5-FC and horseradish.
Some flavonoids markedly downregulate Candida CDR1 (which regulates the efflux pumps and resistances against azoles!):
Flavones, Flavonols, and Glycosylated Derivatives-Impact on Candida albicans Growth and Virulence, Expression of CDR1 and ERG11, Cytotoxicity
The reduction of both fungal virulence and expression of antifungal resistance-linked genes was the most pronounced for apigenin and apigetrin; these results indicate flavonoids' indispensable capacity for further development as part of an anticandidal therapy or prevention strategy.
Here, however, kaempferol's antifungal properties beat apigenin, which exhibits some ambiguous and controversial effects (like upregulating ERG11, inhibition of which is the target for azoles) by miles. Kaempferol seems worth noting down.
Inhibition of Candida albicans extracellular enzyme activity by selected natural substances and their application in Candida infection, 2008
