Re: Minimalist Yeast Abatement Protocol

Why doesn't Candida Albicans produce alcohol like other yeasts? Isn't that the yeasty thing to do?



Somewhere along the evolutionary journey, a mutated strain may have found that it had a survival advantage in mammals by exuding the pyruvate decarboxylase acetaldehyde intermediate from the fermentation process through its membrane instead of completing either its reduction to alcohol or its oxidation to acetate. Candida is certainly capable of dealing with the acetaldehyde enzymatically -- it does have an aldehyde dehydrogenase gene [1] -- but doesn't appear to be using it for internal disposal of this toxic aldehyde [2]. The result is that acetaldehyde becomes a venomous byproduct of yeast pyruvate metabolism.

The modulating impact that the acetaldehyde has upon the immune system of its host as well as its ability to hide its antigenic profile gives this yeast species a comfortable niche in which to reproduce and colonize. This may be one of the reasons, in addition to forming hyphae and invading tissue, that this particular species of yeast, as opposed to yeasts belonging to another species or genus (e.g. Saccharomyces), is considered to be the most pathogenic species of yeast in humans [3]. At the same time it must have learned how to rein in its own pathogenicity so as not to eliminate its host too quickly, even if it did initiate a slow downward spiral towards disease. Commensal parasites, in general, must be very adept at siphoning off enough of the host's resources to satisfy their own needs without taking so much as to kill off the host that sustains them.

The continuous "pushmi-pullyu" dance between yeast cells and the immune system is an ongoing struggle. If the immune system were to diligently go after every microbe populating the body it would soon be exhausted and totally depleted. A certain level of tolerance is exhibited to organisms that are not rapidly and aggressively proliferating because these are not perceived to be an immediate threat to the body's well-being. In fact, many of the resident microbes are beneficial and essential symbiotics. This results in a certain set-point of tolerance that provides a safe haven for yeast colonization. With a doubling time of about an hour [4], Candida Albicans could easily overwhelm a host if conditions were ideal and it did not self-limit its own growth and toxicity. What the immune system doesn't seem to recognize about this yeast, while tolerating it at the macromolecular level, are the devastating effects of the acetaldehyde that is being excreted at the micromolecular level.

One of the steps in the minimalist yeast abatement protocol [5] is an attempt to artificially raise the energetic signal of perceived yeast colonization in the body so as to reawaken the immune system to its presence. This is done with homeopathic Candida Albicans (30C). In a previous post homeopathic acetaldehyde was used to trick the yeast into sensing that there were increased levels of acetaldehyde in the body without actually introducing any of the physical toxic substance. Here the idea is to trick the immune system into sensing that yeast colonization has jumped suddenly beyond its current level of tolerance, without actually introducing any viable yeast cells, and it needs to take action -- a sort of energetic vaccination. Shiitake mushroom "Jump-Start Tea" [6] with its lentinan is also used to attempt to bring adaptive immune system macrophages, in addition to the innate immune system neutrophils, into the fray. You can't fire up the immune system, however, without supporting its voracious nutritional requirements [7]. Mega-dosing on nutrients in the hope that you have everything covered invites both toxicity reactions and cofactor depletion that lead to consequences that are just as harmful as having too little of something essential.

Orthomolecular Psychokinesiology (OPK) techniques [8] and a taste test for vitamin A mobilization [9] are utilized to help support the activity of the immune system according to the real-time dynamics of what is happening in the body. Iodine is used as a halide substrate in the myeloperoxidase killing of phagocytosed yeast cells [10]. Since it can damage mucous membranes in excess dosages, it is supplied externally on the pulse point of the wrist so that the body can absorb it as it needs it. The rate of its disappearance from the wrist is an indication of how active this process is throughout the day.

There are many variables that factor into the dynamic equilibrium point of yeast colonization levels:

• diet including the balance of yeast stimuli (e.g. sugar) versus deterrents (e.g. garlic, coconut oil)

• hormonal status (e.g. menstrual cycle, birth control pills)

• acetaldehyde scavengers (e.g. asparagus MSM)

• innate immune system competence

• availability of resources required by phagocytic cells (e.g. iodine)

• competitive exclusion by beneficial probiotic species

• medications and their side effects (e.g. Antibiotics )

• quorum-sensing limitation of Candida Albicans itself

If any of these variables change, then there may be a shift in the colonization level. If the energy and resources of the body are commandeered to deal with a viral episode such as a bad cold or influenza, for example, then the back-pressure on yeast maintained by the innate immune system may waver. Severe stress or overexertion may divert vital nutrients such as thiamine into other pathways and deplete the vital chi reserves [11] from the body's energy field mechanisms. A course of Antibiotics may selectively remove probiotics from the intestinal tract leaving the yeast to multiply unhindered.

In these situations, even though there may self-limiting aspects involved, imposed by the yeast itself, the overall colonization level may increase dramatically until another higher equilibrium set-point is reached. It is much easier to trigger an increase in yeast colonization levels than it is to bring them back down again -- a ratchet effect. This results in increased amounts of acetaldehyde release with a corresponding upsurge in the downstream cumulative toxicity of daily exposure. Conditions which were marginal prior to such an event may become chronic and conditions which were chronic before may become severe.

The actual symptoms that develop as a result of acetaldehyde exposure may vary from individual to individual and from one yeast tolerance set-point level to another and are subject to the following dependencies and co-dependencies:

• Location of acetaldehyde release
- yeast colonization locales (e.g. esophagus, intestines, blood brain barrier, genital region)

• Amount of acetaldehyde being released
- yeast colonization population levels (e.g. Antibiotic dysbiosis)
- proportion of simple carbohydrates in diet (e.g. high Sugar intake)
- fermentation cofactor availability (e.g. blood thiamine levels)
- morphic phase of yeast (e.g. budding versus hyphal)
- immune system sensitivity to yeast cells (e.g. neutrophils, macrophages)
- immune system cofactor availability (e.g. Iodine for myeloperoxidase support)

• Amount of acetaldehyde available for interference binding
- acetaldehyde scavenging efficacy (e.g. aldehyde dehydrogenase, carnosine)

• Molecular binding sites actively targeted by acetaldehyde
- acetaldehyde proximity (e.g. thyroid TSH receptors, tight junctions, biogenic amines)
- acetaldehyde dispersal (e.g. red blood cell catch and release)
- reactive ingested substances (e.g. food dyes)
- reactive inhaled substances (e.g. hyperventilation -> pulmonary peroxidosis)

• Vulnerability of cells to consequences of acetaldehyde binding
- genetic diversity (e.g. asthma ORMDL3 gene, aldehyde dehydrogenase ALDH2 deficiency)


[1] "Candida Albicans Aldehyde dehydrogenase" in "Candida Genome Database"
http://www.candidagenome.org/cgi-bin/locus.pl?locus=CAL0002252

[2] Gainza-Cirauqui ML et al., "Production of carcinogenic acetaldehyde by Candida albicans from patients with potentially malignant oral mucosal disorders.", J Oral Pathol Med. 2012 Aug 22.
http://www.ncbi.nlm.nih.gov/pubmed/22909057

[3] Jackson et al., "Comparative genomics of the fungal pathogens Candida dubliniensis and Candida albicans.", Genome Res. 2009 Dec;19(12):2231-44.
http://www.ncbi.nlm.nih.gov/pubmed/19745113

[4] Ingham CJ et al., "Rapid susceptibility testing and microcolony analysis of Candida spp. cultured and imaged on porous aluminum oxide.", PLoS One. 2012;7(3):e33818. Epub 2012 Mar 16.
http://www.ncbi.nlm.nih.gov/pubmed/22439000

[5] "Minimalist Approach To The Yeast Problem" and "Yeast Abatment Protocol" in "Astrophysiology... and Yeast", 2011.
http://www.scribd.com/doc/74090699
http://www.epubbud.com/book.php?g=7JQU45V8

[6] "All Hands On Deck", Ibid.

[7] "Immune System Activation Sequence", Ibid.

[8] "Deficient or What?", Ibid.

[9] "Make-A-Face Taste Tests", Ibid.

[10] Daimond RD et al., "Mechanisms of attachment of neutrophils to Candida albicans pseudohyphae in the absence of serum, and of subsequent damage to pseudohyphae by microbicidal processes of neutrophils in vitro.", J Clin Invest. 1978 Feb;61(2):360-9.
http://www.ncbi.nlm.nih.gov/pubmed/340471

[11] "Chi Respiration" in "Astrophysiology... and Yeast", 2011, Op. cit.
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