Re: Minimalist Yeast Abatement Protocol

Even with the ground-breaking work on the sequencing of the human genome completed in 2001, definitive cataloguing of the estimated 20,000-25,000 protein coding genes is ongoing [1]. Superimposed upon this genetic backdrop, the human microbiome consists of more than 10,000 microbial species and 8 million microbial genes [2].

One of these species, ubiquitous in its presence in mammalian hosts, is the yeast Candida Albicans. This is an incredibly complex organism in its own right with over 6,000 genes in its genome [3]. Although it is recognized as a potentially threatening human fungal pathogen, it is usually classified as "opportunistic" only and not dangerous under normal conditions. It has been proposed that during its fermentation of carbohydrates, it is capable of producing and releasing acetaldehyde into its host's environs [4].

In the midst of this overwhelming complexity with its staggering potential for interactions between organisms and genetic material to precipitate human disease, why single out Candida Albicans and one molecule in particular, acetaldehyde, as a major factor in the etiology of so many perplexing disease states.

Isn't this viewpoint so incredibly insular that it verges upon a preposterous and ridiculous fantasy?

It certainly would seem so. Yeast cells with a diameter of around 7.5 micrometers are about the same size as red blood cells but spherically ovoid rather than flattened.




An acetaldehyde molecule measuring about 200 picometers is 37500 times smaller than the yeast cell itself. In the "inner space" of the biochemical milieu, if an acetaldehyde molecule were the size of a marble, a magnification factor of 60 million times, the yeast cell from which it originated would be as big as the Empire State Building is high, and your head would be the same size as the Earth. Acetaldehyde is not a bacterium, not a virus, not a heavy metal, but an organic miniscule molecule. How could such a tiny byproduct of such a tiny organism be a threat to humanity? And if it is, "of all the gin joints in all the towns...", how could it be singled out from such a confusing web of interacting organisms and genes?

As is often the case in apparently unyielding enigmas, serendipity played a role -- and in this situation, double-serendipity...

The case of the miner with an infected cut finger in 1953 [5] prodded the insightful C. Orian Truss to think outside of the box of preconceived notions regarding Candida Albicans. This yeast had been cultured from the patient's sputum but not considered as capable of causing the six months of serious complications that resulted following treatment with the Antibiotic aureomycin. It wasn't until anti-yeast treatment was added to the protocol that the patient experienced full recovery.

Sulphurated linseed oil is mentioned in the 1874 physician's and pharmaceutist's medicinal guide by R. E. Griffith [6]. In the early 1900's a Canadian pioneer undertook to manufacture and market this concoction as a tonic (Wondro) after encountering it on a trip overseas to Scotland. It produced remarkable results [7] but its mode of action remained a mystery. However, its molecular configuration with its salient sulfur atoms [8] would be an irresistible lure for the acetaldehyde emanating from yeast.

Truss's acetaldehyde hypothesis and Wondro's panacea effectiveness fit together like hand and glove.

Acetaldehyde as explored in the "Detoxifying Acetaldehyde" series is certainly capable of provoking any number of different disease processes, including the complications experienced by the miner in 1953, depending upon what biochemical pathways it encounters. It can also be catch and release ferried throughout the body on red blood cells [9] before finally coming to rest. Wondro acting as a scavenger, toxic Miracle-Mineral-Supplement acting as a neutralizer and urinary butane-2,3-diol all suggest that acetaldehyde may be coming from somewhere. But might it not be emanating from another organism, such as helicobacter pylori [10]?

Eye floaters suggest that yeast has migrated into all reaches of the body, far beyond the usual and expected locales, even in healthy individuals. Recent studies have confirmed what Truss suspected decades ago, that the yeast Candida Albicans is capable of producing acetaldehyde in the body [11]. Experiences with lentinan (fungal cell wall glucans), garlic (an antifungal) and the homeopathic sulfur experiment with Candida suggest that we are dealing with a fungal polymorphic organism whose pathogenicity is related to its cellular metabolism.

When individuals are treated with a yeast reduction protocol or when they ingest an acetaldehyde scavenger they improve dramatically! The implication, with evidence that is not just circumstantial anymore, is that pulsed low-dosage exposure to Candida Albicans acetaldehyde emitted from its fermentative processing of dietary carbohydrates is creating cumulative biochemical disruption leading to chronic disease states.

Having finally breached the mental barriers that confined yeast to an opportunistic role only, something that has spawned an entire paradigm of symptom treatment rather than causal treatment, perhaps we can refocus research efforts onto the crux of the problem. However, the yeast/acetaldehyde theory of disease is a deceptively simple idea that may engender the notion that the solution is simple as well. Not so -- while we were unaware of its presence and while we were more or less ignoring it, even after we knew it was there, this organism has honed its evolutionary skills at entrenching itself, hiding itself, propagating itself and controlling its host so as to remain there for the duration. Although reducing its colonization level is certainly a paramount objective, beyond a certain point the best we can hope to do is minimize the impact of its presence.


[1] Stein LD, "Human genome: end of the beginning.", Nature. 2004 Oct 21;431(7011):915-6.
http://www.ncbi.nlm.nih.gov/pubmed/15496902

[2] Human Microbiome Project Consortium, "Structure, function and diversity of the healthy human microbiome.", Nature. 2012 Jun 13;486(7402):207-14.
http://www.ncbi.nlm.nih.gov/pubmed/22699609

[3] van het Hoog M et al., "Assembly of the Candida albicans genome into sixteen supercontigs aligned on the eight chromosomes.", Genome Biol. 2007;8(4):R52.
http://www.ncbi.nlm.nih.gov/pubmed/17419877

[4] Truss CO, "Metabolic abnormalities in patients with chronic candidiasis: the acetaldehyde hypothesis.", Orthomol Psychiatr 1984; 13:66–93.
http://orthomolecular.org/library/jom/1984/pdf/1984-v13n02-p066.pdf

[5] Truss CO, "The Missing Diagnosis", 1983 and "The Missing Diagnosis II", 2009.

[6] Griffith RE, "A Universal Formulary: Preparing And Administering Officinal and Other Medicines." , 1874
http://books.google.ca/books?id=w8EwAAAAYAAJ&pg=PA563

[7] "Wondro Testimonials Pamphlet" , circa 1930's
http://www.scribd.com/doc/76584628
http://www.epubbud.com/book.php?g=W4S59AQF

[8] "Wondro -- Inside Out", 2012
http://www.scribd.com/doc/101099776
http://www.epubbud.com/book.php?g=7D42SJH6

[9] Baraona E, "Transport of acetaldehyde in red blood cells." Alcohol Alcohol Suppl. 1987 1987;1:203-6.
http://www.ncbi.nlm.nih.gov/pubmed/3426680

[10] Salmela KS et al., "Acetaldehyde and ethanol production by Helicobacter pylori." Scand J Gastroenterol. 1994 Apr;29(4):309-12.
http://www.ncbi.nlm.nih.gov/pubmed/8047804

[11] 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

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