Re: Cholesterol sulfate

The singular possibility that the commensal yeast Candida Albicans may be releasing toxic acetaldehyde during its own metabolic processing of dietary carbohydrates (sugar is a simple carbohydrate) requires a complete rethinking of the initiation and manifestation of disease processes. Everything that is ingested, digested, absorbed and excreted has the opportunity of reacting with this molecule and producing something else in the process that may be deleterious to well being. And if this isn't enough, the toxin itself can leech its way through the intestinal walls and take a ferry ride on red blood cells to distant oases far from its origin.

Coloration with both synthetic and natural dyes represents a major part of the food processing and marketing industry, primarily for aesthetic reasons enhancing the perceived flavor that arises from the mental association of a particular color with an expected sensory experience. The link between synthetic food dyes and disease has been given much regulatory attention with the result that some dyes have been delisted and banned from commercial usage.

Let's take a look at some of the known offenders that cause the most allergic and intolerance reactions to see if there is a common feature that might make them targets for acetaldehyde interaction.



A variety of "pseudoallergic" responses have been attributed to ingestion of these food dyes: anxiety, migraine, clinical depression, blurred vision, itching, general weakness, heatwaves, feeling of suffocation, purple skin patches, irritability, hyperactivity, restlessness, sleep disturbance, diarrhea, vomiting, urticaria.

The ones here are all azo compounds which incorporate the functional group R-N=N-R'. Note also that they all have NaSO3 exposed side chains. Now compare these structures with some natural pigments called anthocyanins which are derivatives of anthocyanidins with pendant sugars.



In the assortment of side chains of these natural pigments, which aren't typically associated with the same severity of allergic reactions, there are no SO3 R groups! Consider, then, one of the simplest structures which does contain this configuration, sodium bisulfite, a preservative which is also associated with allergic, sometimes fatal, responses.



What happens when the sulfite structure common to sodium bisulfite and the food coloration azo compounds comes into contact with acetaldehyde? The carbonyl electrophilic carbon finds the nucleophilic sulfur or oxygen an attractive binding site for acetylation.





Food colorings and preservatives have been identified by those with sensitivities as potentially debilitating substances that need to be avoided. But the mechanisms of why they react in this manner have remained elusive. If people are not, in fact, reacting to the substances themselves but a metabolite of the substance's reaction with acetaldehyde, then this could explain why some food coloring s are more allergy-prone than others and why some individuals are more vulnerable.

The temporal release profile of acetaldehyde in areas where it is able to come into contact with and produce the sensitizing byproducts is not only a function of the reactivity of the coloring or preservative with acetaldehyde, but also a function of the temporal agenda of a "creature" with its own evolutionary arsenal of host-control techniques. The level of yeast colonization in certain critical areas, the morphic phase of the yeast at the time of exposure to nutrients, the kind of nutrients that are presented, and other concomitant food intake (such as antifungals) that vary from one individual to another and from one meal to the next all need to be factored into the model.

Avoiding the identifiable substances that trigger potentially debilitating reactions, something that is learned through a tedious process of trial and error, is certainly a positive step. However, this may not be addressing the underlying problem. If the budding phase yeast-released acetaldehyde isn't reacting with the food coloring or preservative, then it will be reacting with something else. And these other reactions may be less obvious but just as harmful in the longer term.

This can make the cause and effect chain murky at best. Hyperactivity, for example, is not just a simple matter of a reaction to a food coloring . Although food coloring may trigger this condition, there are other biochemical pathways subject to acetaldehyde interference that may also produce the same symptoms.

Once a particular molecular structure has surfaced in relation to the formation of acetaldehyde adducts, it is always instructive to search for other essential configurations in the body that might also be subject to attack in a similar manner. If the dots connect with the research of others with respect to disease, then a clearer picture of what is actually transpiring may emerge.

Cholesterol sulfate is a multifunctional sulfolipid that is abundant in human plasma. When looking for chance encounters with rogue acetaldehyde molecules; proximity, reactivity, and concentration all are factors in the likelihood of interactions. What happens subsequently, as a result of these misconfigured biological structures, is as complex and confusing as the chaotic array of diseases that remain a conundrum to modern medical science.



The salient NaO3S feature of this molecule is quite similar to the side chains of the synthetic food coloring agents. The amphiphilic nature of cholesterol sulfate, arising from its negative charge, means not only that it can travel freely in the bloodstream, but also that it might also be an attractive target for acetylation in encounters with acetaldehyde. Such an interaction would remove the cholesterol sulphate molecules thus violated from their vital roles in human metabolism. A deficiency of cholesterol sulphate in association with disease states is just beginning to be explored [1]. Another possible repercussion of this might be an increase of circulating cholesterol levels as the body attempts to compensate for the lossage.

Given the affinity of acetaldehyde for sulfur, it wouldn't be surprising to find interference with the sulfating mechanisms that are responsible for generating the abundant store of circulating cholesterol sulfate. If acetaldehyde is binding to dietary intake of the sulfur-bearing amino acids methionine and cysteine, for instance, then this can create disruption in all of the body's sulfur-dependent metabolic pathways including the important antioxidant glutathione. This may provide a clue as to why intracellular levels of cysteine and glutathione are depressed significantly in children diagnosed with autism [2].

As with all toxic interactions it is imperative not only that the toxin (in this case, unsequestered acetaldehyde) be safely scavenged by side-effect-free molecular policemen patrolling the toxic soup, but also that the source of the toxin (i.e. the yeast Candida Albicans) be addressed at the same time.

[1] Seneff S. et al., "Might cholesterol sulfate deficiency contribute to the development of autistic spectrum disorder?", Med Hypotheses. 2012 Feb;78(2):213-7. Epub 2011 Nov 17.
http://www.ncbi.nlm.nih.gov/pubmed/22098722

[2] Suh JH et al., "Altered Sulfur Amino Acid Metabolism In Immune Cells of Children Diagnosed With Autism", Science Publications (2008).
http://en.scientificcommons.org/46275754
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