Re: Detoxifying acetaldahyde

As if the unscheduled diversion of critical biogenic amines into beta-carbolines and isoquinolines isn't enough trouble already,

See "Serotonin + acetaldehyde" //www.curezone.org/forums/fm.asp?i=1963129

See "Histamine + acetaldehyde" //www.curezone.org/forums/fm.asp?i=1963358

See "Dopamine + acetaldehyde" //www.curezone.org/forums/fm.asp?i=1956462

there are other aspects to these substances that can be disrupted as well by yeast-released acetaldehyde.

Most unrestrained aldehydes in the body are thugs. They beat up whatever they come into contact with. [Pyridoxal (a form of vitamin B6) and retinal (a precursor to retinol -- vitamin A) are exceptions but even these are kept under close enzymatic supervision.] Aldehyde scavengers such as carnosine and aldehyde converters such as aldehyde dehydrogenase patrol to make sure that dangerous aldehydes are kept under control. This is especially important in reactions where the body creates an aldehyde as a byproduct of one of its own enzymatic processes.

The enzyme monoamine oxidase (MAO) is used to regulate the levels of monoamine neurotransmitters and neuromodulators by removing the bioactive profile of these substances through their oxidation to an aldehyde(!):



For example, the concentration of serotonin is controlled by its breakdown into 5-hydroxyindole acetaldehyde by monoamine oxidase:



Although the R-CHO aldehye by-product molecules are much larger than acetaldehyde, they are just as reactive and can participate in neurodegenerative processes such as spawning free radicals [1], creating protein adducts, or forming isoquinoline alkaloid derivatives (neurotoxins) [2]. The potential for oxidative stress and other types of damage is increased if the aldehyde degradation products of the biogenic amines are not dealt with quickly and adequately.

With an endogenous source of acetaldehyde production arising from the fermentative degradation of carbohydrates by Candida Albicans, on-board systems for coping with the aldehydes generated by MAO may already be saturated and overloaded. Hence, there exists the potential for damage not only from the unexpected yeast-released acetaldehyde itself but also from the aldehydes generated by MAO in the normal regulation of monoamine levels. There are just too many aldehyde molecules in the line-up waiting for service and things get ugly!

These unprocessed aldehydes may further react with the biogenic amines creating more beta-carbolines and isoquinolines, thus reducing the levels of necessary neurotransmitters again. However, since beta-carbolines [3] and isoquinolines [4] are themselves inhibitors of monamine oxidase, they can disrupt the bio-regulation of normal biogenic amine degradation leading to a confusing state of either too much or too little of a vital neurotransmitter, depending upon the mode of acetaldehyde interference predominant at any given moment, something influenced by the voracious metabolic appetite of yeast for carbohydrates.

[1] Pena-Silva RA et al., "Serotonin produces monoamine oxidase-dependent oxidative stress in human heart valves", Am J Physiol Heart Circ Physiol. 2009 Oct;297(4):H1354-60..
http://www.ncbi.nlm.nih.gov/pubmed/19666839

[2] Marchitti SA et al., "Neurotoxicity and Metabolism of the Catecholamine-Derived 3,4-Dihydroxyphenylacetaldehyde and 3,4-Dihydroxyphenylglycolaldehyde: The Role of Aldehyde Dehydrogenase", Pharmacological Reviews, June 2007 vol. 59 no. 2 125-150.
http://www.ncbi.nlm.nih.gov/pubmed/17379813

[3] Kim H et al., "Inhibition of monoamine oxidase A by beta-carboline derivatives", Arch Biochem Biophys. 1997 Jan 1;337(1):137-42.
http://www.ncbi.nlm.nih.gov/pubmed/8990278

[4] Bembenek ME et al., "Inhibition of monamine oxidases A and B by simple isoquinoline alkaloids: racemic and optically active 1,2,3,4-tetrahydro-,3,4-dihydro-, and fully aromatic isoquinolines", J Med Chem. 1990 Jan;33(1):147-52.
http://www.ncbi.nlm.nih.gov/pubmed/2296014
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