Neurons in the network talk to each other via neurotransmitters that either excite neuronal firing (glutamate) or inhibit impulse firing (γ-aminobutyric acid or GABA).
Although there are several different aspects to the pathology of epilepsy, let's consider for a moment the specific situation of neurotransmitter receptor malfunction to see if at least one mechanism may be related to acetaldehyde toxicity.
GABA receptors are transmembrane proteins in neurons that respond to GABA molecules. Some of these receptors are ligand-gated ion channels and others are G protein-coupled receptors (GPCRs). Glutamate similarly can activate receptors in both of these classes that are specific to its molecular configuration.
As described in more detail in:
//www.curezone.org/forums/fm.asp?i=1955511
GPCR receptors containing structurally and functionally critical disulfide bridges may be exquisitely sensitive to rogue molecules of acetaldehyde.
Although structurally distinct from GPCRs, ligand-gated ion channel receptors are characterized by a loop formed by a disulfide bond between two cysteine (Cys) residues in a highly conserved (i.e. critical) region of the receptor.
The fact that acetaldehyde is both attracted to and capable of disrupting disulfide bonds has been demonstrated by the staining of disulfide-rich tissues by aldehyde fuchsin, something that glues itself to the molecular configurations that react with its aldehyde group:
See http://ukpmc.ac.uk/abstract/MED/108134
and by the increase of sulfhydryl (-SH) content in proteins rich in disulfide linkages when exposed to acetaldehyde:
See http://www.aaccnet.org/publications/cc/backissues/1960/Documents/CC1960a77.html
This implies that rogue molecules of acetaldehyde may attack the critical disulfide trigger mechanisms of both the GPCR-type and CYS-loop-type receptors in both GABA and glutamate responsive neuronal cells. The result may be like a machine gun that won't fire because its trigger is broken or that is continuously firing because its trigger is jammed -- something that manifests as an epileptic fit. If this model of epilepsy has merit, then there should be confirmation of reduction of episodic seizures by protocols that either scavenge acetaldehyde and/or reduce its production from yeast (antifungals).
The ketogenic diet is a high-fat, low-carbohydrate, adequate-protein diet that was popular in the 1920's and 1930's for the control of epilepsy. It is referred to as a "starvation" diet because it limits the intake of carbohydrates that would normally be converted into "glucose" to such an extent that the body is forced to burn fats for fuel instead (ketogenesis). Often the diet includes a large proportion of medium-chain triglycerides (MCTs) from sources such as coconut oil. The mode of action of the ketogenic diet is unknown...
However, from the perspective of this investigation, not only will the reduction in the amount of available glucose in the ketogenic diet result in less acetaldehyde emission from yeast metabolism,
See //www.curezone.org/forums/fm.asp?i=1954934
but medium-chain triglycerides such as those in coconut oil are antifungal, something that would reduce the yeast levels emitting acetaldehyde.
See http://aac.asm.org/content/45/11/3209.full
Acetaldehyde scavengers such a N-acetyl cysteine have proven to be been effective in some cases:
See http://www.ncbi.nlm.nih.gov/pubmed/8909441
Since users of Wondro back in the 1930's-1950's could restore a healthy equilibrium by ingesting an acetaldehyde scavenger alone without any dietary restrictions, this suggests that for some types of epilepsy, at least, an integrated "yeast abatement protocol" might be able to replace the ketogenic diet with similar favorable results minus the severity of the dietary regimen.
See //www.curezone.org/forums/fm.asp?i=1955272