Date:   8/26/2012 11:44:43 AM ( 12 y ago)
Hits:   27,525
URL:   https://www.curezone.org/forums/fm.asp?i=1978485

Although much attention has been given to the role of heavy metals in the etiology of autism [1], there is considerable controversy and less than definitive results in this regard. Since there are cases of autism where there has been no detectable level of mercury exposure, either environmentally, through mercury fillings, or the vaccine preservative thiomersal [2]; this is used as an argument that mercury doesn't cause autism. However, enzymatic biochemical pathways that are linked to diseases aren't particular about what is interfering with them in relation to manifestations of the disorder, only that they have been inhibited or impaired. This means that mercury may be one of many causes of autism that block certain critical metabolic pathways that are essential to maintaining the mental alertness that is being compromised.

Since mercury does seem to trigger this condition in some individuals, we should be looking for other entities that are also onboard which might share its disruptive profile. Mercury is a heavy metal, a highly electrophilic positive cation that likes to bind to exposed sulfhydryl groups. It can easily drift into and damage cysteine residue enzymatic reaction pockets because of its miniscule size. This behavior can interfere with critical biochemical pathways by shutting down the enzymes responsible for maintaining them.

In a lineup of potential perpetrators, acetaldehyde (the pseudo heavy metal) also matches this profile:

See "Acetaldehyde -- Pseudo Heavy Metal" //www.curezone.org/forums/fm.asp?i=1953097

This is something that everybody is coping with in one way or another as a byproduct of yeast fermentation of carbohydrates with the dosage dependent upon yeast colonization levels. But if everyone has yeast and acetaldehyde can cause autism, then why doesn't everyone have it?

This is where the genetic predisposition comes in. Symptoms from chronic acetaldehyde exposure don't manifest until dosage levels and damage approach disease thresholds. Then each individual begins to display a "known" disease based upon the weakest link in their unique genetic profile. Monozygotic twins are much more likely to develop similar autistic disorders than dizygotic twins [3].

So now we have at least two potential causative agents, mercury and acetaldehyde, sharing similar molecular profiles that may be responsible for the autistic suite of symptoms. What is worse is that they may have a synergistic deleterious effect when combined by competing for the resources in the body designed to deal with this type of toxicity. The body has a natural heavy metal chelator in the form of the protein metallothionein [4].

If an individual is fortunate enough to have low background yeast levels, then they may be able to cope with mercury exposure within reasonable limits without showing any adverse effects -- these are the children who get vaccinated (even with thiomersal-preserved products) and are just fine. However, if an individual has a high background yeast level with acetaldehyde emissions that are saturating their metallothionein competence [5], then any incremental exposure to mercury will set off a cascade of negative consequences, possibly including the autism reported subsequent to vaccinations if they are genetically predisposed to this condition.

The thionein apoprotein of metallothionein has an abundance of sulfhydryl cysteine residues that function as snares for the reactive oxygen species and toxic metals that can bind to them. Sulfur loci available for binding are also prominent in the proposed structure and mode of action of Wondro:

See "Wondro" //www.curezone.org/forums/fm.asp?i=1944518

See "Wondro Mode of Action" //www.curezone.org/forums/fm.asp?i=1944969

Metallothionein is something that the body has to make via protein synthesis from amino acids with a dependence upon dietary cysteine (or methionine). But we have already explored what excess acetaldehyde can do to the body's sulfur-based metabolism:

See "Cysteine + Acetaldehyde" //www.curezone.org/forums/fm.asp?i=1973900

See "Methionine + Acetaldehyde" //www.curezone.org/forums/fm.asp?i=1977201

In other words, functional metallothionein may be in short supply because of limited cysteine availability, something that has also been described in relation to autism [6]. As well, the molecules of this precious protein that there are may be just barely coping with daily levels of acetaldehyde exposure. This is a recipe for disaster when even the minutest levels of mercury are incrementally added to the mixture. A exposure dosage that would normally be tolerated cannot be scavenged by the under-produced and overloaded metallothionein protective mechanism and spills its toxic presence into critical enzymatic interference.

If this trauma concomitantly compromises the immune system's back-pressure on current yeast loads because of neutrophil impairment by mercury [7], then the yeast population may ratchet higher to another tolerance level with a higher daily dosage of acetaldehyde release. Subsequently, even after any detectable levels of mercury have been eliminated [8], the autistic spectrum disorder may persist because of the increased acetaldehyde levels. Mercury (the actual heavy metal), which was the initial trigger of the symptoms may have waned but acetaldehyde (the pseudo heavy metal) remains a daily occurrence.

Disruption of serotonin metabolism is common in autism [9] and the monoamine oxidase pathway that regulates the concentration of this neurotransmitter is exquisitely sensitive to acetaldehyde and its metabolites:

See "Serotonin Catabolism + Acetaldehyde" //www.curezone.org/forums/fm.asp?i=1972530

If the heavy-metal mimicking effects of acetaldehyde are a major factor in the etiology of autism, then we should find situations where autism appears because of treatments that result in higher yeast loads, even in the absence of overt mercury contamination. One such commonality is the prevalence of autism in conjunction with Antibiotic treatment for otitis media [10].

See "Ear Infections + Acetaldehyde" //www.curezone.org/forums/fm.asp?i=1971424

If autism is a genetically modulated disorder related to interference with enzymatic sulfhydryl metabolism, precipitated by mercury (via either dental Amalgam or thiomersal) and/or yeast-released acetaldehyde exposure, then together with ensuring that mercury contamination is no longer an issue, the treatment focus should be shifted to acetaldehyde scavenging and yeast abatement so that the crucial impacted metabolic pathways may resume normal function.

[1] Desoto Master-Cleanse et al., "Sorting out the spinning of autism: heavy metals and the question of incidence.", Acta Neurobiol Exp (Wars). 2010;70(2):165-76.
http://www.ncbi.nlm.nih.gov/pubmed/20628440

[2] Blaxill MF et al., "Thimerosal and autism? A plausible hypothesis that should not be dismissed.", Med Hypotheses. 2004;62(5):788-94.
http://www.ncbi.nlm.nih.gov/pubmed/15082108

[3] Bailey A et al., "Autism as a strongly genetic disorder: evidence from a British twin study.", Pschol Med. 1995 Jan;25(1):63-77.
http://www.ncbi.nlm.nih.gov/pubmed/7792363

[4] Coyle P et al., "Metallothionein: the multipurpose protein.", Cell Mol Life Sci. 2002 Apr;59(4):627-47.
http://www.ncbi.nlm.nih.gov/pubmed/12022471

[5] Hao Q et al., "Aldehydes release zinc from proteins. A pathway from oxidative stress/lipid peroxidation to cellular functions of zinc.", FEBS J. 2006 Sep;273(18):4300-10. Epub 2006 Aug 23.
http://www.ncbi.nlm.nih.gov/pubmed/16930132

[6] 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

[7] Worth RG et al., "Mercury inhibition of neutrophil activity: evidence of aberrant cellular signalling and incoherent cellular metabolism.", Scan J Immunol. 2001 Jan;53(1):49-55.
http://www.ncbi.nlm.nih.gov/pubmed/11169206

[8] Ip P et al., "Mercury exposure in children with autistic spectrum disorder: case-control study.", J Child Neurol. 2004 Jun;19(6):431-4.
http://www.ncbi.nlm.nih.gov/pubmed/15446391

[9] Burgess NK et al., "Hyperserotoninemia and altered immunity in autism.", J Autism Dev Disord. 2006 Jul;36(5):697-704.
http://www.ncbi.nlm.nih.gov/pubmed/16614791

[10] Fallon J, "Could one of the most widely prescribed Antibiotics amoxicillin/clavulanate "augmentin" be a risk factor for autism?", Med Hypotheses. 2005;64(2):312-5.
http://www.ncbi.nlm.nih.gov/pubmed/15607562

 

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