RE: Re: Oral glutathione and others

[Guest guest]

Did you give him MB12 shots and DMG at the same time before? Hyperness may be caused by other issue such as reaction to detox from MB12 shots and chelation or something he has eaten ( most of our kids can't breakdown oxalate and phenol very well, and when these two accumalate too much, it cause hyperness. you may google about phenol or oxalate and find out what type of food are in the high range of phenol or oxalate, basically, most of colorful fruit and vegetable and nuts content high volumn of phenol and oxalate, and you want to avoid them), also hyperness may be caused by yeast.

So, overall, per our experience, to find out what cause hyperness, there are several directions that you may look into:

1) Detoxification reaction ( from chelation or Mb12 shots)

2) Phenol or oxalate intolerance ( you may avoid them from giving your son proper food)

3) Yeast die-off, ( healing regression) if you are cleaning yeast, or virus...( taking anti-virul durgs or OLE or GSE)

4) No junk food content with Food Color, corn syrup, MSG, high sodium, soy, diary, and wheat, these are the triggers of hyperness to everybody.

Folinic acid usually compliments with MB12 shots and may reduce hyperness. But, glutathione is the best thing that we have ever found in terms of calming down my son, and reducing hyperness, and reduce OCD. I can see because glutathione reduce certain level of brain inflammation and also gut inflammation ( he has a better appetite and poop much better, healthest poop that i have seen...) Once his brain inflammation reduce, he is calmer, thinking clear, speak clear, OCD is gone, and happier....

Rei

Sincerely, Rei Founder/Senior Loan Officer

TX State Mortgage Broker License #75036 TX State Loan Officer License #65838 Miles Funding LLC

Rethink Vaccines. Reverse Autism.

From: didilund <shakyleconaol (DOT) com>Subject: Re: Oral glutathione and gut bacteria - Clostridium toxinTo: mb12 valtrex@ yahoogroups. comDate: Monday, July 7, 2008, 10:03 AM

Is the oral glutathione something that you need a prescription for? I really want to start my children on some form of glutathione.Dianne> > > Subject: Oral glutathione and gut bacteria - Clostridium toxin> To: mb12 valtrex@ yahoogroups. com> Date: Monday, July 7,

2008, 8:50 AM> > > > > > > |Hi, there was a thread on this list about non-absorption of oral gsh supplements and how come some kids react well to it anyway. These papers below are quite intriguing as showing glutathione (and nac and few other amino acids) are effective in reducin toxin production by clostridium bacteria!> > I am wondering if this is what is happening here? If anyone here saw good effects of oral glutathione supplements, do you kids have tests or anything showing presence of clostridium? ? please share thoughts> > natasa x> > Infect Immun. 2000 Oct;68(10):5881- 8.> > Toxins, butyric acid, and other short-chain fatty acids are coordinately expressed and down-regulated by cysteine in Clostridium difficile.> > Karlsson S, Lindberg A, Norin E, Burman LG,

Akerlund T. Department of Bacteriology, Swedish Institute for Infectious Disease Control, S-171 82, Solna.> > It was recently found that a mixture of nine amino acids down-regulate Clostridium difficile toxin production when added to peptone yeast extract (PY) cultures of strain VPI 10463 (S. Karlsson, L. G. Burman, and T. Akerlund, Microbiology 145:1683-1693, 1999). In the present study, seven of these amino acids were found to exhibit a moderate suppression of toxin production, whereas proline and particularly cysteine had the greatest impact, on both reference strains (n = 6) and clinical isolates (n = 28) of C. difficile (>99% suppression by cysteine in the highest toxin-producing strain). Also, cysteine derivatives such as acetylcysteine, glutathione, and cystine effectively down-regulated toxin expression. An impact of both cysteine and

cystine but not of thioglycolate on toxin yield indicated that toxin expression was not regulated by the oxidation-reduction potential. Several metabolic pathways, including butyric acid and butanol production, were> coinduced with the toxins in PY and down-regulated by cysteine. The enzyme 3-hydroxybutyryl coenzyme A dehydrogenase, a key enzyme in solventogenesis in Clostridium acetobutylicum, was among the most up-regulated proteins during high toxin production. The addition of butyric acid to various growth media induced toxin production, whereas the addition of butanol had the opposite effect. The results indicate a coupling between specific metabolic processes and toxin expression in C. difficile and that certain amino acids can alter these pathways coordinately. We speculate that down-regulation of toxin production by the administration of such amino acids to the colon may become a novel

approach to prophylaxis and therapy for C. difficile-associate d diarrhea.> > PMID: 10992498 [PubMed - indexed for MEDLINE]> > > of butyric acid - produced by fermentation of sugar or starch> http://www.pubmedce ntral.nih. gov/articlerende r.fcgi?tool= pubmed & pubmedid= 10992498> > > FEBS Lett. 1999 Jun 18;453(1-2): 124-8.> > N-acetylcysteine protects epithelial cells against the oxidative imbalance due to Clostridium difficile toxins.> > Fiorentini C, Falzano L, Rivabene R, Fabbri A, Malorni W. Department of Ultrastructures, Istituto Superiore di Sanitˆ, Rome , Italy . carla.fiorentini@ iss.it> > Toxins A and B from the anaerobic bacterium Clostridium difficile

are the causative agents of the antibiotic-associat ed pseudomembraneous colitis. At the subcellular level, they inhibit the Rho family GTPases, thus causing alterations of the actin cytoskeleton. The cytoskeletal integrity is also controlled by the redox state of cells. Therefore, we have evaluated whether an oxidative imbalance could be involved in the toxin-induced cytopathic effects. Our results indicate that both toxins induce oxidative stress with a significant depletion of protein SH-groups. These responses and the cytoskeleton- dependent cell retraction and rounding are significantly counteracted by N-acetylcysteine but not by alpha-tocopherol. Our study provides the first evidence that the thiol supplier N-acetylcysteine impairs the cellular intoxication by acting on the cytoskeleton integrity. This also suggests a possible beneficial role for this drug during therapeutic>

intervention.> > PMID: 10403388 [PubMed - indexed for MEDLINE]> > >