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Re: Bowel toxins,enzyme peptide conversion of aminos? » raybakes

Posted by Larry Hoover on October 30, 2004, at 8:12:00

In reply to Re: Bowel toxins,enzyme peptide conversion of aminos? » Larry Hoover, posted by raybakes on October 29, 2004, at 11:54:38

> > > if too many detoxification enzymes are used up clearing bowel toxins, there's not enough to regulate neurotransmitters..
> >
> > I can't think of a single case where that is true.
>
> Hi Lar, I was thinking of sulphation and glucuronidation in particular, because of the work on the brain-gut connection with autistic children. I think pathogens also secrete sulphatase and glucuronidase that split conjugated metabolites and toxins,

There are multiple excretory routes into the gut, and thus into feces. One is via bile, the direct excretion from liver to gallbladder to feces. That there are organisms within digestive tracts which can utilize conjugated compounds is of no surprise to me. However, the contents of the gut are outside the body. The issue for me is not that it might happen, but what is the yield? I doubt the proportion of excreted conjugates which are deconjugated and made available for reuptake is large. And even if it is so, the liver and mesenteric enzymes still get another crack at them, via the portal circulation.

> and also break down the glycoproteins that hold the extracellular matrix of the gut wall together.

That is one theory of leaky gut, but as far as I know, the treatments all are about establishing different populations of critters in the gut.

> Also methylation has a strong link with a healthy gut...

It's a circular relationship. A negative feedback loop.

> "The patients with IBD had nearly a six-fold increased incidence of hyperhomocysteinemia - having homocysteine levels above the normal range - compared to controls."

The treatment, then, is to restore methyl donors. That's a core element of my own self-care. Is IBD a cause, or a symptom? Or both? The latter case would hold if it's part of a negative feedback loop.

> Autism and gastrointestinal symptoms., Horvath K, Perman JA., Current Gastroenterology Reports 2002 Jun;4(3):251-8
> " . . . Recent clinical studies have revealed a high prevalence of gastrointestinal symptoms, inflammation, and dysfunction in children with autism. Mild to moderate degrees of inflammation were found in both the upper and lower intestinal tract. In addition, decreased sulfation capacity of the liver, pathologic intestinal permeability, increased secretory response to intravenous secretin injection, and decreased digestive enzyme activities were reported in many children with autism. Treatment of digestive problems appears to have positive effects on autistic behavior. These new observations represent only a piece of the unsolved autism "puzzle" and should stimulate more research into the brain-gut connection. "

I would call those signs of chronic malnutrition. Malnutrition itself can cause malnutrition, by a negative feedback process. For example, lack of methylation capacity can arise from low B12 status. Low B12 status prevents timely and appropriate triggering of stomach HCl release, and of proteolytic enzymes. This reduces the digestive capacity which "exposes" food sources of B12. It may also be related to poor supply of intrinsic factor. The net effect is decreased uptake of B12 from diet, which sets the whole cycle back at the start again.

> > > I'm not sure they would directly aid these enzymes, but it would certainly allow more nutrients available to synthesize them - think it's probably true that bacteria and yeast can degrade important amino acids.
> >
> > Can, but don't have time to do so. Moreover, they much prefer dealing with the energy available in all those carbs and sugars passing by. They turn to amino acid metabolism only when they're starving.
> >
> my line of thought was that they might turn the catecholamines into tyramine, melanin and quinones, making them unavailable for neurotransmitters.

In tiny quantities, if at all, IMHO. For example, look at the tyramine content of high protein foods. It always requires aging. And substantial processing. Consider....milk doesn't develop tyramine as it ages. Curdled milk, dewatered (cheese curds), very slowly develops tyramine as part of fermentation. I really do not think the biotransformations that concern you are at high yield in the gut. Trans-membrane uptake of free aminos is rapid. The gut wall wins the competition, IMHO.

> If they don't then radicals like superoxide generated by immune cells during gut dysbiosis, might oxidise them anyway? What do you think?
>
> Ray

There are degrees of susceptibility to oxidation, and though superoxide is highly reactive, there are substrates that are more vulnerable. Polyunsaturated fatty acids, for example. And then there's superoxide dismutase. Zinc uptake might well be substantially decreased in intestinal inflammatory states. I go back to induced malnutrition as the variable that is amenable to manipulation.

Lar

 

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poster:Larry Hoover thread:407758
URL: http://www.dr-bob.org/babble/alter/20041022/msgs/409084.html