Re: Re: Sandy poops

[Guest guest]

thanks for the heads-up...it's taken me too long to admit my ADD but it's so damn hard to concentrate let alone on these things that are so difficult to understand - that woman should be a school teacher. I think I'll check out that group (because I don't have enough going on lol) Hey, Toni, you're getting to be quite the little nutrition guru, yourself. Have you heard about the failsafe diet? I "ran into" it the other day and it made me think of you as I watch you take your family through this dietary adventure....the person with the blog was a little on the obnoxious side, so it was too irritating for me to continue reading - but it might be something you may want to check out along the line.To: mb12 valtrex Sent: Tue, June 22, 2010 10:00:51 AMSubject: Re: Re: Sandy poops

runs the low oxalate group on yahoo... all her responses are like that :-) It's awesome!On Tue, Jun 22, 2010 at 6:53 AM, T Lynn <t.lynn28@rocketmail .com> wrote:

wow - I wish all the research papers I read were explained just like that! GREAT job!

To: mb12 valtrex@ yahoogroups. comSent: Mon, June 21, 2010 11:36:22 PM

Subject: Re: Sandy poops

Amy,

This will take a bit of explaining, but it is a GREAT question.

Taurine is an osmolyte, and it is most likely that when its levels go up and down in urine or blood, it is a sign that the body has had to adjust to a change in osmolarity. Osmolarity is basically a shift in the water to solute ratio inside the cell or outside the cell. Cells have to adjust their content of solutes because otherwise they will burst or shrivel. Cells also make the same adjustments when they are reacting to oxidative stress.

There is a factor in the nucleus of cells called TonEBP that is signaled either by changes in osmolarity or oxidative stress. Among the changes it initiates is the upregulated expression of taurine transporters which specifically move taurine across the cell membrane.

In some cell types, the signal also initiates the pathway of converting cysteine to taurine so there is more taurine to move across membranes. That diverts the sulfur in cysteine away from glutathione, and away from sulfate.

This adjustment is why you might have a plasma amino acid report or a urine amino acid report that shows elevated or depressed taurine. In autism, it is pretty typical for taurine to be high or low but not as much in the center, which suggests there is a lot of adjustment going on to oxidative stress.

So, whenever you measure taurine, you are basically catching this process on the way up or down, because it represents a cycle that occurs in response to a condition that the body is recognizing.

If this cycle has happened a lot, and especially if oxidative stress has been involved for a long time (such as when large amounts of oxalate have been absorbed through a leaky gut), that can cause glutathione to be depleted, and sulfur in general may be depleted because of this response.

As Veena et al, said (from the text of the study abstracted below), "Studies have pointed out that mitochondria are the major contributor of free radicals in oxalate toxicity, and the contribution of other nonmitochondrial sources is minimal (Khand et al., 2002). Cao et al.

(2004) have also suggested that the mitochondrial dysfunction is

the primary event in oxalate toxicity."

That toxicity and oxidative stress creates the situation that makes it hard, then, for cells to keep making taurine. When that sort of depletion has taken place, that's when taking a supplement of taurine may help the body cope with what has become a bad situation and may spare glutathione and sulfate.

Taurine is also a precursor to some important bile acids. Sometimes, when oxalate is being dumped from cells, the sudden increase in circulating oxalate may induce a LOT of oxidative stress as oxalate is absorbed into cells and then into the mitochondrion, where it does damage, and into the peroxisome, where oxalate is detoxified if it can be. The diversion of taurine to handling the oxidative stress may hurt the manufacture of bile acids, and that may turn the stool light...something we also hear of happening during dumping.

We don't know exactly what salt the sandy stool IS, but we do know that it is a frequent accompaniment to oxalate dumping and the quantity of whatever it is can be really large.

Dumping is the body trying to rid itself of stored oxalate, but that doesn't necessarily mean that the crystals are oxalate, but they are a lot of whatever it is!

This phenomenon is not unique to the low oxalate diet, for if someone has been on a high oxalate diet, it is likely also to happen as the body tries to detoxify when given a little bit of a break from high levels of oxalate input...maybe during fasting or illness. Sandy stools were reported as occuring during the yellow fever epidemic.

This detox process works sort of like DT's, in that people who don't drink lots of alcohol don't get DT's when they aren't drinking alcohol, but those who have been addicted to alcohol and overconsuming it do experience DT's.

Before LOD was introduced to the autism community, we would hear of sandy stools from time to time, but not very often. When I started hearing about them (I've been in autism research for fifteen years) that was during the secretin trials. It ends up secretin is a modulator of transporters that respond to changes in oxalate levels.

Some people who are in a long dumping cycle just keep having sandy stools for quite a bit of time. I haven't yet found an oxalate transporter scientist willing to study and characterize this sandy stool, but I keep asking!

At any rate, some people have told me that taurine may have been able to stop the sandy stool. Stopping the sandy stool might be a good thing, but we don't really know whether stopping it is speeding up or slowing down the detox process.

I do know that the bile acids that DON'T contain taurine tend to make the gut more permeable to any oxalate that is in the diet. Taurocholate, which is made from taurine, has an opposite effect, so it helps reduce the absorption of oxalate. That is why my suspicions are that what the taurine supplement does is a good thing.

I hope that sheds some light on what these issues might mean.

Please check the two references below.

(www.lowoxalate. info)

Mitochondrial dysfunction in an animal model of hyperoxaluria:

A prophylactic approach with fucoidan

Coothan Kandaswamy Veena

phine

Sreenivasan P. Preetha

Nachiappa Ganesh Rajesh

Palaninathan Varalakshmi

Abstract

Oxalate/calcium oxalate toxicity is mediated through generation of reactive oxygen species in a process that partly depends upon events that induce mitochondrial damage...The objective of the present study was to investigate whether mitochondria is a target for oxalate/calcium oxalate and the plausible role of naturally occurring glycosaminoglycans from edible seaweed, fucoidan in ameliorating mitochondrial damage...... .Hyperoxaluria induced a decrease in the activities of TCA cycle enzymes and respiratory complex enzymes. The oxidative stress was evident by the decrease in antioxidant enzymes, glutathione and an increase in reactive species and lipid peroxidation in mitochondria. Mitochondrial damage was evident by increased mitochondrial swelling. ... From the present study, it can be concluded that mitochondrial damage is an essential event in hyperoxaluria. ..

Gastroenterology. 1976 Jun;70(6):1096- 1100.

Effect of bile salts and fatty acids on the colonic absorption of oxalate.

Dobbins JW, Binder HJ.

Abstract

These studies were designed to evaluate the effect of bile salts and fatty acids on colonic oxalate absorption. Five millimolar deoxycholate significantly increased oxalate absorption from 34.2 +/- 9.4 nmoles per min per g dry weight to 330.4 +/- 47.3 (P less than 0.001) and changed water absorption to water secretion. Deoxycholate also increased the absorption of urea, decreased the electrical potential difference, and increased colonic clearance of oxalate, observations which are consistent with an increase in colonic mucosal permeability. In contrast, taurocholate did not increase oxalate absorption. Ricinoleic acid also significantly increased the absorption. These results suggest that bile salts and fatty acids increase colonic absorption of oxalate. Oleic acid had similar effects on oxalate absorption but was less effective than ricinoleic acid. Octanoic acid, a medium chain fatty acid, did not alter oxalate absorption of oxalate by a nonspecific

alteration of mucosal permeability. These observations may further explain many of the clinical phenomena associated with enteric hyperoxaluria.

PMID: 1269869 [PubMed - indexed for MEDLINE]

>

> So does taurine help with oxalates? Does taurine aggravate an already inflammed gut?

>

> Amy A.

-- Toni------Mind like a steel trap...Rusty and illegal in 37 states.