What does high taurine cause/mean?

[Guest guest]

My son's amino acids test came back showing high taurine...and I just

noticed a thread regarding this. I bought taurine to give him

to " calm " him down, and then realized it is already high. Thank

goodness I looked back thru his tests.(that is, if it is the same exact

kind of taurine) He does not have high ammonia though. Can anyone tell

me the significance of taurine being high? Maybe I am missing something

I should be addressing. Still trying to figure things out...especially

with the stimming...otherwise he's basically considered high

functioning (talks very good, social, loving..but school is very hard,

focus is difficult) Thanks everyone... mom to Austin pdd nos and

Jake adhd.

[Guest guest]

Hi,

Some kids who can't handle sulfur very well seem to build up taurine in

their systems. Most of our kids are deficient in taurine, which a lot

of DANs supplement thir programs. Taurine has sulfur in it. How does

your son handle other sulfur based supps, like epsom salts, MSM,

molybdenum? Yasko used to have some info on how high taurine levels

were indicators of brain/gut inflammation. There is testing you can

perform that will sometimes show genetic mutations that may impair your

child from properly processing sulfur.

>

> My son's amino acids test came back showing high taurine...and I just

> noticed a thread regarding this. I bought taurine to give him

> to " calm " him down, and then realized it is already high. Thank

> goodness I looked back thru his tests.(that is, if it is the same

exact

> kind of taurine) He does not have high ammonia though. Can anyone

tell

> me the significance of taurine being high? Maybe I am missing

something

> I should be addressing. Still trying to figure things

out...especially

> with the stimming...otherwise he's basically considered high

> functioning (talks very good, social, loving..but school is very

hard,

> focus is difficult) Thanks everyone... mom to Austin pdd nos and

> Jake adhd.

>

[Guest guest]

i have read in a couple places that high taurine on tests can mean

that it isn't being absorbed properly and just coming straight out

(when supplemented).

jennie

>

> My son's amino acids test came back showing high taurine...and I just

> noticed a thread regarding this. I bought taurine to give him

> to " calm " him down, and then realized it is already high. Thank

> goodness I looked back thru his tests.(that is, if it is the same exact

> kind of taurine) He does not have high ammonia though. Can anyone tell

> me the significance of taurine being high? Maybe I am missing something

> I should be addressing. Still trying to figure things out...especially

> with the stimming...otherwise he's basically considered high

> functioning (talks very good, social, loving..but school is very hard,

> focus is difficult) Thanks everyone... mom to Austin pdd nos and

> Jake adhd.

>

[Guest guest]

----- Original Message -----

From: Fithen

Hi,Some kids who can't handle sulfur very well seem to build up taurine in their systems. Most of our kids are deficient in taurine, which a lot of DANs supplement thir programs. Taurine has sulfur in it.

===>Really, Taurine doesn't contribute to the sulfur load. Most likely it is not being assimilated into the body.

How does your son handle other sulfur based supps, like epsom salts, MSM, molybdenum? Yasko used to have some info on how high taurine levels were indicators of brain/gut inflammation. There is testing you can perform that will sometimes show genetic mutations that may impair your child from properly processing sulfur. >> My son's amino acids test came back showing high taurine...and I just > noticed a thread regarding this. I bought taurine to give him > to "calm" him down, and then realized it is already high. Thank > goodness I looked back thru his tests.(that is, if it is the same exact > kind of taurine) He does not have high ammonia though. Can anyone tell > me the significance of taurine being high? Maybe I am missing something > I should be addressing. Still trying to figure things out...especially > with the stimming...otherwise he's basically considered high > functioning (talks very good, social, loving..but school is very hard, > focus is difficult) Thanks everyone... mom to Austin pdd nos and > Jake adhd.>

[Guest guest]

ekogurl,

This is an issue I've been chasing for years and there is lots on this on

sulfurstories . There are quite a few possibilities.

The first thing to notice is if this was a urinary test (and I'm assuming

it was). Usually when taurine is high in urine, beta-alanine is also high

in urine. Why? That will take some explaining.

Everything that shows up urine has been involved with some subset of three

processes. You start with blood, which goes through the kidney and goes

through a filter that reclaims big molecules like proteins. The rest stays

in the urine. Here is a great explanation of that with a

picture: http://coe.fgcu.edu/faculty/greenep/kidney/Glomerulus.html You

don't want to lose big molecules in the toilet, so that is why the kidney

reclaims most of what is in blood.

The urine, or really " pre-rine " then collects in tubules. A second process

that takes place is reabsorption. When the " pre-urine " passes through the

renal tubules, proteins in the membrane select certain molecules that need

to be recovered that were small molecules and made it past the

filter. These proteins are called transporters, and they selectively

retrieve specific substances for the body to reuse. Taurine and

beta-alanine are reabsorbed via the same transporter. When both are high

in urine, it means something about that transporter has either shut down or

reached its maximum capacity to recover taurine or beta-alanine. A third

process is secretion. Things that are toxic, like oxalate, are supposed to

be secreted actively, but so are a lot of other things that will cause harm

if their levels in blood get too high.

If the capacity of the transporters has been reached, it is really hard to

tell which (taurine or beta-alanine) got high in supply making both

compounds difficult to absorb.

Taurine is an osmolyte. The transporters on cells move taurine in and out

of the cell in order to balance the " saltiness " inside and outside the

cell. Under certain circumstances, more taurine is retained in cells and

in other circumstances, cells are getting rid of excess taurine to kerp in

balance with the rest of he body.

Taurine is known to get elevated in the urine when the body has experienced

oxalate toxicity. A new study looked at this in cancer patients given

platinum oxalate as a drug. The neurotoxicity was accompanied by an

elevation of taurine and glycine, alanine and serine. The study discusses

why they believe this set was elevated as the body tried to deal with the

toxicity of the oxalate. Another study found that feeding rats the

precursor to oxalate also raised urinary taurine.

Other work out of the Nicholson Lab in England by Andy Clayton shows

taurine in urine increasing when the liver is having to deal with certain

types of hepatotoxicity.and that is accompanied by high creatine. See below.

If calcium oxalate crystals form in the body, they can soak up

pyrophosphate. When it gets depleted, urinary taurine levels rise.

And still, after all of this, I think there is probably more to it than

just these things I've mentioned. It isn't simple!

Arch Toxicol. 2003 Apr;77(4):208-17. Epub 2003 Feb 5.[] Links

An hypothesis for a mechanism underlying hepatotoxin-induced hypercreatinuria.

Clayton TA, Lindon JC, Everett JR, Charuel C, Hanton G, Le Net JL, Provost

JP, Nicholson JK.

Biological Chemistry, Biomedical Sciences Division, Imperial College of

Science, Technology & Medicine, Sir Fleming Building, South

Kensington, SW7 2AZ, London, UK. a.clayton@...

As part of a wider metabonomic investigation into the early detection and

discrimination of site-specific hepatotoxicity, male Sprague-Dawley rats

were dosed with the model hepatotoxins allyl formate, ethionine and

alpha-naphthylisothiocyanate (ANIT). Urine samples collected pre- and

post-dose were examined by (1)H nuclear magnetic resonance (NMR)

spectroscopy and the toxin-induced changes in urinary taurine and creatine

excretion were quantified. Hypertaurinuria and hypercreatinuria were

observed following allyl formate dosing, hypertaurinuria with no change in

creatine excretion was observed after ethionine dosing, and hypotaurinuria

and hypercreatinuria were observed after ANIT dosing. These changes are

indicative of different effects on liver and it has been previously

suggested that some hepatotoxin-induced changes in urinary taurine

excretion may be due to altered hepatic cysteine utilisation. A related

hypothesis is now presented that would explain the selective

hypercreatinuria in terms of increased cysteine synthesis.

PMID: 12698236 [PubMed - indexed for MEDLINE]

1: Urol Res. 1986;14(6):299-303.Links

Inhibition of calcium oxalate monohydrate (COM) crystal growth by

pyrophosphate, citrate and rat urine.

Sidhu H, Gupta R, Thind SK, Nath R.

An assay system for the measurement of the rate of Calcium Oxalate

Monohydrate (COM) seed crystal growth in a metastable solution of calcium

chloride and sodium oxalate containing traces of 14C-oxalic acid was used

to assess the inhibitory activity of pyrophosphate (10(-5) M-10(-4) M),

citrate (10(-4) M-10(-3) M) and urines of normal and pyridoxine deficient

rats. Both pyrophosphate and citrate were strong inhibitors of COM crystal

growth and caused a 50% decrease in crystal growth rate at 1.50 X 10(-5) M

and 2.85 X 10(-4) M respectively. Normal rat urine strongly inhibited the

COM crystal growth, while pyridoxine deficient animals showed a significant

(p less than 0.01) decrease in mean inhibitory activity as compared to

pair-fed controls. A lowered urinary inhibitory potential accompanied with

hyperoxaluria and hypercalciuria, which is known to be associated with

pyridoxine deficiency, may be a contributory risk of calcium oxalate

crystallization and stone formation.

PMID: 3027939 [PubMed - indexed for MEDLINE]

Miner Electrolyte Metab. 1990;16(4):216-23.Links

Aminoaciduria of phosphate depletion manifests at the renal brush border

membrane.

Dabbagh S, Epley M, Diven W, Ellis D.

Department of Pediatrics, Children's Hospital of Pittsburgh, University of

Pittsburgh Medical School, Pa.

Vitamin-D deficiency is associated with secondary hyperparathyroidism,

hypophosphatemia, generalized aminoaciduria, phosphaturia and, late in its

course, hypocalcemia. The tubulopathy has been attributed to the elevated

levels of circulating parathyroid hormone. To further delineate the

mechanisms responsible for aminoaciduria, vitamin-D deficiency and/or

phosphate depletion were induced by placing weanling Sprague-Dawley rats on

one of the following diets for 5 weeks: (1) control = 0.7% P, 5.5

micrograms % vitamin D; (2) D-P- = 0.1% P, 0 microgram % vitamin D; (3)

D+P- = 0.1% P, 5.5 micrograms % vitamin D; (4) D-P+ = 0.3% P, 0 microgram %

vitamin D, and (5) D-P++ = 0.7% P, 0 microgram % vitamin D. Short-term P

depletion was produced in a group of animals fed D-P++ for 4 weeks, then

fed D-P- for another week. To study the effects of acute supplementation

with a pharmacological dose of calcitriol on the transport of amino acids

by renal brush border membrane vesicles, the latter experimental group

received 500 pmol of calcitriol (and is known as the SUPP group), or an

equal amount of the vehicle (and is referred to as the ETH group). The

uptake of taurine and proline by renal brush border membrane vesicles was

blunted by 50 +/- 3 and 40 +/- 5%, respectively, at the peak of the

overshoot, in all diets except D-P++. No changes were observed in vesicle

size or Vmax.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID: 2277606 [PubMed - indexed for MEDLINE]

1: Toxicol Appl Pharmacol. 2008 Mar 15;227(3):417-29. Epub 2007 Nov 28.

Toxicological effects of cinnabar in rats by NMR-based metabolic profiling of

urine and serum.

Wei L, Liao P, Wu H, Li X, Pei F, Li W, Wu Y.

Changchun Institute of Applied Chemistry, Chinese Academy of Sciences,

Changchun,

130022, PR China.

Cinnabar, an important traditional Chinese mineral medicine, has been

widely used

as a Chinese patent medicine ingredient for sedative therapy. However, the

pharmaceutical and toxicological effects of cinnabar, especially in the whole

organism, were subjected to few investigations. In this study, an NMR-based

metabolomics approach has been applied to investigate the toxicological effects

of cinnabar after intragastrical administration (dosed at 0.5, 2 and 5 g/kg

body

weight) on male Wistar rats. Liver and kidney histopathology examinations and

serum clinical chemistry analyses were also performed. The 1H NMR spectra were

analyzed using multivariate pattern recognition techniques to show the

time- and

dose-dependent biochemical variations induced by cinnabar. The metabolic

signature of urinalysis from cinnabar-treated animals exhibited an increase in

the levels of creatinine, acetate, acetoacetate, taurine, hippurate and

phenylacetylglycine, together with a decrease in the levels of

trimethyl-N-oxide,

dimethylglycine and Kreb's cycle intermediates (citrate, 2-oxoglutarate and

succinate). The metabolomics analyses of serum showed elevated

concentrations of

ketone bodies (3-d-hydroxybutyrate and acetoacetate), branched-chain amino

acids

(valine, leucine and isoleucine), choline and creatine as well as decreased

glucose, lipids and lipoproteins from cinnabar-treated animals. These findings

indicated cinnabar induced disturbance in energy metabolism, amino acid

metabolism and gut microflora environment as well as slight injury in liver and

kidney, which might indirectly result from cinnabar induced oxidative stress.

This work illustrated the high reliability of NMR-based metabolomic approach on

the study of the biochemical effects induced by traditional Chinese medicine.

PMID: 18164359 [PubMed - indexed for MEDLINE]

Metabolism. 1985 Feb;34(2):97-100.[] Links

Normalization of urinary oxalate by taurine in glycolate-fed rats.

Talwar HS, Madiraju VS, Murthy SR, Nath R, Thind SK.

Oral feeding of sodium glycolate (50 mg/d/rat for ten days) caused a

significant (P less than 0.001) increase in oxalate and taurine excretion

and a decrease in liver protein content (P less than 0.05), glycolic acid

oxidase levels (P less than 0.01), and glycolic acid dehydrogenase levels

(P less than 0.01) as compared to normal untreated rats. Taurine (100

mg/d/rat), when administered along with glycolate, prevented these effects

of glycolate as evident from normal urinary excretion of oxalate, liver

protein content, glycolic acid oxidase, and glycolic acid dehydrogenase

levels in glycolate- plus taurine-fed animals.

PMID: 3881651 [PubMed - indexed for MEDLINE]

Clin Cancer Res. 2007 Nov 1;13(21):6359-68.[] Links

Predictive factors of oxaliplatin neurotoxicity: the involvement of the

oxalate outcome pathway.

Gamelin L, Capitain O, Morel A, Dumont A, Traore S, Anne le B, Gilles S,

Boisdron-Celle M, Gamelin E.

Laboratory of Oncopharmacology-Pharmacogenetics, Institut National de Sante

et de Recherche Medicale U564, Angers, France.

PURPOSE: Oxaliplatin displays a frequent dose-limiting neurotoxicity due to

its interference with neuron voltage-gated sodium channels through one of

its metabolites, oxalate, a calcium chelator. Different clinical approaches

failed in neurotoxicity prevention, except calcium-magnesium infusions. We

characterized oxalate outcome following oxaliplatin administration and its

interference with cations and amino acids. We then looked for genetic

predictive factors of oxaliplatin-induced neurotoxicity. EXPERIMENTAL

DESIGN: We first tested patients for cations and oxalate levels and did

amino acid chromatograms in urine following oxaliplatin infusion. In the

second stage, before treatment with FOLFOX regimen, we prospectively looked

for variants in genes coding for the enzymes involved (a) in the oxalate

metabolism, especially glyoxylate aminotransferase (AGXT), and ( in the

detoxification glutathione cycle, glutathione S-transferase pi, and for

genes coding for membrane efflux proteins (ABCC2). RESULTS: In the first 10

patients, urinary excretions of oxalate and cations increased significantly

within hours following oxaliplatin infusion, accompanied by increased

excretions of four amino acids (glycine, alanine, serine, and taurine)

linked to oxalate metabolism. In a further 135 patients, a minor haplotype

of AGXT was found significantly predictive of both acute and chronic

neurotoxicity. Neither glutathione S-transferase pi nor ABCC2 single

nucleotide polymorphisms we looked for were linked to neurotoxicity.

CONCLUSION: These data confirm the involvement of oxalate in oxaliplatin

neurotoxicity and support the future use of AGXT genotyping as a

pretherapeutic screening test to predict individual susceptibility to

neurotoxicity.

PMID: 17975148 [PubMed - indexed for MEDLINE]

08:13 PM 9/10/2008, you wrote:'

>My son's amino acids test came back showing high taurine...and I just

>noticed a thread regarding this. I bought taurine to give him

>to " calm " him down, and then realized it is already high. Thank

>goodness I looked back thru his tests.(that is, if it is the same exact

>kind of taurine) He does not have high ammonia though. Can anyone tell

>me the significance of taurine being high? Maybe I am missing something

>I should be addressing. Still trying to figure things out...especially

>with the stimming...otherwise he's basically considered high

>functioning (talks very good, social, loving..but school is very hard,

>focus is difficult) Thanks everyone... mom to Austin pdd nos and

>Jake adhd.

>

>

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PM

[Guest guest]

So, if you don't mind me asking...what are you doing to help with the

issue? and is it working?

'

>

> >My son's amino acids test came back showing high taurine...and I

just

> >noticed a thread regarding this. I bought taurine to give him

> >to " calm " him down, and then realized it is already high. Thank

> >goodness I looked back thru his tests.(that is, if it is the same

exact

> >kind of taurine) He does not have high ammonia though. Can anyone

tell

> >me the significance of taurine being high? Maybe I am missing

something

> >I should be addressing. Still trying to figure things

out...especially

> >with the stimming...otherwise he's basically considered high

> >functioning (talks very good, social, loving..but school is very

hard,

> >focus is difficult) Thanks everyone... mom to Austin pdd nos

and

> >Jake adhd.

> >

> >

>

>

> --

> No virus found in this outgoing message.

> Checked by AVG.

> Version: 7.5.526 / Virus Database: 270.6.19/1665 - Release Date:

9/10/2008 7:00 PM

>