Re: Owens

[Guest guest]

Dear ,

I was wondering if this is just a sulphation issue with our kids

then why did it happen " suddenly " . Why is there an upsurge in Autism. I

keep thinking and rethinking and the only thing that fits to make a

complete picture for me is heavy metal toxicity. My son was given his

first shot (HIB)at 7 days old and he also had jaundice. His <billie

rubin sp?> count was starting to normalize but not quite normal(can't

remember the numbers). Autism would have been more prevalent in the past

if it was just a sulphation issue. BTW, I am not making any definite

conclusions, I am just wondering out " loud " . I know Autism is not one

thing so I am not implying that either but what I am saying is that it

SEEMS to me that the sulphation issue could be a consequence of toxicity

and not be an issue otherwise. When I was a child I use to play with

mercury from broken light bulbs and so did most of my school mates.

Before the dangers of metals were known, people were exposed to them

quite a lot and yet there was no upsurge in Autism. I am truly baffled

by the lack of knowledge in the medical community and I am thankful that

people like you are out there trying to help us out. What do think?

Vicky V.

_________________________________________________________

[Guest guest]

Vicki, I am no expert, but I just wanted to give you some of my

thoughts. After Jack, my child with ASD, I had another boy, Luke. I

did not know about the shots being a problem but had some

reservations. I also have two girls older than Jack who have no

problems and had their shots. Before Jack had any problems, he

always had mushy stools. I kept telling the doctor, having it

tested, nothing was found. He is now on a more extensive GF/CF diet

and stools are fine. When LUke, my second son, had normal stools I

was so happy. Then Luke started received his third round of shots

and the stools got mushy. I stopped the shots. Luke's stool are

getting back to normal and he is developing wonderfully but I wonder

if things would be different if I continued w/ the shots. Luke will

be turning two next week. Kids today receive several more shots than

just 6 years ago. If a child is having a detox problem and you keep

adding to the toxic load what happens? Years ago I think kids were

given mor time to detox. I received my MMR at 12. nne

>

> Dear ,

> I was wondering if this is just a sulphation issue with our

kids

> then why did it happen " suddenly " . Why is there an upsurge in

Autism. I

> keep thinking and rethinking and the only thing that fits to make a

> complete picture for me is heavy metal toxicity. My son was given

his

> first shot (HIB)at 7 days old and he also had jaundice. His <billie

> rubin sp?> count was starting to normalize but not quite normal

(can't

> remember the numbers). Autism would have been more prevalent in the

past

> if it was just a sulphation issue. BTW, I am not making any definite

> conclusions, I am just wondering out " loud " . I know Autism is not

one

> thing so I am not implying that either but what I am saying is that

it

> SEEMS to me that the sulphation issue could be a consequence of

toxicity

> and not be an issue otherwise. When I was a child I use to play with

> mercury from broken light bulbs and so did most of my school mates.

> Before the dangers of metals were known, people were exposed to them

> quite a lot and yet there was no upsurge in Autism. I am truly

baffled

> by the lack of knowledge in the medical community and I am thankful

that

> people like you are out there trying to help us out. What do think?

> Vicky V.

>

> _________________________________________________________

>

[Guest guest]

Vicky,

Feel free to " think out loud " . At least here, we can sharpen our concepts

by seeing how others are thinking about the same issues.

I have seen enough reports of children getting better on chelation to

convince me that metal toxicity played a BIG part in those children. Even

so, I am not at all convinced that this is a solitary issue.

I was musing the other day how people studying the genetics of autism feel

very comfortable saying there are multiple genes, but get really excited

when they maybe find only one " susceptibility " gene. They are not put under

the burden of showing this is the solitary cause, or even to show that it

is true of the majority of those with autism, because they can hide behind

the " multiple gene " theory.

We've developed a double standard. We want the environmental issues to be

able to explain the whole can of worms, and that is why the scientists at

the British MRC feel so justified in looking at epidemioligical work. They

like to say that if Wakefield's data can't explain the whole trend, then

his data is WRONG, even if it thoroughly explains the history of the

patient who regressed. No geneticist is put under that burden. We should

be willing to admit that there may be mulitiple environmental issues just

as much as there might be multiple susceptibility genes.

Vicky, I would be surprised if removing the thimerosal from the vaccines

would completely stop the autism epidemic. (I hope it will, and I hope I'm

wrong!) But we can't restrict our investment into singular theories. We

need to examine each piece of work thoroughly, but then invest the effort

to understand how these separate theories might fit together, and be

willing to admit the issues may be complicated.

What seems to be a critical component is the timing of the regression. If

mercury or even having too much activation of the immune system is altering

sulfation issues, we have to remember that sulfation is CRITICAL to brain

development in the first eighteen months in a way that will never be

repeated again. Fortunately, it looks like this process is fairly

forgiving if circumstances change, which I think could be why children with

developmental delay can turn out normal, just late bloomers.

But, Vicky, I also think we may be messing up genetic programs by pushing

the immune system (and related systems) in a way they were never designed

to handle by our use of multiple infant immunizations. I differ from a lot

of researchers because of this opinion, but I fear that by trying to

immunize every child against every known serious illness, we are exposing

people to diseases who may be particularly vulnerable because their

ancestors never encountered those particular germs.

Within ethnic groups who faced these diseases endemically, the genes that

couldn't deal with that germ caught the disease and probably died, and over

many, many centuries or even millenia, if this disease was an illness of

childhood and potentially fatal to people with those genes, then these

children would never have had children, nor have been able to pass those

" weak " genes on. That purging of the " weak genes " for that antigen

wouldn't happen to populations whose ancestors were never exposed to that

disease.

So I think each new vaccine may " select " those people whose cell chemistry

will be put in distress by exposure to only that particular vaccine. These

also would be people who would do poorly with the disease itself, probably,

but their chances of being exposed to that disease were maybe slim, but the

exposure through vaccine was certain, and perhaps, mandatory.

The two most remote populations to Western Disease (the native American

population and the Australian aborigines), now exposed to these diseases

either naturally or through vaccine, now have diabetes and obesity rates

that are staggering...as high as 40% of the population, and no one knows

why this is happening since they apparently did not have these diseases

like this before the rest of us arrived. If you study the way the immune

system interacts with glucose metabolism, it gets scarey.

I also learned that the ish, English and other Northern Europeans have

in their gene pool, an immune system gene that cannot process the hepatitis

B surface antigen that is in this vaccine which has been used in children

for about a decade. This is the same vaccine that had been used in the

" high risk for sexually or blood-transmitted disease " groups for about

twenty years...since about the time we started seeing AIDS rates

increase. Was the introduction of that vaccine in the Northern Europeans

the trigger that made certain people with genes " weak " to hepatitis B more

likely to get AIDS from HIV because it had weakened their immune

response? The huge problem with AIDS in Africa was preceded by a huge

immunization campaign against mainly European diseases...

So, I have plenty of questions, Vicky, and cannot either forget how many

other things have changed in our environment to thwart what our genes were

expecting, like antibiotics that kill off whole populations of gut flora

which can never be restored to whatever they were before the antibiotic

era. Do you know anyone who has never had an antiobiotic, nor their mother

nor grandmother? What happens when we manipulate this inner ecology and

thus change the environment our genes were expecting?

So, I guess I don't see any of this as a simple or singular issue, and I'm

sure there are many other issues we are still missing that reflect changes

we are making in what our bodies and their genes " grew up " to handle. We

have just been very presumptious to think that in a few generations we can

so thoroughly alter our inner and outer ecology, and suppose that our genes

are just supposed to instantly adapt...Actually, it is the PATHOGENS whose

system of genetics work so that they can quickly adapt to change...not ours!

At 3/23/2001 -050004:40 AM, you wrote:

>Dear ,

> I was wondering if this is just a sulphation issue with our kids

>then why did it happen " suddenly " . Why is there an upsurge in Autism. I

>keep thinking and rethinking and the only thing that fits to make a

>complete picture for me is heavy metal toxicity. My son was given his

>first shot (HIB)at 7 days old and he also had jaundice. His <billie

>rubin sp?> count was starting to normalize but not quite normal(can't

>remember the numbers). Autism would have been more prevalent in the past

>if it was just a sulphation issue. BTW, I am not making any definite

>conclusions, I am just wondering out " loud " . I know Autism is not one

>thing so I am not implying that either but what I am saying is that it

>SEEMS to me that the sulphation issue could be a consequence of toxicity

>and not be an issue otherwise. When I was a child I use to play with

>mercury from broken light bulbs and so did most of my school mates.

>Before the dangers of metals were known, people were exposed to them

>quite a lot and yet there was no upsurge in Autism. I am truly baffled

>by the lack of knowledge in the medical community and I am thankful that

>people like you are out there trying to help us out. What do think?

>Vicky V.

[Guest guest]

> ... I am not at all convinced that this is a solitary issue.

>

> I was musing the other day how people studying the genetics of autism feel

> very comfortable saying there are multiple genes, but get really excited

> when they maybe find only one " susceptibility " gene. They are not put

> under the burden of showing this is the solitary cause, or even to show

> that it is true of the majority of those with autism, because they can

hide

> behind the " multiple gene " theory.

>

> We've developed a double standard. We want the environmental issues to be

> able to explain the whole can of worms... They

> like to say that if Wakefield's data can't explain the whole trend, then

> his data is WRONG, even if it thoroughly explains the history of the

> patient who regressed. No geneticist is put under that burden. We should

> be willing to admit that there may be mulitiple environmental issues just

> as much as there might be multiple susceptibility genes.

How true!

This whole 'is it genetic' issue is really misunderstood, in my opinion. It

does seem obvious that there is a genetic component to autism and other

spectrum disorders, but not in the sense of 'predestined' genetics, like one

will have 10 fingers if one's parent's have 10 fingers, but rather that one

may react with some sort of illness to some environmental insult, or

combination of insults, if they are exposed at some critical level at a

critical time. Combine multiple genetic susceptibilities with multiple

environmental insults plus the individual's current health status at the

time of insult (were they infected during the insult for example? already

toxic? poorly detoxing? weakened by a poor nutrition, poor air/water/food

quality, etc.), their age, sex, etc. and you've got a complicated picture.

Can such a complex picture be understood by isolating a single environmental

insult on a relatively non specific population? I don't see how, yet that's

what the researchers continually do when they design their placebo

controlled double blind studies, find no correlation with whatever single

isolated thing they viewed as 'the variable' (in a sea of variables!), then

declare that they've demonstrated that there's no correlation.

(One thing I don't yet understand is what role the media or the journals

plays in this 'overly broad conclusion' business' - it's a huge part of the

problem, I think. They take a baby step on the long journey and declare the

journey complete. Is this just an attempt to market the article or journal,

to make a bigger splash? An attempt to insure their article gets

published?).

The temporal studies, where they attempt to correlate the onset of MMR with

autism for example, are another instance of an overly simplistic approach.

Wouldn't it be nice if the researchers SEARCHED for some way to build on

anecdotal reports of correlation with regression or associated illness, or

searched to understand which sub-populations are most susceptible, rather

than make an assumption about a simple straightforward correlation, not find

it, then declare that no correlation could possibly exist?

Maybe a better way to explore these complex environmental/genetic

interactions would be to could collect tons of info on the current health

status of many study subjects, tons of info on their environmental

exposures, their health history, even their genetic makeup, and then analyze

that data to search for correlations rather than assume a single

cause-effect relationship and not find it. Of course they could always use

anectodal reports and their intuition to help them focus on certain

relationships to speed this process up. Perhaps when the low fruit is

picked and the simplest studies are done (and there's no other way to get

published?) some more courageous researchers will do more probing

investigations - dare we hope?

K.

[Guest guest]

Hi ,

Many thanks from me too!

I really believe that I would not have been able to help my son and

understand his needs so well without your help.

Thank you for all the time you spend writing these messages for us. They are,

at least for me and a few others, very useful, and I hope you know this!

Thank you, !

Valentina

[Guest guest]

hi, ,

I have kept all 's postings. They are so helpful!

Thanks, .

mt

[Guest guest]

Can you forward them to me??? tntpilger@...

Re: [ ] Re: Owens

hi, ,

I have kept all 's postings. They are so helpful!

Thanks, .

mt

[Guest guest]

> I have kept all 's postings. They are so helpful!

I see that everybody's doing this And for sure I understand why )

If somebody is interested, I have some older posts of , very-very good

she's talking about the importance of sulfate in the body - not just for

detoxification, also I have some other files... I think some of them found on

other lists... If anybody is interested, I can share them )

These are for me too very important files.

Valentina

[Guest guest]

Can you forward me the posts as well. Thanks Maureen

[Guest guest]

Roxanne,

I'm so sorry for the delays in answering. My husband's mother died, and we

have been out of state and out of touch!

Years ago, after my first child was still born, and my second pregnancy was

following too much the same sort of mid-pregnancy course, and it became

very obvious to me that my ob/gyn had no source of a gameplan to use to

make choices with a parent with my history. It was not until years later

when I got on the St. s list looking for help for my daughter, that I

finally found a place and people who were dealing with the same sorts of

biological issues. What an answer that was to the deepest sort of heart

cry. It has been a delight (and really quite amazing) to find a community

divided by thousands of miles, but connected nevertheless, which is

determined to " get there " together. I am still convinced that we will be

able to understand WHAT the medical issues really are that cause children

to have delays, and will be able to do something about it, and maybe even

keep it from happening to others like it did for our children.

Since then, much work has brought to light the gut/brain connections and

the involvement of mercury and heavy metal exposures, immune issues, and

maybe even some hereditary issues, and I hope my studies on the sulfur

chemistry have broken some untilled land. But be sure, any work that I do

now is just a payback for all I've learned from other parents over the

years. Thank God we don't have to walk this course alone!

Thanks so much for your kind words.

At 08:51 PM 3/10/2002 -0500, you wrote:

>,

>

>I just wanted to say that I read all of your posts and save EVERY one.

>I find you are SO in tune with the rest of us parents of Autistic

>children, and I just wanted to say Thank You, so very much, for taking

>the time to write to us, and always in such detail. Wow!!!

>

>I have learned alot from your letters and sincerely appreciate all of

>the effort it takes you to put your well worded and educational writings

>together. Being a mother of a special needs child myself, I can

>certainly understand how limited time is each day, and it takes alot

>share what you do. I am so glad you are on this list though, and I just

>wanted you to know that.

>

>That's all....just thanks!

>

>Friends,

>Roxanne

>

>******************************

>

> Owens wrote:

>

> > Valentina,

> >

> > Sorry to be delayed in answering. We've been through a few viruses

> > and

> > bugs over here...not the computer type, either!

> >

> > You asked:

> >

> > > I was reading somewhere that taurine is important

> > f>or the eyes, for a better vision. Is that true?

> >

> > Yes, taurine is important for the eyes. This has been studied the

> > most in

> > cats, because they have an enzyme missing that makes it easy to

> > separate

> > the effects of taurine from other sulfur deficiency issues, but they

> > also

> > have isolated this issue by blocking taurine transport, and the

> > effects are

> > the same. These animals develop problems with the retina, and because

> > poor

> > management of taurine is part of aging, it may account for the

> > tendency

> > towards macular degeneration in the elderly.

> >

> > Taurine deficient cats also develop a cardiomyopathy. I hated

> > learning

> > this as late as I did, for I supplemented epsom salts for my father

> > which

> > improved his quality of life tremendously during the end stages of

> > Alzheimers, but I didn't supplement taurine in him, and he died of

> > heart

> > failure. He had some Parkinsonianisms. Odds are that the same issues

> > that

> > made him need sulfate may have made him need taurine as well!

> >

> > You asked:

> >

> > >Do you think you could find a little time to tell us some things

> > about

> > >taurine? Whatever you think is important and would help in

> > understanding

> > >better the way it works in the body. I would appreciate it very much.

> >

> > Glad to help.

> >

> > I've put below a group of abstracts on many subjects talking about the

> >

> > consequences of taurine deficiency. Taurine deficiency can be caused

> > by

> > the high urinary loss of cystine (cysteine) seen in cystinuria.

> > Cystiene

> > can be lost in urine by being bound to DMSA, as the article below

> > explains

> > in an experiment where they used one single dose of 10.0 mg DMSA/kg

> > po, and

> > that quantity managed to find a LOT of cystine to bind on its way to

> > excretion, but again, this was a single and high dose. It would be

> > interesting to see to what degree the substances being chelated by

> > DMSA may

> > change the sorts of calculations reported in this study, using the

> > sort of

> > dosage schedules that are recommended for chelation..

> >

> > But I've also put below articles talking about auditory evoked

> > potentials,

> > which have been found to be abnormal in many people with autism, and

> > defects in neuronal migration in cell culture. A different article

> > studied

> > this cerebellar issue in vivo, and found a huge disturbance caused by

> > taurine deficiency. Some other things noted in humans have been mental

> >

> > depression not responsive to antidepressant drugs or electroconvulsive

> >

> > therapy, exhaustion, sleep disturbances, and marked weight loss,

> > followed

> > by smptoms of parkinsonism before respiratory failure. In children,

> > rather

> > than weight loss, you would expect to see problems in growth and/or

> > slowed

> > weight gain.

> >

> > You will also find below an aritcle about how taurine deficiency

> > effects

> > the immune system. Another article talks about how astrocytes cope

> > with

> > the sort of sudden changes in osmolarity you might see when someone is

> >

> > ill. Basically, the cell cannot preserve and adjust its size

> > adequately

> > without using taurine as an osmolyte when there are changes in the

> > " saltiness " of the extracellular environment. My impression is that

> > THIS

> > function is the MAIN function of taurine systemically.

> >

> > Plenty to think about.

> >

> >

> >

> > Int J Dev Neurosci 1995 Aug;13(5):491-502

> >

> > Taurine deficiency in dissociated mouse cerebellar cultures affects

> > neuronal

> > migration.

> >

> > Maar T, Moran J, Schousboe A, Pasantes-Morales H.

> >

> > Department of Neurosciences, Institute of Cellular Physiology, UNAM,

> > Mexico

> > City, Mexico D.F.

> >

> > The role of taurine in the process of neuronal migration was studied

> > in a

> > microwell cell culture system. Immunocytochemical analysis of the

> > cellular

> > composition of this culture system revealed the presence of the

> > astrocytic

> > marker GFAP in some structures such as the aggregates of neuronal

> > bodies and in

> > those cables used for migration, resembling what is described in vivo.

> > The

> > neuronal marker gamma-enolase stained practically all structures,

> > including the

> > aggregates and all cables. The intracellular taurine concentration was

> > reduced

> > by 60% in mouse cerebellar granule cells treated with a blocker of

> > taurine

> > transport, guanidinoethane sulfonate (GES). Under these conditions

> > cell

> > migration was markedly reduced to approximately 50% of that in

> > untreated

> > cultures. Both, taurine depletion and impairment of cell migration

> > induced by

> > GES were prevented by adding taurine to the culture medium. Taurine

> > deficiency

> > similarly affected different morphological parameters such as the

> > number of

> > cables suitable for neuronal migration as well as the number of

> > migrating

> > neurons. The number of aggregates of neuronal bodies was significantly

> >

> > increased, by about 30%, as a consequence of the reduced migration.

> > Taurine

> > alone did not exert any effect on the parameters evaluated. GES

> > treatment of

> > granule cells did not affect mitochondrial metabolism or

> > K(+)-stimulated

> > Ca(2+)-dependent [3H]-D-aspartate release. This suggests that the

> > described

> > effects of taurine deficiency were not due to an alteration of

> > neuronal

> > viability and that the action of GES was not simply due to unspecific

> > and

> > deleterious effects. These results are in agreement with those

> > obtained in in

> > vivo studies. This approach represents a useful model to investigate

> > the role

> > played by taurine in the process of neuronal migration.

> >

> > PMID: 7484220 [PubMed - indexed for MEDLINE]

> >

> > Neurochem Res 1994 Apr;19(4):415-20

> >

> > Impaired cell volume regulation in taurine deficient cultured

> > astrocytes.

> >

> > Moran J, Maar TE, Pasantes-Morales H.

> >

> > Institute of Cell Physiology, National University of Mexico, Mexico

> > City.

> >

> > Taurine concentration was reduced by 40 and 65%, respectively in rat

> > cerebellar

> > astrocytes grown in a chemically defined medium or in culture medium

> > containing

> > a blocker of taurine transport (GES). Cell volume in these taurine

> > deficient

> > cells was 10%-16% higher than in controls. When challenged by

> > hyposmotic

> > conditions, astrocytes release taurine and this efflux contributes to

> > the

> > volume

> > regulatory decrease observed in these cells. Taurine deficient

> > astrocytes

> > showed

> > a less efficient volume recovery as compared to controls with normal

> > taurine

> > levels. Exposed to 50% hyposmotic medium, astrocytes with normal

> > taurine

> > concentration recovered 60% of their original volume whereas taurine

> > deficient

> > cells recovered only 30-35%. Similarly, in 30% hyposmotic medium,

> > taurine

> > deficient astrocytes recovered only 40% as compared to 75% in

> > controls. No

> > compensatory increases in the efflux of other osmolytes (free amino

> > acids or

> > potassium) were observed during regulatory volume decrease in taurine

> > deficient

> > astrocytes.

> >

> > PMID: 8065498 [PubMed - indexed for MEDLINE]

> >

> > [Drug-induced seizures in taurine-deficient mice].

> >

> > [Article in Japanese]

> >

> > Shimada C, Tanaka S, Sano M, Araki H.

> >

> > Research and Development Center, Fuso Pharmaceutical Industries, Ltd.,

> > Osaka,

> > Japan.

> >

> > Appearances of pentetrazole-, picrotoxin- and strychnine-induced

> > convulsive

> > seizures in taurine-deficient mice produced by treatment with

> > guanidinoethyl

> > sulfonate (GES), a taurine transport antagonist, were investigated.

> > Mice were

> > fed a taurine-free diet and water containing 1% GES from 2 weeks of

> > pregnancy to

> > weaning. The same feeding condition was applied to male offsprings

> > from 3 weeks

> > of age. At 5 weeks of age, convulsants were administered to some mice

> > and the

> > others were sacrificed for determination of brain amino acids

> > concentrations.

> > The incidences of both seizure and death for strychnine and death for

> > picrotoxin

> > were enhanced by treatment with GES, whereas the latency of

> > pentetrazole-induced

> > tonic extensor was prolonged. Significant decrease of brain taurine,

> > asparaginic

> > acid and GABA concentrations were observed in mice treated with GES.

> > These

> > results suggest that convulsive seizures caused by disinhibition of

> > taurine and

> > GABA system are enhanced by deficiency of brain taurine level.

> >

> > PMID: 1799096 [PubMed - indexed for MEDLINE]

> >

> > Int J Dev Neurosci 1991;9(6):571-9

> >

> > Comparison of the developmental changes of the brainstem auditory

> > evoked

> > response (BAER) in taurine-supplemented and taurine-deficient kittens.

> >

> > Vallecalle-Sandoval MH, Heaney G, Sersen E, Sturman JA.

> >

> > Department of Developmental Biochemistry, Institute for Basic Research

> > in

> > Developmental Disabilities, Staten Island, NY 10314.

> >

> > A similar development of the brainstem auditory evoked response is

> > present in

> > taurine-supplemented and taurine-deficient kittens between the second

> > postnatal

> > week and the third month of life. Between birth and the second

> > postnatal week

> > kittens from mothers fed the 1% taurine diet showed earlier maturation

> > of the

> > brainstem auditory evoked response as indicated by lower threshold,

> > shorter P1

> > latency and shorter central conduction time when compared to the

> > kittens from

> > mothers fed the 0.05% taurine diet. These results suggest an important

> > role of

> > taurine in the anatomical and functional development of the auditory

> > system.

> >

> > PMID: 1803853 [PubMed - indexed for MEDLINE]

> >

> > Arch Gen Psychiatry 2000 Nov;57(11):1077-83 Related Articles, Books,

> > LinkOut

> > [Click here to read]

> > Prolongation of brainstem auditory-evoked responses in autistic

> > probands and their unaffected relatives.

> >

> > Maziade M, Merette C, Cayer M, Roy MA, Szatmari P, Cote R,

> > Thivierge J.

> >

> > or Michel Maziade, MD, FRCP©, Centre de recherche Universite

> > Laval

> > -Giffard, 2601, chemin de la Canardiere, Beauport, Quebec G1J

> > 2G3

> > Canada. michel.maziade@...

> >

> > BACKGROUND: Brain function, as indexed by brain electrical

> > activity,

> > is heritable in humans, and it may be impaired in autism. Autism also

> > has

> > strong genetic determinants, and like all major psychiatric disorders,

> > its

> > complex clinical phenotype renders genetic studies difficult.

> > Innovative

> > strategies focused on alternative biological phenotypes are needed.

> > METHODS: The early brain auditory-evoked response was assessed in 73

> > autistic probands and 251 relatives who were compared with 521 normal

> > controls. RESULTS: We first confirmed in the autistic probands the

> > presence

> > of a slowing in nerve conduction in the auditory system as expressed

> > by the

> > prolongation of early brain auditory-evoked response under the form of

> >

> > I-III interpeak latencies (IPLs). Furthermore, we observed the same

> > I-III

> > IPL prolongation in the unaffected first degree relatives of the

> > autistic

> > probands compared with controls. Despite clear evidence of a

> > coaggregation

> > of autism and I-III IPL prolongation in families, the IPLs did not

> > seem to

> > be the sole liability factor for autism as suggested by the

> > observation of

> > 52% of families in which the autistic proband and relatives showed

> > normal

> > IPLs. CONCLUSION: A prolongation of the early brain auditory-evoked

> > response IPLs may be a marker for one of several deficits underlying

> > autism

> > and deserves further analysis as a potential alternative phenotype for

> > the

> > disorder.

> >

> > PMID: 11074874 [PubMed - indexed for MEDLINE]

> >

> >

> >

> >

> > Toxicol Appl Pharmacol 1989 Feb;97(2):338-49

> >

> > Determination and metabolism of dithiol chelating agents. VI.

> > Isolation and

> > identification of the mixed disulfides of meso-2,3-dimercaptosuccinic

> > acid with

> > L-cysteine in human urine.

> >

> > Maiorino RM, Bruce DC, Aposhian HV.

> >

> > Department of Molecular and Cellular Biology, University of Arizona,

> > Tucson

> > 85721.

> >

> > Virtually nothing is known about the biotransformation of the heavy

> > metal

> > chelating agent, meso-2,3-dimercaptosuccinic acid (DMSA). Two fasted,

> > normal,

> > young men were given 10.0 mg DMSA/kg po, and their urines were

> > collected over a

> > 14-hr period. Urine samples were analyzed, before and after

> > electrolytic

> > reductive treatment, for DMSA and its biotransformants using

> > bromobimane

> > derivatization, HPLC separation, and fluorescence detection.

> > Metabolites were

> > isolated by HPLC, ion-pairing extraction, ion-exchange extraction, and

> > TLC. By

> > 14 hr after DMSA administration, 87% of the total DMSA and 95% of the

> > total

> > L-cysteine found in urine consisted of altered forms of these

> > compounds. The

> > urinary excretion of altered DMSA, at 1, 2, 4, 6, 9, and 14 hr after

> > administration of DMSA, when compared to the urinary excretion of

> > altered

> > L-cysteine had a correlation coefficient of 0.952 and p less than

> > 0.003.

> > Approximately 90% of the altered DMSA excreted in the 2- to 4-hr urine

> > was

> > found

> > in disulfide linkage with L-cysteine. The remaining 10% was found as

> > cyclic

> > disulfides of DMSA. Of the mixed disulfides found in 4- to 6-hr urine,

> > 97%

> > consisted of two L-cysteine residues per one DMSA and the remaining 3%

> >

> > consisted

> > of one L-cysteine per one DMSA. The 2:1 mixed disulfides (97%) were

> > isolated as

> > three distinct species by TLC, consisting of 77, 12, and 8% of the

> > total mixed

> > disulfides found. In addition to the novelty of these biotransformants

> > of DMSA,

> > the DMSA-cysteine mixed disulfides indicate a thiol-disulfide

> > interchange

> > between DMSA and L-cystine. The discovery of the formation of these

> > water

> > soluble DMSA-cysteine mixed disulfides should encourage the evaluation

> > of DMSA

> > in the treatment of cystinuria.

> >

> > PMID: 2538007 [PubMed - indexed for MEDLINE]

> >

> >

> >

> >

> >

> >

> > J Leukoc Biol 1990 Apr;47(4):321-31

> >

> > Immunologic consequences of taurine deficiency in cats.

> >

> > Schuller-Levis G, Mehta PD, Rudelli R, Sturman J.

> >

> > NY State Institute for Basic Research in Developmental Disabilities,

> > Staten

> > Island 10314.

> >

> > Our results show that a lack of taurine in the diet of cats results in

> > a

> > significant leukopenia, a shift in the percentage of polymorphonuclear

> > and

> > mononuclear leukocytes, an increase in the absolute count of

> > mononuclear

> > leukocytes, and a change in the sedimentation characteristics of white

> > cells.

> > Functional studies of polymorphonuclear cells isolated from cats fed

> > taurine-free diets show a significant decrease in the respiratory

> > burst as

> > measured by chemiluminescence as well as a decrease in phagocytosis of

> >

> > Staphylococcus epidermis compared to cats fed the same diet containing

> > taurine.

> > In addition, serum gamma globulin in cats fed taurine-free diets was

> > significantly increased compared to taurine-supplemented cats,

> > indicating that

> > other immune cells may be affected by taurine deficiency. Histological

> >

> > examination of lymph nodes and spleen revealed regression of

> > follicular centers

> > with depletion of reticular cells, mature and immature lymphocytes (B

> > cell

> > areas), as well as mild extravascular hemolysis. These results

> > indicate that

> > there are profound immunologic consequences in cats with prolonged

> > taurine

> > deficiency.

> >

> > PMID: 2319206 [PubMed - indexed for MEDLINE]

> >

> >

> > At 02:41 PM 2/24/2002 +0200, you wrote:

> > > > Sulfate and taurine are products of cysteine, and glutathione is

> > built with

> > > > cysteine as one of its three peptides, so this part is farther

> > down the

> > > > chain of events: sort of second tier.

> > >

> > >

> > >Hi ,

> > >Thank you so much for all the very informative posts you send. I

> > always

> > >read them with interest and learn a lot of things.

> > >The part about taurine got my attention... I don't know a lot about

> > >it and all the things I found on the web are so confusing and

> > sometimes

> > >so hard to " digest " . I have the feeling this is something very

> > important

> > >and am not sure how... I was reading somewhere that taurine is

> > important

> > >for the eyes, for a better vision. Is that true?

> > >Do you think you could find a little time to tell us some things

> > about

> > >taurine? Whatever you think is important and would help in

> > understanding

> > >better the way it works in the body. I would appreciate it very much.

> >

> > >Thank you!

> > >

> > >

> > >Valentina

>

>

>