RE: Re: Group review and editorial comment requested.

[Guest guest]

duh what is the difference between a screening test and a diagnostic test???

[Guest guest]

It is a

22% false positive for the consumption of alchohol, it is zero false positve

for the presence of alcohol.

Re:

Group review and editorial comment requested.

Wow Dainiel, that is

*impressive*! You've put this together elegantly

and articulately.

I remember reading about the Swedish study early in my internet

searches about the EtG test shortly after I flunked it. I think I

scratched my head and said something like " of nine positives, TWO

didn't consume alcohol? It's been several decades since I took

statistics, but isn't that over a 20% false positive rate? That's way

higher than that of any medical test *I* would choose to rely on to

make a diagnosis " . But the overwhelming flood of web-sites claiming

100% reliability overwhelmed my common sense.

What also needs to be brought up is that there is a huge difference

between a screening test and a diagnostic test; the companies

agressively marketing the EtG have obviously either forgotten or chose

to ignore the distinction.

Thanks for writing this.

Judy

>

>

> Helliker

>

> Wall Street Journal

>

> RE: Your article published August 12th, 2006 entitled, A Test for

> Alcohol-And its Flaws

><http://online.wsj.com/article/SB115534928148134109-search.html?KEYWORDS\

> =alcohol & COLLECTION=wsjie/6month>

>

> I wish to add some numbers and introductory statistical definitions and

> methodology supporting your articles premise [snip]

>

[Guest guest]

Dan, Remind me, did you make any mention of endogenous alcohol in your letter? I still feel that endogenous alcohol is a significant factor here and, like inhalation, it is completely beyond one's own control. The studies that the labs base their statement "There is no scientific research to support that the presence of [auto-brewery syndrome] can result in a positive EtG drug screen" is based upon a few studies with very small sample sizes (n=9 or 10).

RE: Re: Group review and editorial comment requested.

It is a 22% false positive for the consumption of alchohol, it is zero false positve for the presence of alcohol.

-----Original Message-----From: Ethylglucuronide [mailto:Ethylglucuronide ] On Behalf Of JudySent: Friday, September 15, 2006 3:02 AMEthylglucuronide Subject: Re: Group review and editorial comment requested.

Wow Dainiel, that is *impressive*! You've put this together elegantlyand articulately.I remember reading about the Swedish study early in my internetsearches about the EtG test shortly after I flunked it. I think Iscratched my head and said something like "of nine positives, TWOdidn't consume alcohol? It's been several decades since I tookstatistics, but isn't that over a 20% false positive rate? That's wayhigher than that of any medical test *I* would choose to rely on tomake a diagnosis". But the overwhelming flood of web-sites claiming100% reliability overwhelmed my common sense.What also needs to be brought up is that there is a huge differencebetween a screening test and a diagnostic test; the companiesagressively marketing the EtG have obviously either forgotten or choseto ignore the distinction.Thanks for writing this.Judy>> > Helliker> > Wall Street Journal> > RE: Your article published August 12th, 2006 entitled, A Test for> Alcohol-And its Flaws><http://online.wsj.com/article/SB115534928148134109-search.html?KEYWORDS\> =alcohol & COLLECTION=wsjie/6month>> > I wish to add some numbers and introductory statistical definitions and> methodology supporting your articles premise [snip]>

[Guest guest]

I did not mention

endogenous alcohol exposure specifically. When controlled studies are done

generating appropriate numbers and controlling for known variables, the

presence of an unknown variable’s influence within that study population

is measured by the examining the likelihood ratios. That is how you answer the

question, “Have we identified everything yet?”

Re:

Re: Group review and editorial comment requested.

Dan, Remind me, did you make any

mention of endogenous alcohol in your letter? I still feel that endogenous

alcohol is a significant factor here and, like inhalation, it is completely

beyond one's own control. The studies that the labs base their statement " There

is no scientific research to support that the presence of [auto-brewery

syndrome] can result in a positive EtG drug screen " is based upon a few

studies with very small sample sizes (n=9 or 10).

Re:

Group review and editorial comment requested.

Wow Dainiel, that is *impressive*! You've put

this together elegantly

and articulately.

I remember reading about the Swedish study early in my internet

searches about the EtG test shortly after I flunked it. I think I

scratched my head and said something like " of nine positives, TWO

didn't consume alcohol? It's been several decades since I took

statistics, but isn't that over a 20% false positive rate? That's way

higher than that of any medical test *I* would choose to rely on to

make a diagnosis " . But the overwhelming flood of web-sites claiming

100% reliability overwhelmed my common sense.

What also needs to be brought up is that there is a huge difference

between a screening test and a diagnostic test; the companies

agressively marketing the EtG have obviously either forgotten or chose

to ignore the distinction.

Thanks for writing this.

Judy

>

>

> Helliker

>

> Wall Street Journal

>

> RE: Your article published August 12th, 2006 entitled, A Test for

> Alcohol-And its Flaws

><http://online.wsj.com/article/SB115534928148134109-search.html?KEYWORDS\

> =alcohol & COLLECTION=wsjie/6month>

>

> I wish to add some numbers and introductory statistical definitions and

> methodology supporting your articles premise [snip]

>

[Guest guest]

dan,one other thought i had is the importance of emphasis on how trivial this deceptively marketed and published as the annointed "direct metabolite of etoh" known as EtG is in the total picture of hepatic alcohol metabolism...only 1 out of 200 etoh molecules will ever be conjugated to EtG,thus there is virtually no chance of this test ever really giving the full picture of what is going on...worse than this any compromise of normal 199/200 of hepatic metabolism will skew exponentially upwards to EtG,causing increased false positives...dr. skipper has recently approved and edited upwards the wikipedia entry on EtG,portions exerpted below.. While <1% of ethanol is converted to EtG, it is known that this metabolic pathway has great inter-individual variability in activity. While there are no studies to provide information

specific for EtG production, other metabolites formed by the same liver isoforms as EtG demonstrate up to a 7-fold difference for one metabolite and a 30-fold difference for another. This said, two people with identical exposures to environmental and dietary unknown/unintentional sources of alcohol may produce very different levels. The question of where to set the cutoff for EtG to increase specificity regarding alcoholic beverage use and to decrease sensitivity to avoid detection of what has come to be called “incidental exposure” is frequently asked. Laboratories are currently offering cutoffs of 100, 250, 500 and 1000 ng/mL. These cutoffs have no scientific foundation in terms of identifying beverage alcohol consumption. Early European studies used the cutoff of 100ng/ml because that was the lowest level at which their

instrumentation was technically reliable. There are no published studies on the effects of non-beverage alcohol (termed "incidental alcohol") on EtG levels. There are no large-scale studies that establish that EtG levels in non-drinkers will consistently fall below 100, 250, or even 500ng/ml. That said, it is recommended that each agency select a cutoff that is appropriate based upon their flexibility (in dealing with investigations of false positive claims), sophistication in understanding the concepts, and severity of consequences from a positive test. Agencies must weigh the potential danger to the public against the possibility of a false accusation and the resulting consequences. As with any laboratory test, EtG is meant to be used as a tool in determining alcohol consumption. Other clinical factors should always be considered. EtG was promoted by the labs to be the be all

to end all...wurst never said it was... it has simply been marketed by the labs as such,worshipping the almighty dollar at the expense of our reputations,lives,and careers...pretty sick stuff,and extremely harmful and legally actionable...regards,r Lorie Garlick <lorieg@...> wrote:

[Guest guest]

Robin,

I added a paragraph in the copy I

submitted to the WSJ addressing the trivial amount of alcohol exposure.

Perhaps I could have chosen a different example than the one I used. We

will see. I like your example. I had not read Wilkepedia.

Thanks for the referral.

On a side note, I find the absence of a

piece of information from any of the posts in this group to be very

significant. It helped me to accept that most,of the people posting are

genuine. The absent information is this: There are known inhibitors

of the enzyme system producing EtG. It is a cheap, readily availble

medication (NO, I will not give up this medications name, for obvious reasons).

For someone testing positive multiple

times, it’s possible to simply shut this enzyme system down. No one

on this group used or advertised to anyone else this action. Instead,

people persisted in attempting to demonstrate their honestry by NEVER losing

their integrity. I found that simply inspiring.

Re:

Re: Group review and editorial comment requested.

dan,one other thought i had is the importance of

emphasis on how trivial this

deceptively marketed and published as the annointed " direct

metabolite of etoh " known as EtG is in the total picture of hepatic

alcohol metabolism...only 1 out of

200 etoh molecules will ever be conjugated to

EtG,thus there is virtually no chance

of this test ever really giving the full picture of

what is going on...worse than this

any compromise of normal 199/200 of hepatic metabolism

will skew exponentially

upwards to EtG,causing increased false

positives...dr. skipper has recently approved

and edited upwards the wikipedia entry on EtG,portions

exerpted below..

While <1% of ethanol is converted to EtG, it is

known that this metabolic pathway has great inter-individual variability in

activity. While there are no studies to pr! ovide information specific for EtG

production, other metabolites formed by the same liver isoforms as EtG

demonstrate up to a 7-fold difference for one metabolite and a 30-fold

difference for another. This said, two people with identical exposures to

environmental and dietary unknown/unintentional sources of alcohol may

produce very different levels.

The question of where to set the cutoff for EtG to

increase specificity regarding alcoholic beverage use and to decrease

sensitivity to avoid detection of what has come to be called “incidental

exposure” is frequently asked. Laboratories are currently offering

cutoffs of 100, 250, 500 and 1000 ng/mL. These cutoffs have no

scientific foundation in terms of identifying beverage alcohol consumption.

Early European studies used the cutoff of 100ng/ml because that was the lowest

level at which their instrumentation was technically reliable. There are no

published studies on the effects of non-beverage alcohol (termed

" incidental alcohol " ) on EtG levels. There are no large-scale studies

that establish that EtG levels in non-drinkers will consistently fall below

100, 250, or even 500ng/ml. That said, it is recommended that each agency

select a cutoff that is appropriate based upon their flexibility (in dealing

with investigations of false positive claims), sophistication in understanding

the concepts, and severity of consequences from a positive test. Agencies

must weigh the potential danger to the public against the possibility of a false accusation and

the resulting consequences. As with any laboratory test, EtG is meant to be

used as a tool in determining alcohol consumption. Other clinical factors

should always be considered.

EtG was promoted by the labs to be the be all to

end all...wurst never said it was...

it has simply been marketed by the labs as

such,worshipping the almighty dollar

at the expense of our reputations,lives,and

careers...pretty sick stuff,and extremely

harmful and legally actionable...regards,r

Lorie Garlick

<lorieglanset> wrote:

[Guest guest]

the wikipedia has the power of common recognition,being used frequently by almost everybody on the web including boards,labs,etc.info also posted edited and reviewed by dr. skipper...as things started to go south on this test,dan,based on the info i have reviewing the information that was deleted,updated, and earlier postings by him and the timeline on all this might be very revealing and of great interest to you... regards,r l DiBona <danieldibona@...> wrote: Robin, I added a paragraph in the copy I submitted to the WSJ addressing the trivial amount of alcohol exposure. Perhaps I could have chosen a different example than the one I used. We will see. I like your example. I had not read Wilkepedia. Thanks for the referral. On a side note, I find the absence of a piece of information from any of

the posts in this group to be very significant. It helped me to accept that most,of the people posting are genuine. The absent information is this: There are known inhibitors of the enzyme system producing EtG. It is a cheap, readily availble medication (NO, I will not give up this medications name, for obvious reasons). For someone testing positive multiple times, it’s possible to simply shut this enzyme system down. No one on this group used or advertised to anyone else this action. Instead, people persisted in attempting to demonstrate their honestry by NEVER losing their integrity. I found that simply inspiring. -----Original Message-----From: Ethylglucuronide [mailto:Ethylglucuronide ] On Behalf Of robin murraySent: Friday, September 15, 2006 12:48 PMEthylglucuronide Subject: Re: Re: Group review and editorial comment requested. dan,one other thought i had is the importance of emphasis on how trivial this deceptively marketed and published as the annointed "direct metabolite of etoh" known as EtG is in the total picture of hepatic alcohol metabolism...only 1 out of 200 etoh molecules will ever be conjugated to EtG,thus there is virtually no chance of this test ever really giving the full picture of what is going on...worse than this any compromise of normal 199/200 of hepatic metabolism will skew exponentially upwards to EtG,causing increased false positives...dr. skipper has recently approved and edited upwards the wikipedia entry on EtG,portions exerpted below.. While <1% of ethanol is converted to EtG, it is known that this metabolic pathway has great inter-individual variability in activity. While there are no studies to pr! ovide information specific for EtG production,

other metabolites formed by the same liver isoforms as EtG demonstrate up to a 7-fold difference for one metabolite and a 30-fold difference for another. This said, two people with identical exposures to environmental and dietary unknown/unintentional sources of alcohol may produce very different levels. The question of where to set the cutoff for EtG to

increase specificity regarding alcoholic beverage use and to decrease sensitivity to avoid detection of what has come to be called “incidental exposure” is frequently asked. Laboratories are currently offering cutoffs of 100, 250, 500 and 1000 ng/mL. These cutoffs have no scientific foundation in terms of identifying beverage alcohol consumption. Early European studies used the cutoff of 100ng/ml because that was the lowest level at which their instrumentation was technically reliable. There are no published studies on the effects of non-beverage alcohol (termed "incidental alcohol") on EtG levels. There are no large-scale studies that establish that EtG levels in non-drinkers will consistently fall below 100, 250, or even 500ng/ml. That said, it is recommended that each agency select a cutoff that is appropriate based upon their flexibility (in dealing with

investigations of false positive claims), sophistication in understanding the concepts, and severity of consequences from a positive test. Agencies must weigh the potential danger to the public against the possibility of a false accusation and the resulting consequences. As with any laboratory test, EtG is meant to be used as a tool in determining alcohol consumption. Other clinical factors should always be considered. EtG was promoted by the labs to be the be all to end all...wurst never said it

was... it has simply been marketed by the labs as such,worshipping the almighty dollar at the expense of our reputations,lives,and careers...pretty sick stuff,and extremely harmful and legally actionable...regards,r Lorie Garlick

<lorieglanset> wrote:

[Guest guest]

Would

you please consider posting the time lines, etc? You seem to be have some

great documentation skills. I think it important to snapshot the testing

facilities websites on a daily basis to document the time of their changing

information, if ever.

“More will be revealed…”

Re:

Re: Group review and editorial comment requested.

!

dan,one other thought i had is the importance of

emphasis on how trivial this

deceptively marketed and published as the annointed " direct

metabolite of etoh " known as EtG is in the total picture of hepatic

alcohol metabolism...only 1 out of

200 etoh molecules will ever be conjugated to

EtG,thus there is virtually no chance

of this test ever really giving the full picture of

what is going on...worse than this

any

compromise of normal 199/200 of hepatic metabolism will skew exponentially

upwards to EtG,causing increased false

positives...dr. skipper has recently approved

and edited upwards the wikipedia entry on EtG,portions

exerpted below..

While <1% of ethanol is converted to EtG, it is

known that this metabolic pathway has great inter-individual variability in

activity. While there are no studies to pr! ovide information specific for EtG

production, other metabolites formed by the same liver isoforms as EtG

demonstrate up to a 7-fold difference for one metabolite and a 30-fold

difference for another. This said, two people with identical exposures to

environmental and dietary unknown/unintentional sources of alcohol may

produce very different levels.

The question of where to set the cutoff for! EtG to

increase specificity regarding alcoholic beverage use and to decrease

sensitivity to avoid detection of what has come to be called “incidental

exposure” is frequently asked. Laboratories are currently offering

cutoffs of 100, 250, 500 and 1000 ng/mL. These cutoffs have no

scientific foundation in terms of identifying beverage alcohol consumption.

Early European studies used the cutoff of 100ng/ml because that was the lowest

level at which their instrumentation was technically reliable. There are no

published studies on the effects of non-beverage alcohol (termed

" incidental alcohol " ) on EtG levels. There are no large-scale studies

that establish that EtG levels in non-drinkers will consistently fall below

100, 250, or even 500ng/ml. That said, it is recommended that each agency

select a cutoff that is appropriate based upon their flexibility (in dealing

with investigations of false positive claims), sophistication in understanding

the concepts, and severity of consequences from a positive test. Agencies

must weigh the potential danger to the public against the possibility of a false accusation and

the resulting consequences. As with any laboratory test, EtG is meant to be

used as a tool in determining alcohol consumption. Other clinical factors

should always be considered.

EtG was promoted by the labs to be the be all to

end all...wurst never said it was...

it has simply been marketed by the labs as

such,worshipping the almighty dollar

at the expense of our reputations,lives,and

careers...pretty sick stuff,and extremely

harmful and legally actionable...regards,r

Lorie Garlick <lorieglanset>

wrote:

[Guest guest]

hi again dan,fyi,an abstract of the latest on the biomarkers presented in sydney 2 days ago...even wurst gives no special significance to EtG,just one of numerous biomarkers of extremely dubious value in the clinical diagnosis of the clinical disease known as relapse.agree with you on the veracity of most of the folks on this site and the drug/enzyme thing...does not seem to be relevant to the major problem,which is deceptive dishonest harmful marketing of EtG by labs and draconian misuse of that misformation by some boards and judges...regards,r Abstract for presentation at ISBRA 2006 World Congress on Alcohol Research Direct ethanol metabolites such as ethyl glucuronide (EtG), ethyl sulfate (EtS), fatty acid ethyl esters (FAEEs) and phosphatidyl ethanol (PEth) - Their use in diagnosis and

treatment PD Dr Friedrich Wurst, Psychiatric University Clinic, Switzerland Prof Gerhard Wiesbeck, Switzerland Dr Steina Aradottir, University of Lund, Sweden Prof Fritz Pragst, University of Berlin, Germany Prof Bankole , University of Virginia Medical School, United States Prof Otto Lesch, University of Vienna, Australia Prof Kate Conigrave, University of Sydney, Australia PD Dr Wolfgang Weinmann, University of Freiburg, Germany Direct ethanol metabolites such as ethyl glucuronide (EtG), ethyl sulfate (EtS), phosphatidylethanol (PEth)and fatty acid

ethyl esters (FAEEs) are formed only when alcohol is present. Each of them remains positive for a characteristic time spectrum after the cessation of ethanol intake – EtG and EtS in serum for hours and in urine up to 5 days, PEth in whole blood more than to 2 weeks. Additionally, EtG and FAEE can be detected in hair for months. PATIENTS AND METHODS: Patients were a ) 50 alcoholics during detoxification, 200 detoxified alcoholics that were monitored for alcohol consumption during a rehabilitation program, c) 453 individuals from the WHO/ISBRA study, d) alcoholics seeking pharmacological treatment to reduce ethanol intake e) 80 patients from an emergency room, f) patients in a methadone maintenance treatment, suffering from Hepatitis C, among others. Methods used include gas chromatography-mass spectrometry (FAEEs), liquid chromatography/tandem mass spectrometry (EtG, EtS, EtP) and high pressure liquid chromatography (PEth), among others. Direct ethanol metabolites are

compared to traditional markers and self reports. RESULTS: Results include new basic aspects (first determination of EtS in serum, data on EtP), and recent clinical findings in various populations: data suggest a) the combined use of EtG and EtS in urine, good potential of identifying hazardous alcohol use by the use of FAEEs in hair and PEth in blood, c) the potential of direct ethanol metabolites in the identification of previous alcohol use in patients in an emergency unit when blood alcohol is zero, furthermore d) the ratio of EtS to EtG in serum around 1:3. Finally, a synopsis for the differential use of the various biomarkers will be given. CONCLUSIONS: The findings suggest, that direct ethanol metabolites have potential in detection of previous ethanol intake in a variety of situations and settings. Their combined use and the conjoint use with traditional markers and self reports might be promising. Conference Organiser - ICMS Pty Ltd DiBona <danieldibona@...> wrote: Robin, I added a paragraph in the copy I submitted to the WSJ addressing the trivial amount of

alcohol exposure. Perhaps I could have chosen a different example than the one I used. We will see. I like your example. I had not read Wilkepedia. Thanks for the referral. On a side note, I find the absence of a piece of information from any of the posts in this group to be very significant. It helped me to accept that most,of the people posting are genuine. The absent information is this: There are known inhibitors of the enzyme system producing EtG. It is a cheap, readily availble medication (NO, I will not give up this medications name, for obvious reasons). For someone testing positive multiple times, it’s possible to simply shut this enzyme system down. No one on this group used or advertised to anyone else this action. Instead, people persisted in attempting to demonstrate their honestry by NEVER losing their integrity. I found that simply inspiring. -----Original Message-----From: Ethylglucuronide [mailto:Ethylglucuronide ]

On Behalf Of robin murraySent: Friday, September 15, 2006 12:48 PMEthylglucuronide Subject: Re: Re: Group review and editorial comment requested. dan,one other thought i had is the importance of emphasis on how trivial this deceptively marketed and published as the annointed "direct metabolite of etoh" known as EtG is in the total picture of

hepatic alcohol metabolism...only 1 out of 200 etoh molecules will ever be conjugated to EtG,thus there is virtually no chance of this test ever really giving the full picture of what is going on...worse than this any compromise of normal 199/200 of hepatic metabolism will skew exponentially upwards to EtG,causing increased false positives...dr. skipper has recently approved and edited upwards the wikipedia entry on EtG,portions exerpted below.. While <1% of ethanol is converted to EtG, it is known that this metabolic pathway has great inter-individual variability in activity. While there are no studies to pr! ovide information specific for EtG production, other metabolites formed by the same liver isoforms as EtG demonstrate up to a 7-fold difference for one metabolite and a 30-fold difference for another. This said, two people with identical exposures to environmental and dietary unknown/unintentional sources of alcohol may produce very different

levels. The question of where to set the cutoff for EtG to increase specificity regarding alcoholic beverage use and to decrease sensitivity to avoid detection of what has come to be called “incidental exposure” is frequently asked. Laboratories are currently offering cutoffs of 100, 250, 500 and 1000 ng/mL. These cutoffs have no scientific foundation in terms of

identifying beverage alcohol consumption. Early European studies used the cutoff of 100ng/ml because that was the lowest level at which their instrumentation was technically reliable. There are no published studies on the effects of non-beverage alcohol (termed "incidental alcohol") on EtG levels. There are no large-scale studies that establish that EtG levels in non-drinkers will consistently fall below 100, 250, or even 500ng/ml. That said, it is recommended that each agency select a cutoff that is appropriate based upon their flexibility (in dealing with investigations of false positive claims), sophistication in understanding the concepts, and severity of consequences from a positive test. Agencies must weigh the potential danger to the public against the possibility of a false accusation and the resulting consequences. As with any laboratory test, EtG is meant

to be used as a tool in determining alcohol consumption. Other clinical factors should always be considered. EtG was promoted by the labs to be the be all to end all...wurst never said it was... it has simply been marketed by the labs as such,worshipping the almighty dollar at the expense of our reputations,lives,and careers...pretty sick

stuff,and extremely harmful and legally actionable...regards,r Lorie Garlick <lorieglanset> wrote:

[Guest guest]

Keep in mind that the Wikipedia article can be edited by anybody and is unreferenced. I've been keeping an eye on it, and it's been edited 6 times since Skipper's last update.

RE: Re: Group review and editorial comment requested.

the wikipedia has the power of common recognition,being used frequently by almost everybody on the web including boards,labs,etc.info also posted edited and reviewed by dr. skipper...as things started to go south on this test,dan,based on the info i have reviewing the information that was deleted,updated, and earlier postings by him and the timeline on all this might be very revealing and of great interest to you...

regards,r

l DiBona <danieldibonamac> wrote:

Robin,

I added a paragraph in the copy I submitted to the WSJ addressing the trivial amount of alcohol exposure. Perhaps I could have chosen a different example than the one I used. We will see. I like your example. I had not read Wilkepedia. Thanks for the referral.

On a side note, I find the absence of a piece of information from any of the posts in this group to be very significant. It helped me to accept that most,of the people posting are genuine. The absent information is this: There are known inhibitors of the enzyme system producing EtG. It is a cheap, readily availble medication (NO, I will not give up this medications name, for obvious reasons).

For someone testing positive multiple times, it’s possible to simply shut this enzyme system down. No one on this group used or advertised to anyone else this action. Instead, people persisted in attempting to demonstrate their honestry by NEVER losing their integrity. I found that simply inspiring.

-----Original Message-----From: Ethylglucuronide [mailto:Ethylglucuronide ] On Behalf Of robin murraySent: Friday, September 15, 2006 12:48 PMEthylglucuronide Subject: Re: Re: Group review and editorial comment requested.

dan,one other thought i had is the importance of emphasis on how trivial this deceptively marketed and published as the annointed "direct metabolite of etoh" known as EtG is in the total picture of hepatic alcohol metabolism...only 1 out of

200 etoh molecules will ever be conjugated to EtG,thus there is virtually no chance

of this test ever really giving the full picture of what is going on...worse than this

any compromise of normal 199/200 of hepatic metabolism will skew exponentially

upwards to EtG,causing increased false positives...dr. skipper has recently approved

and edited upwards the wikipedia entry on EtG,portions exerpted below..

While <1% of ethanol is converted to EtG, it is known that this metabolic pathway has great inter-individual variability in activity. While there are no studies to pr! ovide information specific for EtG production, other metabolites formed by the same liver isoforms as EtG demonstrate up to a 7-fold difference for one metabolite and a 30-fold difference for another. This said, two people with identical exposures to environmental and dietary unknown/unintentional sources of alcohol may produce very different levels.

The question of where to set the cutoff for EtG to increase specificity regarding alcoholic beverage use and to decrease sensitivity to avoid detection of what has come to be called “incidental exposure” is frequently asked. Laboratories are currently offering cutoffs of 100, 250, 500 and 1000 ng/mL. These cutoffs have no scientific foundation in terms of identifying beverage alcohol consumption. Early European studies used the cutoff of 100ng/ml because that was the lowest level at which their instrumentation was technically reliable. There are no published studies on the effects of non-beverage alcohol (termed "incidental alcohol") on EtG levels. There are no large-scale studies that establish that EtG levels in non-drinkers will consistently fall below 100, 250, or even 500ng/ml. That said, it is recommended that each agency select a cutoff that is appropriate based upon their flexibility (in dealing with investigations of false positive claims), sophistication in understanding the concepts, and severity of consequences from a positive test. Agencies must weigh the potential danger to the public against the possibility of a false accusation and the resulting consequences. As with any laboratory test, EtG is meant to be used as a tool in determining alcohol consumption. Other clinical factors should always be considered.

EtG was promoted by the labs to be the be all to end all...wurst never said it was...

it has simply been marketed by the labs as such,worshipping the almighty dollar

at the expense of our reputations,lives,and careers...pretty sick stuff,and extremely

harmful and legally actionable...regards,r

Lorie Garlick <lorieglanset> wrote:

[Guest guest]

Soon the labs may have to start screening for Dan's "mystery substance" with each EtG to ensure that nobody is using it to mask EtG results. Hahaha...That's funny. That could really turn their world upside down.

RE: Re: Group review and editorial comment requested.

hi again dan,fyi,an abstract of the latest on the biomarkers presented in sydney 2 days ago...even wurst gives no special significance to EtG,just one of numerous biomarkers of extremely dubious value in the clinical diagnosis of the clinical disease known as relapse.agree with you on the veracity of most of the folks on this site and

the drug/enzyme thing...does not seem to be relevant to the major problem,which is

deceptive dishonest harmful marketing of EtG by labs and draconian misuse of that misformation by some boards and judges...regards,r

Abstract for presentation at ISBRA 2006 World Congress on Alcohol Research

Direct ethanol metabolites such as ethyl glucuronide (EtG), ethyl sulfate (EtS), fatty acid ethyl esters (FAEEs) and phosphatidyl ethanol (PEth) - Their use in diagnosis and treatment

PD Dr Friedrich Wurst, Psychiatric University Clinic, Switzerland Prof Gerhard Wiesbeck, Switzerland Dr Steina Aradottir, University of Lund, Sweden Prof Fritz Pragst, University of Berlin, Germany Prof Bankole , University of Virginia Medical School, United States Prof Otto Lesch, University of Vienna, Australia Prof Kate Conigrave, University of Sydney, Australia PD Dr Wolfgang Weinmann, University of Freiburg, Germany

Direct ethanol metabolites such as ethyl glucuronide (EtG), ethyl sulfate (EtS), phosphatidylethanol (PEth)and fatty acid ethyl esters (FAEEs) are formed only when alcohol is present. Each of them remains positive for a characteristic time spectrum after the cessation of ethanol intake – EtG and EtS in serum for hours and in urine up to 5 days, PEth in whole blood more than to 2 weeks. Additionally, EtG and FAEE can be detected in hair for months. PATIENTS AND METHODS: Patients were a ) 50 alcoholics during detoxification, 200 detoxified alcoholics that were monitored for alcohol consumption during a rehabilitation program, c) 453 individuals from the WHO/ISBRA study, d) alcoholics seeking pharmacological treatment to reduce ethanol intake e) 80 patients from an emergency room, f) patients in a methadone maintenance treatment, suffering from Hepatitis C, among others. Methods used include gas chromatography-mass spectrometry (FAEEs), liquid chromatography/tandem mass spectrometry (EtG, EtS, EtP) and high pressure liquid chromatography (PEth), among others. Direct ethanol metabolites are compared to traditional markers and self reports. RESULTS: Results include new basic aspects (first determination of EtS in serum, data on EtP), and recent clinical findings in various populations: data suggest a) the combined use of EtG and EtS in urine, good potential of identifying hazardous alcohol use by the use of FAEEs in hair and PEth in blood, c) the potential of direct ethanol metabolites in the identification of previous alcohol use in patients in an emergency unit when blood alcohol is zero, furthermore d) the ratio of EtS to EtG in serum around 1:3. Finally, a synopsis for the differential use of the various biomarkers will be given. CONCLUSIONS: The findings suggest, that direct ethanol metabolites have potential in detection of previous ethanol intake in a variety of situations and settings. Their combined use and the conjoint use with traditional markers and self reports might be promising.

Conference Organiser - ICMS Pty Ltd DiBona <danieldibonamac> wrote:

Robin,

I added a paragraph in the copy I submitted to the WSJ addressing the trivial amount of alcohol exposure. Perhaps I could have chosen a different example than the one I used. We will see. I like your example. I had not read Wilkepedia. Thanks for the referral.

On a side note, I find the absence of a piece of information from any of the posts in this group to be very significant. It helped me to accept that most,of the people posting are genuine. The absent information is this: There are known inhibitors of the enzyme system producing EtG. It is a cheap, readily availble medication (NO, I will not give up this medications name, for obvious reasons).

For someone testing positive multiple times, it’s possible to simply shut this enzyme system down. No one on this group used or advertised to anyone else this action. Instead, people persisted in attempting to demonstrate their honestry by NEVER losing their integrity. I found that simply inspiring.

-----Original Message-----From: Ethylglucuronide [mailto:Ethylglucuronide ] On Behalf Of robin murraySent: Friday, September 15, 2006 12:48 PMEthylglucuronide Subject: Re: Re: Group review and editorial comment requested.

dan,one other thought i had is the importance of emphasis on how trivial this deceptively marketed and published as the annointed "direct metabolite of etoh" known as EtG is in the total picture of hepatic alcohol metabolism...only 1 out of

200 etoh molecules will ever be conjugated to EtG,thus there is virtually no chance

of this test ever really giving the full picture of what is going on...worse than this

any compromise of normal 199/200 of hepatic metabolism will skew exponentially

upwards to EtG,causing increased false positives...dr. skipper has recently approved

and edited upwards the wikipedia entry on EtG,portions exerpted below..

While <1% of ethanol is converted to EtG, it is known that this metabolic pathway has great inter-individual variability in activity. While there are no studies to pr! ovide information specific for EtG production, other metabolites formed by the same liver isoforms as EtG demonstrate up to a 7-fold difference for one metabolite and a 30-fold difference for another. This said, two people with identical exposures to environmental and dietary unknown/unintentional sources of alcohol may produce very different levels.

The question of where to set the cutoff for EtG to increase specificity regarding alcoholic beverage use and to decrease sensitivity to avoid detection of what has come to be called “incidental exposure” is frequently asked. Laboratories are currently offering cutoffs of 100, 250, 500 and 1000 ng/mL. These cutoffs have no scientific foundation in terms of identifying beverage alcohol consumption. Early European studies used the cutoff of 100ng/ml because that was the lowest level at which their instrumentation was technically reliable. There are no published studies on the effects of non-beverage alcohol (termed "incidental alcohol") on EtG levels. There are no large-scale studies that establish that EtG levels in non-drinkers will consistently fall below 100, 250, or even 500ng/ml. That said, it is recommended that each agency select a cutoff that is appropriate based upon their flexibility (in dealing with investigations of false positive claims), sophistication in understanding the concepts, and severity of consequences from a positive test. Agencies must weigh the potential danger to the public against the possibility of a false accusation and the resulting consequences. As with any laboratory test, EtG is meant to be used as a tool in determining alcohol consumption. Other clinical factors should always be considered.

EtG was promoted by the labs to be the be all to end all...wurst never said it was...

it has simply been marketed by the labs as such,worshipping the almighty dollar

at the expense of our reputations,lives,and careers...pretty sick stuff,and extremely

harmful and legally actionable...regards,r

Lorie Garlick <lorieglanset> wrote:

[Guest guest]

yes lorie is right and you can track the entries by their user names on the site...for example a user named gregskipper recently added a new 1000 cutoff now available by lab...very interestin' All active members of Wikimedia projects are invited to vote in the 2006 Election to the Board of Trustees of the Wikimedia Foundation. Ethyl glucuronide From Wikipedia, the free encyclopedia (Difference between revisions) Jump to: navigation, search Revision as of 18:34, 10 September 2006 (edit)66.81.57.227 (Talk)← Older edit Current revision (16:08, 14 September 2006) (edit)69.204.160.167 (Talk) Line 12: Line 12: It’s also important to realize that EtG and EtS can be present in urine from non-beverage alcohol exposure. Following introduction of these tests numerous individuals came forward tenaciously claiming they were falsely accused of drinking because of positive EtG tests. Various products were tested on small numbers of individuals and it was found that ethanol containing mouthwash, sips of communion wine, alcohol free wine and beer, and OTC meds containing ethanol caused low positive EtG tests, up to 300-400ng/ml. A study using alcohol-based hand sanitizing gel (62% ethyl alcohol) indicated that inhalation, not skin absorption, is a major absorption route for ethyl alcohol, producing very

significant EtG levels. Lab experiments utilizing these hand gels have yielded EtG results in the 500-800ng/ml range on multiple occassions. It’s also important to realize that EtG and EtS can be present in urine from non-beverage alcohol exposure. Following introduction of these tests numerous individuals came forward tenaciously claiming they were falsely accused of drinking because of positive EtG tests. Various products were tested on small numbers of individuals and it was found that ethanol containing mouthwash, sips of communion wine, alcohol free wine and beer, and OTC meds containing ethanol caused low positive EtG tests, up to 300-400ng/ml. A study using alcohol-based hand sanitizing gel (62% ethyl alcohol) indicated that inhalation, not skin absorption, is a major absorption route for ethyl alcohol, producing very significant EtG levels. Lab experiments utilizing these hand gels have yielded EtG results in the 500-800ng/ml

range on multiple occassions. - The question of where to set the cutoff for EtG to increase specificity regarding alcoholic beverage use and to decrease sensitivity to avoid detection of what has come to be called “incidental exposure” is frequently asked. Laboratories are currently offering cutoffs of 100, 250, and 500ng/ml. These cutoffs have no scientific foundation in terms of identifying beverage alcohol consumption. Early European studies used the cutoff of 100ng/ml because that was the lowest level at which their instrumentation was technically reliable. There are no published studies on the effects of non-beverage alcohol (termed "incidental alcohol") on EtG levels. There are no large-scale studies that establish that EtG levels in non-drinkers will consistently

fall below 100, 250, or even 500ng/ml. That said, it is recommended that each agency select a cutoff that is appropriate based upon their flexibility (in dealing with investigations of false positive claims), sophistication in understanding the concepts, and severity of consequences from a positive test. Agencies must weigh the potential danger to the public against the possibility of a false accusation and the resulting consequences. As with any laboratory test, EtG is meant to be used as a tool in determining alcohol consumption. Other clinical factors should always be considered. + The question of where to set the cutoff for EtG to increase specificity regarding alcoholic beverage use and to decrease sensitivity to avoid detection of what has come to be called “incidental exposure” is frequently asked. Laboratories are currently offering cutoffs of 100, 250, 500 and 1000 ng/mL. These cutoffs have no scientific foundation in terms of identifying beverage alcohol consumption. Early European studies used the cutoff of 100ng/ml because that was the lowest level at which their instrumentation was technically reliable. There are no published studies on the effects of non-beverage alcohol (termed "incidental alcohol") on EtG levels. There are no large-scale studies that establish that EtG levels in non-drinkers will consistently fall below 100, 250, or even 500ng/ml. That said, it is recommended that each agency select a cutoff that is appropriate based upon their flexibility (in dealing with investigations of false positive claims), sophistication in understanding the concepts, and severity of consequences from a positive test. Agencies must weigh the potential danger to the public against the possibility of a false accusation and the resulting consequences. As with any

laboratory test, EtG is meant to be used as a tool in determining alcohol consumption. Other clinical factors should always be considered. Many studies advise that EtG levels be “normalized” to a creatinine level of 100, which is expressed as “EtG100“. Particularly when levels are critically close to a cutoff level, such an adjustment may have crucial consequences. SAMHSA requires that a creatinine level be measured with all specimens tested for drugs. To normalize the level, use the following formula: “EtG100” = (EtG x 100) / Cr. Many studies advise that EtG levels be “normalized” to a creatinine level of 100, which is expressed as “EtG100“. Particularly when levels are critically close to a cutoff level, such an adjustment may have crucial consequences. SAMHSA requires that a creatinine

level be measured with all specimens tested for drugs. To normalize the level, use the following formula: “EtG100” = (EtG x 100) / Cr. Current revision To meet Wikipedia's quality standards, this article or section may require cleanup.Please discuss this issue on the talk page, or replace this tag with a more specific message. Editing help is available.This article has been tagged since August 2006. This article or section does not cite its references or sources.You can help Wikipedia by introducing appropriate citations. Ethylglucuronide, ethyl glucuronide, or EtG is the name for a chemical marker of recent

alcohol (ethanol) exposure. EtG is a minor non-oxidative metabolite of ethanol. In other words, when you drink alcohol some of it is converted into EtG which is eventually eliminated from the body. The benefit of testing for EtG is that it is present much longer in the body than alcohol itself and thus it can be a more durable and superior marker for recent alcohol exposure. EtG can be found in urine, blood, and all other body tissues (hair, liver, etc). It is only present after exposure to alcohol. EtG is fairly stable in urine (it is degraded by some bacteria, if present in the urine) and is detected by analyzing at a laboratory with either liquid chromatography and mass spectroscopy (LC-MS-MS) or by immunologic testing (ELISA). The ELISA test is relatively new (manufactured by Microgenics). EtG testing is particularly useful in monitoring individuals who have agreed to be abstinent

(professionals who have been allowed to return to their jobs following problems with alcohol at work, who return on condition they will not drink alcohol, custody cases where alcohol use has been an issue, criminal jurisdictions where alcohol has been associated with crime, etc). Ethyl glucuronide, EtG, as well as other non-oxidative metabolites of ethanol, including ethyl sulfate, EtS, and less commonly ethyl phosphate, EtP, are gaining popularity as they can detect ethanol use for up to 7 days post exposure (depending on the person and dose of ethanol). As such, EtG and these other markers should only be used in situations where total abstinence from ethanol is expected or required, such as for employees or licensees (pilots, doctors, etc) who have been allowed to return to work contingent on total abstinence, probationers who’ve agreed to abstinence, monitoring in child custody cases where total abstinence is imposed, or for underage children or young

military recruits, etc. In all other situations drinking ethanol off duty is not prohibited and would cause a positive test but would be meaningless as far as the workplace is concerned. In other words these analytes detect any exposure and therefore having little to do with detection of impairment at work. EtG and/or EtS testing are proving to be very sensitive and specific in detecting exposure to ethanol; however, in the absence of a commitment or expectation of total abstinence (on and off work) they should not be used. It is always important when someone is being tested for these markers that they be advised that incidental exposure to ethanol can cause a positive and they should be advised in detail about products containing ethanol. While <1% of ethanol is converted to EtG, it is known that this metabolic pathway has great inter-individual variability in activity. While there are no studies to provide information specific for EtG production, other

metabolites formed by the same liver isoforms as EtG demonstrate up to a 7-fold difference for one metabolite and a 30-fold difference for another. This said, two people with identical exposures to environmental and dietary unknown/unintentional sources of alcohol may produce very different levels. It’s also important to realize that EtG and EtS can be present in urine from non-beverage alcohol exposure. Following introduction of these tests numerous individuals came forward tenaciously claiming they were falsely accused of drinking because of positive EtG tests. Various products were tested on small numbers of individuals and it was found that ethanol containing mouthwash, sips of communion wine, alcohol free wine and beer, and OTC meds containing ethanol caused low positive EtG tests, up to 300-400ng/ml. A study using alcohol-based hand sanitizing gel (62% ethyl alcohol) indicated that inhalation, not skin absorption, is a major absorption route for ethyl

alcohol, producing very significant EtG levels. Lab experiments utilizing these hand gels have yielded EtG results in the 500-800ng/ml range on multiple occassions. The question of where to set the cutoff for EtG to increase specificity regarding alcoholic beverage use and to decrease sensitivity to avoid detection of what has come to be called “incidental exposure” is frequently asked. Laboratories are currently offering cutoffs of 100, 250, 500 and 1000 ng/mL. These cutoffs have no scientific foundation in terms of identifying beverage alcohol consumption. Early European studies used the cutoff of 100ng/ml because that was the lowest level at which their instrumentation was technically reliable. There are no published studies on the effects of non-beverage alcohol (termed "incidental alcohol") on EtG levels. There are no large-scale studies that establish that EtG levels in non-drinkers will consistently fall below 100, 250, or even 500ng/ml. That said, it is

recommended that each agency select a cutoff that is appropriate based upon their flexibility (in dealing with investigations of false positive claims), sophistication in understanding the concepts, and severity of consequences from a positive test. Agencies must weigh the potential danger to the public against the possibility of a false accusation and the resulting consequences. As with any laboratory test, EtG is meant to be used as a tool in determining alcohol consumption. Other clinical factors should always be considered. Many studies advise that EtG levels be “normalized” to a creatinine level of 100, which is expressed as “EtG100“. Particularly when levels are critically close to a cutoff level, such an adjustment may have crucial consequences. SAMHSA requires that a creatinine level be measured with all specimens tested for drugs. To normalize the level, use the following formula: “EtG100” = (EtG x 100) / Cr. [edit] External links Link page to external chemical sources. This article about an organic compound

is a stub. You can help Wikipedia by expanding it. Retrieved from "http://en.wikipedia.org/wiki/Ethyl_glucuronide" Categories: Cleanup from August 2006 | Articles lacking sources | Glycosides | Organic compound stubs Views Article Discussion Edit this page History Watch Personal tools Qwovadis My talk My preferences My watchlist My contributions Log out Navigation Main Page Community Portal Featured articles Current events Recent changes Random article Help Contact Wikipedia Donations

Search Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this article This page was last modified 16:08, 14 September 2006. All text is available under the terms of the GNU Free Documentation License. (See Copyrights for details.) Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc. Privacy

policy About Wikipedia Disclaimers Lorie Garlick <lorieg@...> wrote: Keep in mind that

the Wikipedia article can be edited by anybody and is unreferenced. I've been keeping an eye on it, and it's been edited 6 times since Skipper's last update. RE: Re: Group review and editorial comment requested. the wikipedia has the power of common

recognition,being used frequently by almost everybody on the web including boards,labs,etc.info also posted edited and reviewed by dr. skipper...as things started to go south on this test,dan,based on the info i have reviewing the information that was deleted,updated, and earlier postings by him and the timeline on all this might be very revealing and of great interest to you... regards,r l DiBona <danieldibonamac> wrote: Robin, I added a

paragraph in the copy I submitted to the WSJ addressing the trivial amount of alcohol exposure. Perhaps I could have chosen a different example than the one I used. We will see. I like your example. I had not read Wilkepedia. Thanks for the referral. On a side note, I find the absence of a piece of information from any of the posts in this group to be very significant. It helped me to accept that most,of the people posting are genuine. The absent information is this: There are known inhibitors of the enzyme system producing EtG. It is a cheap, readily availble medication (NO, I will not give up this medications name, for obvious

reasons). For someone testing positive multiple times, it’s possible to simply shut this enzyme system down. No one on this group used or advertised to anyone else this action. Instead, people persisted in attempting to demonstrate their honestry by NEVER losing their integrity. I found that simply inspiring. -----Original Message-----From:

Ethylglucuronide [mailto:Ethylglucuronide ] On Behalf Of robin murraySent: Friday, September 15, 2006 12:48 PMEthylglucuronide Subject: Re: Re: Group review and editorial comment requested. dan,one other thought i had is the importance of emphasis on how trivial this deceptively marketed and

published as the annointed "direct metabolite of etoh" known as EtG is in the total picture of hepatic alcohol metabolism...only 1 out of 200 etoh molecules will ever be conjugated to EtG,thus there is virtually no chance of this test ever really giving the full picture of what is going on...worse than this any compromise of normal 199/200 of hepatic metabolism will skew exponentially upwards to EtG,causing increased false positives...dr. skipper has recently

approved and edited upwards the wikipedia entry on EtG,portions exerpted below.. While <1% of ethanol is converted to EtG, it is known that this metabolic pathway has great inter-individual variability in activity. While there are no studies to pr! ovide information specific for EtG production, other metabolites formed by the same liver isoforms as EtG demonstrate up to a 7-fold difference for one metabolite and a 30-fold difference for another. This said, two people with identical exposures to environmental and dietary

unknown/unintentional sources of alcohol may produce very different levels. The question of where to set the cutoff for EtG to increase specificity regarding alcoholic beverage use and to decrease sensitivity to avoid detection of what has come to be called “incidental exposure” is frequently asked. Laboratories are currently offering cutoffs of 100, 250, 500 and 1000 ng/mL. These cutoffs have no scientific foundation in terms of identifying beverage alcohol consumption. Early European studies used the cutoff of 100ng/ml because that was the lowest level at which their instrumentation was technically reliable. There are no published studies on the effects of non-beverage alcohol (termed "incidental alcohol") on EtG levels. There are no large-scale studies that establish that EtG levels in non-drinkers will consistently fall below 100, 250, or even 500ng/ml. That said, it is recommended that each agency select a cutoff that is appropriate based upon their flexibility (in dealing with investigations of false positive claims), sophistication in understanding the concepts, and severity of consequences from a positive test. Agencies must weigh the potential danger to the public against the possibility of a false

accusation and the resulting consequences. As with any laboratory test, EtG is meant to be used as a tool in determining alcohol consumption. Other clinical factors should always be considered. EtG was promoted by the labs to be the be all to end all...wurst never said it was... it has simply been marketed by the labs as such,worshipping the almighty dollar at the expense of our reputations,lives,and careers...pretty sick stuff,and extremely harmful and legally actionable...regards,r Lorie Garlick <lorieglanset> wrote:

[Guest guest]

That is

an important revision. The time and date stamping is important as

well. How does one submit requests for entry, such as:

From the Department of

Clinical Neuroscience, Section of Alcohol and Drug Dependence Research, The

Karolinska Institutet, Stockholm, Sweden published initially in a

dissertation written earlier in 2006 by Helen Dahl. Permission to

reproduce her data was not sought as it is publically available on the

internet.

On

page 24 of Ms. Dahl¡Çs dissertation she reports, ¡ÈDuring the placebo period two

of the subjects showed positive results for urinary EtG, albeit at low levels.¡É

Using Ms.

Dahl¡Çs data, the following statistical table is generated. At the time of

this writing Ms. Dahl¡Çs data represents the only published peer reviewed measurements

available for calculation.

ALCOHOL

CONSUMPTION

Present

Absent

TOTALS

EtG

Positive

9

2

11

Test

Negative

0

7

7

Result

TOTALS

9

9

18

Basic

statistical definitions for sensitivity, specificity and predictive values of

positive and negative test results yield the following descriptions:

Sensitivity of EtG testing for

consumed alcohol presence = 100%

Specificity of EtG testing for consumed

alcohol absence = 22%

Predictive value of a positive test for EtG

indicating alcohol consumption = 88%

Predictive value of a

negative EtG test indicating no alcohol consumption = 100%

Likelihood ratio for a

positive test result = 1.28

Likelihood ratio for a

negative test result = zero

Re:

Re: Group review and editorial comment requested.

yes lorie is right and you can track the entries by

their user names on the site...for example a user named gregskipper recently

added a new 1000 cutoff now available

by lab...very interestin'

All

active members of Wikimedia projects are invited to vote in the 2006 Election

to the Board of Trustees of the Wikimedia Foundation.

Ethyl glucuronide

From Wikipedia, the free encyclopedia

(Difference between revisions)

Jump to: navigation,

search

Revision

as of 18:34, 10 September 2006 (edit)

66.81.57.227 (Talk)

¢« Older edit

Current revision

(16:08, 14 September 2006) (edit)

69.204.160.167 (T! alk)

Line 12:

Line 12:

It¡Çs also important to realize that EtG and EtS can

be present in urine from non-beverage alcohol exposure. Following

introduction of these tests numerous individuals came forward tenaciously

claiming they were falsely accused of drinking because of positive EtG tests.

Various products were tested on small numbers of individuals and it was found

that ethanol containing mouthwash, sips of communion wine, alcohol free wine

and beer, and OTC meds containing ethanol caused low positive EtG tests, up

to 300-400ng/ml. A study using alcohol-based hand sanitizing gel (62% ethyl

alcohol) indicated that inhalation, not skin absorption, is a major

absorption route for ethyl alcohol, producing very significant EtG levels.

Lab experiments utilizing these hand gels have yielded EtG results in the

500-800ng/ml range on multiple occassions.

It¡Çs also important to realize that EtG and EtS can

be present in urine from non-beverage alcohol exposure. Following

introduction of these tests numerous individuals came forward tenaciously

claiming they were falsely accused of drinking because of positive EtG tests.

Various products were tested on small numbers of individuals and it was found

that ethanol containing mouthwash, sips of communion wine, alcohol free wine

and beer, and OTC meds containing ethanol caused low positive EtG tests, up

to 300-400ng/ml. A study using alcohol-based hand sanitizing gel (62% ethyl

alcohol) indicated that inhalation, not skin absorption, is a major

absorption route for ethyl alcohol, producing very significant EtG levels.

Lab experiments utilizing these hand gels have yielded EtG results in the

500-800ng/ml range on multiple occassions.

-

The question of where to set the cutoff for EtG to

increase specificity regarding alcoholic beverage use and to decrease

sensitivity to avoid detection of what has come to be called ¡Èincidental

exposure¡É is frequently asked. Laboratories are currently offering cutoffs of

100, 250, and 500ng/ml.

These cutoffs have no scientific foundation in terms of identifying beverage

alcohol consumption. Early European studies used the cutoff of 100ng/ml

because that was the lowest level at which their instrumentation was

technically reliable. There are no published studies on the effects of

non-beverage alcohol (termed " incidental alcohol " ) on EtG levels.

There are no large-scale studies that establish that EtG levels in

non-drinkers will consisten! tly fall below 100, 250, or even 500ng/ml. That

said, it is recommended that each agency select a cutoff that is appropriate

based upon their flexibility (in dealing with investigations of false

positive claims), sophistication in understanding the concepts, and severity

of consequences from a positive test. Agencies must weigh the potential

danger to the public against the possibility of a false accusation and the

resulting consequences. As with any laboratory test, EtG is meant to be used

as a tool in determining alcohol consumption. Other clinical factors should

always be considered.

+

The question of where to set the cutoff for EtG to

increase specificity regarding alcoholic beverage use and to decrease

sensitivity to avoid detection of what has come to be called ¡Èincidental

exposure¡É is frequently asked. Laboratories are currently offering cutoffs of

100, 250, 500 and 1000 ng/mL. These cutoffs have no

scientific foundation in terms of identifying beverage alcohol consumption.

Early European studies used the cutoff of 100ng/ml because that was the

lowest level at which their instrumentation was technically reliable. There

are no published studies on the effects of non-beverage alcohol (termed

" incidental alcohol " ) on EtG levels. There are no large-scale

studies that establish that EtG levels in non-drinkers will consistently fall

below 100, 250, or even 500ng/ml. That said, it is recommended that each

agency select a cutoff that is appropriate based upon their flexibility (in

dealing with investigations of false positive claims), sophistication in

understanding the concepts, and severity of consequences from a positive

test. Agencies must weigh the potential danger to the public against the

possibility of a false accusation and the resulting consequences. As with any

laboratory test, EtG is meant to be used as a tool in determining alcohol

consumption. Other clinical factors should always be considered.

Many studies advise that EtG levels be ¡Ènormalized¡É

to a creatinine level of 100, which is expressed as ¡ÈEtG100¡È. Particularly

when levels are critically close to a cutoff level, such an adjustment may

have crucial consequences. SAMHSA requires that a creatinine level be

measured with all specimens tested for drugs. To normalize the level, use the

following formula: ¡ÈEtG100¡É = (EtG x 100) / Cr.

Many studies advise that EtG levels be ¡Ènormalized¡É

to a creatinine level of 100, which is expressed as ¡ÈEtG100¡È. Particularly

when levels are critically close to a cutoff level, such an adjustment may

have crucial consequences. SAMHSA requires that a creatinine level be

measured with all specimens tested for drugs. To normalize the level, use the

following formula: ¡ÈEtG100¡É = (EtG x 100) / Cr.

Current revision

To meet

Wikipedia's quality standards, this article

or section may require cleanup.

Please discuss this issue on the talk

page, or replace this tag with a more specific message.

Editing help

is available.

This article has been tagged since August

2006.

This article or section does not cite its references or sources.

You can help Wikipedia by

introducing appropriate citations.

Ethylglucuronide,

ethyl glucuronide, or EtG is the name for a chemical marker of

recent alcohol (ethanol)

exposure. EtG is a minor non-oxidative metabolite of ethanol.

In other words, when you drink alcohol some of it is

converted into EtG which is eventually eliminated from the body. The benefit of

testing for EtG is that it is present much longer in the body than alcohol

itself and thus it can be a more durable and superior marker for recent alcohol

exposure. EtG can be found in urine, blood, and all other body tissues (hair,

liver, etc). It is only present after exposure to alcohol. EtG is fairly stable

in urine (it is degraded by some bacteria, if present in the urine) and is

detected by analyzing at a laboratory with either liquid chromatography and

mass spectroscopy (LC-MS-MS) or by immunologic testing (ELISA). The ELISA test

is relatively new (manufactured by Microgenics). EtG testing is

particularly useful in monitoring individuals who have agreed to be abstinent

(professionals who have been allowed to return to their jobs following problems

with alcohol at work, who return on condition they will not drink alcohol,

custody cases where alcohol use has been an issue, criminal jurisdictions where

alcohol has been associated with crime, etc).

Ethyl glucuronide, EtG, as well as other non-oxidative

metabolites of ethanol, including ethyl sulfate, EtS, and less commonly ethyl

phosphate, EtP, are gaining popularity as they can detect ethanol use for up to

7 days post exposure (depending on the person and dose of ethanol). As such,

EtG and these other markers should only be used in situations where total

abstinence from ethanol is expected or required, such as for employees or

licensees (pilots, doctors, etc) who have been allowed to return to work

contingent on total abstinence, probationers who¡Çve agreed to abstinence,

monitoring in child custody cases where total abstinence is imposed, or for

underage children or young military recruits, etc. In all other situations

drinking ethanol off duty is not prohibited and would cause a positive test but

would be meaningless as far as the workplace is concerned. In other words these

analytes detect any exposure and therefore having little to do with detection

of impairment at work. EtG and/or EtS testing are proving to be very sensitive

and specific in detecting exposure to ethanol; however, in the absence of a

commitment or expectation of total abstinence (on and off work) they should not

be used. It is always important when someone is being tested for these markers

that they be advised that incidental exposure to ethanol can cause a positive

and they should be advised in detail about products containing ethanol.

While <1% of ethanol is converted to EtG, it is

known that this metabolic pathway has great inter-individual variability in

activity. While there are no studies to provide information specific for EtG

production, other metabolites formed by the same liver isoforms as EtG

demonstrate up to a 7-fold difference for one metabolite and a 30-fold difference

for another. This said, two people with identical exposures to environmental

and dietary unknown/unintentional sources of alcohol may produce very

different levels.

It¡Çs also important to realize that EtG and EtS can be

present in urine from non-beverage alcohol exposure. Following introduction of

these tests numerous individuals came forward tenaciously claiming they were

falsely accused of drinking because of positive EtG tests. Various products

were tested on small numbers of individuals and it was found that ethanol

containing mouthwash, sips of communion wine, alcohol free wine and beer, and

OTC meds containing ethanol caused low positive EtG tests, up to 300-400ng/ml.

A study using alcohol-based hand sanitizing gel (62% ethyl alcohol) indicated

that inhalation, not skin absorption, is a major absorption route for ethyl

alcohol, producing very significant EtG levels. Lab experiments utilizing these

hand gels have yielded EtG results in the 500-800ng/ml range on multiple

occassions.

The question of where to set the cutoff for EtG to

increase specificity regarding alcoholic beverage use and to decrease

sensitivity to avoid detection of what has come to be called ¡Èincidental

exposure¡É is frequently asked. Laboratories are currently offering cutoffs of

100, 250, 500 and 1000 ng/mL. These cutoffs have no scientific foundation in

terms of identifying beverage alcohol consumption. Early European studies used

the cutoff of 100ng/ml because that was the lowest level at which their

instrumentation was technically reliable. There are no published studies on the

effects of non-beverage alcohol (termed " incidental alcohol " ) on EtG

levels. There are no large-scale studies that establish that EtG levels in

non-drinkers will consistently fall below 100, 250, or even 500ng/ml. That

said, it is recommended that each agency select a cutoff that is appropriate

based upon their flexibility (in dealing with investigations of false positive

claims), sophistication in understanding the concepts, and severity of

consequences from a positive test. Agencies must weigh the potential danger to

the public against the possibility of a false accusation and the resulting

consequences. As with any laboratory test, EtG is meant to be used as a tool in

determining alcohol consumption. Other clinical factors should always be

considered.

Many studies advise that EtG levels be ¡Ènormalized¡É to

a creatinine level of 100, which is expressed as ¡ÈEtG100¡È. Particularly when

levels are critically close to a cutoff level, such an adjustment may have

crucial consequences. SAMHSA requires that a creatinine level be measured with

all specimens tested for drugs. To normalize the level, use the following

formula: ¡ÈEtG100¡É = (EtG x 100) / Cr.

[edit]

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article about an organic compound is a stub. You can help

Wikipedia by expanding

it.

Retrieved from " http://en.wikipedia.org/wiki/Ethyl_glucuronide "

Categories: Cleanup

from August 2006 | Articles lacking sources | Glycosides | Organic compound stubs

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Disclaimers

Lorie Garlick

<lorieglanset> wrote:

Keep in mind that the Wikipedia

article can be edited by anybody and is unreferenced. I've been keeping an eye

on it, and it's been edited 6 times since Skipper's last update.

Re: Re: Group review and editorial comment

requested.

dan,one

other thought i had is the importance of emphasis on how trivial this deceptively mar! keted

and published as the annointed " direct metabolite of etoh " known

as EtG is in the total picture of hepatic alcohol metabolism...only 1

out of

200 etoh

molecules will ever be conjugated to EtG,thus there is virtually no chance

of this

test ever really giving the full picture of what is going on...worse than this

any

compromise of normal 199/200 of hepatic metabolism will skew exponentially

upwards

to EtG,causing increased false positives...dr. skipper has recen! tly

approved

and

edited upwards the wikipedia entry on EtG,portions exerpted below..

While

<1% of ethanol is converted to EtG, it is known that this metabolic pathway

has great inter-individual variability in activity. While there are no studies

to pr! ovide information specific for EtG production, other metabolites formed

by the same liver isoforms as EtG demonstrate up to a 7-fold difference for one

metabolite and a 30-fold difference for another. This said, two people

with identical exposures to environmental and diet! ary unknown/unintentional

sources of alcohol may produce very different levels.

The

question of where to set the cutoff for EtG to increase specificity regarding

alcoholic beverage use and to decrease sensitivity to avoid detection of what

has come to be called ¡Èincidental exposure¡É is frequently asked. Laboratories

are currently offering cutoffs of 100, 250, 500 and 1000 ng/mL. These cutoffs have no

scientific foundation in terms of identifying beverage alcohol consumption.

Early European studies used the cutoff of 100ng/ml because that was the lowest

level at which their instrumentation was technically reliable. There are no

published studies on the effects of non-beverage alcohol (termed

" incidental alcohol " ) on EtG levels. There are no large-scale studies

that establish that EtG levels in non-drinkers will consistently fall below

100, 250, or even 500ng/ml. That said, it is recommended that each agency

select a cutoff that is appropriate based upon their flexibility (in dealing

with investigations of false positive claims), sophistication in understanding the

concepts, and severity of consequences from a positive test. Agencies must

weigh the potential danger to the public against the possibility of a false accusation and

the resulting consequences. As with any laboratory test, EtG is meant to be

used as a tool in determining alcohol consumption. Other clinical factors

should always be considered.

EtG was

promoted by the labs to be the be all to end all...wurst never said it was...

it has

simply been marketed by the labs as such,worshipping the almighty dollar

at

the expense of our reputations,lives,and careers...pretty sick stuff,and

extremely

harmful

and legally actionable...regards,r

Lorie Garlick <lorieglanset>

wrote:

[Guest guest]

NWTox website in which it stated 'Etg is only detected when beverage alcohol has been consumed' is no longer there....the entire website is gone and it is incorporated with Quest web site in which they took out the word 'beverage' I printed out a copy of that website on Aug 17th and within a few days it was gone. DiBona <danieldibona@...> wrote: Would you please consider posting the time lines, etc? You seem to be have some great documentation skills. I think it important to snapshot the testing facilities websites on a daily basis to document the time of their changing information, if ever. “More will be revealed…” -----Original Message-----From: Ethylglucuronide

[mailto:Ethylglucuronide ] On Behalf Of robin murraySent: Friday, September 15, 2006 2:32 PMEthylglucuronide Subject: RE: Re: Group review and editorial comment requested. the wikipedia has the power of common recognition,being used frequently by almost everybody on the web including boards,labs,etc.info also posted edited and reviewed by dr. skipper...as things started to go south on this

test,dan,based on the info i have reviewing the information that was deleted,updated, and earlier postings by him and the timeline on all this might be very revealing and of great interest to you... regards,r l DiBona <danieldibonamac> wrote: Robin, I added a paragraph in the copy I submitted to the WSJ addressing the trivial amount of alcohol exposure. Perhaps I could have chosen a different example than the one I used. We will see. I like your example. I had not read Wilkepedia. Thanks for the referral. On a side note, I find the absence of a piece of information from any of the posts in this group to be very significant. It helped me to accept that most,of the people posting are genuine. The absent information is this: There are

known inhibitors of the enzyme system producing EtG. It is a cheap, readily availble medication (NO, I will not give up this medications name, for obvious reasons). For someone testing positive multiple times, it’s possible to simply shut this enzyme system down. No one on this group used or advertised to anyone else this action. Instead, people persisted in attempting to demonstrate their honestry by NEVER losing their integrity. I found that simply inspiring. ! -----Original Message-----From: Ethylglucuronide [mailto:Ethylglucuronide ] On Behalf Of robin murraySent: Friday, September 15, 2006 12:48 PMEthylglucuronide Subject: Re: Re: Group review and editorial comment requested. ! dan,one other thought i had is the importance of emphasis on how trivial this deceptively marketed and published as the annointed "direct metabolite of etoh" known as EtG is in the total picture of hepatic alcohol metabolism...only 1 out of 200 etoh molecules will ever be conjugated to EtG,thus there is virtually no chance of this test ever really giving the full picture of what is going on...worse than

this any compromise of normal 199/200 of hepatic metabolism will skew exponentially upwards to EtG,causing increased false positives...dr. skipper has recently approved and edited upwards the wikipedia entry on EtG,portions exerpted below.. While <1% of ethanol is converted to

EtG, it is known that this metabolic pathway has great inter-individual variability in activity. While there are no studies to pr! ovide information specific for EtG production, other metabolites formed by the same liver isoforms as EtG demonstrate up to a 7-fold difference for one metabolite and a 30-fold difference for another. This said, two people with identical exposures to environmental and dietary unknown/unintentional sources of alcohol may produce very different levels. The question of where to set the cutoff for! EtG to increase specificity regarding alcoholic beverage use and to decrease sensitivity to avoid detection of what has come to be called “incidental exposure” is frequently asked. Laboratories are currently offering cutoffs of 100, 250, 500 and 1000 ng/mL. These cutoffs have no scientific foundation in terms of identifying beverage alcohol consumption. Early European studies used the cutoff of 100ng/ml because that was the lowest level at which their instrumentation was technically reliable. There are no published studies on the effects of non-beverage alcohol (termed "incidental alcohol") on EtG levels. There are no large-scale studies that

establish that EtG levels in non-drinkers will consistently fall below 100, 250, or even 500ng/ml. That said, it is recommended that each agency select a cutoff that is appropriate based upon their flexibility (in dealing with investigations of false positive claims), sophistication in understanding the concepts, and severity of consequences from a positive test. Agencies must weigh the potential danger to the public against the possibility of a false accusation and the resulting consequences. As with any laboratory test, EtG is meant to be used as a tool in determining alcohol consumption. Other clinical factors should always be considered. EtG was promoted by the labs to be the be all to end all...wurst never said it was... it has simply been marketed by the labs as such,worshipping the almighty dollar at the expense of our reputations,lives,and careers...pretty sick stuff,and extremely harmful and legally actionable...regards,r Lorie Garlick <lorieglanset> wrote:

Stay in the know. Pulse on the new .com. Check it out.

[Guest guest]

Can you please scan the printout into pdf and post it

on the site? That should wake them up and just be

another thing to show the boards or other interested

parties that the labs are backpedaling.

TIA

Ken

--- N <nautiques5@...> wrote:

> NWTox website in which it stated 'Etg is only

> detected when beverage alcohol has been consumed' is

> no longer there....the entire website is gone and it

> is incorporated with Quest web site in which they

> took out the word 'beverage' I printed out a copy

> of that website on Aug 17th and within a few days it

> was gone.

>

> DiBona <danieldibona@...> wrote:

> Would you please consider posting the time

> lines, etc? You seem to be have some great

> documentation skills. I think it important to

> snapshot the testing facilities websites on a daily

> basis to document the time of their changing

> information, if ever.

>

> “More will be revealed…”

>

> Re: Re: Group review and

> editorial comment requested.

>

>

>

> !

> dan,one other thought i had is the

> importance of emphasis on how trivial this

> deceptively marketed and published as the annointed

> " direct metabolite of etoh " known as EtG is in the

> total picture of hepatic alcohol metabolism...only 1

> out of

>

>

> 200 etoh molecules will ever be conjugated to

> EtG,thus there is virtually no chance

>

>

> of this test ever really giving the full

> picture of what is going on...worse than this

>

>

> any compromise of normal 199/200 of hepatic

> metabolism will skew exponentially

>

>

> upwards to EtG,causing increased false

> positives...dr. skipper has recently approved

>

>

> and edited upwards the wikipedia entry on

> EtG,portions exerpted below..

>

>

>

>

>

>

> While <1% of ethanol is converted to EtG, it

> is known that this metabolic pathway has great

> inter-individual variability in activity. While

> there are no studies to pr! ovide information

> specific for EtG production, other metabolites

> formed by the same liver isoforms as EtG demonstrate

> up to a 7-fold difference for one metabolite and a

> 30-fold difference for another. This said, two

> people with identical exposures to environmental and

> dietary unknown/unintentional sources of alcohol may

> produce very different levels.

>

>

>

>

>

>

>

>

>

>

>

> The question of where to set the cutoff for!

> EtG to increase specificity regarding alcoholic

> beverage use and to decrease sensitivity to avoid

> detection of what has come to be called “incidental

> exposure” is frequently asked. Laboratories are

> currently offering cutoffs of 100, 250, 500 and 1000

> ng/mL. These cutoffs have no scientific foundation

> in terms of identifying beverage alcohol

> consumption. Early European studies used the cutoff

> of 100ng/ml because that was the lowest level at

> which their instrumentation was technically

> reliable. There are no published studies on the

> effects of non-beverage alcohol (termed " incidental

> alcohol " ) on EtG levels. There are no large-scale

> studies that establish that EtG levels in

> non-drinkers will consistently fall below 100, 250,

> or even 500ng/ml. That said, it is recommended that

> each agency select a cutoff that is appropriate

> based upon their flexibility (in dealing with

> investigations of false positive claims),

> sophistication in

> understanding the concepts, and severity of

> consequences from a positive test. Agencies must

> weigh the potential danger to the public against the

> possibility of a false accusation and the resulting

> consequences. As with any laboratory test, EtG is

> meant to be used as a tool in determining alcohol

> consumption. Other clinical factors should always be

> considered.

>

>

>

>

>

> EtG was promoted by the labs to be the be all

> to end all...wurst never said it was...

>

>

> it has simply been marketed by the labs as

> such,worshipping the almighty dollar

>

>

> at the expense of our reputations,lives,and

> careers...pretty sick stuff,and extremely

>

>

> harmful and legally actionable...regards,r

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

> Lorie Garlick <lorieg@...> wrote:

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

> ---------------------------------

> Stay in the know. Pulse on the new .com. Check

> it out.

__________________________________________________

[Guest guest]

Do not

lose information like this. Keep it secure in a non-modifiable format

stored in a combination of personal media and on-line storage. If

litigation ever occurrs, the integrity of the information will be challenged

exhaustively. This is not a “slam-dunk” liability situation,

but it is becoming more attractive. I believe the future holds either

large scale litigation or quiet damage control. Either way, be prepared

for how slowly time moves in situations like this (ie, the speed of a

glacier). Time mellows and clarifies, but also rots good information if

not compulsively recorded, documented, cross-referenced and stored securely.

Re:

Re: Group review and editorial comment requested.

!

dan,one other

thought i had is the importance of emphasis on how trivial

this deceptively marketed and published as the annointed " direct

metabolite of etoh " known as EtG is in the total picture of hepatic

alcohol metabolism...only 1 out of

200 etoh

molecules will ever be conjugated to EtG,thus there is virtually no chance

of this test

ever really giving the full picture of what is going on.! ..worse than this

any compromise

of normal 199/200 of hepatic metabolism will skew exponentially

upwards to

EtG,causing increased false positives...dr. skipper has recently

approved

and edited

upwards the wikipedia entry on EtG,portions exerpted below..

While <1%

of ethanol ! is converted to EtG, it is known that this metabolic pathway has

great inter-individual variability in activity. While there are no studies to

pr! ovide information specific for EtG production, other metabolites formed by

the same liver isoforms as EtG demonstrate up to a 7-fold difference for one

metabolite and a 30-fold difference for another. This said, two people

with identical exposures to environmental and dietary unknown/unintentional

sources of alcohol may produce very different levels.

The question

of where to set the cutoff for! EtG to increase specificity regarding alcoholic

beverage use and to decrease sensitivity to avoid detection of what has come to

be called “incidental exposure” is frequently asked. Laboratories

are currently offering cutoffs of 100, 250, 500 and 1000 ng/mL. These cutoffs have no

scientific foundation in terms of identifying beverage alcohol consumption.

Early European studies used the cutoff of 100ng/ml because that was the lowest

level at which their instrumentation was technically reliable. There are no

published studies on the effects of non-beverage alcohol (termed

" incidental alcohol " ) on EtG levels. There are no large-scale studies

that establish that EtG levels in non-drinkers will consistently fall below 100,

250, or even 500ng/ml. That said, it is recommended that each agency select a

cutoff that is appropriate based upon their flexibility (in dealing with

investigations of false positive claims), sophistication in understanding the

concepts, and severity of consequences from a positive test. Agencies must

weigh the potential danger to the public against the possibility of a false accusation and

the resulting consequences. As with any laboratory test, EtG is meant to be

used as a tool in determining alcohol consumption. Other clinical factors

should always be considered.

EtG was

promoted by the labs to be the be all to end all...wurst never said it was...

it has simply

been marketed by the labs as such,worshipping the almighty dollar

at the expense

of our reputations,lives,and careers...pretty sick stuff,and extremely

harmful and

legally actionable...regards,r

Lorie Garlick

<lorieglanset> wrote:

Stay in the know. Pulse

on the new .com. Check it

out.

[Guest guest]

dan,one other thought i had is the importance of emphasis of how trivial this deceptively marketed and published as the annointed "direct metabolite of etoh" known as EtG is in the total picture of hepatic alcohol metabolism...only 1 out of 200 etoh molecules will ever be conjugated to EtG,thus there is virtually no chance of this test ever really giving the full picture of what is going on...worse than this any compromise of normal 199/200 of hepatic metabolism will skew exponentially upwards to EtG,causing increased false positives...dr. skipper has recently approved and edited upwards the wikipedia entry on EtG,portions exerpted below.. While <1% of ethanol is converted to EtG, it is known that this metabolic pathway has great inter-individual variability in activity. While there are no studies to provide information specific for EtG production, other metabolites

formed by the same liver isoforms as EtG demonstrate up to a 7-fold difference for one metabolite and a 30-fold difference for another. This said, two people with identical exposures to environmental and dietary unknown/unintentional sources of alcohol may produce very different levels.Lorie Garlick <lorieg@...> wrote: Dan, Remind me, did you make any mention of endogenous alcohol in your letter? I still feel that endogenous alcohol is a significant factor here and, like inhalation,

it is completely beyond one's own control. The studies that the labs base their statement "There is no scientific research to support that the presence of [auto-brewery syndrome] can result in a positive EtG drug screen" is based upon a few studies with very small sample sizes (n=9 or 10).

RE: Re: Group review and editorial comment requested. It is a 22% false positive for the consumption of alchohol, it is zero false positve for the presence of alcohol. -----Original Message-----From: Ethylglucuronide [mailto:Ethylglucuronide ] On Behalf Of JudySent: Friday, September 15, 2006 3:02 AMEthylglucuronide Subject: Re: Group review and editorial comment requested. Wow Dainiel, that is *impressive*! You've put this together elegantlyand articulately.I remember reading about the Swedish study early in my internetsearches about the EtG test shortly after I flunked it. I think Iscratched my head and said something like "of nine positives, TWOdidn't consume alcohol? It's been several decades since I

tookstatistics, but isn't that over a 20% false positive rate? That's wayhigher than that of any medical test *I* would choose to rely on tomake a diagnosis". But the overwhelming flood of web-sites claiming100% reliability overwhelmed my common sense.What also needs to be brought up is that there is a huge differencebetween a screening test and a diagnostic test; the companiesagressively marketing the EtG have obviously either forgotten or choseto ignore the distinction.Thanks for writing this.Judy>> > Helliker> > Wall Street Journal> > RE: Your article published August 12th, 2006 entitled, A Test for> Alcohol-And its Flaws><http://online.wsj.com/article/SB115534928148134109-search.html?KEYWORDS\> =alcohol & COLLECTION=wsjie/6month>> > I wish to add some numbers and introductory statistical definitions and> methodology supporting your articles premise [snip]>

[Guest guest]

I hope my letter to the WSJ did just that. If not, perhaps you could offer some

words that you believe may more clearly convey the same information.

On Saturday, September 16, 2006, at 07:44PM, robin murray <remurraymd@...>

wrote:

>

><<Original Attached>>

dan,one other thought i had is the importance of emphasis of how trivial this deceptively marketed and published as the annointed "direct metabolite of etoh" known as EtG is in the total picture of hepatic alcohol metabolism...only 1 out of 200 etoh molecules will ever be conjugated to EtG,thus there is virtually no chance of this test ever really giving the full picture of what is going on...worse than this any compromise of normal 199/200 of hepatic metabolism will skew exponentially upwards to EtG,causing increased false positives...dr. skipper has recently approved and edited upwards the wikipedia entry on EtG,portions exerpted below.. While <1% of ethanol is converted to EtG, it is known that this metabolic pathway has great inter-individual variability in activity. While there are no studies to provide information specific for EtG produ!

ction,!

other metabolites

formed by the same liver isoforms as EtG demonstrate up to a 7-fold difference for one metabolite and a 30-fold difference for another. This said, two people with identical exposures to environmental and dietary unknown/unintentional sources of alcohol may produce very different levels.Lorie Garlick <lorieglanset> wrote: Dan, Remind me, did you make any mention of endogenous alcohol in your letter? I still feel that endogenous alcohol is a significant factor here and, like inhalation,

it is completely beyond one's own control. The studies that the labs base their statement "There is no scientific research to support that the presence of [auto-brewery syndrome] can result in a positive EtG drug screen" is based upon a few studies with very small sample sizes (n=9 or 10). ----- Original Message ----- From: DiBona Ethylglucuronide Sent: Friday, September 15, 2006 7:23 AM Sub!

ject:

RE: Re: Group review and editorial comment requested. It is a 22% false positive for the consumption of alchohol, it is zero false positve for the presence of alcohol. -----Original Message-----From: Ethylglucuronide [mailto:Ethylglucuronide ] On Behalf Of Judy!

Sent: Friday, September 15, 2006 3:02 AMEthylglucuronide Subject: Re: Group review and editorial comment requested. Wow Dainiel, that is *impressive*! You've put this together elegantlyand articulately.I remember reading about the Swedish study early in my internetsearches about the EtG test shortly after I flunked it. I think Iscratched my head and said something like "of nine positives, TWOdidn't consume alcohol? It's been !

severa!

l decades since I

tookstatistics, but isn't that over a 20% false positive rate? That's wayhigher than that of any medical test *I* would choose to rely on tomake a diagnosis". But the overwhelming flood of web-sites claiming100% reliability overwhelmed my common sense.What also needs to be brought up is that there is a huge differencebetween a screening test and a diagnostic test; the companiesagressively marketing the EtG have obviously either forgotten or choseto ignore the distinction.Thanks for writing this.Judy>> > Helliker> > Wall Street Journal> > RE: Your article published August 12th, 2006 entitled, A Test for> Alcohol-And its Flaws><http://online.wsj.com/article/SB115534928148134109-search.html?KEYWORDS\> =alcohol & COLLECTION=wsjie/6month>> > I wish to add some numbers and introductory statistical definitions and> methodology supporting your articles premise [snip]>