liver metabolizing of AAS (info found)

[skinnykenney]

here is something i googled, copied and pasted for everyone to read.
I dod not do the research so don't blame me!

Oral steroids are more difficult for the liver to metabolize
than injectable steroids . Liver cells are damaged as the
liver attempts to break down the oral agents.(3) There are
changes in the structure of the liver with continued use, and the
liver's ability to rid the body of wastes (excretory function) is
decreased.(4) In one type of toxicity, blood-filled pockets
open inside the liver as a result of steroid use . This is known
medically as "peliosis hepatitis," and although rare, is not
restricted to high doses or long-term use of steroids. (2,5,6)

I just found this for you to read.
see the part about orals being more difficult to metabolize than injectable steroids

[Dog-Slime]

[Big]

for info, he's attempting to continue his discussion from here:
how do i know when the test enth and eq have kicked in?
(read the entire thread)

[LATS60]

for info, he's attempting to continue his discussion from here:
how do i know when the test enth and eq have kicked in?
(read the entire thread)

Thanks big, thats the funniest thread i have read for ages, god help us all.
Even skinneykenney, no: especially skinneykenny LOL.

[JiGGaMaN]

What a dumb thing to say. Orals are structured in a way that they cant be metabolized in the first pass, adding stress to the liver. I dont understand.

[skinnykenney]

What a dumb thing to say. Orals are structured in a way that they cant be metabolized in the first pass, adding stress to the liver. I dont understand.

jigga......I did not say this re read the post.
it was copied and pasted from an article on liver metabolization THAT I FOUND ( I DID NOT WRITE THE ARTICLE )

i WAS JUST TRYING TO HELP PEOPLE UNDERSTAND THAT ALL LIVERS DO NOT RESPOND THE EXACT SAME WAY. AND THAT THE AAS WILL HIT PEOPLE AT DIFFERENT TIMES THAN OTHER PEOPLE. REGARLESS OF THE ESTER USED!

i GUESS WITH THE EXPERIENCE OF 2 DOCS AND THE RESEARCH I DID/ THAT THIS IS WAY OVER PEOPLES HEAD OR THEY JUST SIMPLY DO NOT WANT TO BELIEVE THIS. I DON'T UNDERSTAND THAT!

[JiGGaMaN]

jigga......I did not say this re read the post.
it was copied and pasted from an article on liver metabolization THAT I FOUND ( I DID NOT WRITE THE ARTICLE )

i WAS JUST TRYING TO HELP PEOPLE UNDERSTAND THAT ALL LIVERS DO NOT RESPOND THE EXACT SAME WAY. AND THAT THE AAS WILL HIT PEOPLE AT DIFFERENT TIMES THAN OTHER PEOPLE. REGARLESS OF THE ESTER USED!

i GUESS WITH THE EXPERIENCE OF 2 DOCS AND THE RESEARCH I DID/ THAT THIS IS WAY OVER PEOPLES HEAD OR THEY JUST SIMPLY DO NOT WANT TO BELIEVE THIS. I DON'T UNDERSTAND THAT!

I think its what you said regarding to german people metabolizing steroids faster that pissed people off. You are correct, not everyone will metabolize at the same rate. Unfortunately that rate won't be so large that there is a noticeable difference. You may also be interested in the fact that the faster you metabolize something the less of an effect you will get. Think about it: If you dont metabolize a given steroid at all, then its in you forever. Make sense? I think you are trying to claim that people of german descent metabolize it slower then? Either way heres a google search to start you on your bizarre claim: http://www.google.ca/search?hl=en&q=...G=Search&meta=

[skinnykenney]

I think its what you said regarding to german people metabolizing steroids faster that pissed people off. You are correct, not everyone will metabolize at the same rate. Unfortunately that rate won't be so large that there is a noticeable difference. You may also be interested in the fact that the faster you metabolize something the less of an effect you will get. Think about it: If you dont metabolize a given steroid at all, then its in you forever. Make sense? I think you are trying to claim that people of german descent metabolize it slower then? Either way heres a google search to start you on your bizarre claim: http://www.google.ca/search?hl=en&q=...G=Search&meta=

the post about liver metabolizing was COPIED AND PASTED OFF OF AN ARTICLE I FOUND ON GOOGLE!
I NEVER SAID GERMANS I MEANT ACORDING TO THE STUDY, WHITE PEOPLE THAT HAVE THE SLOW METABLIZATION, A RECURING ROLE WAS PERCIEVED.A PRODOMINENT AMOUNT OF THE STUDY PATIENTS WITH THIS HAVE GERMAN IN THEM.
this is well known in the medical field and I have two doctors saying the same thing!
and I know my body well, I have had it all my life.
my liver does not metabilize all aas corectly!

AGAIN I WAS NOT PICKING ON GERMAN PEOPLE!

JUST WHITE PEOPLE THAT HAVE GERMAN IN THIER GENES.LOL! ( JOKE! )

Thanks for the tip on the google link, Bro! But i hav'nt liked to it yet.
I will look at it now.
thanks!

[Big]

What a dumb thing to say. Orals are structured in a way that they cant be metabolized in the first pass, adding stress to the liver. I dont understand.

JiGGa-you know more about this stuff than I do, if you don't mind read skinnykeney's posts in the thread I linked above and respond back here, I would LOVE to hear your opinion on his theory...

[Drake Hotel]

Old news. If someone can dig up info what happens at the cellular level and the dynamics of orals damaging the liver, it'd be interesting for real. What you quoted is just statement of fact.

[JiGGaMaN]

JiGGa-you know more about this stuff than I do, if you don't mind read skinnykeney's posts in the thread I linked above and respond back here, I would LOVE to hear your opinion on his theory...

I did. First, what i was trying to say was the article skinnykenney is showing us has nothing to do with anything in terms of race. Another thing I would like to note is that people of different races do have certain genetic differences. But that being said, you cant say something like specifically people of German decent. It would have to be more generalized, like a region for example western Europe as genetics dont have anything to do with man made divisions in the geography. Also, I have not heard anything about what hes talking about specifically, but ill take a look into it. one last thing, theres nothing that will make steroids specifically be absorbed any more or less quickly than other drugs that are also metabolized hepatically.

[skinnykenney]

I did. First, what i was trying to say was the article skinnykenney is showing us has nothing to do with anything in terms of race. Another thing I would like to note is that people of different races do have certain genetic differences. But that being said, you cant say something like specifically people of German decent. It would have to be more generalized, like a region for example western Europe as genetics dont have anything to do with man made divisions in the geography. Also, I have not heard anything about what hes talking about specifically, but ill take a look into it. one last thing, theres nothing that will make steroids specifically be absorbed any more or less quickly than other drugs that are also metabolized hepatically.

then why does certain drugs ( from my doc ) build up in my system and basically put me in a catatonic state and so much so i checked into the hospital and they took me off of my meds and let the liver catch up.I even wrecked a vehicle from the med build up.
my bloodwork showed a build up of lexapro in my system.
I would have soon over dosed if I did not stop the med imediately.
I was so screwed up I could not even get my own shirt on!
thay said if I keep taking that med I will need a new liver before I am 45-50 years old! I am 36 now.
i looked at the google link. where is the info that I am talking about? i did not see anything that contradicted my docs!

[JiGGaMaN]

then why does certain drugs ( from my doc ) build up in my system and basically put me in a catatonic state and so much so i checked into the hospital and they took me off of my meds and let the liver catch up.I even wrecked a vehicle from the med build up.
my bloodwork showed a build up of lexapro in my system.
I would have soon over dosed if I did not stop the med imediately.
I was so screwed up I could not even get my own shirt on!
thay said if I keep taking that med I will need a new liver before I am 45-50 years old! I am 36 now.
i looked at the google link. where is the info that I am talking about? i did not see anything that contradicted my docs!

ever heard of half-lifes?

[WARMachine]

Oh i remember you...

You were saying somethin like 20% of white people with German genes metabolize test faster than other races?

Suuuuurrreee.....

[MuscleScience]

Oh i remember you...

You were saying somethin like 20% of white people with German genes metabolize test faster than other races?

Suuuuurrreee.....

I am of German decent, And us Germans do not need steroids to get big......hehehehehehe

[skinnykenney]

I am of German decent, And us Germans do not need steroids to get big......hehehehehehe

I know I cant tell the men from the women LOL!

[spywizard]

Regeneration of the Liver

The liver has a remarkable capacity to regenerate after injury and to adjust its size to match its host. Within a week after partial hepatectomy, which, in typical experimental settings entails surgical removal of two-thirds of the liver, hepatic mass is back essentially to what it was prior to surgery. Some additional interesting observations include:

• In the few cases where baboon livers have been transplanted into people, they quickly grow to the size of a human liver.
• When the liver from a large dog is transplanted into a small dog, it loses mass until it reaches the size appropriate for a small dog.
• Hepatocytes or fragments of liver transplanted in extrahepatic locations remain quiescent but begin to proliferate after partial hepatectomy of the host.

These types of observations have prompted considerable research into the mechanisms responsible for hepatic regeneration, because understanding the processes involved will likely assist in treatment of a variety of serious liver diseases and may have important implications for certain types of gene therapy. A majority of this research has been conducted using rats and utilized the model of partial hepatectomy, but a substantial body of confirmatory evidence has accumulated from human subjects.
The Dynamics of Liver Regeneration

Partial hepatectomy leads to proliferation of all populations of cells within the liver, including hepatocytes, biliary epithelial cells and endothelial cells. DNA synthesis is initiated in these cells within 10 to 12 hours after surgery and essentially ceases in about 3 days. Cellular proliferation begins in the periportal region (i.e. around the portal triads) and proceeds toward the centers of lobules. Proliferating hepatocytes initially form clumps, and clumps are soon transformed into classical plates. Similarly, proliferating endothelial cells develop into the type of fenestrated cells typical of those seen in sinusoids.
It appears that hepatocytes have a practically unlimited capacity for proliferation, with full regeneration observed after as many as 12 sequential partial hepatectomies. Clearly the hepatocyte is not a terminally differentiated cell.
Changes in gene expression associated with regeneration are observed within minutes of hepatic resection. An array of transcription factors (NF-kB, STAT3, fos and jun) are rapidly induced and probably participate in orchestrating expression of a group of hepatic mitogens. Proliferating hepatocytes appear to at least partially revert to a fetal phenotype and express markers such as alpha-fetoprotein. Despite what appears to be a massive commitment to proliferation, the regenerating hepatocytes continue to conduct their normal metabolic duties for the host such as support of glucose metabolism.
Stimuli of Hepatic Regeneration

Hepatic regeneration is triggered by the appearance of circulating mitogenic factors. This conclusion was originally supported by experiments demonstrating that quiescent fragments of liver that had been transplanted to extrahepatic sites would begin to proliferate soon after partial hepatectomy, and also that hepatectomy in one of a pair of parabiotic rats led to hepatic proliferation in the other of the pair.
As might be expected, liver regeneration seems to be supported by a group of mitogens and growth factors acting in concert on several cell types. Some of the major and well-studied players that act together in this process include:

• Hepatocyte growth factor (scatter factor) levels rise to high levels soon after partial hepatectomy. This is the only factor tested that acts by itself as a potent mitogen for isolated hepatocytes cultured in vitro. This factor is also of critical importance in development of the liver, as target deletions of its gene lead to fetal death due to hepatic insufficiency.
• TNF-alpha, which stimulates proliferation of hepatic endothelial cells.
• Interleukin-6, which acts as a biliary epithelial mitogen.
• Epidermal growth factor.
• Norepinephrine potentiates the mitogenic activity of EGF and HGF.
• Insulin is required for regeneration but appears to play a permissive rather than mitogenic role.

The processes and signals involved in shutting down the regenerative response are less well studied than those that stimulate it. TGF-beta1, which is known to inhibit proliferative responses in hepatocytes, is one cytokine involved in this process, but undoubtedly several others participate.



http://www.vivo.colostate.edu/hbooks...ver/regen.html

[skinnykenney]

Regeneration of the Liver

The liver has a remarkable capacity to regenerate after injury and to adjust its size to match its host. Within a week after partial hepatectomy, which, in typical experimental settings entails surgical removal of two-thirds of the liver, hepatic mass is back essentially to what it was prior to surgery. Some additional interesting observations include:

• In the few cases where baboon livers have been transplanted into people, they quickly grow to the size of a human liver.
• When the liver from a large dog is transplanted into a small dog, it loses mass until it reaches the size appropriate for a small dog.
• Hepatocytes or fragments of liver transplanted in extrahepatic locations remain quiescent but begin to proliferate after partial hepatectomy of the host.

These types of observations have prompted considerable research into the mechanisms responsible for hepatic regeneration, because understanding the processes involved will likely assist in treatment of a variety of serious liver diseases and may have important implications for certain types of gene therapy. A majority of this research has been conducted using rats and utilized the model of partial hepatectomy, but a substantial body of confirmatory evidence has accumulated from human subjects.
The Dynamics of Liver Regeneration

Partial hepatectomy leads to proliferation of all populations of cells within the liver, including hepatocytes, biliary epithelial cells and endothelial cells. DNA synthesis is initiated in these cells within 10 to 12 hours after surgery and essentially ceases in about 3 days. Cellular proliferation begins in the periportal region (i.e. around the portal triads) and proceeds toward the centers of lobules. Proliferating hepatocytes initially form clumps, and clumps are soon transformed into classical plates. Similarly, proliferating endothelial cells develop into the type of fenestrated cells typical of those seen in sinusoids.
It appears that hepatocytes have a practically unlimited capacity for proliferation, with full regeneration observed after as many as 12 sequential partial hepatectomies. Clearly the hepatocyte is not a terminally differentiated cell.
Changes in gene expression associated with regeneration are observed within minutes of hepatic resection. An array of transcription factors (NF-kB, STAT3, fos and jun) are rapidly induced and probably participate in orchestrating expression of a group of hepatic mitogens. Proliferating hepatocytes appear to at least partially revert to a fetal phenotype and express markers such as alpha-fetoprotein. Despite what appears to be a massive commitment to proliferation, the regenerating hepatocytes continue to conduct their normal metabolic duties for the host such as support of glucose metabolism.
Stimuli of Hepatic Regeneration

Hepatic regeneration is triggered by the appearance of circulating mitogenic factors. This conclusion was originally supported by experiments demonstrating that quiescent fragments of liver that had been transplanted to extrahepatic sites would begin to proliferate soon after partial hepatectomy, and also that hepatectomy in one of a pair of parabiotic rats led to hepatic proliferation in the other of the pair.
As might be expected, liver regeneration seems to be supported by a group of mitogens and growth factors acting in concert on several cell types. Some of the major and well-studied players that act together in this process include:

• Hepatocyte growth factor (scatter factor) levels rise to high levels soon after partial hepatectomy. This is the only factor tested that acts by itself as a potent mitogen for isolated hepatocytes cultured in vitro. This factor is also of critical importance in development of the liver, as target deletions of its gene lead to fetal death due to hepatic insufficiency.
• TNF-alpha, which stimulates proliferation of hepatic endothelial cells.
• Interleukin-6, which acts as a biliary epithelial mitogen.
• Epidermal growth factor.
• Norepinephrine potentiates the mitogenic activity of EGF and HGF.
• Insulin is required for regeneration but appears to play a permissive rather than mitogenic role.

The processes and signals involved in shutting down the regenerative response are less well studied than those that stimulate it. TGF-beta1, which is known to inhibit proliferative responses in hepatocytes, is one cytokine involved in this process, but undoubtedly several others participate.



http://www.vivo.colostate.edu/hbooks...ver/regen.html

good post, but i am not talking about liver regeneration.

[spywizard]

good post, but i am not talking about liver regeneration.

don't care,

point being, the liver is one of the most and easiest to repair of all the organs..

it's more relevant to this board then many of the posts here...

[TranscriptionFactor]

(I have been sick with the flu for the past 3 days, haven't gone to the gym)
Long boring discourse follows:

There do exist genetic polymorphisms, they are particularly important with respect to enzymatic activity as they will affect the speed and ease of metabolism of certain drugs. This is well known in medicine, but it is difficult to generalize about populations and ultimately better to do specific genetic testing on the individual.

We see this in one example that many (not all) people of Asian heritage are lactose intolerant. It becomes problematic to try to use "nationalities" as they are man made boundaries and there CAN be great deal of heterogeneity within a specific nation, even though in reality some "nations" are less diverse than others. Without getting into the statistical anaylsis of each persons genome with the population, one can see that a nation such as South Korea is more homogenous in its population than the United States, or for that matter Germany, who's boundaries have been drawn and redrawn so many times and wars, immigration have infused some greater degree of diversity.

There are certain polymorphisms which are more prevalent (but nothing being absolute) in people of so called "Northern European" heritage. Most of these would be deemed to offer some Darwinian advantage by the fact that they propagate and remain well represented. Some of them seem to offer no advantage and in fact a disadvantage, but to explain their continued survival one has to posit that there was at least at some time and advantage and this has not been outweighed by any disadvantage.

Two examples that come to mind are

1) the cystic fibrosis gene. It is estimated that 1 in 25 people of Northern European descent are carriers for this gene. The possible believed advantage is that it may have offered some defense against the Bubonic Plague. However when 2 carriers mate there is a good chance of their offspring having full blown Cystic Fibrosis, which is an awful disease.

2) Something like 5% of people of NE descent have a higher tendency to form blood clots because of a polymorphism in their Factor V, one of the clotting factors. This is called Factor V Leiden (b/c discovered in Leiden Germany). It is possible this was an advantage when people were trying to violently kill each other with swords and spears and the better clotters survived, and people rarely lived past 40 anyway - however in this relatively safe day and age a blood clot can get you killed and prevent you from living to 80.

I believe what the most august and esteemed Mr. SkinnyKenney is trying to say is that he may have a subset of liver enzymes which behave differently from the "average" population, and that this subset is more commonly found in people with German and/or Irish ancestry. This is plausible.

As an aside, medically speaking there is no such thing as "race". There is only one species of man, and some degree of heterogeneity within the species, which for humans is so so incredibly insignificant when compared to intraspecies variety in other animals.

Whether we are able to tolerate these minor differences and work together with the parts equaling more than the whole is a spiritual question, not one of science.

[skinnykenney]

(I have been sick with the flu for the past 3 days, haven't gone to the gym)
Long boring discourse follows:

There do exist genetic polymorphisms, they are particularly important with respect to enzymatic activity as they will affect the speed and ease of metabolism of certain drugs. This is well known in medicine, but it is difficult to generalize about populations and ultimately better to do specific genetic testing on the individual.

We see this in one example that many (not all) people of Asian heritage are lactose intolerant. It becomes problematic to try to use "nationalities" as they are man made boundaries and there CAN be great deal of heterogeneity within a specific nation, even though in reality some "nations" are less diverse than others. Without getting into the statistical anaylsis of each persons genome with the population, one can see that a nation such as South Korea is more homogenous in its population than the United States, or for that matter Germany, who's boundaries have been drawn and redrawn so many times and wars, immigration have infused some greater degree of diversity.

There are certain polymorphisms which are more prevalent (but nothing being absolute) in people of so called "Northern European" heritage. Most of these would be deemed to offer some Darwinian advantage by the fact that they propagate and remain well represented. Some of them seem to offer no advantage and in fact a disadvantage, but to explain their continued survival one has to posit that there was at least at some time and advantage and this has not been outweighed by any disadvantage.

Two examples that come to mind are

1) the cystic fibrosis gene. It is estimated that 1 in 25 people of Northern European descent are carriers for this gene. The possible believed advantage is that it may have offered some defense against the Bubonic Plague. However when 2 carriers mate there is a good chance of their offspring having full blown Cystic Fibrosis, which is an awful disease.

2) Something like 5% of people of NE descent have a higher tendency to form blood clots because of a polymorphism in their Factor V, one of the clotting factors. This is called Factor V Leiden (b/c discovered in Leiden Germany). It is possible this was an advantage when people were trying to violently kill each other with swords and spears and the better clotters survived, and people rarely lived past 40 anyway - however in this relatively safe day and age a blood clot can get you killed and prevent you from living to 80.

I believe what the most august and esteemed Mr. SkinnyKenney is trying to say is that he may have a subset of liver enzymes which behave differently from the "average" population, and that this subset is more commonly found in people with German and/or Irish ancestry. This is plausible.

As an aside, medically speaking there is no such thing as "race". There is only one species of man, and some degree of heterogeneity within the species, which for humans is so so incredibly insignificant when compared to intraspecies variety in other animals.

Whether we are able to tolerate these minor differences and work together with the parts equaling more than the whole is a spiritual question, not one of science.

Thanks for the info and help!
very good post!
This is what I would have said, if my vocabulary would have allowed it LOL!
again thanks.

JUST TO GO ON RECORD:I WAS NOT PICKING ON ANY SPECIFIC RACE.
JUST POINTING OUT THE FACT THAT NOT ALL PEOPLE WILL RESPOND TO THE SAME COMPOUNDS AS OTHERS EVEN IF SAID PEOPLE ARE BROTHERS!

personal example:
My brothers ( 2 ) do not have this condition just me.
one of my brothers has 3 siblings ( 2 are twins but not identical ) and they are always in the same place they do the same things and live in the same home. One of the twins has a build up of lead in his system and the 2 other kids are fine.