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IMPORTANT Info on KEY hep/liver nutrient: PPC
I found this incredibly informative page on PhosChol (phosphatidyl choline...use the purified PhosChol PC NOT lecithin).
This stuff is backed by medical research...and I can tell it is helping my liver metabolism for a fact. I (my liver that is) am handling fats MUCH better since I've been taking 3-4 of these 900 mg PPC capsules...go to Nutricity.com for the best price.
Here's the link to find out WHY PPC is so gosh darn important:
http://www.woodmed.com/Phos%20Choline.htm
This stuff is backed by medical research...and I can tell it is helping my liver metabolism for a fact. I (my liver that is) am handling fats MUCH better since I've been taking 3-4 of these 900 mg PPC capsules...go to Nutricity.com for the best price.
Here's the link to find out WHY PPC is so gosh darn important:
http://www.woodmed.com/Phos%20Choline.htm
From my Journal, good info!
PPC study as adjunct to SOC
Apr 14, 2008 12:13PM - 0 comments - (Public)
PROLONGED PPC THERAPY GIVEN TO RESPONDERS BEYOND THE CESSATION
OF INTERFERON THERAPY TENDED TO INCREASE THE RATE OF SUSTAINED RESPONDERS AT WEEK
48 IN PATIENTS WITH HEPATITIS C (41% VERSUS 15% IN THE CONTROL GROUP; p = 0.064).
BACKGROUND/AIMS: Polyunsaturated phospatidyl-choline (PPC) has been shown to
reduce serum aminotransferases in experimental hepatitis. This multi-center,
randomized, double-blind, placebo-controlled trial evaluated the effects of PPC
in patients with chronic hepatitis B and C in combination with interferon alpha
2a or 2b. The diagnosis of chronic viral hepatitis was based on an abnormal serum
alanine aminotransferase (ALT) value (more than twice the upper value of normal),
viral replication and chronic hepatitis found on liver biopsy. METHODOLOGY:
Patients received 5 million I.U. (Hepatitis B) and 3 million I.U. (hepatitis C)
interferon s.c. thrice weekly for 24 weeks, respectively, and were randomly
assigned to additional oral medication with either 6 capsules of PPC (total daily
dose: 1.8 g) or 6 capsules of placebo per day for 24 weeks. Biochemical response
to therapy was defined as a reduction of ALT by more than 50% of pre-treatment
values. The responders were treated for further 24 weeks after cessation of
interferon therapy with either PPC or placebo. RESULTS: 176 patients completed
the study protocol (per-protocol population: 92 in the PPC and 84 in the placebo
group). A biochemical response (> 50% ALT reduction) was seen in 71% of patients
who were treated with PPC, but only in 56% of patients who received placebo (p <
0.05). PPC increased the response rate in particular in patients with hepatitis
C: 71% of those patients responded in the PPC group versus 51% in the placebo
group (p < 0.05). PROLONGED PPC THERAPY GIVEN TO RESPONDERS BEYOND THE CESSATION
OF INTERFERON THERAPY TENDED TO INCREASE THE RATE OF SUSTAINED RESPONDERS AT WEEK
48 IN PATIENTS WITH HEPATITIS C (41% VERSUS 15% IN THE CONTROL GROUP; p = 0.064).
In contrast, PPC did not alter the biochemical response to interferon in patients
with hepatitis B. PPC did not accelerate elimination of HBV-DNA, HBeAg and
HCV-RNA.
CONCLUSIONS:
In conclusion,
PPC may be recommended in patients with
chronic hepatitis C in combination with interferon and after termination of
interferon in order to reduce the high relapse rate.
PPC may not be recommended
for patients with chronic hepatitis B. In contrast to IFN and other antiviral
agents PPC does not carry major risks and is tolerated very well.
----------------------------------------------------------
It would be naive to assume that PPC by itself can halt the progression of fibrosis. But it certainly is one very useful component of a multiprong/complex approach in that direction. HR
--------------------------------------------------------
If my child had cirrhosis I would advise him to take 4 of these capsules a day (as part of quite a few other things that I would advise to take/do ( better do/take!) my child in that setting). I would of course advise him to understand that this is just a nutritional supplement possibly beneficial to his general health and that no claim can or should be made that it has any capacity to cure or mitigate his cirrhotic liver disease at this point in time, until, by randomized, properly powered clinical trials whose results have been analyzed and scrutinized by an expert advisory panel a decision is made by the proper authority that such disease specific claims can be attached to such a substance.I would explain to him, that while he is in need of immediate treatment, the strict rules to attach such claims must be followed in a world that is filled with quackery claims by people trying to financially profit from the need of the despaired. HR
-------------------------------------------------------------
-The knowledge regading PPC is mainly from Dr. Charles Liebers work, he has published several animal studies on the antifibrotic effect of this compound. It is also from abstracts at prior liver meetings, posters viewed there and a personal, over an hour discussion wit Dr. Lieber which allowed me to better judge his qualifications, trust his conclusions and get his ovrall " feel" for this compound. The rest is from what publications are available on Pubmed and the overall trend re lack of any toxicity, likelihood of contribution to liver health by concept and role in membrane biology. There are no further large human trials, since none will pay for those, since this is not an item where you can charge $20 per pill as with the antivirals and if you did, patients would obtain it from other sources once you would have spent the money to further prove its usefulness. I fully realize that this is not enough to convince any authorities in Germany or here ("evidence based medicine") to allow it to be officially labeled and indicated as antifibrotic , indeed, its contribution in this regard might be smaller that we think or even worst case, nonexistent. However, weighing all the available evidence, combined with the virtually nonexistent toxicity, the availability and its low cost it seems a valuable component to someone with inflammatory liver and/or fibrosis. Please also note, that the above PPC trial tested its efficac y re SVR% improvement, not antifibrosis, and it seemed well conducted to me. HR
PPC study as adjunct to SOC
Apr 14, 2008 12:13PM - 0 comments - (Public)
PROLONGED PPC THERAPY GIVEN TO RESPONDERS BEYOND THE CESSATION
OF INTERFERON THERAPY TENDED TO INCREASE THE RATE OF SUSTAINED RESPONDERS AT WEEK
48 IN PATIENTS WITH HEPATITIS C (41% VERSUS 15% IN THE CONTROL GROUP; p = 0.064).
BACKGROUND/AIMS: Polyunsaturated phospatidyl-choline (PPC) has been shown to
reduce serum aminotransferases in experimental hepatitis. This multi-center,
randomized, double-blind, placebo-controlled trial evaluated the effects of PPC
in patients with chronic hepatitis B and C in combination with interferon alpha
2a or 2b. The diagnosis of chronic viral hepatitis was based on an abnormal serum
alanine aminotransferase (ALT) value (more than twice the upper value of normal),
viral replication and chronic hepatitis found on liver biopsy. METHODOLOGY:
Patients received 5 million I.U. (Hepatitis B) and 3 million I.U. (hepatitis C)
interferon s.c. thrice weekly for 24 weeks, respectively, and were randomly
assigned to additional oral medication with either 6 capsules of PPC (total daily
dose: 1.8 g) or 6 capsules of placebo per day for 24 weeks. Biochemical response
to therapy was defined as a reduction of ALT by more than 50% of pre-treatment
values. The responders were treated for further 24 weeks after cessation of
interferon therapy with either PPC or placebo. RESULTS: 176 patients completed
the study protocol (per-protocol population: 92 in the PPC and 84 in the placebo
group). A biochemical response (> 50% ALT reduction) was seen in 71% of patients
who were treated with PPC, but only in 56% of patients who received placebo (p <
0.05). PPC increased the response rate in particular in patients with hepatitis
C: 71% of those patients responded in the PPC group versus 51% in the placebo
group (p < 0.05). PROLONGED PPC THERAPY GIVEN TO RESPONDERS BEYOND THE CESSATION
OF INTERFERON THERAPY TENDED TO INCREASE THE RATE OF SUSTAINED RESPONDERS AT WEEK
48 IN PATIENTS WITH HEPATITIS C (41% VERSUS 15% IN THE CONTROL GROUP; p = 0.064).
In contrast, PPC did not alter the biochemical response to interferon in patients
with hepatitis B. PPC did not accelerate elimination of HBV-DNA, HBeAg and
HCV-RNA.
CONCLUSIONS:
In conclusion,
PPC may be recommended in patients with
chronic hepatitis C in combination with interferon and after termination of
interferon in order to reduce the high relapse rate.
PPC may not be recommended
for patients with chronic hepatitis B. In contrast to IFN and other antiviral
agents PPC does not carry major risks and is tolerated very well.
----------------------------------------------------------
It would be naive to assume that PPC by itself can halt the progression of fibrosis. But it certainly is one very useful component of a multiprong/complex approach in that direction. HR
--------------------------------------------------------
If my child had cirrhosis I would advise him to take 4 of these capsules a day (as part of quite a few other things that I would advise to take/do ( better do/take!) my child in that setting). I would of course advise him to understand that this is just a nutritional supplement possibly beneficial to his general health and that no claim can or should be made that it has any capacity to cure or mitigate his cirrhotic liver disease at this point in time, until, by randomized, properly powered clinical trials whose results have been analyzed and scrutinized by an expert advisory panel a decision is made by the proper authority that such disease specific claims can be attached to such a substance.I would explain to him, that while he is in need of immediate treatment, the strict rules to attach such claims must be followed in a world that is filled with quackery claims by people trying to financially profit from the need of the despaired. HR
-------------------------------------------------------------
-The knowledge regading PPC is mainly from Dr. Charles Liebers work, he has published several animal studies on the antifibrotic effect of this compound. It is also from abstracts at prior liver meetings, posters viewed there and a personal, over an hour discussion wit Dr. Lieber which allowed me to better judge his qualifications, trust his conclusions and get his ovrall " feel" for this compound. The rest is from what publications are available on Pubmed and the overall trend re lack of any toxicity, likelihood of contribution to liver health by concept and role in membrane biology. There are no further large human trials, since none will pay for those, since this is not an item where you can charge $20 per pill as with the antivirals and if you did, patients would obtain it from other sources once you would have spent the money to further prove its usefulness. I fully realize that this is not enough to convince any authorities in Germany or here ("evidence based medicine") to allow it to be officially labeled and indicated as antifibrotic , indeed, its contribution in this regard might be smaller that we think or even worst case, nonexistent. However, weighing all the available evidence, combined with the virtually nonexistent toxicity, the availability and its low cost it seems a valuable component to someone with inflammatory liver and/or fibrosis. Please also note, that the above PPC trial tested its efficac y re SVR% improvement, not antifibrosis, and it seemed well conducted to me. HR
the 2003 escaped my eyes. Made me curious and I googled 'Phosphatidylcholine HCV' and found some newer stuff. Obviously some scientists are working on checking it out.
Originally published In Press as doi:10.1074/jbc.M706160200 on November 14, 2007
J. Biol. Chem., Vol. 283, Issue 2, 849-854, January 11, 2008
Long Chain Acyl-CoA Synthetase 3-mediated Phosphatidylcholine Synthesis Is Required for Assembly of Very Low Density Lipoproteins in Human Hepatoma Huh7 Cells*
Hongbing Yao and Jin Ye1
From the Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, Texas 75390
Hepatocytes play a crucial role in regulating lipid metabolism by exporting cholesterol and triglyceride into plasma through secretion of very low density lipoproteins (VLDL). VLDL production is also required for release of hepatitis C virus (HCV) from infected hepatocytes. Here, we show that long chain acyl-CoA synthetase 3 (ACSL3) plays a crucial role in secretion of VLDL and HCV from hepatocytes. In cultured human hepatoma Huh7 cells, ACSL3 is specifically required for incorporation of fatty acids into phosphatidylcholine. In cells receiving small interfering RNA targeting ACSL3, secretion of apolipoprotein B, the major protein component of VLDL, was inhibited and the lipoprotein was rapidly degraded. This inhibition in secretion was completely eliminated when these cells were treated with phosphatidylcholine. Treatment of cells with small interfering RNA targeting ACSL3 also inhibited secretion of HCV from Huh7-derived cells. These results identify ACSL3 as a new enzymatic target to limit VLDL secretion and HCV infection.
Received for publication, July 26, 2007 , and in revised form, November 13, 2007.
* This work was supported by National Institutes of Health Grant HL-20948 and the Perot Family Foundation. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Marcia
Originally published In Press as doi:10.1074/jbc.M706160200 on November 14, 2007
J. Biol. Chem., Vol. 283, Issue 2, 849-854, January 11, 2008
Long Chain Acyl-CoA Synthetase 3-mediated Phosphatidylcholine Synthesis Is Required for Assembly of Very Low Density Lipoproteins in Human Hepatoma Huh7 Cells*
Hongbing Yao and Jin Ye1
From the Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, Texas 75390
Hepatocytes play a crucial role in regulating lipid metabolism by exporting cholesterol and triglyceride into plasma through secretion of very low density lipoproteins (VLDL). VLDL production is also required for release of hepatitis C virus (HCV) from infected hepatocytes. Here, we show that long chain acyl-CoA synthetase 3 (ACSL3) plays a crucial role in secretion of VLDL and HCV from hepatocytes. In cultured human hepatoma Huh7 cells, ACSL3 is specifically required for incorporation of fatty acids into phosphatidylcholine. In cells receiving small interfering RNA targeting ACSL3, secretion of apolipoprotein B, the major protein component of VLDL, was inhibited and the lipoprotein was rapidly degraded. This inhibition in secretion was completely eliminated when these cells were treated with phosphatidylcholine. Treatment of cells with small interfering RNA targeting ACSL3 also inhibited secretion of HCV from Huh7-derived cells. These results identify ACSL3 as a new enzymatic target to limit VLDL secretion and HCV infection.
Received for publication, July 26, 2007 , and in revised form, November 13, 2007.
* This work was supported by National Institutes of Health Grant HL-20948 and the Perot Family Foundation. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Marcia
Welcome to the forum.
Are you currently on treatment fo hep c?
The study looks interesting. I wonder if anyone else has any experience in or heard of taking this supplement while on tx.
Anyway, you should always discuss with your treating Physician, which supplements to take during tx.
Marcia
Are you currently on treatment fo hep c?
The study looks interesting. I wonder if anyone else has any experience in or heard of taking this supplement while on tx.
Anyway, you should always discuss with your treating Physician, which supplements to take during tx.
Marcia
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