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formation of fibrosis/cirrhosis due to cholesterol/fat

http://archive.mail-list.com/hbv_research/message/20110405.145457.f0c1d708.en.html

please check if red yeast rice and cholesterol lowering drugs or liposomal glutathione inactivate LXR receptors
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Avatar universal
Liposomes used to enclose drug, by itself I don't think it has any use.
http://liposomalglutathione.com/wp/
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Avatar universal
lipo gsh
Prevention of excess collagen formation and cross-linking (wrinkles and scarring)

http://lyposphericvitamin-c.com/lypo-spheric-gsh/116/

this is the only thing i have found
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Avatar universal
Ok. Liposomal glutathione(GXL) greatly increases absorption, no need to use IV. I think Liposomes have no effects on cholesterol. GXL is heavily marketed, like all the other health products.

STRUCTURE

Liposome
A liposome is an extremely small (1/2 the width of a human hair) bubble, which is also called a vesicle. Liposomes have a fat-soluble exterior and an interior that is watery. This watery interior can combine with water soluble materials such as glutathione. Our liposomes are multi-layered, as you can see in the diagram to the right.

Liposomes are made from the same type of material as our cell membranes, phospholipids.  The phospholipids in our liposomes are derived from lecithin, which comes from oil extracted from soy, not soy protein.

The unique structure of liposomes allows them to encapsulate biologically active ingredients. In this case the liposomes keep glutathione in its “reduced”, or biologically active state.  The liposomes in our product are very stable, which allows use in an oral drink.
HOW THEY WORK

Because they are made of the same type of material as our cell membranes, liposomes penetrate mucosal tissues allowing for rapid release into the blood stream.  Nutrients that are not in liposomes have to pass through the stomach to reach the liver where they are metabolized and released into the bloodstream.  Some nutrients are destroyed or compromised by stomach acids.  Liposomes avoid the digestive system by penetrating the mucosal tissue.

A scientific article published in 1965 in the Journal of Molecular Biology (Bangham, A.D.et al) described these vesicles for the first time and explained their similarity to human membranes. Since that time liposomes have been the subject of great interest and study. Because of their adaptability, liposomes have a wide range of applications – from delivering anti-cancer drugs to providing gene therapy and skin care. To date, more than 35,000 articles have been published in scientific journals regarding liposomes.
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Avatar universal

check arteroscelorosis studies and cholesterol about liposomal glutathione.no meaning for liver or detoxifier just check effect of liposomal gsh on cholesterol, we dont know clear if it is liposoms or gsh to make the trick on cholesterol and arterosclerosis regression

glutathione if not IV was useless, no absorption, so all those studies if not IV or liposomal were trash
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Avatar universal
I am a bit lost: what is the connection between liposomal gluthatione and Liver X Receptors and fibrosis?

A lot of people sell gluthatione (MAX-GXL). A person on the hblist approached me to be his GXL sub-seller in Australia. It claims to be:
A GREAT DETOXIFIER

Your liver harbors the most concentrated source of glutathione because it is the organ of detoxification. Your body uses glutathione to protect you from pollution, radiation, drugs, carcinogenic chemicals and heavy metals. Modern living even exposes us to toxins in our water and food. Dealing with this onslaught is especially difficult for people with certain neurological conditions such as autism, because they have difficulty ridding their bodies of toxins.

THE MOST IMPORTANT ANTIOXIDANT

Oxidative stress in the outside world is the chemistry that causes things to rust. Inside your body, oxidative stress causes damage to the proteins that keep the cells and their membranes running. Glutathione protects your cells against free radicals that cause oxidative stress.

Free radicals, formed when oxygen interacts with molecules, must be neutralized or they will cause cells to “rust”, meaning they will die or perform poorly. Studies have shown that oxidative stress increases with aging, and over time, free radicals can lead to degenerative diseases: heart disease, memory problems, cancer, diabetes, arthritis.

Glutathione is considered the most important antioxidant because it is the only antioxidant capable of working with enzymes. One enzyme, glutathione peroxidase, works with glutathione to prevent membranes from being “rusted” or oxidized. Glutathione also helps activate the better-known antioxidants, vitamin C and vitamin E.
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Avatar universal
Yes, I remember reading your post a few months back on vit c.

Thank you for clearing it up.
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Avatar universal

taking normal gsh or normal coq10 is useless because they doont get to blood

also vit C as a cure is useless if not liposoaml, by only 2 bags of liposomal vit c of 2g you reach 20g and vit C is reported to start being really effective at >20g
by the way it is also reported to lower chol to healthy levels but only liposomal high dose or IV high dose
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Avatar universal
It is said that most of liposomal gluthatione is destroyed in the digestive processes

the normal GSH gets destroied, not the glutathione it all gets thru by liposoms


for example 1g of liposomal vit c gets the same level of 10g of normal vit C, liposomoes gets thru cellular barrier and gets inside the cells, infact i said combo of red yeast rice and liposomal gsh because the first can lower only serum chol since it can t get inside the cells and liposomal gsh because it lowers chol from inside the cells

red yeast rice is super checked it is nothing new while the effects of liposomals are new
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Avatar universal
And of course, I must apologize for interrupting your thread and also because your question was addressed to StephenCastlecrag.
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Avatar universal
This sounds very promising, doesn't it? I think that it is definitely better to try using this, instead of experimenting with some other ingredients which sound rather suspicious (although I must admit that I do believe in some herbs since I've had the benefits from them).

There are many many people who would try anything regarding their health. I was reading this site's old posts and came to that conclusion: for example, there were many fakers posting "cures" for HBV, and each time, there were many responses saying that they would try the same thing.

My point is, I've read the numeral benefits of liposomal gluthatione and don't see a reason why not to try it. But know I have a question:

It is said that most of liposomal gluthatione is destroyed in the digestive processes (if taken orally), and that the best way to administer it is intravenously or as patches. Only recently have they developed it not to be destroyed in the process of digestion, but how would someone be completely sure about the newly "enhanced liposomal gluthatione"?  

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Avatar universal

at this point my question would be:

is it ok for all hbvers to use liposomal glutathione (no dose since no toxicity at any dose, very high doses have antiviral effects) and low dose red yaest rice (monacolins 5mg day) to lower  cholesterol without sides effect and preserve liver from damage and weaken virus?
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Avatar universal
http://www.pnas.org/content/99/18/11896.full

this also explains some of liver X receptors and macrophages but linked to atherosclerosis
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Avatar universal
http://www.jimmunol.org/content/early/2011/03/11/jimmunol.1000585.abstract

Liver X Receptors Inhibit Macrophage Proliferation

so it all looks pointed to immune system inhibition blocking macrophage and virus replication and liver damage henancment, i guess at this point we have so many suggestions for hbvers to lower cholesterol production
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Avatar universal
Author: ******
Date: 2011-04-05 16:54 +200
To: hbv_research
Subject: FYI...Cholesterol Regulator Plays Key Role in Development of Liver Scarring, Cirrhosis



Cholesterol Regulator Plays Key Role in Development of Liver Scarring, Cirrhosis

ScienceDaily (Apr. 4, 2011) — UCLA researchers have demonstrated that a key regulator of cholesterol and fat metabolism in the liver also plays an important role in the development of liver fibrosis -- the build-up of collagen scar tissue that can develop into cirrhosis. Cirrhosis, in turn, is a major cause of premature death and is incurable without a liver transplant.

Published in the March issue of the journal Gastroenterology, the study shows that liver X receptors (LXRs), master regulators of cholesterol, fat and inflammatory gene expression, also control the fibrosis-making cells of the liver, known as hepatic stellate cells.

In the face of chronic liver injury -- due to excess fat, chronic viral hepatitis or alcohol abuse, for example -- stellate cells become activated and launch an inflammatory and fibrotic cascade that eventually results in the build-up of collagen scar tissue in the liver.

LXRs, when stimulated, "turn on" several hundred genes that hold instructions to create proteins for carrying out bodily processes in cells, from transporting and excreting cholesterol to synthesizing fat in the liver. They have also been shown to suppress inflammatory processes in several contexts.

"Our work sets the stage for looking at new ways to modulate cholesterol and/or fat metabolism in order to have therapeutic potential for the treatment of fibrosing liver diseases," said lead author Dr. Simon Beaven, an assistant professor of digestive diseases at the David Geffen School of Medicine at UCLA.

The research was done in the laboratory of senior author Dr. Peter Tontonoz, a professor of pathology and laboratory medicine at the Geffen School of Medicine and a Howard Hughes Medical Institute investigator.

Beaven noted that the recent rise in obesity has resulted in a surge in the prevalence of a condition known as fatty liver, which can be a precursor to fibrosis and chronic liver disease. Simple fatty liver, also known as non-alcoholic fatty liver disease, or NAFLD, is one of the most common reasons patients consult a liver doctor in the United States. Cirrhosis due to fatty liver is skyrocketing and within a decade may become the most common indication for liver transplantation.

Beaven said the need to find better treatments for liver disease is crucial.

"A 'holy grail' for liver researchers is to develop anti-fibrotic treatments that target activated stellate cells in order to slow or prevent the development of cirrhosis," Beaven said. "Our study offers the first detailed look at how LXRs specifically impact the activation of hepatic stellate cells and the subsequent development of liver fibrosis in animal models."

UCLA researchers have found that LXRs normally play a role in helping to reduce the collagen-producing actions of stellate cells when the cells are "activated" by liver damage. For the study, UCLA scientists first tested how activated stellate cells taken from mice would react when a chemical that induces LXR activity was added to the cell culture.

In stellate cells from normal mice, LXRs suppressed the inflammatory and fibrosis-promoting program. But in those taken from mice genetically lacking LXRs, that same program of genes significantly increased because the inhibitory effect of LXRs was no longer present.

"We showed that LXRs dampen stellate cell activation by repressing inflammatory and collagen-producing genes," Beaven said.

To further gauge the strength of the response, scientists took the medium from the cultures of LXR-deficient cells and added it to stellate cells from normal mice. These cells then showed a markedly exaggerated inflammatory and collagen-producing response, suggesting that LXR-deficient stellate cells are secreting signals to promote fibrosis.

The researchers noted that these experiments demonstrate that LXRs control a fibrotic response in stellate cells that can have a wide influence on neighboring cells.

The scientists also found that after replicating chronic liver injury, mice without LXRs had dramatically more liver fibrosis than normal mice.

"The genetic loss of LXRs rendered the mice susceptible to developing fibrotic liver disease," Beaven said.

But LXRs are also known to have important functions in the immune system. The researchers then wanted to know whether the effects they were seeing in animals were due to changes in stellate cell activity specifically or whether immune cells -- derived from bone marrow -- accounted for most of the effect. After extensive testing, the researchers found no differences

in the level of liver fibrosis among normal mice and animals lacking LXRs, suggesting that the contribution from the immune system was negligible.

"This finding, along with the cell culture studies, suggests that LXRs' influence on fibrosis most likely resides in altering stellate cell function in the liver," Beaven said. "This is a critical finding and opens an entire new field of study for stellate cell biologists."

Additional studies will further identify which genes in stellate cells are activated by LXRs and help researchers better understand the role of cholesterol metabolism in the fibrotic response.

This study was funded primarily by grants from the National Institutes of Health and the Howard Hughes Medical Institute. Collaborators from the University of Southern California were funded by core grants from the NIH and the Southern California Research Center for ALPD and Cirrhosis.

Other study authors included senior investigator Dr. Peter Tontonoz of the Howard Hughes Medical Institute; Kevin Wroblewski and Cynthia Hong from Tontonoz's lab; Jiaohong Wang and Hide Tsukamoto of the Southern California Research Center for ALPD and Cirrhosis, USC's Keck School of Medicine and the Department of Veterans Affairs Greater Los Angeles Healthcare System; and Steven Bensinger of the department of pathology at the David Geffen School of Medicine at UCLA.
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