« March 2006 | Main | June 2006 »
April 18, 2006
Milk Thistle Extract and Its Effect on Liver Fibrosis
A commonly prescribed medicinal plant, milk thistle's protective properties to the liver have been supported by literally hundreds of research studies around the world. A recent article discusses one such study involving the milk thistle extract, Silybin Phytosome®, and its ability to prevent hardening of the liver, a sign of advancing liver disease.
Silybin Phytosome® to Prevent Fibrosis
April 10, 2006
Liversupport.com
Nicole Cutler, L.Ac.
Regardless of its cause, the progression of liver disease is typically measured by the suppleness, and in turn, the functionality of the liver. Recent studies demonstrate the ability of the milk thistle extract, Silybin Phytosome®, to inhibit the hardening of liver tissue.
Some types of liver disease respond well to prescribed therapy, while others take on a chronic status. In addition to addressing the underlying cause of dysfunction, these chronic liver diseases require vigilance to support liver tissue health. While each disease has a preferred conventional treatment standard, an increasing number of clinicians are predominantly concerned with fibrosis prevention.
According to the Merck Manual, Fibrosis is an accumulation of fibrous tissue in the liver resulting from an imbalance between production and degradation of the extracellular matrix, and accentuated by the collapse and condensation of preexisting fibers. In more general terms, fibrosis is the hardening of liver tissue, occurring when the liver is impaired and thus, unable to break down fibrous material.
The liver is touted as the most dynamic organ in the body. This title is not only a result of the numerous functions for which it is responsible, but also for its self-restorative capability. The liver is the only organ capable of regenerating parts of itself to repair any sustained damage.
Helping maintain the liver’s texture is akin to supporting this organ’s health. To prevent or inhibit fibrosis, all individuals with liver disease would benefit from an accelerated regeneration of damaged liver tissue.
In Europe, silymarin, the purified extract of the fruits of S. marianum, and its main constituent, silybin, are used to maintain liver health. Worldwide, milk thistle is, deservedly, one of the most commonly prescribed medicinal plants.
S. marianum is a medicinal plant which has been widely used in traditional European medicine for centuries. Commonly known as milk thistle, St. Mary’s thistle and lady’s thistle, it is native to southern Europe, southern Russia, Asia Minor and North Africa. It has been naturalized to North and South America.
Literally hundreds of research studies, mostly conducted in Europe, have confirmed the remarkable ability of milk thistle to protect the liver against virtually all types of damage: from accidental exposure to chemical pollutants, toxic side effects of medications and even the self-inflicted damage from overindulgence of rich food and alcohol.
The United States National Library of Medicine has catalogued more than 300 scientific studies of milk thistle and its active compounds in their medicine database.
The active ingredients of milk thistle are not very bioavailable, especially in their purified or standardized forms. This means one would need to ingest large amounts to experience beneficial effects. Not only impractical, it could be quite expensive.
A recent study published in Digestive and Liver Disease, clearly demonstrates the ability of Silybin Phytosome® to inhibit liver fibrosis. This study confirmed Silybin Phytosome’s® hepatoprotective abilities by proving it counteracts the progression of liver fibrosis typically seen in chronic liver diseases.
On a molecular level, fibrosis is marked by excessive accumulation of extracellular matrix with collagen. The hepatic stellate cells activate this cumulus. In the referenced study, Silybin Phytosome® reduced hepatic stellate cell activation and proliferation. It also significantly reduced the synthesis and deposition of collagen in liver tissue. The authors of this study concluded that Silybin Phytosome® could inhibit liver fibrosis by reducing the synthesis of collagen and by interfering with excessive accumulation of extracellular material.
Additional evidence of silybin’s value in preventing fibrosis is garnered from a 1984 study demonstrating that silybin accelerates the rate of protein synthesis in the liver, leading to faster cell regeneration. A 1997 German study also reported results where silybin reduced the proliferation of hepatic stellate cells by 50 to 75 percent, which again, is highly indicative of its anti-fibrotic effect.
By their very nature, chronic liver diseases are persistent and stubborn to known modern treatments. Chronic liver disease summons our attention to provide every bit of hepatic support possible, until our medical expertise can catch up with us and ameliorate the offending disease. Years of research point to the ability of Silybin Phytosome® to meet this demand, by preventing the damage that liver diseases typically cause.
For more information on supplements containing Silybin Phytosome®, visit LiverSupport.com.
Posted by Editors at 03:33 PM --- Printer-friendly version | Comments (0)
A New Study on HIV/HCV Co-Infection and Race
A new study on HIV and HCV co-infection confirms a significantly greater mortality rate for individuals infected with both viruses than those infected with only one. Researchers also reported that for yet unexplained reasons, white people are twice as likely to die from co-infection than black people.
Whites fare poorly with HIV and hepatitis C
Will Boggs, MD
Reuters
April 18, 2006
NEW YORK (Reuters Health) - Liver disease and death rates are worse with hepatitis C virus (HCV) infection on top of HIV infection than with just HIV or HCV, especially among white patients, according to a new report.
"We need to better understand why the co-infected patients do so poorly and the underlying mechanism for apparent racial disparity in their outcome," Dr. Kyong-Mi Chang, told Reuters Health.
"We also need better drugs that directly target HCV," added Chang, from the University of Pennsylvania and Philadelphia Veterans Affairs Medical Center.
Chang's team examined the impact of dual infection and race in 265 veterans with HCV/HIV co-infection, 251 infected with HCV only, and 227 others with HIV only.
Over a three-year period, mortality was significantly greater among HCV/HIV-co-infected patients than among patients mono-infected with either HCV or HIV, the researchers report in the American Journal of Gastroenterology.
Specifically, after taking into account a variety of factors, mono-infected patients were only about one-third as likely to die as dual-infected patients.
During the study period, twice as many white patients died compared to black patients, the report indicates.
Also, the average age at death in white patients (46 years) was significantly younger than that in black patients (52 years).
Since dual-infected patients fare so poorly, Chang said, the team aims to treat them "as much as possible and monitor them closely for liver dysfunction." He said specialists in liver disease and infectious diseases "as well as pharmacists (also social work and mental health support), is needed to optimize therapy for these complex patients."
SOURCE: American Journal of Gastroenterology, April 2006.
Posted by Editors at 03:27 PM --- Printer-friendly version | Comments (0)
April 14, 2006
Replication Discovery Provides New Treatment Approach
The recent discovery that the Hepatitis C virus needs a small part of RNA found only in the liver to replicate itself has sparked new treatment approaches. If researchers can determine whether lowering the amount of this RNA decreases viral load without adversely affecting the liver we may see a promising breakthrough.
April 5, 2006
Stanford Office of Communication and Public Affairs
STANFORD, Calif. — Last year Peter Sarnow, PhD, professor of microbiology and immunology at the Stanford University School of Medicine, identified a previously unknown mechanism that the hepatitis C virus uses to replicate, yielding a promising new approach to combating the disease-causing virus. On April 5 at the Experimental Biology meeting in San Francisco, Sarnow will discuss recent developments in this work—including his partnership with two pharmaceutical companies that seeks to use the new understanding of the virus to develop treatments.
According to the World Health Organization, hepatitis C virus infects 170 million people worldwide. About 70 percent of those infected develop liver disease, including cirrhosis and liver cancer. In the United States, it is the most common blood-borne viral infection, killing more than 10,000 people each year. Currently available treatments are expensive and do not work in about half of the cases.
“Normally with an RNA virus like hepatitis C, resistance to antivirals very quickly emerges, so the drug is not effective any more,” said Sarnow, who has been studying the virus for years, sorting out how the viral RNA amplifies in cultured liver cells.
In the normal sequence of events, genetic information is stored in DNA and then is copied into RNA, which serves as a template to create proteins. With RNA viruses such as hepatitis C, the genetic information is stored in RNA instead of DNA.
RNA is genetically more unstable than DNA, resulting in the accumulation of many mutations. These mutations allow the virus to outwit the immune system and develop resistance to antiviral medication.
Sarnow’s group has shown that a small fragment of RNA found in the liver, known as a microRNA, is necessary for hepatitis C to grow and reproduce. Their work, published in September 2005 in the journal Science, is the first to link the presence of a specific microRNA with a major infectious disease.
When the researchers inactivated the microRNA, called miR-122, the amount of hepatitis C virus RNA was reduced by approximately 80 percent. “The cool thing is that here, an antiviral is encoded by a host function and not by the virus — so it cannot change,” said Sarnow. In other words, because the virus needs miR-122 to replicate, there is no way the virus could develop resistance to a strategy that inactivates miR-122.
A couple of years ago, Sarnow learned that other scientists had discovered miR-122, found only in the liver. He knew that there could be up to 65,000 copies of miR-122 per cell in the liver. “And we know that the virus can persist in the liver for as long as 30 years, so we made the hypothesis that the virus might interact with miR-122 in some way,” he said. “It turns out that yes, the virus grabs it for its own good.”
“This is a completely different way for microRNA to interact with its target from what is known and it brings up the idea that other microRNAs might work like that,” said Catherine Jopling, PhD, a postdoctoral researcher in Sarnow’s laboratory who spearheaded the work. “But nobody’s been looking for that.”
The researchers think that their findings may have therapeutic potential for a new antiviral target that does not attack the virus directly.
“If you can lower the amount of the microRNA in the liver without affecting liver function maybe this will help lower the viral load,” said Sarnow. Stanford has entered into a licensing agreement with Alnylam Pharmaceuticals and Isis Pharmaceuticals to explore the possibility of using miR-122 as a novel therapeutic against hepatitis C.
The big question is what does this microRNA normally does in the liver. It is possible that lowering microRNA levels in the liver might produce an undesirable outcome, such as cancer, said Sarnow. However, recent promising reports from researchers at Rockefeller University, Alnylam and Isis have demonstrated that miR-122 can be inactivated in mouse liver for some time without impairing liver function.
The Experimental Biology meeting is an annual gathering of groups covering a range of scientific disciplines, including anatomy, biochemistry, molecular biology, pharmacology and pathology. This year 12,000 scientists are expected to attend the event at the Moscone Center in San Francisco.
Posted by Editors at 12:26 PM --- Printer-friendly version | Comments (0)