Doctor Jason Simmons-New York Colon Review Board Founder The amount of dangerous colon cleansing products out on the market today is FRIGHTENING!

I'm Dr. Jason Simmons. My foundation and I have spent the last 8 months testing and researching 62 different colon cleansing products. Through extensive clinical research, using over 4300 clinical trial participants, we have found only 2 colon cleansing products that have exceeded our highest standards and are worthy of our seal of approval.

Review looked at six decades of studies on cancer, physical activity

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Title: Norovirus Outbreak Traced to Reusable Grocery Bag
Category: Health News
Created: 5/9/2012 10:05:00 AM
Last Editorial Review: 5/9/2012 12:00:00 AM

Rid your body of weight and toxins. Not all colon cleansers are safe and effective.
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Review looked at six decades of studies on cancer, physical activity

Rid your body of weight and toxins. Not all colon cleansers are safe and effective.
Read our recommendations BEFORE you buy!

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Title: ursodiol, Actigall, Urso Forte, Urso 250
Category: Medications
Created: 10/20/2001 11:31:00 PM
Last Editorial Review: 5/4/2012 12:00:00 AM

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Title: ursodiol, Actigall, Urso Forte, Urso 250
Category: Medications
Created: 10/20/2001 11:31:00 PM
Last Editorial Review: 5/4/2012 12:00:00 AM

Rid your body of weight and toxins. Not all colon cleansers are safe and effective.
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Rid your body of weight and toxins. Not all colon cleansers are safe and effective.
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Viral Hepatitis at a Crossroad

Every May, Gastroenterology publishes a supplementary issue, the “13th Issue”, that is devoted to a specific topic or theme. When the 2012 theme was discussed by the new Board of Editors (each member of which desperately tried to avoid having his or her favorite topic be chosen, as this would undoubtedly mean a considerable amount of additional work), the topic of viral hepatitis emerged unanimously. It must be acknowledged that no other field in Hepatology and Gastroenterology has grown more rapidly than viral hepatitis during the past 15 years, thanks to the considerable interest of the scientific community for diseases that involve over 500 million patients worldwide, active support for research from governments in the United States, Europe, Japan, and Australia, among other regions, and major drug industry investment for what promises to be an incredibly rewarding market for antiviral drugs. Viral hepatitis care and research are now at a crossroad. After many years of investigation aimed at understanding the life cycle of hepatitis viruses, the immunology of acute and chronic infection and the pathophysiology of related liver and extra-hepatic disorders, the field is poised with powerful therapeutic and preventive strategies that will efficiently control these infections. With entecavir and tenofovir now approved in most areas of the world, hepatitis B virus (HBV) replication can be controlled in the long-term in the vast majority of chronically infected patients. In addition, the universal HBV vaccination of newborns in high endemic areas has proven to reduce not only HBV infection but also HBV-related hepatocellular carcinoma (HCC). After some false starts, the search for antiviral drugs targeting hepatitis C virus (HCV) is now moving at an incredible pace with more than 100 compounds currently at the preclinical, or early-to-late clinical developmental stages. After 10 years of stagnation with pegylated interferon alfa and ribavirin therapy, 2 specific inhibitors of the HCV NS3/4A protease, telaprevir and boceprevir, were approved in 2011 in the United States and Europe for the treatment of patients infected with HCV genotype 1. Many other compounds are likely to be approved within the next 5 years. Most importantly, the hope that very high rates of viral eradication will be achieved soon with all-oral, interferon-free regimens is no longer a fantasy. Reasonably, one can now foresee that most chronic HCV infections will be cured, at least in countries that will be able to afford the high price of the new drug combinations.

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Most cases of hepatocellular carcinoma (HCC) are associated with cirrhosis related to chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection. Changes in the time trends of HCC and most variations in its age-, sex-, and race-specific rates among different regions are likely to be related to differences in hepatitis viruses that are most prevalent in a population, the timing of their spread, and the ages of the individuals the viruses infect. Environmental, host genetic, and viral factors can affect the risk of HCC in individuals with HBV or HCV infection. This review summarizes the risk factors for HCC among HBV- or HCV-infected individuals, based on findings from epidemiologic studies and meta-analyses, as well as determinants of patient outcome and the HCC disease burden, globally and in the United States.

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No one would argue with the notion that chronic infection with hepatitis C virus (HCV) causes hepatocellular carcinoma (HCC). Early observations of the association between post-transfusion non-A, non-B hepatitis and HCC in Japan from the 1980s have, unfortunately, proved to be all too true, and in many industrialized countries (including the United States and Japan), HCV infection is now the leading risk factor for HCC. The age-adjusted incidence rate of HCC has tripled in the United States over the past 30 years, reflecting the spread of HCV among Americans decades earlier. Most cases occur in patients with well-established cirrhosis, by itself a very strong risk factor for liver cancer. However, this is not always the case. Eight percent of patients developing HCC in the prospective Hepatitis C Antiviral Long-term Treatment against Cirrhosis (HALT-C) study lacked any evidence of cirrhosis, although all had an Ishak fibrosis score of at least 3 when enrolled in the study. Adjusting for other risk factors, such as alcohol intake, active HCV infection increases the risk of HCC about 18-fold. Thus, the question is not whether HCV infection causes liver cancer, but rather how it does this. Is HCV directly carcinogenic? Or does infection simply set in motion a brisk inflammatory and profibrotic response that causes cancer?

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Hepatitis C virus (HCV) causes liver-related death in more than 300,000 people annually. Treatments for patients with chronic HCV are suboptimal, despite the introduction of directly acting antiviral agents. There is no vaccine that prevents HCV infection. Relevant animal models are important for HCV research and development of drugs and vaccines. Chimpanzees are the best model for studies of HCV infection and related innate and adaptive host immune responses. They can be used in immunogenicity and efficacy studies of HCV vaccines. The only small animal models of robust HCV infection are T- and B- cell deficient mice with human chimeric livers. Although these mice cannot be used in studies of adaptive immunity, they have provided new insights into HCV neutralization, interactions between virus and receptors, innate host responses, and therapeutic approaches. Recent progress in developing genetically humanized mice is exciting, but these models only permit studies of specific steps in the HCV life cycle and have limited or no viral replication.

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