MCP Helps Cardiovascular Disease, Fibrosis & Inflammatory Conditions

Posted on May 20, 2011 | 5 comments

MCP Helps Cardiovascular Disease, Fibrosis & Inflammatory Conditions

In a new important research study out of the UK, scientists found that Modified Citrus Pectin (MCP) of the correct molecular weight interrupts deadly kidney fibrosis by binding to and blocking Galectin-3 molecules. By disabling the Galectin-3 molecules, MCP decreased the effects of inflammation and fibrosis in a kidney injury model.

New Uses for MCP

Modified Citrus Pectin is a form of pectin that has been altered so that it can be more easily absorbed by the digestive tract. Pectin is found in most plants and is particularly plentiful in the peels of apples, citrus fruits and plums. The latest research study demonstrates an exciting new use for Modified Citrus Pectin. It is now understood that unhealthy levels of Galectin-3 molecules in the body can be involved in the progression of numerous serious diseases, beyond what we already knew about cancer progression.

Fibrosis is responsible for many chronic and deadly disease states because of the overproduction of excessive scar tissue within various organs and systems. Conditions such as cardiovascular & heart disease, pulmonary fibrosis (lung disease), cirrhosis of the liver, kidney disease and many other serious health problems involve inflammation and fibrosis.

By binding to the Galectin-3 molecules, Modified Citrus Pectin prevents Galectin-3 from fostering harmful inflammation, excessive scar tissue build up and abnormal cellular growth. This new discovery shows MCP has enormous potential for prevention and treatment of inflammation and fibrosis related conditions for which there are currently limited or no treatments available. As a pioneer in the field of Modified Citrus Pectin research, I want to emphasize that this new research is truly exciting because Modified Citrus Pectin is turning out to be much, much more versatile than anyone imagined.

In this new pre-clinical study, scientists at the Nephro-Urology Dept. of UCL Institute of Child Health in London, UK, researched the effects of my unique form of Modified Citrus Pectin (MCP) in induced kidney fibrosis disease. The findings demonstrate the potential of using Modified Citrus Pectin as a new compound for acute kidney injury and its potential role in protection from other inflammatory and fibrosis related conditions.

Because this citrus pectin is modified to a specific low molecular weight range and structure, it can easily be absorbed into the circulation and reach specific organs and tissues affected by this dangerous inflammation and fibrosis process. Now that we understand more about the role of Galectin-3 in inflammation and fibrosis, we can use Modified Citrus Pectin to target various conditions involved in abnormal cellular growth and fibrosis, as well as apply it for preventative purposes.

New FDA-Approved Blood Test for Galectin-3

A new blood test which measures circulating levels of Galectin-3 has been approved by the FDA and most health insurance as a useful tool in helping to determine cardiovascular disease risk and prognosis, as well as risks of cancer metastasis. The development and use of this simple blood test by conventional medicine means that Galectin-3 is now on its way to being widely accepted and used as a therapeutic target in conditions from congestive heart failure to metastatic cancer and more. Modified Citrus Pectin remains the leading natural Galectin-3 inhibitor, able to get into the blood stream and bind to Galectin-3 throughout the body.

As more research continues on the role of Galectin-3 in a wide range of diseases, the extreme usefulness of Modified Citrus Pectin will continue to grow as well, offering new hope to patients seeking safe and effective therapies for fighting disease and restoring health naturally. For more information about the research study, click here.

Source: Kolatsi-Joannou M, Price KL, Winyard PJ, Long DA. Modified Citrus Pectin Reduces Galectin-3 Expression and Disease Severity in Experimental Acute Kidney Injury. PLoS ONE 2011 April 6(4): e18683. doi:10.1371/journal.pone.0018683

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