A Clear Path to Address Cardiovascular Disease—with Modified Citrus Pectin

A Clear Path to Address Cardiovascular Disease—with Modified Citrus Pectin

An anti-inflammatory diet… Moderate physical activity…Mind-body exercises…

Not long ago, these heart-healthy strategies were considered alternative approaches that might reduce your risks of cardiovascular disease.

But today, thanks to an outpouring of research, these strategies are standard recommendations for preventing and managing heart disease—given to patients by board-certified physicians and specialists.

That’s because these lifestyle approaches are shown to manage some of the primary risks of cardiovascular disease (CVD) and heart failure, such as high blood pressure and chronic inflammation. Other advancements, such as minimally-invasive surgical interventions, have led to minor improvements in overall CVD statistics.

But even these developments aren’t enough. Cardiovascular disease is still the number one cause of death worldwide, and accounts for one out of every three deaths in the US each year. (1)

The truth is, available treatments for heart failure are still largely disappointing. We need more sophisticated tools to detect and manage CVD and prevent deaths. We need targeted, researched interventions that are proven safe, effective, and easy to use.

A fast-growing body of independent research suggests that Modified Citrus Pectin (MCP) can help to fulfill this growing demand. Third-party data continues to show how this researched form of MCP offers targeted benefits for safe and effective cardiovascular disease prevention and management.

Today, 25+ independent studies show how this form of MCP halts and reverses deadly inflammation and fibrosis in the cardiovascular system, promotes flexible blood vessels, and protects the heart. MCP is shown to stop the destructive, fibrotic remodeling of cardiac tissue that leads to heart failure, and support healthy cardiovascular function.

These unparalleled benefits are due to the unique ability of this form of MCP to bind and block a master alarm protein in the body, called galectin-3.

With over 3,000 published clinical and preclinical studies, galectin-3 is gaining significant attention as a culprit biomarker and treatment target for cardiovascular disease, as well as a myriad of pro-inflammatory and profibrotic conditions. (2)

Galectin-3 and the Progression of Heart Failure

Heart failure is a chronic disease that develops over time. Following a heart attack or other ischemic (blocked blood flow/oxygen) event, the heart undergoes a process of scarring / tissue remodeling. This scarring can also result from ongoing hypertension, aka high blood pressure.

During this destructive remodeling process, functional muscle is replaced with fibrotic, non-functional tissue (scar tissue). Just as with fibrotic changes in other organs like the kidneys, lungs, and liver, the vicious cycle of fibrosis continues, and end-stage heart failure is generally unavoidable. (3)

Researchers have repeatedly shown that out-of-control galectin-3 is a primary driver in the initiation and progression of cardiovascular disease. galectin-3 is directly involved in numerous disease processes associated with heart failure, including inflammation, fibrosis, and blood vessel and tissue remodeling. In large-scale clinical studies, circulating galectin-3 concentrations are associated with an increased incidence of heart failure.  (4,5)

Modified Citrus Pectin: The Most-Researched Galectin-3 Inhibitor Why is this specific form of modified citrus pectin earning so much attention from independent medical researchers—especially in the study of cardiovascular disease?

Because it’s recognized as the most-researched, and ONLY available galectin-3 inhibitor, shown to enter the circulation, bind to galectin-3, and block its deadly disease processes to restore normal tissue function.

Over the last 10 years, numerous studies have emerged demonstrating the unique protective actions of MCP in halting the effects of galectin-3 in the treatment of cardiovascular disease. Published data in cardiovascular studies show that MCP works to actively promote

· Healthy heart tissue and cardiac function

· Arterial flexibility and integrity 

· Optimal circulation

· Metabolic function 

· Antioxidant activity 

· and more… 

One 2018 study showed how galectin-3 promotes metabolic changes associated with obesity. Results of the study showed the ability of MCP to halt these effects, and protect cardiovascular function against the inflammatory impacts of unhealthy weight gain. (6)

Other Cardiovascular Benefits of MCP

In addition to controlling the impacts of galectin-3 in cardiovascular health, MCP also helps to promote healthy cholesterol balance. Furthermore, published clinical data shows that MCP safely removes heavy metals including lead, mercury, arsenic and other toxins that threaten cardiovascular function.

The ONLY Researched Modified Citrus Pectin

It’s important to know that not all MCPs are alike. According to the research, there is only one MCP that has been proven effective—the original and only positively researched form of modified citrus pectin, developed over 25 years ago. This MCP is produced with a highly specific modification process to ensure the correct molecular weight and structure (between 5-15 kDa and <10% esterification) to enter the bloodstream and be effective—as shown in published research. Unmodified citrus pectin does not have the same short polysaccharide chains as MCP to enter the circulation, and other “modified” pectins could indicate that the pectin has been altered in some way, but not necessarily containing the correct specifications to achieve the results shown in the growing body of research.

With clinical studies underway at prominent research institutes for CVD and other indications, MCP is quickly becoming a respected therapy offering unparalleled benefits for numerous conditions—including and especially, cardiovascular health and treatment.

Sources:

1. Benjamin, E.J., et al, Circulation, 2017;135(10): e146-e603].

2. Newlaczyl A.U., et al. Cancer Lett, 2011;313(2):123-8

3. Segura, A.M., et al. Heart Fail Rev, 2014;19(2):173-85.

4. Nayor, M., et al. J Am Heart Assoc, 2016;5(1)].

5. Meijers W.C., et al. Am Heart J. 2014;167(6):853-60.e4.

6. Marin-Royo, G., et al., Dis Model Mech, 2018. 11(2).