Cardiovascular disease will kill nearly 2.5 million people in the United States this year, according to the Centers for Disease Control. Over time, inflammation, collagen deposition and scar tissue formation can cause blood vessels to stiffen, a process called vascular fibrosis. Though researchers have known that the hormone aldosterone (Aldo) plays a role in this process, the precise mechanisms have been poorly understood.
Now, an international study published in Arteriosclerosis, Thrombosis, and Vascular Biology: Journal of the American Heart Association is providing new insights into cardiovascular disease. Particularly significant, the study illuminates how Aldo and the protein galectin-3 jointly contribute to vascular remodeling and congestive heart failure by fueling the processes of inflammation, fibrosis and collagen deposition.
The findings indicate that galectin-3 is required for inflammatory and fibrotic responses to Aldo, suggesting a key role for galectin-3 in vascular fibrosis. Equally important, the study proves that modified citrus pectin (MCP), a preparation derived from the pith of citrus peels, prevents these effects by binding to galectin-3 and controlling Aldo induced elevated galectin-3 levels.
MCP is a form of citrus pectin modified to a specific molecular weight and structure for enhanced absorption and bioactivity. Regular pectin goes through the gastrointestinal tract unabsorbed, whereas MCP is readily absorbed and has been demonstrated in published research to perform multiple beneficial functions. MCP's small molecular weight and unique structure allow it to bind and block excess galectin-3 throughout the body. Elevated serum galectin-3 has been linked to high mortality rates in heart failure and metastatic cancer. MCP slows cancer progression and metastasis, blocks inflammation, helps prevent fibrosis, and offers other critical benefits related to the inhibition of galectin-3. It also supports immunity and safely chelates heavy metals.
Aldo and Galectin-3
The researchers in this study sought to understand exactly how Aldo and galectin-3 work together to affect vascular remodeling. In small quantities, Aldo and galectin-3 perform necessary biological functions. Aldo regulates blood pressure and electrolyte balance; galectin-3 facilitates cell-to-cell communication and cell growth. However, high levels of Aldo are linked to arterial stiffness and heart failure. Similarly, high levels of galectin-3 play a direct role in chronic inflammation, fibrosis and subsequent tissue remodeling in the kidneys, liver, heart and other organs; as well as cancer formation and metastasis.
In 2011, the Food and Drug Administration approved a serum galectin-3 test to assess the risk and progression of congestive heart failure and heart disease. This test is widely available and covered by most health insurances for cardiovascular screening. Practitioners also use this test to assess the risk and progression of cancer and other galectin-3 related diseases.
Dr. Isaac Eliaz, a recognized expert in the field of galectin-3 and the use of modified citrus pectin states, "The results of this study have enormous implications for the prevention and treatment of heart disease and fibrosis related conditions. Because it functions as an active, culprit biomarker, galectin-3 serves as a therapeutic target in multiple life-threatening conditions. According to the scientific literature, this is achievable with the oral application of MCP, a galectin-3 inhibitor without side effects. This approach offers a new solution to numerous chronic conditions related to inflammation, fibrosis and metastatic cancer for which there are limited conventional treatments."
In the study, rats were given Aldo and sodium chloride salt, which increased blood pressure, inflammation, fibrosis and galectin-3 levels. Using MCP, the research team blocked excess galectin-3 with significant results. Collagen type 1 deposition, blood pressure, inflammation, fibrosis and aortic wall thickness were all reduced. Spironolactone, a pharmaceutical Aldo inhibitor, achieved similar results.
However, the side effects of spironolactone are significant while MCP is proven to achieve greater results without toxicity or side effects. Specifically, the MCP was shown to outperform spironolactone in a few key areas related to inflammation and fibrosis. MCP achieved better suppression of fibrotic markers. Importantly, MCP completely inhibited the cytokine interleukin-6 (IL-6) which plays a key role in inflammation, fibrosis, immune response and cancer/metastasis. Spironolactone only partially blocked the Aldo induced IL-6.
The team went on to test the impact of increasing Aldo in regular mice as well as in galectin-3 knockout mice unable to produce the protein. When given Aldo, the normal mice experienced the inflammation and overabundant collagen formation associated with vascular remodeling. However, the knock-out mice experienced no ill effects, supporting the conclusion that Aldo requires galectin-3 to induce the collagen type 1 synthesis and deposition associated with vascular fibrosis.
Beyond Heart Disease
This new research confirms a number of earlier studies which implicate galectin-3 in numerous conditions related to inflammation and fibrosis. In particular, it substantiates research published in the journal PLoS One in 2011 demonstrating the role that galectin-3 plays in acute fibrosis-related kidney injuries. That study also shows that MCP blocks the harmful effects of excess galectin-3 and helps to reverse related damages.
This recent study marks a critical step toward understanding the mechanisms behind vascular fibrosis, and the role MCP can play in inhibiting these and other factors associated with heart failure and organ fibrosis. More research must be done to further illuminate the role of galectin-3 in cardiovascular and chronic diseases. Further research including clinical trials are being planned to explore MCP as a safe and natural preventative and treatment for congestive heart failure and metastatic cancer.