Mitigating the harmful effects of Galectin-3 with Modified Citrus Pectin

The AANP Conference Planning Team would like to introduce Issac Eliaz, MD, LAc, MS, as a guest blogger for the 2013 Annual Conference Blog. He will be leading a Vendor Workshop, Friday, July 12, from 11:15am to 12:00pm, in Keystone, Colorado.

As an integrative physician who treats cancer and chronic illness, my practice is rooted in the concept of individualized, patient-driven medicine. This means we work closely with each patient to design a protocol tailored to their unique needs, in order to build health while simultaneously fighting disease. Rightly, one size does not fit all. In conventional medicine this approach has been slow to take hold because it requires a truly holistic perspective. That is why I enjoy working with Naturopathic Doctors. We speak the same language of holistic, patient-driven medicine and we understand deeply the importance of integrating leading research advancements with traditional healing wisdom.

An excellent example of this integration of traditional botanical wisdom and science is the exciting and fast-growing body of research on galectin-3 molecules and the role of Modified Citrus Pectin (MCP) as a proven natural galectin-3 inhibitor. So while integrative, patient-driven medicine is highly individualized, there are also certain natural therapies that can have universal benefit, and the body of scientific literature is showing MCP to be one of these therapies. This is due in large part to its unique relationship with a protein called galectin-3.

Worldwide epidemiological studies over the last several years have revealed a strong correlation between many chronic and life-threatening diseases and elevated levels of circulating galectin-3. At normal levels, galectin-3, produced by the body, is beneficial—it is a signaling molecule that aids in regulating the cell cycle, cellular growth, development, and cell to cell communication. It is also part of the inflammation and repair process, and that's where it can become problematic when uncontrolled. Serious conditions such as cancer metastasis, heart disease, chronic inflammation and fibrosis, kidney injury, ulcerative colitis, cirrhosis of the liver, arthritis, and a host of other chronic conditions have been shown to be triggered and exacerbated by high levels of galectin-3 in the blood. Experts in this field project that in the near future a new class of diseases known as “Elevated Galectin-3 Diseases” will be established for diagnostic and treatment purposes.

Screening for Galectin-3
In 2011, the U.S. Food and Drug Administration (FDA) approved a serum assay to measure galectin-3 levels as a way to evaluate cardiovascular disease risk and progression. This is an easy and inexpensive test, covered by most health insurances for cardiovascular screening and prognosis. Since elevated galectin-3 is recognized as a “culprit” biomarker -- rather than a “bystander” biomarker such as CRP -- this test serves as an invaluable tool providing insight into the risks and progression of numerous chronic, degenerative illnesses. As a culprit, active biomarker, elevated galectin-3 is both a cause and an effect of metastatic cancer and inflammatory/fibrosis-related conditions.

A naturally occurring beta-galactoside binding protein, elevated galectin-3 fuels the development of diseases related to chronic inflammation and the progression of inflammation to fibrosis, in addition to cancer tumor formation and metastasis. This process can affect every organ and system in the body. A large scale population study presented in 2012 showed that elevated levels of galectin-3 increase overall mortality 3-fold in the general population. The Role of Galectin-3 in Cancer and Chronic Disease Galectin-3 can circulate freely through the blood system, or be expressed in the nucleus, cytoplasm, mitochondrion, cell surface, and extracellular space. The role of galectin-3 in the formation and spread of cancer is well documented and accepted throughout the medical community. Cancer cells are commonly found to have an abundance of galectin-3 on their surface. The galectin-3 acts as a cell binder, allowing cancer cells to aggregate, attach to endothelium and metastasize. Galectin-3 has also been shown to be a major factor in angiogenesis—the formation of new blood vessels to feed the tumor.

The surprising news that has emerged over the last several years is the expanding body of evidence demonstrating that elevated galectin-3 plays a direct role in the formation of numerous other life-threatening diseases beyond cancer. We now know that galectin-3 in excess works to advance chronic inflammation and the progression of inflammation to fibrosis within organs and tissues. Studies on hepatic, renal, cardiac, gastrointestinal, musculoskeletal, and other organs/systems have shown that galectin-3 plays an active role in activating fibroblasts—the cells responsible for fibrogenesis and fibrosis. Galectin-3 activates resting fibroblasts into matrix-producing fibroblasts after being secreted into the extracellular space. Matrix-producing fibroblasts are characterized by increased expression of certain proteins within and around the fibroblasts, a mechanism of action demonstrated in the scientific literature.

Elevated levels of circulating galectin-3 correlate significantly with increased risk of death in populations experiencing acute decompensated heart failure, as well as chronic heart failure. We now know that excess galectin-3 is directly involved in processes associated with heart failure fibrogenesis, myofibroblast proliferation, adverse ventricular and tissue remodeling, and others.

This link between galectin-3 and a significant number of chronic and acute conditions demonstrates the critical importance of closely tracking galectin-3 levels, particularly in patients with cardiovascular disease and/or cancer. As research continues to expand our understanding of these connections, the diagnostic and prognostic value of the galectin-3 serum assay is becoming more widely accepted throughout the medical community and many labs now offer the galectin-3 serum assay.

Modified Citrus Pectin (MCP): Proven natural galectin-3 blocker
Clearly, blocking the effects of galectin-3 in the body is paramount in preventing the formation and progression of a large number of chronic, life-threatening diseases. According to the literature, this is achievable with Modified Citrus Pectin (MCP): a naturally occurring soluble fiber from the peels of citrus such as lemons, limes, oranges, and grapefruits. Many people are already aware of the benefits of regular pectin in helping cleanse the digestive tract, where it can bind with and remove environmental toxins such as heavy metals -- even radioactive isotopes as demonstrated in the tragic Chernobyl aftermath.

The problem has been that regular, unmodified pectin molecules are too big to enter the bloodstream. This has been solved with the development of Modified Citrus Pectin (MCP)—a significantly smaller form of pectin molecule with enhanced molecular characteristics. Due to its specific size and structure, MCP is shown to provide a number of therapeutic benefits throughout the body, including selective immune enhancement, as well as protection against organ fibrosis and metastatic cancer.

MCP is naturally attracted to galectin-3 molecules and has the unique ability to bind with excess galectin-3 and effectively block the inflammatory, fibrotic and pro-cancer effects of this “rogue molecule.” In doing so, MCP is shown in multiple studies to inhibit the growth and metastasis of cancer cells, as well as reverse features of illnesses related to chronic inflammation and fibrosis, including kidney injury, vascular fibrosis and others.

Galectin-3 and Kidney Disease
A 2011 study has shown that MCP binding with galectin-3 was effective in reducing kidney injury. Animal subjects were pretreated with either water or MCP for one week, then folic acid was introduced to simulate kidney injury. Typical kidney injury symptoms were reduced in the subjects receiving MCP. Reduced galectin-3 levels, decreased kidney fibrosis, and a decrease in macrophages, pro-inflammatory cytokines and apoptosis were all observed in the MCP group.