Unmasking Galectin-3: The Hidden Protein Linked to Cancer & Inflammatory Diseases
The Hidden Protein Linked to Cancer & Inflammatory Diseases
Dr. Isaac Eliaz, MD
Isaac Eliaz, MD, MS, LAc, has been a pioneer in integrative medicine since the early 1980s, focusing on cancer, immune health, detoxification, and mind-body medicine. He’s a respected clinician, researcher, author, and educator. He is the author of The Survival Paradox, founder and Medical Director of Amitabha Medical Clinic and Healing Center, and founder and CEO of Eliaz Therapeutics, a medical device company dedicated to transforming the treatment of sepsis and other life-threatening diseases.
Dr. Eliaz is a lifelong student and practitioner of Buddhist practices. One of them is Tonglen Meditation, a method that involves the art of exchanging suffering with love and compassion After decades of study, Dr Eliaz created Open Heart Medicine, a modality that combines science, meditation, and a unique understanding of the heart’s physiology and its inherent ability to engage in meditation. Through Open Heart Medicine, he offers a clear pathway to wellness that honors both the scientific and spiritual dimensions of human experience
For more information, see the Helpful Links page at the end of this PDF.
Uncover the Source of Your Symptoms
As a physician and researcher steeped in integrative medicine, I’ve spent 30 years studying the protein Galectin-3 and its central role in inflammation and fibrosis.
Under normal physiological conditions, Galectin-3 is important for wound healing and tissue repair. But when the body makes too much of it, this protein transforms from helpful to harmful I’ve seen firsthand how it accelerates diseases and how blocking it restores balance and healing.
I believe Galectin-3 overproduction is a hidden health crisis of our time. I’m working to combat this through research, education, and more recently, the development of a medical device that selectively targets and removes Galectin-3 from the bloodstream (more on this ahead).
Please join me in learning about this critical yet overlooked biomarker for disease, including the causes behind Galectin-3 dysfunction and what helps disrupt its inflammatory cascade.
Warm regards,
IsaacEliaz,MD,LS,LAc
What Is Galectin-3?
Galectin-3 is a carbohydrate-binding protein normally present in the body at low concentrations. Its chief role is that of a “survival protein.” When your body faces a physical or emotional threat, trauma, or illness, it goes into survival mode. As the body’s chief “survival protein,” Galectin-3 is activated and triggers a short-term inflammatory response designed to stimulate the healing repair process.
I want to emphasize the word short-term because Galectin-3 is not meant to be circulating in your system in elevated levels on a regular basis. It’s only when you are dealing with a serious health crisis that the production of this protein spikes the body should stop making excessive amounts of it once the danger has been resolved.
Why Your Body Can’t Turn Off Its Galectin-3 Switch
As the saying goes, too much of a good thing is never good. This is especially true in the case of Galectin-3. This protein has the ability to spike very quickly and start a cascade of immune and inflammatory responses. This is normal and necessary when the body needs healing urgently. Problem is, Galectin-3 can get stuck in the “on” position imagine a car alarm that never shuts off or a jammed on/off switch. That’s what we are dealing with here.
What causes this protein to go haywire? Our modern lifestyles bear a lot of the blame. Most of us are living in a constant state of survival or “crisis mode” these days, causing our bodies to artificially stay on high alert and continue pumping out Galectin-3.
When Galectin-3 fails to deactivate, it sets off multiple pathways that initiate inflammation and the process of fibrosis (uncontrolled scar tissue build-up). This can lead to hardening of tissues, organs, and systems in the body. This then drives up Galectin-3 production, forming a perpetually closed-loop system that is among one of the greatest threats to our health.
How Modern Life Keeps Your Body in Constant Crisis Mode
Most of us live high-stress lifestyles inundated with electronic and other forms of stimulation. It’s not an exaggeration to say that our modern society is in a state of overwhelm.
The continual barrage of stimuli from every direction, the onslaught of environmental toxins, the ongoing physical and emotional stress we’ve grown accustomed to throw us into survival mode and keep us stuck there.
As a result, our systems are on constant high alert, like that alarm that never stops.
It’s important to note that the condition of our body’s “alarm system” and its response to various stressors depend upon the condition of multiple other systems. It’s influenced by the neurological, circulatory, and metabolic systems, as well as mitochondrial function. Our diet and lifestyle affect it too.
Diseases Associated with High Galetin-3 Levels
Elevated levels of the protein Galectin-3 have been associated with many diseases and health conditions there are literally thousands of studies (over 10k) showing a strong link between the two. Here are the conditions most commonly tied to high Galectin-3 levels:
Fibrosis
Elevated Galectin-3 levels are strongly associated with heart failure, particularly in cases of cardiac fibrosis and remodeling. It is considered a biomarker for predicting the progression and severity of heart failure.
Galectin-3 plays a significant role in the development of fibrosis in various organs, including the heart, liver, kidneys, and lungs It promotes the activation of fibroblasts and the deposition of extracellular matrix components, leading to tissue scarring.
Heart Failure
A long-term study linked elevated Galectin-3 levels among the general public with increased odds of allcause mortality compared to people with lower circulating Galectin-3 in their bloodstream.
Diseases Associated with High Galetin-3 Levels (cont.)
Galectin-3 is implicated in renal fibrosis and inflammation, contributing to the progression of CKD High levels are associated with worse outcomes in kidney disease patients Chronic Kidney Disease Research suggests that Galectin-3 is involved in neuroinflammation and neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis.
Neurological Disorders
Galectin-3 contributes to chronic inflammation in conditions such as rheumatoid arthritis, inflammatory bowel disease (IBD), and asthma by modulating immune responses and promoting inflammatory pathways.
Inflammatory Diseases
Galectin-3: A Common Thread in Alzheimer’s Studies
Alzheimer’s patients tend to have higher levels of Galectin-3 than healthy people, according to research. In one study, researchers found elevated Galectin-3 in those with Alzheimer’s and people with mild cognitive impairment. Other studies back this up with similar findings.
Diseases Associated with High Galetin-3 Levels (cont.)
Liver Diseases
Elevated Galectin-3 levels are associated with liver fibrosis, cirrhosis, and non-alcoholic steatohepatitis (NASH) It plays a role in the activation of hepatic stellate cells, which drive fibrotic changes in the liver
Diabetes and Metabolic Syndrome
Galectin-3 is linked to insulin resistance, obesity, and metabolic syndrome. It may contribute to the development of type 2 diabetes and its complications.
Cancer
Galectin-3 is involved in tumor progression, metastasis, and immune evasion. It is overexpressed in various cancers, including breast, prostate, thyroid, and pancreatic cancers, and is linked to poor prognosis (more on this soon).
Galectin-3 promotes vascular inflammation and plaque formation, contributing to the development of atherosclerosis and increasing the risk of cardiovascular events.
Atherosclerosis
Galectin-3 and Cancer
Often called “the guardian of the tumor microenvironment,”
Galectin-3 is over-expressed on the surface of cancer cells, acting as a sticky surface molecule that allows cancer cells to aggregate, disseminate throughout the circulatory system, evade immune surveillance, and establish themselves at distant sites. It is also involved in angiogenesis. Essentially, cancer is hijacking Galectin-3 for its own growth and survival.
Put another way, Galectin-3 allows cancer cells to clump together, create blood supply to feed themselves, metastasize to other areas, and hide from the immune system. Galectin-3 also protects cancer by preventing apoptosis (programmed cell death) of cancer cells, and forms a protective barrier around tumors to shield them from immune attack.
But when we remove and block unhealthy Galectin-3, we can stop, slow and sometimes even reverse cancer growth, prevent metastasis, and enhance immune system function.
Galectin-3 as a Biomarker for Cancer and Disease
Research reveals that Galectin-3 levels are significantly elevated compared to control groups in cancer patients with breast, gastrointestinal, lung, ovarian, melanoma, and nonHodgkin’s lymphoma. Higher levels are also seen in patients with metastatic disease, compared to with localized tumors.
These and similar findings demonstrate that circulating Galectin-3 levels play a significant role in tumor progression, making the protein an important biomarker for early-stage cancer and a predictor of metastasis.
This problematic protein also serves as the backbone of biofilm formations in the body—biofilms sequester toxins and pathogens in inflamed, isolated areas shielded from immune surveillance and treatments. They creates an environment where bacteria, viruses, and toxins can thrive. This shows that Galectin-3 isn’t just a biochemical marker—it’s also an active participant in disease pathology.
Nature’s Best Galectin-3 Blocker
Research shows that controlling Galectin-3 delivers significant benefits to tissues and organs, helping prevent cancer progression and other diseases. Modified Citrus Pectin (MCP), an extract of orange, lemon, and lime piths, is the most-researched inhibitor of Galectin-3, with powerful anti-inflammatory and anti-fibrotic properties. Studies show that MCP works synergistically with certain chemotherapy drugs, with no known drug interactions.
Getting Your Galectin-3 Levels Tested
Galectin-3 is a specific blood test. It’s generally not included on routine blood tests (e.g., CBC and metabolic panels), but you can request it from your doctor as a separate or add-on test.
If you have never heard of a Galectin-3 test, you are not alone. Despite this large and fast-growing body of data on Galectin-3, most people including many healthcare professionals are not familiar with this pro-inflammatory molecule. But as the research on Galectin-3 continues, more people and doctors are starting to recognize it as a critical biomarker for health.
The chart below gives you an overview of Galectin-3 ranges. Both Quest Diagnostics and LabCorp offer Galectin-3 blood tests. REGISTER NOW
XGal-3®: CuttingEdge Treatment for Removing Excess Galectin-3
XGal-3® is a novel medical device that works like dialysis but with a crucial difference. It combines therapeutic apheresis (a wellestablished procedure) with targeted removal of Galectin-3. Using proprietary anti-Galectin3 ligand traps, the device selectively eliminates this key inflammatory protein from the bloodstream, potentially halting sepsis progression.
By disrupting the pathological process early, XGal-3® aims to prevent the devastating sequence of inflammation and organ damage, helping to save lives. This targeted strategy addresses the root cause of inflammatory diseases, particularly cancer and sepsis, providing a breakthrough solution and new hope for millions.
The technology has shown remarkable results in our research. In large animal studies, XGal-3® rapidly demonstrated the incredible ability to halt the devastating cascade of sepsis in hours, an achievement that no currently approved treatment has been able to accomplish.
Breakthrough Designation Granted to XGal-3®
The FDA recently awarded XGal-3® its Breakthrough Device Designation for the treatment of sepsis. This is a highly coveted label in the medical world that validates technologies tackling urgent, unmet medical needs. It gives patients timely access to innovative treatments that are highly vetted for safety and effectiveness. And often, it offers hope where there is none.
This patented technology, supported by two prestigious NIH grants and protected by over 60 patents across 34 countries, has the potential to transform the treatment of sepsis and other inflammatory and fibrotic diseases.
Explore This
Topic Further
Visit EliazTherapeutics.com to learn more about XGal3®, including how the technology works and the research behind this cutting-edge medical device. Interested in learning about investing in XGal-3®? See what existing investors have to say about the opportunity.
Final Thoughts: Unraveling the Complexities of Galectin-3
Given that each of us have complex biochemical structures and unique genetic tendencies, there is no standard, predictable response when it comes to Galectin-3. This protein can be at different levels in different people and trigger different responses even if they have the same condition.
For example, some people’s bodies are hypervigilant and respond to a stimulus or trigger with lots of inflammation. Others may not have a good “survival sense” and therefore are unable to mount the proper inflammatory response. Instead, they might shut down and with suppressed immunity or increased fibrosis. There is also an adaptive response with Galectin-3 the reaction is amplified due to previous physical, emotional, or psychological trauma.
What is clear is that by removing and blocking excess levels of Galectin-3, we can disarm its harmful effects and help render it inactive, decreasing unhealthy inflammation in the process. This makes targeting Galectin-3 one of the most important therapeutic strategies available today for treating and disease and restoring health.
For More Information
Website: dreliaz.org
Book: The Survival Paradox: Reversing the Hidden Cause of Aging and Disease by Isaac Eliaz, MD (available on Amazon)
YouTube: Videos and Free Webinars
Eliaz Therapeutics and XGAL-3®: eliaztherapeutics.com
Medical Clinic: Amitabha Medical Clinic & Healing Center
Free Weekly Meditations: Community Meditations, a virtual to gather “live” at 7am and 5pm U.S. Pacific Time, Monday through Friday. (Register using link above.)
Dr. Eliaz CV: https://dreliaz.org/curriculum-vitae/
References
Sun H, Peng J, Cai S, Nie Q, Li T, Kellum JA, Eliaz I, Peng Z A translational study of Galectin-3 as an early biomarker and potential therapeutic target for ischemicreperfusion induced acute kidney injury. J Crit Care. 2021 Oct;65:192-199. Epub 2021 Jul 2.
Sun H, Jiang H, Eliaz A, Kellum JA, Peng Z, Eliaz I. Galectin-3 in septic acute kidney injury: a translational study. Crit Care. 2021 Mar 18;25(1):109.
Rudd KE, Johnson SC, Agesa KM, et al Global, regional, and national sepsis incidence and mortality, 1990-2017: analysis for the Global Burden of Disease Study Lancet 2020 Jan 18;395(10219):200-211
Prud’homme M, Coutrot M, Michel T, Boutin L, et al. Acute Kidney Injury Induces Remote Cardiac Damage and Dysfunction Through the Galectin-3 Pathway. JACC Basic Transl Sci. 2019 Oct 28;4(6):717-732.
Navarro-Alvarez N, Goncalves B, Andrews AR, Wang Z, Wang Z, Harrington E, Shah J, Sachs DH, Eliaz I, Huang CA The effects of galectin-3 depletion apheresis on induced skin inflammation in a porcine model J Clin Apher 2018 Aug;33(4):486-493 Epub 2018 Mar 23
Eliaz I, Patil A, Navarro-Alvarez N, Wang Z, Eliaz A, Weil E, Wilk B, Sachs DH, Huang CA. Methods for the detection and serum depletion of porcine galectin-3. J Clin Apher. 2017 Oct;32(5):335-341.
Eliaz, I The Role of Galectin-3 as a Marker of Cancer and Inflammation in a Stage IV Ovarian Cancer Patient with Underlying Pro-Inflammatory Comorbidities Case Rep Oncol 2013 Jul 3;6(2):343-9
Wang X, Zhang S, Lin F, Chu W, Yue S. Elevated Galectin-3 Levels in the Serum of Patients With Alzheimer's Disease. Am J Alzheimers Dis Other Demen. 2015 Dec;30(8):729-32. Epub 2013 Jul 2.
de Boer, RA, et al. The fibrosis marker galectin-3 and outcome in the general population J Intern Med 2012 Jul;272(1):55-64
