The Root Cause of Aging and Chronic Disease

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Controlling this master alarm protein helps halt and reverse life-threatening conditions 

Your body has deep-rooted survival and repair mechanisms to keep you safe from danger, orchestrate your defenses, and direct critical repair processes. And leading these survival mechanisms is one protein in particular: Galectin-3… your master alarm protein.  

As an alarm protein, galectin-3 is activated when your body faces a threat… whether that’s a pathogen, stress, injury, illness—even normal aging processes. The threat triggers your body to ramp up galectin-3, which unleashes a cascade of biochemical inflammatory signals and chain reactions that reach all the way down to the cellular level.   

The problem is this: With all we face in today’s world—from stress, to toxins, to increasingly aggressive pathogens—our alarm systems stay dialed up. This comes with a heavy cost that includes inflammation and fibrosis (uncontrolled scar tissue build up) that severely damages organs and tissues. And it’s all driven by galectin-3. Furthermore, levels of galectin-3 tend to rise with age. 

The long-term inflammatory damage triggered by out-of-control galectin-3 creates problems throughout the body—from fueling cancer and cardiovascular disease, to arthritis, immune suppression and sepsis. 

This is why galectin-3 is considered an instigator and driver of virtually all chronic disease states… from diabetes to arthritis to cancer.1 Today, galectin-3 represents one of the fastest growing fields of medical research, with over 3,000 published studies showing its far-reaching impacts in our most critical areas of health.  

From Survival Protein to Silent Killer 

Why does the body produce something so harmful? Like so many other things, it all comes down to balance and moderation. In small amounts inside the cell, galectin-3 is good. It supports cell development, growth, and communication.2 Galectin-3 directs cells to respond to threats (like viruses and toxins) and injuries.3  

But when galectin-3 is circulating outside the cell, it becomes a destructive force and can overreact to threats. It can also hide pathogens from detection by your immune system, and prevent immunity from working properly.  

Even more serious, galectin-3’s alarm signals can unleash a deadly cytokine storm, where your immune system goes haywire and starts attacking organs and tissues—with potentially life-threatening consequences. 

Galectin-3 Impacts Your Whole Body 

Galectin-3 can affect nearly every area of health. Research shows it plays a primary role in fueling our most deadly diseases by triggering: 

  • system-wide inflammation 
  • immune overreactions or immune suppression 
  • oxidative stress 
  • fibrosis (uncontrolled scarring) 

Galectin-3 is also called “The Guardian of the Tumor Microenvironment” because it promotes tumor growth, protects cancer cells from the immune system, and helps cancer cells metastasize.  

Worse, too much circulating galectin-3 can block proper healing, making it harder to manage or recover from disease.  

6 Major Diseases Fueled by Galectin-3 

Here are some of the main ways that galectin-3 can take a serious toll on your health and longevity: 

Cardiovascular disease: By driving inflammation and fibrosis, galectin-3 plays a key role in the progression of cardiovascular diseases, including atherosclerosis (thickened, hardened arteries), stroke damage,  and heart failure.4 In fact, many doctors now use galectin-3 as a biomarker to help diagnose and monitor heart conditions, and predict patient outcomes.5  

Cancer: Galectin-3 is cancer’s best friend. It helps fuel cancer through numerous mechanisms, interferes with treatment efficacy, and makes it much harder for the body to fight the disease.6,7 

Diabetes and Metabolic SyndromeGalectin-3 fuels diabetes and pre-diabetes by making it harder for your body to balance blood sugar (aka glucose homeostasis), partly by increasing insulin resistance.8,9  

Alzheimer’s disease: Galectin-3 triggers damaging inflammation in the brain that fuels Alzheimer’s disease. Galectin-3 is also shown to promote the formation of plaques in the brain, another hallmark of Alzheimer’s disease.10  

Endometriosis: Galectin-3 plays a major role in the debilitating condition of endometriosis. Researchers showed that blocking galectin-3 may be a viable treatment for the painful symptoms of endometriosis.11 

Arthritis: Galectin-3 plays a driving role in rheumatoid arthritis and osteoarthritis.12 Research shows it  increases joint swelling, pain and deterioration.13 

There is good news. Scientists continue to show that controlling galectin-3 with a proven galectin-3 blocker is a powerful strategy for halting and reversing deadly disease processes and restoring normal function to cells, tissues and organs.  

Even more importantly, new research shows that unhealthy galectin-3 can show up very early in the disease development process—before other signs and symptoms. By addressing galectin-3 early, before it causes extensive damage, it’s possible to protect against the development of chronic diseases. And for existing conditions, halting galectin-3 is a powerful strategy to support optimal healing, repair and recovery.14   

Blocking Galectin-3: The Secret to Lasting Health 

A fast-growing body of published research shows that blocking  galectin-3 can slow, stop, reverse, and prevent the progression of nearly every inflammatory degenerative condition.  

But in order to do that, you need the one proven galectin-3 blocker available today: Clinically researched  opens in a new windowModified Citrus Pectin (MCP).   

With over 65 published studies, this form of Modified Citrus Pectin is the most-researched and only available agent shown to effectively bind and block galectin-3, delivering powerful results: 

  • Less inflammation and oxidative stress15 
  • Greater cardiovascular health and reduced risk of cardiovascular disease16 
  • Improved immune responses17 
  • Healthy aging and increased longevity18 

With continued published research, MCP is earning a well-deserved reputation as one of the most important agents for preventing and treating a broad range of conditions—thanks to its unique ability to block galectin-3 and in doing so, dramatically improve health.  

This is also why it’s important to choose the  opens in a new windowonly researched and proven effective form of MCP…   

With Modified Citrus Pectin—Size Matters  

Most citrus pectin contains very big molecules—too big to absorb into your circulation from your GI tract.  

That’s where the “M” in MCP comes in. This modified form of citrus pectin is made using a specialized enzyme process that creates tiny, easily absorbed pectin molecules which enter the circulation and bind to galectin-3 proteins, effectively disarming them.  

MCP has been studied for 25+ years, and is shown to deliver a remarkable range of benefits including: 

  • Powerful immune system balance and support19 
  • Safe detoxification of heavy metals and environmental toxins20 
  • Prebiotic nourishment for a healthy microbiome21 
  • Synergistic properties that increase the effectiveness of other medical treatments, including cancer treatments and antibiotics22 

Most important, MCP is THE antidote to galectin-3. By binding to unhealthy galectin-3 and halting its devastating activity,23 MCP is proving to be a fundamental strategy for deep healing and optimal long-term wellness.24   


  1. Sciacchitano S, Lavra L, Morgante A, et al. Galectin-3: One Molecule for an Alphabet of Diseases, from A to Z. Int J Mol Sci. 2018;19(2):379.  

  1. Arthur CM, Baruffi MD, Cummings RD, Stowell SR. Evolving mechanistic insights into galectin functions. Methods Mol Biol. 2015;1207:1-35. doi:10.1007/978-1-4939-1396-1_1 

  1. Díaz-Alvarez L, Ortega E. The Many Roles of Galectin-3, a Multifaceted Molecule, in Innate Immune Responses against Pathogens. Mediators Inflamm. 2017;2017:9247574. doi:10.1155/2017/9247574 

  1. Zhong X, Qian X, Chen G, Song X. The role of galectin-3 in heart failure and cardiovascular disease. Clin Exp Pharmacol Physiol. 2019;46(3):197-203.  

  1. Amin HZ, Amin LZ, Wijaya IP. Galectin-3: a novel biomarker for the prognosis of heart failure. Clujul Med. 2017;90(2):129-132. doi:10.15386/cjmed-751 

  1. Amin HZ, Amin LZ, Wijaya IP. Galectin-3: a novel biomarker for the prognosis of heart failure. Clujul Med. 2017;90(2):129-132. doi:10.15386/cjmed-751 

  1. Farhad M, Rolig AS, Redmond WL. The role of Galectin-3 in modulating tumor growth and immunosuppression within the tumor microenvironment. Oncoimmunology. 2018;7(6):e1434467.  

  1. Yilmaz H, Cakmak M, Inan O, Darcin T, Akcay A. Increased levels of galectin-3 were associated with prediabetes and diabetes: new risk factor?. J Endocrinol Invest. 2015;38(5):527-533. doi:10.1007/s40618-014-0222-2 

  1. Menini S, Iacobini C, Blasetti Fantauzzi C, Pesce CM, Pugliese G. Role of Galectin-3 in Obesity and Impaired Glucose Homeostasis. Oxid Med Cell Longev. 2016;2016:9618092. doi:10.1155/2016/9618092 

  1. Boza-Serrano A, Ruiz R, Sanchez-Varo R, et al. Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer’s disease. Acta Neuropathol. 2019;138(2):251-273. doi:10.1007/s00401-019-02013-z 

  1. Mattos RM, Machado DE, Perini JA, et al. Galectin-3 plays an important role in endometriosis development and is a target to endometriosis treatment. Mol Cell Endocrinol. 2019;486:1-10. doi:10.1016/j.mce.2019.02.007 

  1. Hu Y, Yéléhé-Okouma M, Ea HK, Jouzeau JY, Reboul P. Galectin-3: A key player in arthritis. Joint Bone Spine. 2017;84(1):15-20. doi:10.1016/j.jbspin.2016.02.029 

  1. Weinmann, D., Schlangen, K., André, S. et al. Galectin-3 Induces a Pro-degradative/inflammatory Gene Signature in Human Chondrocytes, Teaming Up with Galectin-1 in Osteoarthritis Pathogenesis. Sci Rep6, 39112 (2016). 

  1. Hara A, Niwa M, Noguchi K, et al. Galectin-3 as a Next-Generation Biomarker for Detecting Early Stage of Various Diseases. Biomolecules. 2020;10(3):389.  

  1. Ramachandran C, Wilk B, Melnick SJ, Eliaz I. Synergistic Antioxidant and Anti-Inflammatory Effects between Modified Citrus Pectin and Honokiol. Evid Based Complement Alternat Med. 2017;2017:8379843. doi:10.1155/2017/8379843 

  1. Li S, Li S, Hao X, Zhang Y, Deng W. Perindopril and a Galectin-3 Inhibitor Improve Ischemic Heart Failure in Rabbits by Reducing Gal-3 Expression and Myocardial Fibrosis. Front Physiol. 2019;10:267.  

  1. Caniglia JL, Guda MR, Asuthkar S, Tsung AJ, Velpula KK. A potential role for Galectin-3 inhibitors in the treatment of COVID-19. PeerJ. 2020;8:e9392.  

  1. Gao Z, Liu Z, Wang R, Zheng Y, Li H, Yang L. Galectin-3 Is a Potential Mediator for Atherosclerosis. J Immunol Res. 2020;2020:5284728.  

  1. Ramachandran C, Wilk BJ, Hotchkiss A, Chau H, Eliaz I, Melnick SJ. Activation of human T-helper/inducer cell, T-cytotoxic cell, B-cell, and natural killer (NK)-cells and induction of natural killer cell activity against K562 chronic myeloid leukemia cells with modified citrus pectin. BMC Complement Altern Med. 2011;11:59. Published 2011 Aug 4. doi:10.1186/1472-6882-11-59 

  1. Eliaz I, Weil E, Wilk B. Integrative medicine and the role of modified citrus pectin/alginates in heavy metal chelation and detoxification–five case reports. Forsch Komplementmed. 2007;14(6):358-364. doi:10.1159/000109829 

  1. Larsen N, Bussolo de Souza C, Krych L, et al. Potential of Pectins to Beneficially Modulate the Gut Microbiota Depends on Their Structural Properties. Front Microbiol. 2019;10:223. Published 2019 Feb 15. doi:10.3389/fmicb.2019.00223 

  1. Conti S, Vexler A, Hagoel L, et al. Modified Citrus Pectin as a Potential Sensitizer for Radiotherapy in Prostate Cancer. Integr Cancer Ther. 2018;17(4):1225-1234. doi:10.1177/1534735418790382 

  1. 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;6(4):e18683. Published 2011 Apr 8. doi:10.1371/journal.pone.0018683 

  1. Eliaz I, Raz A. Pleiotropic Effects of Modified Citrus Pectin. Nutrients. 2019;11(11):2619. Published 2019 Nov 1. doi:10.3390/nu11112619

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