Lufenuron bioaccumulates. 

http://www.syngenta.co.nz/msds/syngentanz/MATCH_24106015.pdf

 

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The studies above demonstrate that Lufenuron can cause intestinal cell line damage and leaky gut. One benefit of the intestinal cells is that they regenerate quickly, thus demonstrating their ability to heal and restore the intestinal barrier. Lufenuron has the ability to block this regeneration. It's role in serine protease inhibition could lead to chronic inflammatory conditions, food allergies, autoimmune diseases, etc. 

Lufenuron can also interfere with absorption of N-Acetylglucosamine, necessary for the formation of the cell walls in many beneficial bacteria. 

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Disturbance of the epithelial barrier and epithelial transport processes is often discussed to be a major factor in the pathogenesis of intestinal inflammation and inflammatory bowel disease. Increased permeability of the epithelial barrier in ulcerative colitis was first reported in 1973 [11]. 

How Bacteria-Induced Apoptosis of Intestinal Epithelial Cells Contributes to Mucosal Inflammation

http://www.hindawi.com/journals/iji/2010/574568/

 

The intestinal epithelium provides a critical protective barrier against enteric pathogens, food antigens, and physiochemical stresses caused by digestive and microbial products, and yet must be selectively permeable to beneficial nutrients and fluids. Tightly regulated control of barrier function and integrity is critical, as the pathogenesis of intestinal diseases such as Crohn's disease, ulcerative colitis, inflammatory bowel diseases (IBD), and autoimmune diseases are linked to intestinal barrier dysfunction and increased intestinal permeability (1). The intestinal epithelium is a single layer of linked columnar epithelial cells that regulates, through the paracellular pathway, the selective passage of ions, fluid, and macromolecules from the intestinal lumen into the underlying tissues. 

 

The intestinal epithelium serves as a major protective barrier between the mammalian host and the external environment. Here we show that the transmembrane serine protease matriptase plays a pivotol role in the formation and integrity of the intestinal epithelial barrier. St14 hypomorphic mice, which have a 100-fold reduction in intestinal matriptase mRNA levels, display a 35% reduction in intestinal transepithelial electrical resistance (TEER). Matriptase is expressed during intestinal epithelial differentiation and colocalizes with E-cadherin to apical junctionalcomplexes (AJC) in differentiated polarized Caco-2 monolayers. Inhibition of matriptase activity using a specific peptide inhibitor or by knockdown of matriptase by siRNA disrupts the development of TEER in barrier-forming Caco-2 monolayers and increases paracellular permeability to macromolecular FITC-dextran. Loss of matriptase was associated with enhanced expression and incorporation of the permeability-associated, “leaky” tight junction protein claudin-2 at intercellular junctions.  These results support a key role for matriptase in regulating intestinal epithelial barrier competence, and suggest an intriguing link between pericellular serine protease activity and tight junction assembly in polarized epithelia.

http://www.pnas.org/content/107/9/4200.full

 

 

“Mechanisms terminating the short physiological life cycle of epithelial cells are supposed to have an impact on these essential functions and have influence on inflammatory reactions in the intestinal mucosa. A disturbance of the epithelial barrier is thought to be a major factor in the pathogenesis of inflammatory bowel disease.

Disturbance of the epithelial barrier and epithelial transport processes is often discussed to be a major factor in the pathogenesis of intestinal inflammation and inflammatory bowel disease.”

http://www.hindawi.com/journals/iji/2010/574568/

 

 

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One website that sells lufenuron has pictures of inflammatory skin conditions that responded to lufenuron treatment. A deficiency of serine protease inhibitors can play a role in creating such inflammatory skin conditions. The website implies that the healing seen in the pictures was created by lufenuron's anti-fungal affect against candida. It is much more likely that this was due to its serine protease inhibition effect. I've talked frequently about how people misinterpret what they see and notice. This would be a classic example.

 

Lufenuron has demonstrated the ability to damage intestinal cells and intestinal cell junctions. Intestinal cells play a critical role in the maintenance of the homeostasis of the intestinal tract. Lufenuron can also interfere with the structure of healthy intestinal bacteria. It has demonstrated a possible role in affecting candida fungal growth. The goal of any approach in restoring balance to the intestinal flora, immune responses, and candida overgrowth, should not also present known risks to the body. Based on this, I would never recommend lufenuron.