ButturZym contains an “adaptogenic” mixture of enzymatic fermented herbal compounds including parthenolide, valproic acid and plant enzymes in a synergistic proprietary formula designed for the treatment of cancer and autoimmune diseases.
Pharmacological control of interleukin-12 (IL-12) production may be a key therapeutic strategy for modulating immunological diseases dominated by type-1 cytokine responses. IL-12 plays a pivotal role in the pathogenesis of Th1 cell-mediated autoimmune diseases. Rheumatoid arthritis is a chronic, progressive autoimmune disease that is characterized primarily by inflammatory joint damage producing chronic pain, loss of function and disability. The condition affects approximately 1% of the worldwide population. Given the inflammatory nature of this disease, numerous candidate molecular targets exist. These include T-cell and B-cell surface molecules. IL-12 is a novel cytokine cloned from B-cell lines and has a broad array of potent biologic activities, acting as the master regulator of the Th1 pathway, which drives major chronic inflammatory diseases, including rheumatoid arthritis.
Uncontrolled mucosal immunity in the gastrointestinal tract of humans results in chronic inflammatory bowel disease (IBD), such as Crohn’s disease (CD) and ulcerative colitis (UC). Patients present symptoms that include abdominal pain, diarrhea, and rectal bleeding, caused by immune cell attack on the small or large intestine. These diseases affect about 2 million people in the United States, and that number is rapidly increasing. For decades, researchers had been looking for the pathogenic strains of bacteria responsible for IBD, to no avail. But several recent studies had pointed to the role of commensal—not pathogenic—bacteria in triggering IBD. The thousands of bacteria, fungi and other microbes that live in our gut are essential contributors to our good health. They break down toxins, manufacture some vitamins and essential amino acids, and form a barrier against invaders. Bacteria can influence the oral tolerance response, in which the immune system is less sensitive to an antigen (including those produced by gut bacteria) once it has been ingested. This tolerance, mediated in part by the gastrointestinal immune system and in part by the liver, can reduce an overreactive immune response like those found in auto-immune disease.
Thus, the intestinal microflora is essential for the protection mechanism to work optimally. In fact, not having the correct balance of bacteria in the gut has been associated with a number of conditions including inflammatory bowel disease (IBD). Changes to diet and eating patterns, and the use of antibiotics can have a harmful effect on the balance of the gut microflora. These can combine to shift the balance of the gut microflora away from potentially beneficial or health-promoting bacteria such as the lactobacilli and bifidobacteria, towards an increase in the harmful or pathogenic micro-organisms (e.g: certain clostridia and enteroccocci).
Current and novel therapies are designed to dampen these over-active responses. Analysis of the types of immune responses ongoing in diseased mucosa of inflammatory bowel disease (IBD) patients has revealed that CD and UC are fundamentally different diseases. The former has the molecular imprints of a Th1 dominant cell-mediated hypersensitivity response whereas the latter appears to involve antibody-mediated hypersensitivity.
In early clinical trials, IL-12 has been implicated as a major mediator of these diseases based on the ability of anti-p40 mAb treatment to reverse intestinal inflammation. The cytokine IL-23 shares the same p40 subunit with IL-12, and the anti-p40 mAbs used in human IBD studies neutralized the activities of both IL-12 and IL-23. Autoimmune inflammatory responses and the diseases that develop as a consequence are now thought to be driven through a novel non-Th1 pathway. A novel T helper (Th) cell lineage, Th17, that exclusively produces the proinflammatory cytokine IL-17 has been reported to play important roles in various inflammatory diseases. IL23 is also focused upon for its potential to promote Th17. IL-23 play important roles in controlling the differential Th1/Th17 balance in both UC and CD, although Th17 cells may exist in both diseases.
IL-23, together with additional factors including TGF-β1 and IL-6, collectively generate and sustain a distinct CD4+ ‘Th17 inflammation effector’ T-cell subset characterized by its production of inflammatory chemokines and cytokines, including IL-17. With this paradigm shift in understanding of autoimmune inflammation pathogenesis comes exciting opportunities to identify and to target therapeutically molecules within the IL-23/Th17 axis that are key to disease development.
Psoriasis is a chronic skin disease mediated, at least partially, by the body’s T-cell inflammatory response mechanisms. Two interleukins (IL) in particular, IL-12 and IL-23, have been specifically implicated as key players in the pathogenesis of psoriasis secondary to their role in linking the innate and adaptive immune responses. Both IL-12 and IL-23 bind to the b1 receptor of T cells and natural killer cells via their shared p40 subunit. IL-12/IL-23 inhibition is an important target for therapeutic intervention against rheumatoid arthritis, IBD (inflammatory bowel disease) and other autoimmune diseases.
ButterZym has inhibitory effects on IL-12/IL-23 synthesis, prostaglandin (PG) synthesis and various components of the inflammatory response such as IL1β, IL-6, TNF-α and COX-2. ButtturZym is the only product in the world that has perfect solubility and bioavailability of parthenolide and phenolics enough to modulate autoimmune responses. ButturZym is synergistic with BosturZym, TeanZym, HydranZym and GinolZym.
They are called “master cells” and hard to kill. It is only recently that a clear link has been established between stem cells and cancer in a variety of cancer types since cancers often arise from the transformation of normal stem cells. There is a lot of evidence to suggest now that cancer stem cells are responsible for many of the recurrences that are observed after treatment has stopped. Most cancer cells are NOT important because they have a limited growth potential. It is the small population of cancer stem cells, primitive self renewing cells, that maintains the tumor mass.
For details please read the following article.
Bioavailable Parthenolide is a specific Histone Deacetylase (HDAC) Inhibitor, Part 2
ButterZym contains: Proprietary blend of Organic Feverfew Extract (leaf) 98g providing 3% Pure Parthenolide (2.9g), valproic acid, Plant Enzymes, Natural Phyto-compounds. Free of alcohol, soy, corn, gluten, dairy, egg, and is formulated without the use of artificial preservatives, flavors or colors. 100% Pure & Natural
SCIENCE BASED BIOAVAILABILITY: Bioactive Butterzym greatly improve the cellular uptake of Parthenolide, the healthful extract from fresh organic feverfew leaves, with clinically validated efficacy in for helping headache, migraine and inflammatory conditions. It is recognized that the therapeutic effectiveness of parthenolide is limited due to its poor absorption from the GI tract, so the use of the natural fermentation to enhance its uptake is particularly beneficial.
