Tumor cells don’t just use glucose/sugar as their only source of fuel, especially when we may be restricting sugars because we heard that tumor cells only consume sugars, but this is a half truth. Glucose is usually their primary fuel source, however, when it’s not available such as when being restricted by FENBENCUR™ or FLUBENCUR™ and/or in late stage progression, the tumor cells have devised an ingenious way of changing their metabolism to grab fuel from there other sources: Glutamine (proteins) , Fatty Acid Synthesis (FASN) & Autophagy.
These 3 main fuel pathways exploited by Tumors are a popular strategy used by Care Oncology (COC) for using Re-purposed drugs such as Metformin, Doxycyline, Dipyridamole, Niclosamide, Aspirin and a statin to target and inhibit these pathways which drive the TCA cycle within each cancer cell with the aim of to weakening them over time.
However, should you have difficulty being prescribed the drugs described, we have developed a herbal formula which aims to target similar Fatty Acid Synthesis pathways of: Acetate, SREB1/2, FAO, ACLY, FASN and HMGCR which we have named FASNHIB™.
[To better understand these concepts, See our MFI Strategy here – Werone Private Herbal Health Trust Members only]
FASNHIB™ is a broad-based nutraceutical formula containing herbal extracts and other nutrients which have individually been shown to reduce fatty acid availability. [source]. Our other formula GLUTAHIB™, is aimed at inhibiting Glutamine uptake by cells and will follow shortly.
First observed in the 1950s, de novo Fatty Acid synthesis is a major source of Fatty Acid (FAS) fuel for Tumor cells [When Fats Commit Crimes]. Rapidly growing Tumor cells require relatively large amounts of Fatty Acids to support processes such as membrane formation and signaling.
The mechanism was further confirmed by blocking FAS and FAO with siRNAs which induce ROS (free radicals) production resulting in the disruption of simultaneous FAS and FAO, causing NADPH (energy) depletion. NADPH also protects Tumor cells against metabolic stress and hypoxia (suffocation), this is an important target.
So as well as choosing supplements which help target various oncogenes and tumor surpressors, the other aspects driving the Tumor is metabolic syndrome, this is how the Tumor gets it’s fuel, when you starve the cells and weaken them, you can then go in for the kill and be more effective than attacking strong growing Tumor cells.
Preferential exploitation of aerobic glycolysis by Tumor cells is a key issue of reprogrammed metabolism. It is becoming clear that other metabolic pathways or mediators may play a fundamental role in Tumors. The availability of recent sophisticated experimental approaches to study the metabolic profile of Tumor cells has allowed identification of an impressive number of alterations. They essentially concern levels of expression/accumulation or status of enzymes or intermediate substrates involved in several anabolic pathways.
ATP-citrate lyase (ACLY) is a cytosolic enzyme that catalyzes the generation of acetyl CoA from citrate. Acetyl CoA is a vital building block for the biosynthesis of fatty acids and cholesterol and is involved in isoprenoid-based (Vit E, Vit A) protein modifications of the bacteria found in our guts. Acetyl CoA is also required for acetylation reactions that modify proteins, such as histone acetylation. ACLY is upregulated or activated in several types of cancers, and its inhibition is known to induce proliferation arrest in cancer cells both in vitro and in vivo.
ACLY is a cross-link between glucose and/or glutamine metabolism and fatty acid synthesis and/or mevalonate pathways. When tumor cells that have functioning mitochondria are grown under normoxic conditions, the glycolytic pathway mainly provides citrate for acetyl-CoA production via an ACLY-catalyzed reaction. In tumor cells with defective mitochondria or in cancer cells proliferating under hypoxic conditions, reductive carboxylation of glutamine-derived a-KG provides citrate for acetyl-CoA synthesis (red arrows)
The following diagram shows the specific metabolic pathways which the BiohackIT herbal formulas seek to inhibit.
Take 2-3 x caps with water in the morning after food (if not fasting), 2-3 x Caps after lunch and 2-3 x Caps in the evening after food or as directed by your health professional. For greater effect, increase the dosage. FASNHIB™ may best be supported with GLUTAHIB™ Glutamine metabolic fuel supply inhibiting formula, AUTOPHIB™, EGAMMA™, CURCUBOS™, FENBENCUR™, CURCUMEL™, ZERO Sugar/Fat Diet, METFORMIN, LD/ASPIRIN and/or STATIN, DIPYRIDAMOLE & MILDRONATE. Avoid White Rice, Sesame Oils & Flax-oils. FASNHIB™ may be made more effective by combining with intermittent fasting. It is also possible that in the beginning low energy levels and altered immune T-cell response may be experienced, this may improve over a period of days/ weeks, weight-loss may also be experienced.
Berberine Note: Berberine HCL content is 8% of the Coptis extract, therefore 2 capsules = 80mg Berberine HCL and may not need to be pulsed as you would with a Berberine isolate.
Quality Assurance Declaration
Werone.co endeavors to use the most potent source materials within our formulas. Our herbal extracts are sourced and tested by the only Government-certified large scale producer of crude herb (powder-free) TCM concentrates in Asia who manufacture to GMP / ISO 9001/2000 pharmaceutical grade and also operate an ISO17025/TAF-certified laboratory where they subject all plant extracts to strict quality inspections free from heavy metals, pesticides or microbes before release to the clinics all over the world. The formulas and tinctures are assembled without fillers in small batches by a BHMA member herbal dispensary.
Nutraceutical DisclaimerThese statements have not been evaluated by the Food and Drug Administration or MHRA and the items are not intended to diagnose, treat, cure, or prevent any disease nor are they associated, endorsed, affiliated or sponsored by Anthony William, Medical Medium® Joe Tippens, Jane McLelland or Jim Gordon.
When fats commit crimes: fatty acid metabolism, cancer stemness and therapeutic resistance
THE EMERGING HALLMARKS OF CANCER METABOLISM (2016)
ATP-Citrate Lyase: A Key Player in Cancer Metabolism
Unsaturated Fatty Acids Maintain Cancer Cell Stemness
Astragalus Polysaccharides Lowers Plasma Cholesterol through Mechanisms Distinct from Statins
Chinese Herbal Medicine on Dyslipidemia: Progress and Perspective