This website presents research and analysis which demonstrate causal mechanism and ability to prevent and alleviate all disease and detrimental outcomes.

This site is now the Research documents Website, follow the Capsule Shaped Button at the Top of the Page to Proceed to the Primary Website. The complete List of training Data for specific areas of Pathology and for the Health Industry Generally is located as Training Data Documents on the Primary Website.  The Data listed here is applicable to all Pathology in a General Context as a General Set of Training Data or Remediating Activity for any Disease or Condition. The Research Content is being Gradually relinked to their positions on the Pages of Content. The username and Password to the Research Content Pages are as follows.


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The summary of the research seems to be that all disease and detrimental behavior emerge from impaired or inhibited function of PEMT1, PEMT2, PEMT3, its supplying pathways, its supply of diverse fatty acids for LPCAT/MBOAT activity, and correlated inadequate Hydride, Methyl Group and Choline availability.  Certainly, allow inadequate satisfaction of Human and Social requirements modulate the ways in which such factors emerge as outcomes.

Therapeutics Optimally are Derived from Diagnoses Conducted at the following levels











Local Area of Pathology or Biopsy





or other levels

Subsequently, Diagnoses of causal factors in these contexts constitute complete Diagnosis

How or Why the Condition Emerged

How orWhy the Condition Persists

Why or How the Condition Progresses

Why or How the Condition Imparts Detriment

How or Why the Condition Eludes Biological Capabilities of Prevention, Alleviation, Repair or Allelivation

Subsequently, Therapeutic management or alleviation of the following Diagnosed causal factors in these contexts constitute complete Diagnosis

One or More Factors Required for How or Why the Condition Emerged

One or More Factors Required for How or Why the Condition Persists

One or More Factors Required for Why or How the Condition Progresses

One or More Factors Required for Why or How the Condition Imparts Detriment

One or More Factors Required for How or Why the Condition Eludes Biological Capabilities of Prevention, Alleviation, Repair or Allelivation

Summary of the Recommendations include those presented here. The details are located inside the Amehsi Website

  1. Protecting the Home, Environment and Physiology from Energy and Communications Fields

  2. Protecting Physiology from Chlorine and Fluorine in water and other supplies

  3. Avoiding Typical Tables Salt which can have abrasives that impair vasculature

  4. Alleviating Choline Deficiency and assuring Hydride Transfer into Physiology and Methyl Group availability

  5. Assuring the function of the Phosphatidylethanolamine

  6. Managing C-Reactive Protein with inhibitors including Curcumin

  7. Managing Homocysteine to below 6 Micromoles per Liter

  8. Managing S-Adenosyl Homocysteine to below 0.012 Micromoles per Liter

  9. Enabling BHMT with Trimethylglycine, Zinc and 5678 Methyltetrahydrofolate

  10. Enabling BHMT2 with S-Methylmethionine, Zinc and 5678 Methyltetrahydrofolate

  11. Using Dimethylacetothetin, Trimethylselenonium+ to potential Trimethylsulfonium, or Trimethylsulfonium to enable Thetin-Homocysteine Methylpherase

  12. Assuring obtainment of Sodium Each Day as Pink Himalayan Sea Salt to obtain diverse minerals and enable Sodium Coupled Choline Transport

  13. Assuring the Function of Homocysteine Hydrolase, Apoptosis Pathways, Biosynthesis and Stability with NAD+

  14. Managing Trimethylamine-N-Oxide with 3,3 DMB, Grapeseed Extract, Broad Spectrum Antibiotic during Emergency, Post/Pro/PreBiotic

  15. Managing Trimethylamine-N-Oxide with Laxatives, Fasting, Water, Balsamic Vinegar, Fruity Olive Oil

  16. Assuring Plasticity and Slow Wave Potential of Digestive Pathways by providing the complete factors presented here and Potassium Water each day such as Bai unflavored Water or Superwater from Bodyarmour

  17. Assuring the regulation of Choline Kinase Alpha

  18. Securing Cholesterol availability for Star Protein enabled Shielded Transfer or Cholesterol to the Mitochondria for Steroidogenesis

  19. Assuring Sulfur Obtainment such as Methylsulfonyl Methane, assuring Diverse Minerals including Sulfur Eluting Alkali, Molybdenum for Sulfur Toxicity

  20. Securing availability of Selenium such as Selenomethionoine and Glutathione

  21. Regulating Inducible Nitric Oxide Synthase to prevent depletion of Ca2+, uncoupling, impairing LANDs, CDP, Fatty Acid and other Pathways

  22. Regulating Uncoupled Nitric Oxide Synthase to prevent Infarct using L-Arginine, Tetrahydrobiopterin, Vanadium, Sapropterin, others

  23. Managing AP1 with inhibitors or Berberine

  24. Securing SP1 with Curcumin

  25. Securing PD1, and PDL1, while managing, also, Indoleamine 2,3 Dioxygenase,

  26. Managing Uncoupling of NOS by inhibiting Nitrosamine with Kolaviron/Garcinia Kola Seed Extract, managing Hypochlorite

  27. Managing Uncoupling of NOS by managing Superoxide with Superoxide Dismutase, managing H2O2 with Catalase, managing Peroxynitrite

  28. Managing nSMase/aSMase, SP1, SP1 Lyase

  29. Using Vistide, HPMPC, Favipiravir Phenols, Egyptian Artichoke, and Microbial RNA Polymerase Inhibitors to disrupt Microbe function and retroactivity

  30. Diverse Vitamin Supplement with all B Vitamins and B12 Methylcobalamin

  31. Scavenging Methylglyoxal with L-Arginine

  32. Scavenging Oxalate with Magnesium, Trimethylglycine, Beet Powder from Beta Vulgaris, and Water

  33. Monitoring and Managing L Lactate and L Lactic Acid

  34. Managing and Monitoring D Lactate and D Lactic Acid

  35. Diverse Nucleotides with DNA/RNA Nucleotides

  36. Management of Poly (ADP) Ribose with inhibitors or Nucleotides to assist in PARP/PARS DNA/RNA Repair/replication/Transcription

  37. Ribose/Deoxyribose

  38. Managing impaired Histidine, Cysteine and Methionine from Carbonate Buffering System activity because using these as buffering capabilities impairs methionine metabolism and impairs the Histidine, Cysteine, Aspartic Acid locus of Cysteine Protease Catalytic Activation used by Caspases

  39. Organic NonGMO Nutritional Regimen

  40. Avoiding Amino Acid Supplements unless 800 mg of Choline is obtained each day

  41. Regular and Moderate Exercise

  42. Regular Rest and Sleep Schedule

  43. Assured Housing

  44. Access to proactive and comprehensive Health, Behavior, Cognitive and Therapeutics Services Coverage

  45. Access to Health Services which analyze, diagnose, and intervene how detrimental outcomes emerge, persist, impart detriment, progress and escape physiological capabilities which prevent and repair such outcomes

  46. Assured Nutrition

  47. Economic and Social Security

The Major Axis of Pathology and Metabolic Syndrome to Consider Analytically when reviewing these enzymes.

  1. Choline Deficiency

  2. Inhibited PEMT1/PEMT2

  3. Increase in S-Adenosyl Homocysteine and Homocysteine Resultant of Impaired PEMT activity

  4. Upregulation of Choline Kinase and CDP Choline Pathway

  5. Upregulation of P53 which inhibits Glycolysis, Pentose Phosphate Pathway, NADPH Synthesis, Supply of CoA to Krebs Cycle, DNA Synthesis, RNA Synthesis, Insulin Receptor, Endocytosis of Sugar or Glucose through GLUT 1/3/4, Synthesis of Ethanol through Acetaldehyde Dehydrogenase, and Pyruvate Pathway to produce Anaerobic Glycolysis in tissues except for Actively Exercising Muscle Tissue. Available, but decreased, pyruvate is directed toward Lactate Anion to produce more NAD+ from NADH, depriving other pyruvate metabolic pathways but also produces additional NAD+ as PARP signaling occurs persistently 1 million instances each day in each cellular entity for DNA Repair waiting for DNA Nucleotides to become available while PARS also waits for RNA to be available more often than 1 million instances each day in each cellular entity to conduct Gene Transcription while waiting for enough RNA to be available.

  6. iNOS from particular factors in environment, water and Electromagnetic/Magnetic fields, as well as particular sound characteristics, depletes Ca2+, produce apertures in Plasma Membrane, depletes extracellular Ca2+ and depletes extracellular L-Arginine, while causing Sarcolemma to Collapse, sequestering Ca2+ away from eNOS and nNOS, and causes the principle Loci of cellular endocytosis, secretion and signal transduction in the Caveolae to become impaired through constriction of the Caveolae.

  7. Phospholipase C is active, catabolizing cellular membranes to free choline, freeing Ca2+ from around the Headgroups of Membranes Phospholipids to replace iNOS depletion of Calcium, both resultant of Choline inadequacy, change in gravitational fields, massive apoptosis of cellular entities required the immune system to require being instrument to prevent tissue collapse, electromagnetic/magnetic/sound influences including artificial light and energy/communications infrastructure, as well as particular factors in water and atmosphere.

  8. Phospholipase D is also active, causing negative curvature of cellular membranes utilized in fission and fusion of membranes. Phospholipase D also enables fission of Membranes which produce endosomes that allow viruses or microbes to escape the membrane interstitial space where toxic reactive molecular species would prevent their continued biological activity and where MHC Histocompatibility reporter complexes wound integrate with their proteins and conduct antigen presentation on lipid rafts of CD4 and CD8 to allow T Cellular entities to copy these to their own DNA using V(D)J Recombination, followed by migration to the Thymus for T Cellular Replication, Priming and readying of monitoring and immune cascade which are components of adaptive Cellular Immunity as well as components of Humoral Immunity. Every Virus Requires the Expression of iNOS in some capacity, including incipient activity and continued exhibition as well as continued pathology.

  9. Natural Cytotoxic Cellular entities utilized in Oncological therapy inhibit PEMT, stimulated Phospholipase A2 versions which have Ankyrin moieties which inhibit P53 and thus decreases the ability of p53 to cause apoptosis and clear senescent cellular entities affected by disease. T Cellular entities inhibit PEMT and exacerbate the other pathologies presented here. Adaptive Immunity Cytotoxic T Cellular Entities rely upon P53 to cause Apoptosis in Oncology exhibiting Cellular Entities while innate immunity Natural Cytotoxic Cellular Entities Rely upon P53 in Neoplasms to upregulate PD-L1, FA/APO1 and MHC I. Inhibition of P53 and inhibition of Natural Cytotoxic Cellular Entities resulted in expansion of inflammatory Neoplasm Potential Cellular Entities, such that P53 exhibition without Natural Cytotoxic Cellular Entities was more efficient in producing apoptosis in these inflammatory cellular entities than both P53 and Natural Cytotoxic Cellular Entities together. However, PD1 and PDL1 integration at the locus of Inflammation may protect P53 from Natural Cytotoxic Cellular entities similarly to the way that PTEN Protects P53 from Deterioration through the action of MDM2. PD-1 is required to expressed to be presented on the extracellular surface of Antigen Presenting Cellular entities such that when Adjacent to PD-L1, these ligands link to each other, preventing Ligand activation of PDL1, MHCp and B7 by Natural Cytotoxic T Cellular Entities. T Cellular Entity Therapy or CART Therapy relies upon functional modulation of PDL1, MHCp and B7 using PD-1, inhibitors of PD1, inhibitors of PDL1 management of any of these, and assurance of Methylation Pathways with the important caveat that inhibition of P53 is essential to Natural Cytotoxic Cellular Entity Production, CD16 is essential because it activation can stimulate production Ca2+ Independent Phospholipase A2 version that have Ankyrin Inhibitors of P53,although P53 is impaired from NAD+ depletion along with impairment of large aspects Phospholipase, Acyltransferase, Aldehyde Dehydrogenase, and other factors involved in LANDs Cycle, Fatty Acid and optimal Phospholipid metabolism. Although Natural Cytotoxic Cellular Entity Therapy is known as CART therapy, it is also known as Immune Checkpoint Blockade Therapy and also can involve modulation of CTLA4 which competes with BL7/BL2 activation of CD28 as PD1 interaction with PD-L1/PD-L2 which is important because when PD1 interacts with PD-L1 or PD-L2 there is an activation of SHP2 that includes inhibition of Bl7/Bl2/CD28, inhibition of pMHC/TCR Complex, and ancillary pathway inhibition including downregulation of PI3K and AKT signaling that would occur resultant of outcomes in Immune Checkpoint Ligand activation.

  10. The exhibition of iNOS depletion of Ca2+, the providing of Ca2+ by Ca2+ independent Phospholipases, the depletion of Store Operated Ca2+ by PIK3 and IP3 which perforate Endoplasmic Reticulum Membranes and Perforate Plasma Membranes to allow systemic gradients of Ca2+ to supply persistent iNOS signaling with Ca2+ from even the Bones, can also include the observation that Ca2+ in intracellular environment can stimulate apoptosis or necrosis while decreases can also cause substantial changes that also potentiate pathology, apoptosis or necrosis. The potential that functioning iNOS can produce a pumping mechanism to supply Ca2+ when Ca2+ is to inadequate for iNOS function, a mechanism of enhanced influx using systemic Ca2+ to supply intracellular environment with Ca2+, and the tunneling mechanism which supplies Ca2+ directly to subcellular locations where iNOS is operational, all potentiate a circumstantial depletion and circumstantially enhanced availability of Ca2+. N-Methyl-D-Aspartate NMDA Receptors cause Neurotoxicity through increased Ca2+ by activation of NMDA which results progressive activation of 1beta-Converting Enzyme (ICE)/CED-3-Associated Protease known as CPP32/Yama/Apopain which is also known as Caspase 3. PARP is segmented and deteriorated by Caspase 3. Calpain is a Ca2+ reliant Cysteine Protease that function as enhancers of cellular hypertrophy toward Lysis and Apoptosis, such that inhibiting Calpain results in deterioration of IkB alpha, activates Calcineurin and prevents apoptosis. Tuberculosis Microbes, for instance, depletes NAD+ to cause Macrophage Necroptosis. Depleting NAD+ with FK866 surmounts Bortezomib Resistance and enhances Multiple Myeloma Cellular Entity Clearing, Caspase 8/9/3 Activation, Poly (ADP-Ribose) Polymerase upregulation, Mcl-1 inhibition, NAD+ depletion, downregulation of Proteases varieties Chymotrypsin, Caspase, and Trypsin, as well as disruption of Angiogenesis. NAMPT inhibition mimicked or enhanced the effect of NAD+ depletion with FK866 along with Bortezomib. It must be asserted again, that, NAD+ depletion causes completely differentiated cellular entities to exhibit apoptosis and causes emerging, undifferentiated and progenitor cellular entities to exhibit impaired apoptosis, such that circulating proliferating cellular entities would ordinarily exhibit impaired apoptosis pathways. Why NAD+ supplementation was not utilized in the study of Bortezomib is not known, and depletion of NAD+ to be lower than NADH causes metabolic change would could possibly be distinct from Catastrophic Depletion of NAD+. Regardless, Poly (ADP-Ribose) Polymerase activity causes depletion of NAD+ and leads directly impaired DNA Repair, inhibition of P53 activity, inhibition of the Pentose Phosphate Pathway and Glycolysis Pathway, thereby can introduce Aerobic Glycolysis, results in S-Adenosyl Homocysteine increased by increasing Nicotinamide Methyltransferase activity and Impairment of S-Adenosyl Homocysteine Hydrolase, while also causing the paradigm of differentiate cellular entity apoptosis along with impaired apoptosis among emerging, undifferentiated, progenitor cellular entities.

  11. Ankyrin Protein expression is known to inhibit P53 and exhibition of Ankyrin proteins in molecules or upregulated expression of Ankyrin Protein is correlated to increased Viral Load in Herpes Simplex Viral Condition, although downregulation of Ankyrin with the same health condition is correlated to exhibition of a different version of the condition. Natural Demise Cellular Entities, Natural Cytotoxic, are known to upregulate Acetylcholine synthesis suggesting that Natural Cytotoxic Cellular Entities alleviate Anaerobic Glycolysis, Cause Aerobic Glycolysis, upregulates the availability of Pyruvate for being directed toward Acetyl-CoA a precursor to Acetylcholine Synthesis, thus enables decarboxylation of Pyruvate to occur. The directing of Pyruvate to Acetyl-CoA and Acetylcholine seems to the mechanisms by which Natural Cytotoxic Cellular entities prevent emergence of neoplastic activity and neoplasm in P53 deficient cellular entities, although the correlation between stored Choline and downregulation of Choline Kinase Alpha, the CDP-Ethanolamine Pathway and inhibition of Phosphocholine availability as well as inhibition of the Xenobiotic Histamine response changes to plasticity produced by upregulation of the CDP-Ethanolamine Pathway, all seems to be relevant. Natural Cytotoxic Cellular Entities other than T Cellular Entities required Methyl Groups and Methylation pathways to function, as well as reconstitute Acetyl-Choline storage by upregulating Pyruvate availability or changing rate at which Pyruvate is directed toward Acetyl-CoA for interaction into Acetylcholine.P53, SIR, PARP and Fatty Acid Synthesizing Alcohol Dehydrogenases ALDH3B2, ALDH1B1, ALDH3A2 are each reliant upon NAD+ while the first enzyme in Beta Oxidation of Fatty Acids is also reliant upon NAD+ similarly to reliance of S-Adenosyl Homocysteine Hydrolase or SAH on the redox enabled by NAD+.  Importantly, this suggests that a somewhat culminating phase of physiological changes that comprise typical emergence of pathology is NAD+ depletion which introduces impairment of P53 which is actively produces changes the way that cellular entities emerge, mature, develop and experience programmed deterioration as well as impairs P53 in ways that constitute exhibition of Aerobic Glycolysis. The Hydride Potential of NAD+ are pervasive factors in existentialist contexts, angular or vector contexts that interact in dimensions of space and time, linkage to celestial entities which use hydride to enhance mass and provide energy resources.  SAH transforms S-Adenosyl Homocysteine into Homocysteine which can depleted by Autophagy, Proteolysis, Transsulfuration pathway, BHMT, BHMT, Methionine Synthase and Thetin-Homocysteine Methylpherase as well as functional PEMT1/PEMTS and functional PEMT2/PEMTL.NAD+ inadequacy can impair Acetyl-CoA cycling and enabled impaired storage of Acetylcholine, impair the first phase of the Pentose Phosphate and Glycolysis Pathway, and cause differentiated cellular entities to exhibit Parthanatos version Apoptosis while emerging cellular entities have impaired apoptosis. Ca2+ depletion adds to this by causing misregulation of apoptosis.

  12. Inhibitors of PEMT such as AP1, SP1, Indoleamine 2,3 dioxygenase IDO, iNOS, Uncouple Nitric Oxide Synthase, Chlorine, Fluorine, Monocyte Chemoattractant Protein 1, Thrombin, Trimethylamine-N-Oxide, S-Adenosyl Homocysteine, Homocysteine, Nitrosamine, C – Reactive Protein and other factors are primary inhibitors of PEMT and each promote misregulation of Cyclins and requirement being preventing from inhibiting PEMT in pervasive microbial or other conditions, including diseases, persistent impairment and behavioral conditions.

  13. PEMT relies upon newly produce Phosphatidylethanolamine first from Decarboxylation of Phosphatidylserine into Phosphatidylethanolamine and then from Choline Phosphotransferase, preferring newly produced phosphatidylethanolamine that is the least glycosylated, while the preference for DHA, Oleoyl, first fatty acid in Beta Oxidation Palmitoyl, Extended Length Arachidonate, Omega-3 Ether Linked Polyunsaturated Fatty Acids seems to be resultant of substrate availability according to Ca2+, NAD+, Choline, Lands Cycle Phospholipase/Aldehyde Dehydrogenase/Lysophospholipid Acyltransferase function which shuffles fatty acids for diversity. However, nSMase and aSMase as well as S1P and S1P Lyase status are important because the upregulation of the Choline Kinase Alpha, CDP-Choline, Phosphatidylcholine, nSMase/aSMase, S1P, SPL pathway determines if this upregulation results in diverse survival signaling that can include G Proteins or if these are directed through S1P Lyase toward endogenous Hexadecenal toward Hexadecenal Trimethylsulfonium conjugates that inhibit Choline Kinase Alpha as well as S1P Lyase directing of S1P toward endogenous synthesis of Ethanolamine as Phosphoethanolamine which is shunted into the CDP-Ethanolamine Pathway two enzymic interactions away from production of Phosphatidylethanolamine.

  14. Impairment of cyclins emerges when DNA repair becomes impaired, Choline is deficient, PEMT is inhibited by any factor including S-Adenosyl Homocysteine, Homocysteine, Trimethylamine-N-Oxide, AP1, SP1, Thrombin, iNOS, uNOS, Peroxynitrite, Indoleamine 2,3 Dioxygenase, Nitrosamine, C-Reactive Protein, Choline Deficiency, or other factor. PEMT then results in P53 upregulation, and Natural Cytotoxic Cellular Entities must downregulate P53 using NAD+ inadequacy, Phospholipase IPLA2 with Ankyrin moieties, and adequate Methyltransferase Activity to exhibit their ability to cause Cytotoxicity or enhance survival when PD1 is integrated into PDL1 or PD1 is integrated into PDL2.Cytotoxic T Cellular entities of Adaptive Immunity inhibit PEMT and utilize P53 to determine cellular outcomes while innate Immunity Natural Cytotoxic Cellular Entities inhibit P53, upregulated Acetylcholine Storage to sequester Energy molecules as Phosphate and Choline away from Choline Kinase which supplies the CDP Ethanolamine Pathway with energy for survival signaling, histamine response, xenobiotic response and increase of less than optimal membrane phosphatidylcholine. T Cellular entities inhibit PEMT and exacerbate the other pathologies presented here. Adaptive Immunity Cytotoxic T Cellular Entities rely upon P53 to cause Apoptosis in Oncology exhibiting Cellular Entities while innate immunity Natural Cytotoxic Cellular Entities Rely upon P53 in Neoplasms to upregulate PD-L1, FA/APO1 and MHC I.Phosphatidylcholine, however, if adequate, results in abatement of cellular cycle while Omega-3, Ether Link Fatty Acids, including Polyunsaturated Fatty Acids such as DHA, EPA, Oleoyl and others, promote deterioration of pathology exhibiting cellular entities. Upregulation of the CDP-Ethanolamine Pathway begins with impaired synthesis of Acetyl-CoA occurring after PEMT inhibition upregulates P53 and pyruvate levels and Glucose available to Pentose Phosphate and Glycolysis pathways slow to a trickle in all but actively exercisable Muscle Tissue or actively functioning muscle tissue. The slowing of Glucose entry into intracellular environment occurs from P53 inhibition of endocytosis of Sugar absorption and metabolisms by inhibiting Insulin Receptor and GLUT 1/3/4 while also inhibiting Glucose 6 Phosphate metabolism toward pyruvate, decrease directing of Pyruvate to Acetyl-CoA Krebs Cycle and Acetylcholine Synthesis, as well as inhibits Acetaldehyde and Ethanol synthesis to prioritize directing of Pyruvate toward Lactate Anion, resulting transformation of NADH to NAD+.  Pyruvate directed toward Krebs and Acetyl-CoA does not potentiate increases in NAD+ and directing of Pyruvate toward Acetaldehyde may result in NAD+ but requires cofactors as gating mechanisms. Lactate Anion is among the strong Ions and can disrupt strong Ion Balance as well as potentiate Lactic Acid. Challenges to the strong Ions balance invoke the Carbonate Buffering Systems which places additional disruption of Pyruvate direction in Glycolysis Pathways as well as causes Cysteine and Histidine in the Cysteine Protease Catalytic Activation Loci to become utilized along with methionine for Carbonate buffering, potential impairing Cysteine Protease Activity and programmed Apoptosis. pRb, Cyclins and CDKIs are all affected by Choline Kinase Upregulation, AP1, SP1, Phosphatidylcholine exhibition in Membranes, upregulation of S1P which supplies signals for diverse G Protein, Cyclin and other Survival Signaling, while nSMase/aSMase, Ceramide, S1P signaling also affects numerous mechanisms required for cellular cycle checkpoint, DNA replication, and other Mitotic regulation factors. AP1 and SP1 oppositely regulate Telomerase Reverse Transcriptase repair of Telomere depletion.AP1 inhibits PEMT activity.

Where to Begin for Oncology

     Although Phenotyping the Metabolome and Genome of Biopsied Diagnostics are optimal for oncology, beginning therapeutics without a reference point can be challenging.  Crispr Cas perfect genetic therapy is emerging is essential in this context.  However, the pathology stack presented here I likely to represent a comprehensive group of causal factors which can be expanded using the other Amehsi Research, Diagnostic Factors, and other information.

Similarly, the factors presented in this page already and details within the website should enable clinicians and patients to outperform the market and the industry in assuring therapeutically optimal outcomes, the following information provides a reference point to begin. However, the factors presented heretofore are known to be of such influence in improving outcomes that each has been recommended because they introduce a requirement for change of practice in a wide array of therapeutic fields.

      A Study produced by practicing health providers observes that among diverse oncology there may be a less than 20 percent response level for Suramin, Amobarbital, Quinine, Metformin, Silibinin, Ketoconazole, Quinacrine, and Tolbutamide, whereas a greater than 20 percent response level was observed for PKM2 Activation using D – Fructose 1,6 Bisphosphate, PEP Carboxykinase Inhibition using Albendazole, Lipolysis Inhibition using Simvastatin, LDH Inhibition using Gossypol, Phospholipase D Inhibition using Farnesyl, Phospholipase C Gamma Inhibition using Genistein, management of NADH Dehydrogenase activity using Capsaicin, Hexokinase Inhibition using Lonidamine, PDH activation using Dimercaprol, Lipotropic Homocysteine depleting and Choline potentiating Betaine, ATP Citrate Lyase activation using Hydroxycitrate which constitutes a Krebs Metabolite, Inhibition of Anhydrase Carbonic Factors using Acetazolamide, Choline Kinase inhibition by Miltefosine, PDHK1 inhibition by Dichloroacetate and PDHK1 inhibition by Lipoic Acid.  These confirm the finding of the Amehsi Specification.  The article presents diverse oncology factors in a two separate lists, although the most effective therapeutic in the study were a combination of Alpha Lipoic Acid 600 mg Intravenous, Vitamin D Hydroxycitric Acid 500 mg Solgar along with variable addition of Capsaicin/Octreotide for Melanoma correlated conditions, or evening Administration of Naltrexone Revia for Chemoresistant Advanced Metastatic Oncology otherwise.


     Other factors included in the study were Glutaminase inhibitor 6-Diazo-5-Oxo-l-norleucine, Polyamine Synthesis Inhibition by Agmatine, Citrate Synthase Inhibition by Alpha Ketoglutarate, Na+/H+ Antiport Inhibition by Amiloride, IGFBP activation by Apigenin, IGFBP Activation by Bicalutamide, Hypothalamic D2 Receptor Agonist activity by Bromocriptine, HDAC Inhibition by Butyrate Sodium, PK-M2 inhibition by Chitosan, Choline Chloride which supplies Hydride along with Methylation and Betaine, Citrate which inhibits Citrate Synthase, PEP Carboxykinase inhibition by Cryogenine, AID/iNOS/SP1 inhibition by Curcumin, D-Alanine which inhibits Alanine Transaminase, Epigallocatechin Gallate which regulates PK-M1/M2 Splicing, NSAID Ibuprofen, Indole 3 Carbinol which enables Triglyceride reduction, Fluoxetine which enables Serotonin Reabsorption Inhibition, Ketoconazole which inhibits Cytochrome P450 Demethylase, Lactoferrin which decreases Oxidative distress, Letrozole which inhibits Aromatase, L-Norvaline which inhibits Arginase, Melatonin’s Antioxidant/Antiproliferative, Menadione Tyrosine Kinase Receptor Inhibition, Omeprazole which activates IGFBP, Oxythiamine which inhibits Transketolase, PEG8000 activation of PK, Pegvisomant GH Receptor Inhibitor, Pralidoxime which inhibits Alanine Transaminase, Retinoic Acid activation of Cellular differentiation, Sulpiride which inhibits GH Secretion, Suramin which inhibits Citrate Synthase, Vitamin B12 which assists transforming Homocysteine to Methionine, Valproate Sodium which inhibits HDAC. The study presenting this information is essential to read for practicing providers.

Methanol extracts of Myoga Flowers and Labdane Diterpene Galanol inhibit IDO while Galanol Exhibited a 7.7 Micromole IC50 while cellular level IC50 was 45 Nanomoles per Liter.  IDO has its catalytic activity extensively inhibited by Quercetin, Luteolin, Curcumin, Galanol, Andrographolide Angelica, Chrysanthemums, Burdock, Zedoary, Andrographis.

Sources of information include

    Metabolic Treatment, the Example of Oncology. 




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