Chronic Diseases - Epigenetics
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1 Chronic Diseases - Epigenetics As explained in the website because minerals and elements are the foundation of the epigenome, epigenetic modeling requires new thought processes that are supported by quantum mechanics and physical science. The new resulting epigenetic modeling process has been transposed into biologically-friendly terms for independent verification by anyone with knowledge of biology 101. Copy error mutations can be proven to be responsible for approximately 2/3 of cancer mutations. With that said, if an interest truly exists in gaining access to verifiable modeling tools that can be used to verify the causes of chronic diseases, interested parties must set aside the time to enable MCFIP to use these slides to bridge communications between flawed genomic theories and epigenetics.
2 Chronic Diseases - Epigenetics Research has validated the fact that, as cells divide, copy error mutations can prevent DNA repair. The following slides will address the primary cause of copy errors that have been validated by recent research as being the cause of approximately 2/3 of cancer mutations. During verbal discussions, the role of neuropeptides (neuropeptide Y, pancreatic polypeptide and peptide YY) relative to the causes of copy error mutation can be explained for independent verification. The following will be used during the discussions to explain key verifiable cellular mechanisms that are the foundation for epigenetic modeling that, if disrupted, can result in copy error mutations. %20Errors%20-%20Neuropeptides.pdf Note: Epigenetic modeling will allow interested parties to understand how copy error mutations are the underlying cause of most chronic diseases and not only cancers.
3 Chronic Diseases - Epigenetics Individuals who are astute in any bioscientific discipline can use the facts outlined in the website to verify the following as irrefutable facts: 1. Current genomic sequencing based on the A C T and G alphabet is flawed 2. Minerals and elements are the foundation for intra and intercellular signaling 3. The epigenome that encompasses agonistic and antagonistic aspects of minerals and elements provides the basis from which an explicit and replicable model can be used to identify the causes of chronic diseases
4 Maxim of The Center for Modeling Optimal Outcomes : Unless you know what you are looking for, you will never find it. Bioinformatic search methods have failed to look for minerals and elements as well as interactions, imbalances and homeostasis that are the foundation for epigenetics. 4
5 Chronic Diseases - Epigenetics Concise examples for the roles of minerals and elements that form the foundation for cellular signaling (typically in conjunction with amino acids to regulate on off activities) are provided here: Calcium Magnesium %20Causes%20of%20Chronic%20Diseases%20x.pdf Sodium Potassium %20Potassium%20Imbalances.pdf %20Sodium%20(Flawed%20Theory).pdf
6 Overview of B Vitamins Reference to vitamins usually triggers a cynical response from biomedical researchers. However, when reduced to their elemental constituents and their epigenetic roles defined; they can be verified as being part of one of the DNA repair mechanisms. As outlined in the following slides for verification by individuals who are seeking to identify causes of chronic diseases, the following are roles of several vitamins that can be discussed as part of explanations for the epigenome. Vitamins B1 B2 and B3 are anabolic (binding) Vitamins B5 B6 and B7 are catabolic (autophagy disassembly) Using lay terms, as cells divide, tact knowledge dictates that their contents must be disassembled (catabolic activity) and then reassembled within the two cells (anabolic activity). The MCFIP processes for the epigenome provide the scientific foundation from which the anabolic and catabolic activities can be subjected to validation. 6
7 Vitamin B1: Three Forms of Thiamin (Triphosphate Diphosphate and Monophosphate) Triphosphate (Glutamic acid) IL-16 (Iron Sulfur based) Monophosphate (Glycine) Diphosphate (Proline) 7
8 Vitamin B2: Three Forms of Glutaminase (i.e. 1 2 and 3) Glutaminase 1 (Leucine) IL-16 (Iron Sulfur based) Glutaminase 3 (Valine) Glutaminase 2 (Isoleucine) The p53 binding protein family is another designation for the three forms of vitamin B2; i.e. p53bp1 p53bp2 cathepsin and so is the binding protein family known as IGFBP4-8
9 Understanding Vitamin B2 Access to an Internet search engine can verify riboflavin (vitamin B2) as being adenosine triphosphate. Catabolic activity cleaves it into adenine dinucleotide (FAD) and flavin mononucleotide (FMN). Collectively, these three isoforms represent one of the binding mechanisms for the anabolic activity necessary to perform DNA repair as cells divide. Shortcomings in the original DNA modeling by Watson and Crick due to inadequate technology resulted in the designation of adenosine as a nucleoside and eventually as a nutritional supplement; aka a vitamin. 9
10 Vitamin B3: Three Forms of Abl (i.e. Abl1 Abl2 and BCR-Abl) Abl-1 (Phenylalanine) IL-16 (Iron Sulfur based) BCR- Abl (Tryptophan) Abl-2 (Tyrosine) Note: Phenylalanine, tyrosine and tryptophan are three of the 4 aromatic amino acids that absorb UVB light 280 nm. The 4 th one can be verified as being histidine. Tyrosine kinases (the inability to disassemble and convert the three primary aromatic amino acids) is designated as tyrosine kinase and it is one of the primary causes of aggressive cancers. 10
11 Vitamins B5 B6 and B7: Catabolic Activity for DNA Repair To Prevent Copy Error Mutations To avoid complexity and avoid confusion, we have opted to set aside explanations for the copper zinc based byproducts of IL-18 (aka neuropeptide PYY) that forms vitamins B5 B6 and B7 when subjected to catabolic activity. These catabolic epigenetic signal molecules can be verified as regulating autophagy; the mechanism that is crucial to prevent copy error mutations that can disrupt DNA repair. 11
12 Summary These slides have been provided to serve as a basic introduction to epigenetics. As outlined in the information provided, the discipline of epigenetics provides a means of rectifying flawed genomic modeling and it establishes an explicit and replicable tool to identify the causes of chronic diseases. DNA repair encompasses a variety of cellular mechanisms beyond copy error modeling that rely on homeostasis to prevent chronic diseases. The following provides insight into several of these epigenetic activities that can be discussed with individuals who are seeking to apply or commercialize aspects of the epigenome. meostasis.pdf Interested parties are encouraged to contact William McFaul: WJMcFaul@Aol.com to discuss how access to the model for epigenetics based on the principles of physical science can be provided. 12
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