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Epigenome Modulation

Process - and it's Science

The Epigenome Modulation Process is designed to take advantage of the fact that genetic expression is not set in stone but is rather alterable or even programable so as to optimize the epigenetic or effective expression of the human DNA for maximum health, performance and well-being. 


Epigenetics is defined as cellular and physiological phenotypic (characteristic) trait variations that are caused by external (that is, external to the DNA) or environmental factors that switch genes on and off and can affect how cells read genes and even retranslate their instructions to our mind and body instead of being caused or determined solely by changes in our regular DNA sequence.


Epigenesis seeks to describe dynamic alterations in the transcriptional potential of the cells-- that is, how they replicate and express themselves both in and beyond our physiology. Some, perhaps many, of these alterations are proving to be heritable. Unlike genetics based on changes to the DNA sequence (the genotype), the changes in gene expression or cellular phenotype of epigenetics have other causes, thus the use of the prefix epi- (Greek: επί- over, outside of, around) not the least of which are our interpretations and perceptions of our environment.


Epigenetics has emerged as a new focal point in the fields related to biological and genomic science. When the Human Genome Project [e.g. a consortium project tasked with the identification and mapping of the active human DNA structure] was nearing completion it was heralded as destined to be the greatest achievement of our time. It was indeed a tremendous step forward in the understanding of the human body and its health challenges. However, since its completion in April 2003 the luster of this accomplishment has been dimmed by its limitations. The actual stars of the show—the genes themselves—esentially failed in the fullest sense to be the actual physiological and biochemical control mechanisms everyone expected—rather anticlimactic.


Not only did the heralded miraculous health benefits remain elusive but it had become even more perplexing that, as suspected, at least

98 % of human genes fell into an apparently useless category often referred to as “junk DNA.” This was DNA purportedly left over from eons of evolution that appeared to have no real purpose. (1)  It seemed that possibly that genetic science was missing something. Consequently, to address this puzzle (and because we were still far from the holy grail of DNA mastery) the National Human Genome Research Institute (NHGRI) launched a follow-on public research consortium named ENCODE already that September [2003] to carry out a project for the identification of all possible functional elements in the human genome sequence with particular attention to what was considered as noncoding DNA. (2)  Though results of this project have proven a bit controversial (such as what exactly constitutes the term "functional") at least two interesting facts have emerged from the project: 1) essentially 80 % of this so-called “junk” DNA is actually biologically active and, 2) that an increasing percentage of these supposed non-entity genes are being found to actually perform regulatory epigenetic like functions involving the expression of our regular DNA. In fact, we now know from other studies that over 50 % of our human genome contains what have been termed "jumping genes" which possess an amazing built-in intelligence that is not yet clearly understood. Which means this, what is now more appropriately named non-coding DNA doesn't look quite so much like junk anymore. (3) 


It has now become increasingly clear to science that the non-coding DNA is in fact very active in playing a complex support role for our regular DNA. In fact, even the term noncoding has become an inaccurate misnomer (there is, in fact genertic coding present). (4)  Even more confounding to mainstream science is that after all this investment in resources aimed at mastering the genome it turns out that our genes are not the sole determinants of our physical expression as previously understood, nor is their relationship to our environment the controlling factor in our health or behavior. Other related fields of study had to step in to address this emerging knowledge vacuum. So that, rather than telling our body what to do, they [e.g. the genes] are actually told what to do by other processes over which we mortals actually have some degree of control. Which is one reason why the spotlight has now turned to the field of Epigenetics. (5) “Epi” meaning “above,” the field of epigenetics is the study of the mechanisms that operate “above” and in conjunction with the genome by which our genetic pairs of DNA get turned on and off and are subsequently expressed in thousands of variations in the real world complex in which we live and experience life. (6)


Rather than determining our fate it turns out that DNA is like an array of blueprints locked in a set of drawers to which our epigenome has the keys. And there is, in fact, a considerable set of epigenetic “keys” in the form of proteins, peptides and various chemical compounds which allow and facilitate variations in carrying out details of the blueprints. In conjunction with this blueprint interpretation our epigenome is very much responsive to our neurological and emotional reactions to and perceptions of our ongoing environment. It is constantly receiving and managing signals from external and internal sources and refers in a rather interpretative manner to the blueprints when necessary. In fact, our interpretations of the totality of our environmental stimuli and our epigenetic functioning are intertwined in a marvelous dance that plays out as the unique expressions of a personal life path. But it doesn’t stop there. The epigenome is a two-edged sword. Besides the opportrunity it presents to manage our destiny we now understand, for example, that ancestral experiences including the effects of diet, disease and even emotional states are being passed down to later generations in a manner that cannot be accounted for by traditional genetic science and that at least some of these effects follow emerging patterns that also involve the epigenome. (7)


In consequence of this we also now know, both profoundly and scientifically, that at least some of the aspects of our behavior and habits carry a responsibility well beyond their immediate effects on ourselves and those in our mortal orbit. From studies of twins we know that one twin may experience cancer or other serious diseases to which the other appears immune despite having the exact same DNA and essentially the same early life “imprinting” experiences. The effect of nurture or environment, long thought to be the explanation for such discrepancies, has eventually been ruled out as the only primary cause. The difference in these twins is the manner in which the same set of genes is epigenetically expressed. A number of carefully controlled studies of certain populations stressed by such things as famine, constant threat to life or sexual abuse have demonstrable biochemical health and emotional effects upon later generations.  And, though it is not confined to them, we are particularly affected, for example, by the living habits and experiences of our grandparents—the effects varying for each grandchild. (8)


So what bearing does this have on our work? A great deal. This realm is important because the epigenetic processes by which our genes are expressed are in some measure alterable and programmable. So are the morphic and energetic fields that also play a significant role in this human dance of life expression. There is potentially programmable signaling at every juncture. We are not essentially the victims of our genes. Our environment and our perceptions and interpretations of our environment not only have a powerful effect upon our epigenome but they [e.g. our perceptions] are themselves changeable and programmable. Our epigenome is constantly receiving, digesting and responding to the plethora of environmental signals [entering through the filters in our Reticular Activating System] including generational factors while managing our DNA and its expression. In combination with the central and peripheral nervous systems (e.g. Brain), conscious and unconscious mental states, the intestinal nervous system (Biome), the epigenome constitutes a fourth leg of highly programmable health related signaling systems that operate together like the sections of an orchestra. This orchestra can play a symphony, a love song, or even a funeral dirge. (9)


Sages and motivational teachers have been telling us this [e.g. change our attitude, change our world] for a lifetime, but seldom with any lasting effect. Quantum physics is now telling us essentially the same thing. The common failure to successfully apply this knowledge is due to the fact that intellectual and even spiritual knowledge does not necessarily reach our core or change our unconscious programs. Even if a powerful motivating teacher can get us earnestly invested it almost always soon dissipates—our unconscious programming takes over. Our perceptions and their life controlling or altering effects must be changed at levels motivational speakers can’t reach and spiritual gurus cannot sustain. If we can actually change the nature of the input/incoming signals and/or, importantly, the significance or data interpretation attributed to them our genome is there to support it. The opposite, unfortunately, is also true. However, the object of personal and enduring change of a higher order must have some value that corresponds with our higher life purposes, and therefore taps into the Source of all life. Anything less than a head-heart-spirit congruence in partnership with God is a formula for anxiety and affliction—versus peaceful assurance (and, in this regard, we have found that a certain amount of grounding in verifiable science also assists to avoid misinformation and temptation to flights of fantacy).


The Epigenome Modulation Process employs all presently known epigenetic avenues to optimum gene expression. Epigenetic factors determine which inherited genes are actually available as well as how they are subsequently expressed in the mind/body. From a physiological perspective this includes energetic/informational normalization of the various cromatin [gene package] and gene expression mythylation cycles, nucleosome, RNA (ribonucleac acid) and histone behavior as well as the crucial regulatory, support through Intron and various other RNA (gene transfer, splicing and assemblage) functions of what are termed noncoding (so-called junk) DNA (10) including all environmental signaling effects and any upregulation that is required according to the intelligence contained within the body itself as well as the standards established by the mind/body templates contained in the Universal Information Field (UIF or Zero Point Field). Additionally it is imperative to include all other generational, energetic, informational, wave form and quantum factors that impact stress processing and life purpose including coordination with neurological circuits (including important cardiac, enteric and glial cell participation) (11) and with particular attention to the HPA axis (see RESEARCH 2) and the interpretative and filtering functions of the Reticular Activating System (RAS, see SCIENCE 3). Such incursions into the mind/body must ultimately be goverened and guided by the Intelligence that created it and normalized and optimized as much as possible in accordance to the same.


In this quest the client is our partner (also see: Methodology in the Background section page).  For details of the actual NG Epigenome Process steps see:

1) One of the puzzels for traditional or Darwinian science has been why the human and other mammalian organisms would retain large portions of apparently unusable DNA over the supposed eons of evolution. Evolutionary theory would dictate that it would have been jettisoned along the evolutionary path. On the other hand New Ager's seize upon its existence as evidence that man's higher intelligence is locked away in there somewhere waiting to be liberated by some spiritual elixir, perhaps even in the form of additional strands of operative DNA (like the 2 that are already seemingly doing all the work). Despite considerable speculation on the Internet and elsewhere there is, unfortunately, no scientific evidence to support this idea. The various so-called authorities cited turn out not to be valid authorities and their purported research constitute un-replicatable pseudo-science. As it is turning out now in emerging science restructuring the non-coding or the formerly so-called junk DNA to provide additional strands would actually negate the brilliant intelligence that is already built into our genome including its previously overlooked so-called non-coding or junk components. See also footnotes #'s 2 - 4 &  9 -10 below.

(2) In the absence of good information of noncoding DNA the ENCODE project set out to map and further understand what might be the function, if any, with this vast amount of inexplicable genetic material. Though still far from a comprehensive understanding it has became clear that significant portions of the noncoding or so-called "junk" DNA are actually biochemically active with some very much engaged with the regular strands of DNA in terms of support and regulation as well as with disease. It also appears that what is termed non-coding DNA constitutes a support system that provides regulatory, ordering and adaptability to changing human environments. Kellis, et. al., Defining functional DNA elements in the human genome, Proceedings of the National Academy of Sciences, 2014, ; See also: Ponting, Hardison, What fraction of the human genome is functional? Genome Research, 2011, 21(11):1769–1776. See also Footnotes #'s 3 & 4 below.

3) Woodmorappe, Junk DNA Indicted, 2004, ResearchGate TJ 1(18),pp1, 32-33; "Discoveries of function in erstwhile junk DNA are occurring at an ever-increasing pace. It is now realized that DNA has numerous functions beyond that of encoding peptides. A previously unsuspected world of widespread non-coding RNA, transcribed from intergenic DNA, introns and pseudogenes, has been discovered. This form of RNA appears to regulate many genes, and may even be the very foundation of human development. Antisense transcription of DNA is far more common in humans than supposed until recently. DNA that appears to lack conservation of sequence is probably nevertheless functional in terms of serving as ‘background’ for proper gene function, as a spacer between genes and their long-distance  regulatory elements, and, in the case of introns, in terms of physical length alone. Monotonous DNA repeats (STRs) probably serve a regulatory function for certain genes. Still other potential functions for junk DNA,  such  as those related to ‘epigenetic’ control of DNA, await clarification. It  is  easy  to  see  that  the  junk  DNA concept, whose longevity owes at least partly to tacit evolutionary assumptions, has very much delayed our understanding of the genome.... One can only wonder how much sooner the functions of noncoding DNA would have been discovered had the genome been recognized asthe pre-planned product of an Intelligent Designer instead of the long-term outcome of purposeless evolutionary processes." (emphasis ours) This overview also points out that many so-called non-coding genes actually do code for shorter-chain peptides and proteins. See also: Park, Junk DNA — Not So Useless After All: Researchers report on a new revelation about the human genome: it’s full of active, functioning DNA, and it's a lot more complex than we ever thought, Sep. 2012, See also New functions for 'junk' DNA? See also Lieff, Jumping Genes versus Epigenetics: The Real Drivers of Evolution Nov. 2012, evolution#sthash.kZCkyjW1.UdcgLAf5.dpuf

4) The following are some of the studies that underscore the importance of non-coding or junk DNA in the overall genomic scheme of health. SInger, A Surprise Source of Life's CodeEmerging data suggests the seemingly impossible—that mysterious new genes arise from “junk” DNA, Quanta Magazine, Scientific American, Aug. 2015; Mehler, Mattick, Non-coding RNA in the nervous system,  "Increasing evidence suggests that the development and function of the nervous system is heavily dependent on RNA editing and the intricate spatiotemporal expression of a wide repertoire of non-coding RNAs, including micro RNAs, small nuclear RNAs and longer non-coding RNAs. Non-coding RNAs may provide the key to understanding the multi-tiered links between neural development, nervous system function, and neurological diseases." The nervous system genomic interface is unique among organs in its precise and sophisticated patterns of regional cellular morphogenesis, cellular diversity, membrane electrical properties, responses to changing environmental inputs and perturbations, neural network connections, and dynamic activity-dependent alterations in synaptic strength underlying higher order cognitive functions including learning and memory (Abrous et al., 2005). These functional properties are, in turn, orchestrated by a corresponding set of multilayered developmental mechanisms (Mehler, 2002a, b), including neural induction, neural patterning and axis formation within the evolving neural plate and neural tube, elaboration of stem cell generative zones throughout the neuraxis and the evolution of connections between specialized regional neuronal and glial cell types. Alterations of specific components of these developmental stages and maturational processes result in a broad spectrum of neurodevelopmental disorders and predispose to an equally complex array of adult neurological and neuropsychiatric disorders, underscoring the levels of complexity in developmental and mature brain-behavior relationships. Although only about 1.2% of the mammalian genome encodes proteins, most of the genome is transcribed, in complex patterns of interlacing and overlapping transcripts from both strands (Carninci et al., 2005; Cheng et al., 2005a; Frith et al., 2005; Katayama et al., 2005; Engstrom et al., 2006; Mattick & Makunin, 2006), at least some of which are processed to form small regulatory RNAs such as microRNAs and small nucleolar RNAs (reviewed in (Mattick & Makunin, 2005). A range of evidence suggests that these RNAs form complex networks that direct the trajectories of differentiation and development, via regulation of chromatin modification, transcription, RNA modification, splicing, mRNA translation, and RNA stability (Mattick & Gagen, 2001; Mattick, 2003, 2004a) as well as other mechanisms (Prasanth et al., 2005; Willingham et al., 2005). It is also clear that multiple classes of non-coding RNAs (ncRNAs) are overly represented in the central and peripheral nervous system (Hsieh & Gage, 2004; Kim et al., 2004; Rogelj & Giese, 2004; Cheng et al., 2005b; Davies et al., 2005; Klein et al., 2005; Rogaev, 2005; Cao et al., 2006; Ravasi et al., 2006), underscoring the likelihood that nervous system development and function is heavily dependent on RNA regulatory networks the include the noncoding genome. The non-coding source miRNAs are short 21-23 nucleotide regulatory sequences that inhibit the translation or stability of target RNAs (Mattick & Makunin, 2005; Zamore & Haley, 2005). In mice, there are numerous brain-specific miRNAs (Krichevsky et al., 2003; Cheng et al., 2005b; Lim et al., 2005; Xie et al., 2005), a significant subset of which have been directly implicated in human neural development and neural cell differentiation (Kawasaki & Taira, 2003; Smirnova et al., 2005). A wide variety of miRNAs are localized to neuronal subtypes with the highest concentration in the cerebral cortex and the cerebellum (Kosik & Krichevsky, 2005; Krichevsky et al., 2006). Additional miRNAs are present within glial cell subtypes with others exhibiting more ubiquitous or neural progenitor cell-specific patterns of expression (Krichevsky et al., 2003; Klein et al., 2005; Smirnova et al., 2005).  miRNAs are also abundantly expressed in the adult brain and appear to regulate the maintenance of mature neural traits and synaptic plasticity (Krichevsky et al., 2003; Jin et al., 2004; Sempere et al., 2004; Cheng et al., 2005b; Kosik & Krichevsky, 2005; Smirnova et al., 2005; Conaco et al., 2006; Schratt et al., 2006). Numerous studies suggest that miRNAs are intimately involved in synaptic function and input specificity during memory formation (Martin & Kosik, 2002; Schaeffer et al., 2003; Kim et al., 2004; Lugli et al., 2005; Ashraf et al., 2006; Schratt et al., 2006). Moreover, transcripts encoding synapse-associated proteins also comprise the largest subgroup of predicted miRNA targets, including synapsin 1 and the fragile X mental retardation protein (FMRP) (John et al., 2004). A novel RNA called dsNRSE (double-stranded neuron-restrictive silencing element) that resembles a miRNA in structure and length acts as a transcriptional activator of neuronal differentiation genes by converting the neuronal silencer factor (REST/NRSF) from a transcriptional repressor in undifferentiated and non-neuronal cells to a transcriptional activator during neuroblast differentiation (Kuwabara et al., 2004). Also tens of thousands of larger ncRNAs, both polyadenylated and nonpolyaden-ylated are transcribed from the mammalian genome (Carninci et al., 2005; Cheng et al., 2005a; Kapranov et al., 2005; Engstrom et al., 2006), At least some of these miRNAs show differential expression in different areas of the brain, such as the hippocampus and amygdala, areas associated with learning and memory, and are transiently modulated during contextual memory consolidation (fear conditioning) (Rogelj et al., 2003). Human homologs of these snoRNAs are also highly enriched in brain (Cavaille et al., 2000). So-called noncoding imprinted genes have essential roles in both neural development and adult CNS functioning, and alterations in their expression profiles are associated with a spectrum of complex neurodevelopmental and neuropsychiatric disorders (Costa, 2005; Davies et al., 2005; Davies et al., 2006). These allele-selective genes exhibit preferential and exquisite cell-specific patterns of expression within the brain, and are frequently processed from larger transcriptional units encompassing multiple tandemly repeated snoRNAs and miRNAs (Sleutels et al., 2000; Seitz et al., 2004; Davies et al., 2005; Lewis & Reik, 2006). These imprinted loci also generate a complex spectrum of spliced and unspliced larger ncRNAs (Sleutels et al., 2000; Davies et al., 2005; O'Neill, 2005; Furuno, 2006). Additional ncRNAs associated with imprinted loci include the production of antisense RNAs to reciprocally imprinted neighbouring protein-coding genes (Sleutels et al., 2000; Davies et al., 2005). Noncoding imprinted genes play a role in regulating distinct brain signalling systems and in mediating brain-behaviour relationships and when disrupted in neurological diseases associated with autism, schizophrenia, attention deficit hyperactivity disorder, bipolar disorder and Tourette’s syndrome (see Davies et al., 2004; Wang et al., 2004b; Davies et al., 2005; Davies et al., 2006).

5) Epigenetics actually extends far beyond the emerging role of non-coding DNA. Epigenetics describes a variety of features of the human genome that extend beyond the primary DNA sequence, such as chromatin packaging, histone modifications and DNA methylation which are important in regulating gene expression, replication and other cellular processes. Epigenetic markers strengthen and weaken transcription of certain genes without altering the sequence of DNA nucleotides. DNA methylation, a major form of epigenetic control over gene expression, is one of the most highly studied topics in epigenetics. During development, the human DNA methylation process experiences dramatic changes. In early germ line cells, the genome has very low methylation levels. These low levels generally describe active genes. As development progresses, parental imprinting tags lead to increased methylation activity. Epigenetic patterns can be identified between tissues within an individual as well as between individuals themselves. Diet, toxins, and hormones impact the epigenetic state. Studies in dietary manipulation have demonstrated that methyl-deficient diets are associated with hypomethylation of the epigenome. Such studies have concluded that epigenetics as an important interface between the environment and the mammalian genome. Scheen, Junien, Epigenetics, interface between environment and genes: role in complex diseases. Revue Médicale De Liège 67 (5-6): 250–7. See also: Misteli, Beyond the sequence: cellular organization of genome function. Cell May/Jun 2012, 128 (4): 787–800; Zuckerlandl, Why so many non-coding nucleotides ? The eukaryote genome as an epigenetic machine, Institute of Molecular Medical Sciences, Stanford, CA, Genetica115: 105–129, 2002. Electromagnetic and other wave forms and quantum considerations must also play a role.

6) The fact that there are so many examples emerging of so-called non-coding DNA actually coding or, more importantly, producing various forms of epigenetically potential forms of RNA is overturning long standing understandings of the human genome. "The failure to recognize the full implication of  this—particularly  the  possibility that  the  intervening  non-coding  sequences may be transmitting parallel information in the form of RNA molecules—may well go down as one of the biggest mistakes in the history of molecular biology." No one  knows just what the big picture of genetics will look like once this hidden layer of information is made visible. “Indeed, what was damned as junk  because it was not understood may, in fact, turn out to be the very basis of human complexity”, J S Mattick, quoted in Gibbs, The unseen genome: gems among the junk, Scientific American 289 (5): 48–53, 2003, pp. 49-50, 53. See also: Mattick, Challenging the dogma: the hidden layer of non-proteincoding RNAs in complex organisms, BioEssays 25:931, 2003.

7) Rodgers, et. al., Transgenerational epigenetic programming via sperm microRNA recapitulates effects of paternal stress, Sep. 2015, Proceedings of the National Academy of Sciences of USA; Rodgers, et. al., Paternal stress exposure alters sperm microRNA content andreprograms offspring HPA stress axis regulation, Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania; Journal of Neuroscience, 2013 May 22; 33(21): 9003–9012; Zama, Uzumcu, Epigenetic effects of endocrine-disrupting chemicals on female reproduction: An ovarian perspective, Department of Animal Sciences, School of Environmental and Biological Sciences, Rutgers, NJ, Front Neuroendocrinol. 2010 Oct.; 31(4): 420–439. See also: The transgenerational transmission of holocaust trauma: Lessons learned from the analysis of an adolescent with obsessive-compulsive disorder, Attachment & Human Development Volume 1, Issue 1, 1999.

8) Hurley, Grandma's Experiences Leave a Mark on Your Genes: Your ancestors' lousy childhoods or excellent adventures might change your personality, bequeathing anxiety or resilience by altering the epigenetic expressions of genes in the brain.; Hughes, Epigenetics: The sins of the father: The roots of inheritance may extend beyond the genome, but the mechanisms remain a puzzle, Nature 05 March 2014. See also Gray, Phobias may be memories passed down in genes from ancestors: Memories may be passed down through generations in DNA in a process that may be the underlying cause of phobias, Dec. 2013, Dr. Samuel Hannemann already recognized transgenerational effects of certain dispositions and diseases over 200 years ago. His groundbreaking work also contributed to the development of the Neuro-Genix Generational MIasm Process. See PROCESSES 1.

9) Taken as a whole there are many indications within the realm of science that point to conclusions that many mainstream scientists are unable to see, let alone embrace. When quantum physics is brought into the equation many of the new discoveries in biological and medical science take on a new perspective and one not necessarily welcome in all sectors of an entrenched health and wellness profession and marketplace. It is not only our feeling but also our clinical experience that the methodology incorporated in the Neuro-Genix processes are well researched and proven effective well beyond anything explainable by the Placebo Effect. The works cited in our reading list of books contain many pertinent principles that are unfortunately often taken to some excess position. In this vein see also Bruce Lipton, PhD, The Biology of Belief, Hay House, Inc. 2005/2008. There are many good points in Dr. Lipton's books and  seminars--however, without providing necessary methods or tools to accompany his increasingly esoteric notions. There is a good deal of agreement here [e.g. within Neuro-Genix] with many principles that are embraced by self-help advocates while considering that so-called self-help and enlightenment programs seldom have any genuine lasting effect. Consequently, we have taken our own path. Results must be the proof of procedure and there is no lasting room in the principles of progression for half-truths or self-deception. There are belief systems that exalt and there are those that simply promise it in company with a temporary release of feel-good endorphins. It is perhaps unfortunate that many true as well as apparently true principles are employed or usurped by impostors as well as well-meaning health proponents for ends and destinations that just do not pan out. For clarity on our position we refer the reader to Principle # 5 on our Home Page.

10) See Epigenetics and introns: Life beyond DNA Impact: Cell Biology, May 2, 2010,,  Zuckerkandl, Cavalli, Combinatorial epigenetics, "junk DNA", and the evolution of complex organisms. Gene. 2007 Apr 1;390(1-2):232-42. Epub 2006 Dec 9, Dept of Biological Sciences, Stanford University, Among the growing roles for non-coding DNA are that of negating retroviruses and sequestering potentially damaging mutant genes. Also, for a more comprehensive list of identified and potential functions of non-coding or so-called junk DNA see footnote # 4 above.

11) Glial cells may be considered to also operate in a quasi-epigenetic manner as they control and regulate neural synaptic transmission in a similar or analogous manner to epigenetic control mechanisms that regulate gene expression. Regarding cardiac and enteric factors see RESEARCH 2.

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