Alpha genomics (for those unfamiliar with their spelling)
Re: On this team, Dr. Hani El Shawa, is also first author of Prenatal Ethanol Exposure Disrupts Intraneocortical Circuitry, Cortical Gene Expression, and Behavior in a Mouse Model of FASD. The Journal of Neuroscience, 27 November 2013, 33(48): 18893-18905.

Excerpt: “Changes in gene expression reported in this study may be caused by altered DNA methylation, an epigenetic modification that cells use to mediate gene expression (Moore et al., 2013), cell differentiation, and embryonic development (Monk et al., 1987; Feng and Fan, 2009). Methylation occurs at the fifth position of cytosine and is driven by three conserved enzymes, DNA methyltransferase 1 (DNMT1), DNMT3A, and DNMT3B, which together are responsible for its deposition and maintenance, a function required for normal development (Li et al., 1992; Okano et al., 1999). Methyltransferase activity can be modified by exposure to ethanol; chronic exposure to ethanol is associated with reduced DNMT3B mRNA expression and hypermethylation in adults (Bönsch et al., 2006). Embryonic exposure to ethanol has been shown to alter DNA methylation patterns at neurulation, with increased methylation of genes on chromosome 10 and X correlating with an increase in neural tube defects (Liu et al., 2009). Furthermore, ethanol exposure impacts methyl donors (Mason and Choi, 2005), highlighting a possible mechanism by which ethanol, through methylation, can drive downstream epigenetic modifications and alter gene expression, as we have seen in this study (Haycock, 2009).”
My comment: The article establishes his extraordinary understanding of biologically-based cause and effect. He has already integrated current information from across the disciplines of physics, chemistry, and molecular biology and made a cohesive representation that differentiates healthy embryonic development from the pathology associated with ethanol uptake during pregnancy. The clear link is from epigenetic effects of chemicals on gene activation to affects on behavioral development via DNA methylation
Similarly, Jennifer Doudna’s works with others led to detailed aspects of RNA-directed DNA methylation and cell type differentiation that show up in the 2014 Nobel Prize in Physiology or Medicine. It was awarded to John O’Keefe, 75, a British-American scientist, who will share the prize of $1.1 million with May-Britt Moser, 51, and Edvard I. Moser, 52,  for their works. They detailed how the experience-dependent development of different cell types involved in learning and memory can be linked to humans from model organisms like the honeybee. See: Epigenomics and the concept of degeneracy in biological systems
Jennifer Doudna is already well on her way to winning a Nobel Prize for her works. See for examples: 1) DNA interrogation by the CRISPR RNA-guided endonuclease Cas9 and 2) Programmable RNA recognition and cleavage by CRISPR/Cas9
Conclusion from 2): “The ability to recognize endogenous RNAs within complex mixtures with high affinity and in a programmable manner paves the way for direct transcript detection, analysis and manipulation without the need for genetically encoded affinity tags.”
That ability to recognize endogenous RNAs within complex mixtures shows up in Alpha Genomix testing, which represents a quantum leap forward from what many experts inaccurately attribute to mutations, natural selection, and evolution. Instead, Alpha Genomix is leading the way by incorporating what is currently known about RNA-directed DNA methylation and RNA-mediated events that link enzymes to amino acid substitutions that differentiate cell types.
The RNA-mediated amino acid substitutions differentiate all cell types of all individuals of all species. Testing to determine the differences in enzymes and other factors that alter cell types enables predictions to be made about how an individual may respond to specific medications based on their unique genotype and its phenotypic expression at the level of cellular metabolism.
At the level of differences in cell type metabolism, RNA-mediated events occur outside the context of ridiculous misrepresentations made by evolutionary theorists and evolutionary theists who have never described a biologically-based evolutionary event. They still think in terms of genetically-determined cause and effect as if their theories had any explanatory power in the context of what’s been learned about cell type differentiation since 1973, when Dobzhansky wrote: “…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla.”
Until then, the theorists and evolutionary theists were stuck trying to explain how ecologically adapted organisms somehow evolved over hundreds of millions of years, despite clear indications that ecological variation in nutrient availability leads to the metabolism of the nutrients via receptor-mediated events and enzymes, which link the metabolism of nutrients to species-specific pheromones that control the physiology of reproduction. The result is the species specificity of morphological and behavioral phenotypes that clearly are ecological adaptations, not mutations that lead to perturbed protein folding, diseases, and disorders. For example, dietary differences markedly alter how much coumadin (characterized as a ‘blood thinner’) will regulate the potential for blod clot formation. Too much coumadin combined with poor diet or altered diet may lead to toxicity associated with morbidity and mortality. Beneficial effects and toxicity have been linked to amino acids.
For examples of the difference a single amino acid substitution makes in species from microbes to man see: Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Note, however, that even I was stuck with use of the term evolution, since too few people recognize the difference between controlled ecological adaptations and mutation-driven evolution.
Mutation-driven evolution does not occur for reasons that should be obvious. Fixation of amino acid substitutions occurs across populations; fixation of mutations may appear to temporarily occur across some lineages for a few generations, but only the amino acids substitutions contribute to organized genomes. The idea that mutations organize genomes in different species is ridiculous. It was invented based on assumptions made more than 80 years ago.
Alpha genomix has left those assumptions behind, and other companies may also now begin to do so when the biological facts become better known than the ridiculous theory about evolution. For examples of how serious scientists like Dr. El Shawa have moved away from a ‘one size fits all’ model of health and treatment, see: Hypothalamic PGC-1α Protects Against High-Fat Diet Exposure by Regulating ERα reported as: Male and female brains aren’t equal when it comes to fat.
Excerpt:  “…differences in the brain lead to greater inflammation and increased health risks in males that indulge on fatty foods in comparison to females, a new study in mice shows.  Earlier data from Clegg’s team and others had suggested that inflammation in the brain is tied to overeating, blood sugar imbalances, and increased inflammation in other parts of the body, including fat tissue.” We have always had ‘one size fits all’ with respect to our nutritional information and our pharmaceutical approach,” Clegg said. “Our data begin to suggest that sex should be factored in, and men should be more closely monitored for fat intake and inflammation than women.”
My comment: My co-authors and I may have been the first to publish on RNA-mediated sex differences in cell types in species from microbes to man. In our 1996 Hormones and Behavior review article From Fertilization to Adult Sexual Behavior, we wrote: “Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”
If not for the incessant touting of evolutionary theory — as if it had the explanatory power to link molecular epigenetics to sex differences in cell types across all species — other serious scientists would have been moving forward since 1973, instead of living in the past as also indicated by Dobzhansky 50 years ago when he wrote:  “…the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists!”
Among the serious scientists who remain in the category of astute bird-watchers, but also understand molecular epigenetics, are those associated with Donna L. Maney’s group. They continue to present their findings in the context of nutrient-dependent pheromone-controlled hormone-organized and hormone-activated behaviors that are linked from sexual differentiation of cell types in yeasts via insect models of life history transitions to sex differences and individual differences in the cell types of all vertebrates. The differences in the behavioral morphs of white-throated sparrows are obviously nutrient-dependent, but the direct link from differences in feeding patterns parallels what others have reported in other models of developmental differences in morphological and behavioral phenotypes that will lead others to ask: “What about birds?”
That was the question asked when I presented my model to Jay R. Feierman in 1995. Like many other self-proclaimed experts, he refuses to accept any experimental evidence that links the birds and the bees to cell type differentiation in all cells of all tissues of all organs and all organ systems via the conserved molecular mechanisms the enable increasing organismal complexity. Instead, Feierman claims: “Random mutations are the substrates on which directional natural selection acts.” — as if any evidence of biologically-based cause and effect has ever confirmed the pseudoscientific nonsense touted by evolutionary theorists, or by human ethologists.
It is past time to leave ridiculous theories behind and enter the real world of personalized medicine heralded by Alpha Genomix.
See also: Combating Evolution to Fight Disease. Know who the enemy is and see: RNA and dynamic nuclear organization.
Ask if any member of the Society for Neuroscience and the Society for Integrative and Comparative Biology still believes in theories about mutations that lead from natural selection to the evolution of biodiversity. Dr. El Shawa is a member of both societies. If others still believe in ridiculous theories they may be among those who Denis Noble addressed when he said:  “If you learnt evolutionary biology and genetics a decade or more ago you need to be aware that those debates have moved on very considerably, as has the experimental and field work on which they are based.” (p 1014) Everything currently known about biologically-based cause and effect links ecological variation to ecological adaptations.
For example: Reverse ecology describes the use of genomics to study the impact of ecological factors on the partitioning of genomic variation in one or more natural populations.
This approach can be used to link enzymes and other factors from epigenetic effects across human life histories that determine their pharmacogenomic response (i.e., their response to different prescription pharmaceuticals.) The responses are becoming more predictable based on what is known about enzymes that link nutrient-uptake and metabolism to RNA-directed DNA methylation and RNA-mediated events that alter the organized genomes of insect, like the honeybee and mammals like humans. The most recent example of biologically-based cause and effect was reported 15 October 2014 as House Fly Genome Reveals Expanded Immune System.
Excerpt 1): “The genome, roughly twice the size of the fruit fly’s genome, revealed an expanded number of immune response and defense genes. The researchers also discovered an expansion in the number of cytochrome P450s, which help the flies metabolize environmental toxins. “House flies have a lot more of these enzymes than would be expected based on other insects they are related to,” said Scott, noting that the house fly’s close relative, Glossina morsitans (tsetse fly), has half as many cytochrome P450s. These enzymes are more ancient than insecticides.”
Excerpt 2): The M. domestica genome also revealed many genes for chemoreceptors, which detect certain chemical stimuli in the environment. These receptors are important in sensing food and moving in ways critical for survival, allowing house flies to detect a wide variety of different things, Scott said.”
Their focus is on chemoreceptors involved in taste. My focus is on chemoreceptors that link food odors to the de novo creation of olfactory receptors that link nutrient uptake to cell type differences in all cells of all individuals of all species via the conserved molecular mechanisms that show up in the testing provided by Alpha Genomics. Their results attest to the unique features of each individual’s metabolism and will help medical practitioners know how to personalize your treatment and avoid some of the hazards associated with medications, like coumadin toxicity.

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