Definition of BEIRBO
Glossary
BEIRBO:
God designed our DNA to react and adapt to our environent and our behavior — even that which we think about. The term I coined to describe this phenomenon is BEIRBO, An acronym for Behavioral and Environmental Input, Reactive Biological Output. Is there any scriptural evidence to support this belief?
In Genesis 30:25-36, we read of Jacob’s colored rods or, as I like to call them, his BEIRBO rods. After working for Laban (the father of his future bride, Rachel) and greatly multiplying Laban’s flocks of sheep, Jacob agreed to take as his wages the spotted, striped, speckled, and black sheep of Laban’s flocks. Unbeknownst to Jacob, however, Laban instructed his sons to sequester all of those types of sheep far away from all the others so that only white sheep remained. Let’s pick up the story from there. We read:
Then Jacob took fresh rods of poplar and almond and plane, and peeled white streaks in them, exposing the white of the rods. He set the rods which he had peeled in front of the flocks in the runnels, that is, the watering troughs, where the flocks came to drink. And since they bred when they came to drink, the flocks bred in front of the rods and so the flocks brought forth striped, speckled, and spotted. And Jacob separated the lambs, and set the faces of the flocks toward the striped and all the black in the flock of Laban; and he put his own droves apart, and did not put them with Laban’s flock. Whenever the stronger of the flock were breeding Jacob laid the rods in the runnels before the eyes of the flock, that they might breed among the rods, but for the feebler of the flock he did not lay them there; so the feebler were Laban’s, and the stronger Jacob’s. (Gen. 30:37-42).
Furthermore, all Scripture passage hat discuss the fathers sins visiting his children to the third and fourth generation are all a consequence of the process described as BEIRBO (cf., Ex 20:5, 34:7; Num. 14:18; Deut. 5:9). What are some examples of BEIRBO in action? Some of the environmental factors that initiate the epigenetic mechanism (see Figure 1 above)? The following research represents a small sample of all triggers for epigenetic change, often leading to transgenerational heredity. They are:
1. Food and drink (see “The Epigenetics of Food and Drink” below);2. Repeated behaviors that trigger fight, flight, or stress hormones such as norepinephrine, epinephrine, adrenaline, and cortisol (see “The Epigenetics of Substance Abuse and Addiction” below);3. Repeated behaviors that result in the production of reward hormones/neurotransmitters such as dopamine (often associated with addictions), oxytocin, endorphins, and serotonin;4. Repeated behaviors that feed the three lusts described by St. Paul — lust of the flesh, lust of the eyes, and the boastful pride of life (1 Jn. 2:16). Typically, behaviors of this nature are also closely involved with numbers 2 and 3 above;5. Traumatic experiences with parents, loved ones, and/or others;6. Experiences that result in unhealthy and/or chronic levels of fear, stress, etc.;7. Both Electromagnetic Energy and Sound Waves, and:8. Various Environmental Factors.
The Epigenetics of Food and Drink
1). Studying the genetics and epigenetics behind obesity, Johns Hopkins researcher Dr. Andrew Feinberg and his colleagues studied seventy–four older adults in Iceland. Over eleven years, they sought to find out if epigenetics played a role in susceptibility to obesity. They found that there were thirteen changes to the genes of the obese participants. They also discovered that those changes were due to chemical tags called methyl groups (part of the epigenetic triggering mechanism). Researchers said those changes began in childhood and remained stable until the eleven–year study was concluded. Furthermore, Feinberg and his colleagues suggest that autism, bipolar disorder, and asthma may also be due to epigenomic changes.[1] The study did not look at the heritability of said changes, but we know from other research and from the mouse study cited elsewhere that they likely are.[2] Our subsequent study will also help to support this belief;2). In a study performed by Kartik Shankar et al. and published in the February 2008 issue of the American Journal of Physiology –– Regulatory, Integrative and Comparative Physiology, Shankar and his team used rat dads, all of which were lean (in weight). They then mated them with rat moms (called dams). Some of the moms were kept lean by not altering their normal diet. Others were fattened up by overfeeding before conception and through their pregnancy. It is important to note all of the moms were lean before the experiment started. Any weight gain and any subsequent change to the functioning of the mother’s genes would have had to occur due to epigenetic–driven modifications to the functioning of their genes. All of the offspring were of normal weight at birth and during weaning. After that, however, they were all given free access to high–fat rations. The progeny from the overweight mothers showed great sensitivity to the high–fat food. They gained more weight, and more of the weight consisted of fat mass when compared to the offspring from the mothers that had not been fattened up. Researchers strongly suggest that the dams’ obesity was the sole factor responsible for the inherited changes to the body’s metabolism and body–weight control mechanisms;[3]3). Recent studies have shown that a man’s diet affects both his sperm count and the ability of the sperm to move spontaneously. The male’s diet plays a much more significant role than previously thought on the health of subsequent generations of his children. Suzanne Young, a researcher at UC Berkeley’s School of Public Health, tells us, “Our study is the first to look at the effects of diet on chromosomal abnormalities in sperm. These abnormalities would cause either miscarriages or children with genetic syndromes if the sperm fertilized an egg.” The culprit here is folate, a B–vitamin found in the liver, leafy green vegetables, citrus fruit, etc. Folate is necessary for the synthesis of DNA, RNA, and proteins. A man’s low folic acid intake diet could produce chromosomal abnormalities in his sperm that could result in Down’s Syndrome, Klinefelter Syndrome, or boys born with learning or behavioral problems. A word of caution: according to Andrew Wyrobek, chair of the Radiation Biosciences Department at Lawrence Berkeley National Laboratory, “We can’t yet say that increasing folate in your diet will lead to healthier sperm but we did come up with enough evidence to justify a larger, clinical and pharmacological trial in men to examine the causal relationships between dietary folate levels and chromosomal abnormalities in their sperm;”[4]4). Research performed at Duke University by Drs. Robert A. Waterland and Randy L. Jirtle looked at the effects of diet on identical twin mice. Identical twins share the exact same DNA. You could say that identical twins are, sort of, clones of each other, but not in a manner consistent with a strictly scientific definition of the term. Suppose two identical twin mice have different outer appearances, e.g., one having a brown coat versus the other with a yellow coat. In that case, the phenotype difference is most likely due to differing regulation in the expression of particular genes (via the epigenome. Falling back on our previous analogy: the twins have the same computer hardware, but the software running in each of them differed, thus producing different outputs. In the study, one of the identical twins was fat, had a yellow coat, and was prone to diabetes and cancer; the other twin was skinny and with a brown coat. It also lacked the health risks of its twin. Why the difference? Both twins contained an identical gene called the agouti. The agouti of the fat mouse was turned on all the time, resulting in obesity and different coat color.[5] Why is that? According to Nova ScienceNOW host Neil DeGrasse Tyson, a chemical tag of carbon and hydrogen is attached directly to the fat mouse’s agouti gene, causing it to produce a particular protein unceasingly.[6] When the epigenome was not altered to fix the agouti problem, the female obese mouse would continue to produce succeeding generations of offspring with the same problem. When the problem was fixed by altering the diet, the successive generations returned to the brown coat and normal weight. According to Jirtle, we are what we ate, what our parents ate, and even what our grandparents ate — to the third and fourth generation.[7]5). After a similar epigenetic study on humans, Manel Estellar of the Spanish National Cancer Center in Madrid concluded: the function of our epigenome can change in response to such seemingly inconsequential things, such as what we drink, smoke, eat, etc.[8]6). Fernando Gómez–Pinilla, a UCLA professor of Neurosurgery and Physiological Sciences, analyzed over one–hundred sixty studies relating to the effects of diet on the human body. Here are only a few of the conclusions he wrote about in Nature Review Neuroscience. What we eat and drink will positively or negatively affect the likelihood of experiencing depression, mood disorders, dyslexia, schizophrenia, learning disabilities, dementia, brain function, and changes in the genetic expression of specific proteins that affect the brain’s cognitive and metabolic regulation. Like the previous study, he also reported that what we eat today will potentially affect our descendants’ physical and mental health. He further concludes what we eat will affect the brain function of our grandchildren. A long–term study performed on three hundred Dutch families showed an individual’s risk for diabetes and an early death were increased or decreased depending on the abundance or shortage of food existing when their paternal grandparents were in their childbearing years.[9]
Bible authors (Divinely inspired by the Holy Spirit) were right when they warned us that changes caused by epigenetic methylation could be passed along to succeeding generations — up to the third or fourth generation (Ex 20:5, 34:7; Num. 14:18; Deut. 5:9; as well as Gen 30:25–36, i.e., Jacob’s colored rods). All of the research cited in the previous section, which only represents a small percentage of the available science, strongly supports the statement’s validity: we are what we eat — which would include the Eucharist!
Brief Note About the Eucharist
The following is slightly off–topic, but since we are talking about the science of food and drink, it would be appropriate to talk about the science of Sacred Food and Drink. Jesus tells us, “Truly, truly, I say to you, unless you eat the flesh of the Son of man and drink his blood, you have no life in you; he who eats my flesh and drinks my blood has eternal life.” (Jn. 6:53–54). Why? As Dr. Randy L. Jirtle tells us: we are what we eat and drink; what we eat and drink changes us — right down to the molecular and quantum level! Jesus tells us he is real food and real drink. He tells us, “For my flesh is food indeed, and my blood is drink indeed. He who eats my flesh and drinks my blood abides in me, and I in him” (John 6:55-56).The Epigenetics of Environmental Factors
Is food the only factor that triggers epigenetic changes? Professor Wolf Reik, Associate Director at the Babraham Institute and Professor of Epigenetics at the University of Cambridge, writes, “It is now well established that epigenetics is the ‘integrator’ between the environment [SML] and the genome [SML].”[10] So let’s look at the consequences of some environmental factors on the salt of our DNA in current and future generations of our children.
· “Some colorectal cancers are known to develop when a key DNA–repair gene called MHL1 becomes coated in methyl groups [epigenetically changed], preventing it from working. In 2007, Ward and her colleagues published a study of a woman with colorectal cancer and her three children. The MHL1 gene was active in two of the children, but one son had a heavily methylated, silenced gene like his mother (The New England Journal of Medicine, vol. 356, p 697). The paper caused a sensation among cancer researchers because it suggested an entirely new way in which disease risk might be inherited … Since the paper came out, though, direct inheritance is starting to look more likely. Other teams have identified similar families, and in all cases, the effect seems to be transmitted down the maternal line via the egg. The MHL1 gene in the sperm of affected men appears normal;”[11]
· According to the National Institutes of Health, Exhaust from cars and trucks is a significant source of outdoor air pollution. When we breathe in high levels of the particles present in the exhaust, these particles can irritate the lungs and cause breathing disorders. … breathing in fine particles has been associated with epigenetic changes that may increase the risk of disease. Epigenetic changes are alterations in the way genes are switched on and off without a change in the DNA sequence. The type of epigenetic change associated with air pollution is DNA methylation, the attachment of methyl groups to DNA.”[12] While not a part of this particular research project, DNA methylation was identified as the epigenetic modification factor strongly indicates the likelihood of transgenerational inheritance. And;
· “Some epigenetic marks may also be inherited from fathers, however. In a now–classic study published in 2005, Matthew Anway at the University of Idaho in Moscow and colleagues showed that male rats exposed to the common crop fungicide vinclozolin in the womb were less fertile and had a higher than normal risk of developing cancer and kidney defects. Not only were these effects transmitted to their offspring, they were passed from father to son through the three following generations as well (Science, vol. 308, p 1466). The team found no DNA changes, only altered DNA methylation patterns in the sperm of these rats, suggesting that epigenetic factors were to blame.”[13]
The Epigenetics of Substance Abuse and Addiction
· A team at the University of Maryland in Baltimore found that male mice who had inhaled cocaine passed memory problems onto their pups. Again, their sperm showed no apparent DNA damage, but in the seminiferous tubules, where sperm are produced, the researchers found changes in the levels of two enzymes involved in methylating DNA.[14]
· Researchers at Wake Forest University Baptist Medical Center wanted to determine the effects of cocaine use on the genome. They chose monkeys as the subjects because the genetic and behavioral similarities with humans are significant. They used a state–of–the–art proteomic technology that allows researchers to compare the proteome (all proteins produced by the genes within an organism at a given time) of two groups of monkeys. One that self–administered cocaine. The other did not. By way of background, proteins are what genes produce. Proteins are the chemical language of our DNA. A protein is a messenger delivering instructions that tell cells or the genes within cells to start or stop a particular action — to build or destroy something. According to lead researcher Dr. Nilesh Tannu, a consequence of cocaine usage, the changes to the structure, functioning, and communications of neurons (nerve cells) within the subjects’ brains were very significant. Furthermore, the resulting changes were not prone to reversal.[15]
Changing the structure, metabolism, and signaling of the neuron could only be accomplished by altering our salt of DNA’s very function — down to the molecular and quantum level. In other words, epigenesis can lead to profound biological changes to the functioning of the body. As seen through our following study, the conclusions reached from this research apply to other types of addictions such as pornography, alcoholism, gambling, smoking, etc.
· Researchers at the University of Texas demonstrated how addictions change our DNA’s functioning and do so permanently. Starting with a single dose of an addictive drug, a protein identified as ∆FosB (delta Fos B) begins to be produced by our salt of DNA and is accumulated in the neurons. Every time the drug(s) are used, it causes more ∆FosB to be stored in the cells. When a sufficient quantity is present, a genetic switch is flipped that, more or less, permanently alters which genes are expressed (turned on) and which ones are not (turned off). As a consequence of this functional change, the brain’s system for handling dopamine (the “reward” hormone associated with addictions) is irreversibly damaged. This process is not limited to drug addictions. Repeated activities such as jogging and consumption of sugared drinks also lead to the accumulation of ∆FosB and permanent changes to the dopamine system.[16]
The Epigenetics of Fear and Stress
· Over the years, there has been much research on the effects of the Holocaust on the survivors’ children. Survivors suffered from what is now called Post Traumatic Stress Disorder (PTSD). The children of these survivors showed physiological effects similar to those of their parents. Like their parents, their bodies produced higher levels of the stress hormone cortisol. The symptoms were assumed to be learned. Neurobiologist Isabelle Mansuy of the University of Zurich set out to study the role epigenetics’ plays in the inheritance of trauma symptoms by subsequent generations of Holocaust survivors. Mansuy’s team raised male mice from birth. They were subjected to frequent but unpredictable, stress–inducing separations from their mothers. This stress period continued from day one to day fourteen. Next, they were reared, fed, and nurtured by their non–stressed mothers (the males of this species have no part in their offspring’s upbringing, and the mothers were never subjected to stress — so any symptoms of stress could not have been learned). As adults, these mice (equivalent to first–generation Holocaust survivors) exhibited all the classic symptoms of PTSD. Researchers targeted the functioning of five different genes responsible for PTSD behavior, including genes that regulated the production of stress hormones and neurotransmitters such as serotonin. They found that all of the genes in question were either over–reactive or under–reactive. “They then fathered young [the second generation from stressed fathers] … [the father] had nothing to do with their upbringing. Their mothers raised the second generation pups with none of the trauma and separation their fathers had suffered. When they grew up, not only did they exhibit the same anxious behavior [as their stressed fathers], but they also had the same signature gene changes. ‘We saw the genetic differences both in the brains of the offspring mice and in the germline – or sperm – of the fathers,’ says Mansuy.”[17] In other words, the children of the children (what would be the third generation) of the original male mice were biologically positioned to inherit the same genetic problems as their grandfather;
· The following research can see further evidence of the role of stress in epigenetic inheritance. “There is recent evidence that abnormal epigenetic patterns play a role in mental health disorders. In March, Arturas Petronis at the Centre for Addiction and Mental Health in Toronto, Canada, and colleagues reported the first epigenome–wide scan of post–mortem brain tissue from thirty–five people who suffered from schizophrenia. They found a distinctive epigenetic pattern, controlling the expression of roughly forty genes (The American Journal of Human Genetics, vol. 82, p 696). Several genes were related to neurotransmitters, brain development, and other processes linked to schizophrenia. These findings lay the groundwork for a new way of understanding mental illness, says Petronis, as a disease with a significant epigenetic component. Yet there are also hints that the people with schizophrenia might instead have inherited them from their parents – and that they, in turn, might pass the marks on to their children …. the abnormalities in DNA methylation [part of the epigenetic mechanism] in Petronis’s subjects were not restricted to their frontal cortex: they were also present in their sperm [emphasis mine]. ‘[This] suggests that it is possible that inherited epigenetic abnormalities may be contributing to the familial nature of schizophrenia and bipolar disorder,’ says team member Jonathan Mill at the Institute of Psychiatry at King’s College London;”[18]
· According to science writer Mariette Le Roux, “Lab mice trained to fear a particular smell can transfer the impulse to their unborn sons and grandsons through a mechanism in their sperm, a study said Sunday. The research claims to provide evidence for the concept of animals ‘inheriting’ a memory of their ancestors’ traumas, and responding as if they had lived the events themselves. It is the latest find in the study of epigenetics, in which environmental [SML] factors are said to cause genes to start behaving differently without any change to their underlying DNA encoding.”
Later, they tested the extent to which the animals’ offspring startled when exposed to the same smell. The younger generation had not even been conceived when their fathers underwent the training, and had never smelt the odour before the experiment. The offspring of trained mice were “able to detect and respond to far less amounts of odour ... suggesting they are more sensitive” to it, Ressler told AFP of the findings published in the Journal Nature Neuroscience.
They did not react the same way to other odours, and compared to the offspring of non–trained mice, their reaction to the cherry blossom whiff was about 200 percent stronger, he said. The gene, inherited through the sperm of trained mice, had undergone no change to its DNA encoding, the team found. But the gene did carry epigenetic marks that could alter its behaviour and cause it to be ‘expressed more’ in descendants, said Dias. This in turn caused a physical change in the brains of the trained mice, their sons and grandsons, who all had a larger glomerulus—a section in the olfactory (smell) unit of the brain.”[19][20]
· Scientists from the Max Planck Institute of Psychiatry in Munich studied the effects of repeated and/or severe abuse on both children and adult victims. Of the approximately two thousand subjects tested, about one–third of them had been found to have experienced an epigenetic change to the FKBP5 gene as a direct result of the abuse (other illnesses were ruled out as a potential cause). The FKBP5 gene regulates the stress hormone system within the body. Interestingly, researchers believe that these abuse–responsive changes to the function of the FKBP5 gene and the resultant stress hormone system dysfunction would likely last for the rest of the victim’s life.[21] The particular study did not ascertain whether or not the malfunction was passed on to succeeding generations. However, many other studies (including the previous and subsequent cited studies) have shown that epigenetic changes to DNA are frequently inherited by succeeding generations of each subject’s offspring.
· Does mild to moderate family problems (e.g., argumentative environment, some emotional abuse, lack of affection, etc.) encountered on a chronic basis also lead to genetic–based developmental changes? A study conducted by the University of Cambridge and the Medical Research Council Cognition and Brain Sciences Unit found that children between birth and 11 years old exposed to this challenging environment developed a smaller cerebellum (area of the brain associated with sensory–motor control, stress regulation, and skill learning). According to the study’s leader, Dr. Nicholas Walsh, this finding is significant. Childhood adversities are the biggest risk indicator for the development of psychiatric illness in later life. Interestingly, adolescents whose exposure to similar environments did not begin until around fourteen developed larger cerebellums than normal, as seen when scanned 3–4 years after onset. This evidence indicates a possible inoculating effect that helps them better cope with stress in later life.[22]
The Epigenetics of Electromagnetic Energy & Sound Waves
Within the scientific literature, it is now well–established that living organisms react sensitively to electromagnetic fields in a range of frequencies and strengths. The human body emits electromagnetic fields in a range of frequencies, including microwave and optical (although too weak to be seen by the naked eye).[23] Even of weak and extremely low frequency, these fields are used by humans on a molecular level for information exchange.[24][25] One example of this comes from a study published in Nature Biotechnology in 2002 and Discovery News in 2011. By simply emitting photons at a particular wavelength, scientists initiated specific genes within yeast cells to produce proteins through epigenetic–driven mechanisms. When they stopped emitting the photons, the protein production stopped.[26] These experiments demonstrate that electromagnetic energy (light) triggers epigenetic mechanisms.
Trace Dominquez writes:
Scientists have used a computer to "talk" to yeast in a Zurich laboratory. In the conversation, the researchers created a communication loop between regular brewers yeast and a computer, giving control to the computer over protein production in the yeast cell. This "feedback control" between the computer and the yeast is the first of its kind and opens the door to use a computer to manage genetically altered microorganisms.
In 2002, a study in Nature Biotechnology found that when a red light was shone onto basic yeast (called Saccharomyces cerevisiae), it would become active and produce a protein. A deeper red light would deactivate the cells.
Now the team has taken the research a step farther by tying a "reporter molecule" to a gene that activates the production of the protein. When the yeast begins protein production, the fluorescent reporter molecule actives as well. This molecule can be seen by a computer to confirm that the yeast are active. Once the desired level of protein is reached, the computer can flash a deeper red light, deactivating the yeast.
Using this "feedback control" system, the mechanism of control is moved outside of the cell to the computer, which controls the level of protein production in these S. cerevisiaei cells.
The science is complex, but the idea is straightforward; computerized control of a bacteria [via light at a particular wavelength—SML] could revolutionize biotechnology. Bacteria are used for a number of industrial purposes, from making pharmaceutical products to creating biofuels to digesting trash. By shining lights onto the cells, computers could maximize this bacteria activity.[27]
Speaking at a webinar, Dr. Carlo Ventura states, “You’re somehow reprogramming … cells backward to [a] certain state in which any kind of decision [leading to cell differentiation] is somehow possible; even the decision to become virtually any kind of cell of the organism. And just think about the tremendous potential of this discovery. This is why the two guys that made this discovery, Shinya Yamanaka and John Gurdon, got the Nobel Prize in medicine for their discovery that even non–stem adult cells can be epigenetically reprogrammed [all emphasis SML] backward to a state where they can eventually give rise to neural cell, cardiac cells, skeletal muscle cells, or insulin–producing cells. So this is really relevant, a step forward in science. … Another issue that makes the role of physical energy and the environment even more consistent … [is] the potential of affecting cell reprogramming and epigenetics [through] vibration, the acoustic vibration, the sound vibration.”[28]
An example of this biological and quantum (light) mix comes from cell biologist and chemist Vladimir Voeikov. He informs us that DNA, RNA, and proteins (polymers) undergo chemical transformations resulting from exposure to the energy of audible sound (e.g., voice) and ultrasound.[29] In other words, the sound waves of the voice impact the function and signaling of the salt of DNA and all of its products (e.g., proteins and cell membranes). Furthermore, the electromagnetic radiation caused by the beating heart is co-mingled with the sound waves from that same beating heart.
There is another level to the depth of this heart—sound wave mystery. The internal matrix of the cell is permeated by a sort of scaffolding that is made up of fibers. These fibers continuously vibrate at specific frequencies, which change in response to environmental factors. The entire world of cells is vibrating in resonance with the cells scaffold matrix.[30] Until the development of Atomic Force Microscopy, these nanomechanical vibrations could not be detected. Is the phenomenon of cell vibration important? Drs. Carlo Ventura and James K. Gimzewski have been investigating the issue of cell vibration. These vibrations can be recorded as sound. They are now investigating whether or not the vibrations recorded from a beating heart affect the differentiation of stem cells[31] exposed to that sound (recall Adam’s rib). Initial results are promising.[32] ENDNOTES:
[1]. Andrew P. Feinberg, Rafael A. Irizarry, Delphine Fradin, Martin J. Aryee, Peter Murakami, Thor Aspelund, Gudny Eiriksdottir, Tamara B. Harris, Lenore Launer, Vilmundur Gudnason, and M. Daniele Fallin, “Personalized Epigenomic Signatures That Are Stable Over Time and Covary with Body Mass Index,” Science Translational Medicine, 15 Sep 2010: Vol. 2, Issue 49, pp. 49ra67 DOI: 10.1126/scitranslmed.3001262.
[2]. Daniel J. DeNoon, "Gene Switches May Turn Obesity On; Obesity Linked to Chemical Changes in 13 Genes," WebMD Health News, https://www.webmd.com/diet/news/20100915/gene-switches-may-turn-obesity-on: WebMD, LLC., Sept. 15, 2010 (accessed 09/22/2010).
[3]. USDA/Agricultural Research Service, "Baby's Obesity Risk: What's the Mother's Influence?," ScienceDaily.com, https://www.sciencedaily.com/releases/2010/03/100315125551.htm?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+sciencedaily=Google+Feedfetcher: ScienceDaily L.L.C., April 5, 2010 (accessed April 5, 2010).
[4]. University of California – Berkeley, "Genetic Abnormalities In Sperm Linked To Dietary Folate Intake, Study Shows," ScienceDaily, https://www.sciencedaily.com/releases/2008/03/080319193036.htm: ScienceDaily, March 20, 2008 (accessed Mar. 20, 2008).
[5]. Robert A. Waterland, Randy L. Jirtle, "Transposable Elements: Targets for Early Nutritional Effects on Epigenetic Gene Regulation," Molecular and Cellular Biology, Vol. 23, n. 15, doi: 10.1128/MCB.23.15.5293–5300.2003, http://mcb.asm.org/content/23/15/5293.full: August 2003 (accessed 02–02–2007).
[6]. Nova scienceNOW, "Epigenetics," http://www.pbs.org/wgbh/nova/transcripts/3411_sciencen.html.
[7]. Nova scienceNOW, "Epigenetics," http://www.pbs.org/wgbh/nova/transcripts/3411_sciencen.html.
[8]. Ibid.
[9]. Gómez–Pinilla et al., "Brain foods: the effects of nutrients on brain function," Nature Reviews Neuroscience (Nature Publishing Group) 9 (July 2008).
[10] The Babraham Institute, "New insight into reprogramming of cell fate," ScienceDaily, https://www.sciencedaily.com/releases/2010/01/100127111105.htm?+%28ScienceDaily%3A+Latest+Science+News%29&utm_content=Google+Feedfetcher: ScienceDaily L.L.C., February 1, 2010 (Retrieved February 1, 2010).
[11]. Emma Young, "Rewriting Darwin: The new non–genetic inheritance," New Scientist, https://www.newscientist.com/article/mg19926641-500-rewriting-darwin-the-new-non-genetic-inheritance/: Reed Business Information Ltd., July 09, 2008 (accessed 02/15/2012).
[12]. NIH Research Matters, “Combatting epigenetic effects from outdoor air pollution,” National Institutes of Health, https://www.nih.gov/news-events/nih-research-matters/combatting-epigenetic-effects-outdoor-air-pollution, March 21, 2017 (accessed 03/29/2021).
Journal Source: Zhong J, Karlsson O, Wang G, Li J, Guo Y, Lin X, Zemplenyi M, Sanchez-Guerra M, Trevisi L, Urch B, Speck M, Liang L, Coull BA, Koutrakis P, Silverman F, Gold DR, Wu T, Baccarelli AA. B vitamins attenuate the epigenetic effects of ambient fine particles in a pilot human intervention trial. Proc Natl Acad Sci U S A. 2017 Mar 28;114(13):3503-3508. doi: 10.1073/pnas.1618545114. Epub 2017 Mar 13. Erratum in: Proc Natl Acad Sci U S A. 2017 Apr 18;114(16):E3367. PMID: 28289216; PMCID: PMC5380085.
[13]. Emma Young, "Rewriting Darwin: The new non–genetic inheritance," New Scientist, https://www.newscientist.com/article/mg19926641-500-rewriting-darwin-the-new-non-genetic-inheritance/: Reed Business Information Ltd., July 09, 2008 (accessed 02/15/2012).
[14]. Young, "Rewriting Darwin: The new non–genetic inheritance," New Scientist, https://www.newscientist.com/article/mg19926641-500-rewriting-darwin-the-new-non-genetic-inheritance/: Reed Business Information Ltd., July 09, 2008 (accessed 02/15/2012).
[15]. The Wake Forest University Baptist Medical Center, “Molecular Fingerprint Of Cocaine Addiction Revealed,” ScienceDaily, https://www.sciencedaily.com/releases/2008/05/080527113200.htm: ScienceDaily L.L.C., May 29, 2008 (accessed 05/29/2008).
[16]. Dr. Norman Doidge, The Brain That Changes Itself, (New York , NY , Penguin Books, 2007), 107.
[17]. Jeffrey Kluger, "Genetic Scars of the Holocaust: Children Suffer Too," Time, http://content.time.com/time/health/article/0,8599,2016824,00.html: Time, Inc., September 9, 2010 (accessed 09/13/2010).
[18]. Emma Young, "Rewriting Darwin: The new non–genetic inheritance," New Scientist, https://www.newscientist.com/article/mg19926641-500-rewriting-darwin-the-new-non-genetic-inheritance/: Reed Business Information Ltd., July 09, 2008 (accessed 02/15/2012).
[19]. Mariette Le Roux , “Mice can 'warn' sons, grandsons of dangers via sperm,” Medical Xpress, https://medicalxpress.com/news/2013-12-mice-sons-grandsons-dangers-sperm.html, December 1, 2013 (accessed 3/21/21).
Journal Source: Szyf, M., “Lamarck revisited: epigenetic inheritance of ancestral odor fear conditioning,” Nature Neuroscience 17, 2–4 (2014). https://doi.org/10.1038/nn.3603.
[20]. Franklin, Tamara B., Holger Russig, Isabelle C. Weiss, Johannes Graff, Natacha Linder, Aubin Michalon, Sandor Vizi, and Isabelle M. Mansuy. "Epigenetic Transmission of the Impact of Early Stress Across Generations." Biological Psychiatry 68, 5 (September 1, 2010): 408–415.
[21]. Max–Planck–Gesellschaft, “Childhood Trauma Leaves Mark On DNA Of Some Victims: Gene–Environment Interaction Causes Lifelong Dysregulation Of Stress Hormones,” Science Daily, https://www.sciencedaily.com/releases/2012/12/121202164057.htm: ScienceDaily L.L.C., December 2, 2012 (accessed 11/04/12):
Journal Source: Torsten Klengel, Divya Mehta, Christoph Anacker, Monika Rex–Haffner, Jens C Pruessner, Carmine M Pariante, Thaddeus W W Pace, Kristina B Mercer, Helen S Mayberg, Bekh Bradley, Charles B Nemeroff, Florian Holsboer, Christine M Heim, Kerry J Ressler, Theo Rein, Elisabeth B Binder. “Allele–specific FKBP5 DNA demethylation mediates gene–childhood trauma interactions.” Nature Neuroscience, 2012; https://doi.org/10.1038/nn.3275, https://pennstate.pure.elsevier.com/en/publications/allele-specific-fkbp5-dna-demethylation-mediates-gene-childhood-t.
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[24]. Ibid., Kindle Locations 2500–2501.
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[28]. Dr. Ventura’ findings (upon which this webinar was based) were published in Federation of American Societies for Experimental Biology (FASEB) Journal in 2004 and 2005. Ventura, “DNA and Cell Reprogramming Via Epigenetic Information Delivered By Magnetic Fields, Sound Vibration and Coherent Water,” Webinar transcript available at https://www.scribd.com/document/161598761/Dna-and-Cell-Reprogramming-Transcript.
Dr. Ventura’s brief biography: Prof. Carlo Ventura, is MD, Cardiologist, and Ph.D. in Biochemistry. He was Researcher at the “Laboratory of Cardiovascular Science”, N.I.A./N.I.H., Baltimore, MD, U.S.A. from 1988 to 1992, and then for repeated periods until 1994. He is Full Professor of Molecular Biology at the School of Medicine of the University of Bologna, Italy, and Chief of the National Laboratory of Molecular Biology and Stem Cell Engineering of the National Institute of Biostructures and Biosystems (NIBB – INBB) – ELDOR LAB, at the Innovation Accelerators of CNR (National Research Council), in Bologna. Carlo Ventura is member of the American Society of Biochemistry and Molecular Biology (ASBMB), and of the Cell Transplant Society. He discovered nuclear endorphin receptors and small peptide signaling responsible for cardiogenesis in mouse embryonic stem cells, paving the way to the new field of “intracrine” regulation of cell biology.
He developed new molecules harboring differentiating and paracrine logics for cardiovascular regeneration. He found that “extremely–low frequency” and asymmetrically–conveyed radioelectric fields were able to enhance stem cell expression of pluripotency, and afford a direct reprogramming of human skin fibroblasts towards myocardial, neuronal and skeletal muscle lineages. He has also discovered that cells are sensitive to acoustic vibrations and patented the cell ability to express “vibrational” signatures of their health and differentiating potential. These findings opened a new perspective based upon the use of physical energy in stem cell science. He published more than 150 full papers in the top journals of cellular and molecular biology.
[29]. Vladimir L. Voeikov, “Fundamental Role of Water in Bioenergetics,” ed. L.V. Beloussov;V.L. Voeikov;V.S. Martynyuk. Biophotonics and Coherent Systems in Biology (Kindle Location 1297-1298). Kindle Edition.
[30]. Ventura, "DNA and Cell Reprogramming Via Epigenetic Information Delivered By Magnetic Fields, Sound Vibration and Coherent Water," Webinar transcript, https://www.scribd.com/document/161598761/Dna-and-Cell-Reprogramming-Transcript.
[32]. Ventura, "DNA and Cell Reprogramming Via Epigenetic Information Delivered By Magnetic Fields, Sound Vibration and Coherent Water," Webinar transcript, https://www.scribd.com/document/161598761/Dna-and-Cell-Reprogramming-Transcript.