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Born With It: Does God Will It? Part 1 of 3

Born With It: Does God Will It?

Part 1 of 3 Parts

The Science of Epigenetic–driven Biological Change: Using Science & Theology to Refute a Logical Fallacy



The epigenome and its mechanisms are another of the thirty–four mysteries of cutting–edge science that are hidden within the books of Scripture. These mysteries are not written in the form of  textbooks, but in the genre of applied sciences. The Bible’s human authors (who are Divinely inspired by the Holy Spirit) wrote about these scientific mysteries thousands of years ago. Scientists, by comparison, are only now beginning to discover them, but only at a rudimentary level. Why did God choose to use applied science as the method by which to reveal them? Simply stated, the knowledge to be gained from reading the Bible is not meant only for the intellectual elite. It is for everyone.
Before we attempt to answer the question posed in this blog’s title, it is essential to talk about the science behind biological change that occurs at the level of genomic function. The level at which the clay of our physiology is moldable (e.g., Job 10:9, Sirach 33:13, and Jer 18:1-10). We must first know a bit about epigenetics and its effect on each phenotype.[1] Ultimately, this blog series aims to address the arguments used by many who are trying to compel us to accept a link between the genetic roots of same–sex attraction and God's will. The argument goes like this: Gayness is entirely a product of our genetic makeup. Therefore, God makes people with same–sex attraction. Therefore, God wills people to be gay. Therefore, same–sex attraction is normal and healthy. Of course, this is a logical fallacy which we will more fully address at another time. Part Three of this blog series will answer the question: does born with it mean that God wills it?
The science we will be discussing is relatively young. Dr. Conrad Waddington only introduced epigenetic–driven modification as a hypothetical in 1942. It wasn’t until around the year 2000 that research became more refined and developed and became more focused.
The word epigenetic translated literally, means above the genome. A more precise definition comes from Dupont et al. He writes, “Over the following years, with the rapid growth of genetics, the meaning of the word [epigenetic] has gradually narrowed. Epigenetics has been defined and today is generally accepted as ‘the study of changes in gene function that are mitotically[2] and/or meiotically[3] heritable and that do not entail a change in the DNA sequence.[4] To help visualize the epigenome’s role, think in terms of our DNA as being a computer. The genes within the DNA molecule are the hardware of the computer. The epigenome is the software, which tells the computer (the genes) what to do. In our biology, the software (the epigenome) will alter the computer’s function without changing the hardware (the DNA sequencing of the nucleotides, aka the steps of the DNA ladder). The epigenome tells the cells to divide and what types of cells they are to become (e.g., heart cell, muscle cell, neuron, etc.). It’s the epigenome that turns on the genes needed for a particular cell type to function correctly and turns off the unneeded genes (i.e., tells them to stop making proteins).
Since we compare our DNA (and the genes within it) to computer hardware, binary code is an excellent way to understand the epigenetic (software) mechanism. A computer’s software uses bits and bytes to give the computer its marching orders. A bit is a single transistor (aka junction) with two potential states — ON (represented by the number one) or OFF (represented by the number zero). The epigenetic mechanism functions much the same way. Chemical tags called methyl groups (see Figures below), working in conjunction with histones, will turn a gene’s production (expression) of proteins on or off. In laymen’s terms, “on” means the gene sends out instructions to other genes to do something; “off” means it does not.
Initially, it was felt that all epigenetic change resulted, primarily from the diet. Current research shows a much more comprehensive range of environmental and behavioral factors (both sense–able and meta–sense–able) will also epigenetically alter gene function, possibly for several generations, aka transgenerational heredity.
Figure 1: Graphic courtesy of National Institutes of Health
Figure 2: Histones (blue) & DNA (orange)
BEIRBO — Behavioral & Environmental Input, Reactive Biological Output
What are 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 (see “The Epigenetics of Substance Abuse and Addiction” below);
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 (see “The Epigenetics of Fear and Stress” below), and;
7. Both light (see “The Epigenetics of Electromagnetic Energy and Sound Waves” below), and:
8. Environmental Factors (see “The Epigenetics of Environmental Factors” below).

The Epigenetics of Food and Drink

  • 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.[5] 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.[6] Our subsequent study will also help to support this belief;
  • 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;[7]
  • 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;”[8]
  • 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.[9] 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.[10] 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.[11]
  • 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.[12]
  • 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.[13]
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 entire section above, “The Epigenetics of …,” shows us how the epigenetics of food and drink can make us weak, ill, or healthy depending upon what we eat and drink. St. Paul tells us, “Whoever, therefore, eats the bread or drinks the cup of the Lord in an unworthy manner will be guilty of profaning the body and blood of the Lord … For any one who eats and drinks without discerning the body eats and drinks judgment upon himself. That is why many of you are weak and ill, and some have died [SML]” (1 Cor 11:27-30). A case can be made that covenants of salt with fallen man directly involve epigenetic plasticity (think moldable clay in Scripture).  
When thinking about covenants of salt, consider this: Luke writes, “And eating together with them, he commanded them, that they should not depart from Jerusalem, but should wait for the promise of the Father” (Acts 1:4: Douay-Rheims 1899 American Edition). Pope Benedict XVI places great significance on Luke’s wording when talking about Jesus’ eating with his Apostles before his Ascension. According to Pope Benedict XVI, the word that Luke used is synalizômenos. Benedict tells us this wording must have been very important to Luke, so much so that he must have deliberately chosen to employ it. The literal translation of the phrase in question is “eating salt with them.” Why is the word significant? It is because all food is salt. All food is composed of the salt and dust of DNA. Benedict interprets this wording as a direct reference to the Eucharist, which is the final fulfillment of the Old Testament Covenant of Salt.[14] Jesus describes himself as REAL food. All food is the salt of DNA.
All the Old Covenant Jews were required to add salt to all their offerings to God. What happens at Mass? We have to join Jesus on the Cross (via the Eucharist) as a pure and acceptable offering to our Father. Also, all of those offerings had to be eaten. After an oblation was offered to God on the altar, it had to be eaten (the offering was not valid otherwise). The early Jews believed that by eating the offering, the offeror would become one with that offering and thus participate in the altar sacrifice’s benefits.[15] Becoming one with the offering is precisely the theology behind the Mass and the Eucharist. Now we know why salt (a type of our salt of DNA) was required to be added to the unblemished Lamb offering. Now we know the deeper meaning of the crucifixion. The unblemished Lamb was nailed to that Cross, thus becaming one with the salt of DNA of the wood of the Cross. Both Elijah’s (1 Kgs 17:21-22) and Elisha’s (2 Kgs 4:32-35) resurrecting two children by laying outstretched upon their dead bodies is a type of Jesus’ crucifixion on the wooden Cross.
In the biblical sense, a covenant is a solemn oath (sacratemtum in Latin) and a gift of persons. To appreciate the gravity of a Divine/sacramental covenant, Dr. Scott Hahn tells us the Trinity is a covenant relationship of three Persons in one God. Therefore, a covenant is a family oath, as can be seen by the very names given to the different Persons of the Trinity, i.e., Father, Son, and Spirit. The covenantal relationship of the Trinity is not a covenant of salt. Only man is formed from the salt/dust of the earth. Hahn tells us that God designs a covenant to forge bonds of sacred kinship, to turn people into spouses, sons, daughters, and parents — both to each other and to Himself.
A covenant forms a sacred kinship with God. One type of family covenant is the solemn oath exchanged in the Sacrament of Matrimony. The institution of sacramental marriage is the most complete image possible of the Holy Trinity existing within creation. A sacramental marriage (as opposed to a civil marriage) is a covenant through which a man and a woman become one–flesh (Mt. 19:5-6, Mk. 10:8). Incidentally, science is now showing that a one–flesh relationship is not merely symbolic. It is a gift between two persons that is both unitive and fruitful. Man is made in the image and likeness of God, consisting of Three Persons in a covenantal relationship. One God; Three Persons.
Scripture refers to covenants of salt (aka salt covenants). What, if any, is the difference between a “covenant” and a “covenant of salt”? Nowhere in Scripture can a passage be found in which God is quoted as establishing a covenant with man that is specifically referred to as a salt covenant. Yet, we know that salt covenants exist. Three passages refer to them (2 Chron. 13:4-5, Lev. 2:12-14, Num. 18:18-20). All Scripture passages in which covenants of salt are mentioned, are done so in the context of a previously entered into event — a covenant already in effect. Never as something that is in the current process of being established. There is also no specific text in Scripture directly defining a covenant of salt.
Due to their eternal nature (among other reasons), all covenants are salt covenants. In Scripture, we read, “Do you not know that the LORD God of Israel gave the kingship over Israel forever to David and his sons by a covenant of salt” (2 Chronicles 13:5)? This generational handing down of kingship occurred through a covenant of salt. In other words, this kingship involved the salt of DNA. All generational covenants involve, by definition, the salt of DNA. After all, it is the salt/dust of DNA that the parents give to their offspring. Who was the final recipient of the Old Covenant of Salt? Jesus, whose body (salt/stone of DNA) is the rebuilt/resurrected temple (John 2:19-21). The case can be made that a covenant of salt is the only type of covenant of salvation that God could enter into with fallen man.
Covenants of Salt tell us a great deal about the Sacraments, including the Eucharist. The Eucharist is the fulfillment of God’s covenant of salt with man. Marriage is a covenant of salt. In Marriage, man and women become one flesh. St. Paul tells us, “Do you not know that he who joins himself to a prostitute becomes one body with her? For, as it is written, ‘The two shall become one’” (1 Cor 6:16). Obviously, St. Paul is referring to the sex act outside of marriage, which in no way involves a solemn oath. In both cases, the participants become one body. One Salt.
When we receive His body and blood as our sacred nutrition, He purifies the heart and heals the salt of our DNA — cleansing it in the manner prophetically shown to Ezekiel (chapter 47). In his dream, the water flowing out from the New Covenant Temple flowed down to the Salt/Dead Sea and purified it, making it alive, not dead. Making it fruitful, not barren. If it is true that Jesus’ body and blood are real food and real drink, then the changes to our salt of DNA promised in Scripture are also true. The function of his risen body affects the epigenome of all those who faithfully and worthily receive him.
I haven’t done any research on the dietary laws imposed on the Israelites by God. I can’t help but wonder if there were much deeper reasons, other than simply fostering an attitude of obedience to God’s Laws, for God to have imposed them. The Chosen People were chosen by God to preserve Abraham’s intergenerational seed from decay and corruption. In light of the research discussed above, this is an especially intriguing question. God told St. Hildegard that the flesh of animals conceived through hormone–induced intercourse can inflame the lusts of the humans who eat it.[16] All hormones are delivered to their target cells through the bloodstream. Not only were Jews forbidden from eating the flesh and blood of certain animals, but they were also prohibited from consuming the blood of any animal, even though allowed to eat the flesh. Life is in the blood (Lev. 17:11). This prohibition is one of the reasons why the Jews were so horrified when told by Jesus they must eat his flesh and drink his blood.

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].”[17] 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;[18]
  • 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.”[19] 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.[20]

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.[21]
  • 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.[22]
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.[23]

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.”[24] 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;”[25]
  • 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.”[26][27]
  • 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.[28] 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.[29]

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).[30] Even of weak and extremely low frequency, these fields are used by humans on a molecular level for information exchange.[31][32] 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.[33][34] These experiments demonstrate that electromagnetic energy (light) triggers epigenetic mechanisms.
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.”[35]
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Updated 05/24/2021


[1] According to the California Academy of Sciences, “An organism's genotype is the set of genes that it carries. An organism's phenotype is all of its observable characteristics [both sense–able and meta–sense–able] which are influenced both by its genotype and by the environment.” https://evolution.berkeley.edu/evolibrary/article/genovspheno_01.
[2] Mitosis involves the division of body cells.
[3] Meiosis involves the division of sex cells (gametes), i.e., sperm or egg cells.
[4] Dupont C, Armant DR, Brenner CA (September 2009). "Epigenetics: definition, mechanisms and clinical perspective". Seminars in Reproductive Medicine. 27 (5): 351–7. doi:10.1055/s–0029–1237423. PMC 2791696. PMID 19711245.
[5] 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.
[6] 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).[7] USDA/Agricultural Research Service, "Baby's Obesity Risk: What's the Mother's Influence?," ScienceDaily.com, http://www.sciencedaily.com/releases/2010/03/100315125551.htm?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+sciencedaily+%28ScienceDaily%3A+Latest+Science+News%29&utm_content=Google+Feedfetcher: ScienceDaily L.L.C., April 5, 2010 (accessed April 5, 2010).
[8] University of California – Berkeley, "Genetic Abnormalities In Sperm Linked To Dietary Folate Intake, Study Shows," ScienceDaily, http://www.sciencedaily.com/releases/2008/03/080319193036.htm: ScienceDaily, March 20, 2008 (accessed Mar. 20, 2008).
[9] 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).
[12] Ibid.
[13] Gómez–Pinilla et al., "Brain foods: the effects of nutrients on brain function," Nature Reviews Neuroscience (Nature Publishing Group) 9 (July 2008).
[14] Joseph Ratzinger (Pope Benedict XVI), "Jesus of Nazareth Part Two, Holy Week: From the Entrance Into Jerusalem To The Resurrection," (Kindle Locations 3436-3437), Ignatius Press.
[15]. Burge, Gary M. (2012-08-07). Jesus and the Jewish Festivals (Ancient Context, Ancient Faith) (Kindle Locations 1184-1187). Zondervan. Kindle Edition.
[16] Hildegard, Scivias, 281.
[17] The Babraham Institute, "New insight into reprogramming of cell fate," ScienceDaily, http://www.sciencedaily.com/releases/2010/01/100127111105.htm?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+sciencedaily+%28ScienceGoogle+Feedfetcher: ScienceDaily L.L.C., February 1, 2010 (Retrieved February 1, 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] 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.
[20] Emma Young, "Rewriting Darwin: The new non–genetic inheritance," New Scientist, http://www.newscientist.com/article/mg19926641.500–rewriting–darwin–the–new–nongenetic–inheritance.html: Reed Business Information Ltd., July 09, 2008 (accessed 02/15/2012).
[22] The Wake Forest University Baptist Medical Center, “Molecular Fingerprint Of Cocaine Addiction Revealed,” ScienceDaily, http://www.sciencedaily.com/releases/2008/05/080527113200.htm: ScienceDaily L.L.C., May 29, 2008 (accessed 05/29/2008).
[23] Doidge, The Brain That Changes Itself, 107.
[24] 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).
[26] 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.
[27] 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.
[28] Max–Planck–Gesellschaft, “Childhood Trauma Leaves Mark On DNA Of Some Victims: Gene–Environment Interaction Causes Lifelong Dysregulation Of Stress Hormones,” Science Daily, http://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; DOI:10.1038/nn.3275, https://pennstate.pure.elsevier.com/en/publications/allele-specific-fkbp5-dna-demethylation-mediates-gene-childhood-t
[29] University of East Anglia. “Family problems experienced in childhood and adolescence affect brain development.” ScienceDaily. https://www.sciencedaily.com/releases/2014/02/140219075213.htm (accessed February 19, 2014);
Journal source: Nicholas D. Walsh, et al. “General and Specific Effects of Early–Life Psychosocial Adversities on Adolescent Grey Matter Volume.” NeuroImage: Clinical, 2014; 4: 308 DOI: 10.1016/j.nicl.2014.01.001 <http://dx.doi.org/10.1016/j.nicl.2014.01.001>.
[30] N.A. Temuryants, V.S. Martynyuk, and E.N. Chuyan. “Influence of Electromagnetic Fields Of Extremely Different Frequency Diapason on Infradian Rhythms of Physiological Processes.” Biophotonics and Coherent Systems in Biology. ed. L.V. Beloussov, V.L. Voeikov, V.S. Martynyuk. (Kindle Locations 2499–2500). Kindle Edition.
[31] Ibid., Kindle Locations 2500–2501.
[32] Werner R. Loewenstein. The Touchstone of Life: Molecular Information, Cell Communication, and the Foundations of Life (Kindle Locations 547-549; 627-628; 786-787; 2357-2359). Kindle Edition.
[33] Sae Shimizu–Sato et al., “A Light–Switchable Gene Promoter System,” Nat Biotech 20, no. 10 (October 2002): 1041–44, https://pubmed.ncbi.nlm.nih.gov/12219076/.
[34] Trace Dominguez, "Scientists 'Talk' to Yeast." Discovery News. https://www.seeker.com/computers–talk–to–yeast–1765506125.html: Discovery Communications, LLC, Nov 15, 2011 (accessed 11/16/2011).
Journal Source: Milias–Argeitis, A., Summers, S., Stewart–Ornstein, J. et al. In silico feedback for in vivo regulation of a gene expression circuit. Nat Biotechnol 29, 1114–1116 (2011). https://doi.org/10.1038/nbt.2018.
[35] 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 here: 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.

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