Definition for Epigenetics
Glossary
Epigenetics
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.
Epigenetics is the field of science that studies heritable changes caused by the activation and deactivation of genes without any change in the underlying DNA sequence of the organism. In comparison, the genome is the complete genetic material existing within an organism. 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. 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 with two potential states — ON (represented by the number 1) or OFF (represented by number 0). 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.
BEIRBO — Behavioral & Environmental Input & Reactive Biological Output
What are some of the environmental factors that initiate the epigenetic mechanism? 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 https://www.stossbooks.com/blog/index.php?id=00000003D);3. Repeated behaviors that result in the production of reward hormones/neurotransmitters such as dopamine (often associated with addictions), oxytocin, endorphins, and serotonin (see https://www.stossbooks.com/blog/index.php?id=00000003D);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 https://www.stossbooks.com/blog/index.php?id=00000003D), and;7. Both Electromagnetic Energy and Sound Waves (see https://www.stossbooks.com/blog/index.php?id=00000003D), and:8. Environmental Factors (see https://www.stossbooks.com/blog/index.php?id=00000003D).
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 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;
- 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]
- 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
- 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]
- 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]
- 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 these statement’s validity: we are what we eat — which would include the Eucharist!
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, 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).
[4] 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).
[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] Ibid.
[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).