Tuesday, May 9, 2017

By Dr. Gary Isaacs

When I was growing up as a preacher’s kid in the small town of Lincoln, Delaware, it was my weekly duty to hold the door for people arriving at church each Sunday morning. Amidst the typical greetings, I would invariably hear a comment from an appreciative, elderly individual stating that I “looked just like my father” or that I “had my mother’s eyes.” This began a process of thought in my own mind where my identity was linked to my parents, my appearance, my personality, and my talents. It seemed that even aspects of my future fell on a continuum between my father and mother.

This idea of our identity stemming from our genome is not limited to the scientific community, as it shows up in daily conversations concerning health and fitness. There are times where a “genetic blame game” is played out in our society, sometimes with medical data to support, but many times without. We understand that our DNA holds the information for life within each of our cells. We understand that our DNA can confine us within various biological limits (e.g., height, weight, color of our hair and skin) and that these limits extend to more than just attributes of appearance. Most relevant for the mindset of our culture are the pervasive limits that are stamped on each of our cells; we use our genome as an excuse: “This is simply how I was made.” That is how the blame game is played. The structure of DNA and the process of its replication to daughter cells ensures a faithful rendering of the original. This suggests that our identity has been forged; it is steadfast and concrete, and written with permanence in cell and tissue.

Not only do we view ourselves as the product of our DNA, but we also project our understanding of identity, of our human brokenness, on the DNA itself. As scientists have sequenced the 3.2 billion bases of the human genome we discovered vast stretches of DNA (hundreds of thousands of bases) between genes which were referred to in many circles as “junk DNA.” This label seemed appropriate because researchers could not ascribe a specific function for these DNA sequences, and it was believed that they were the garbage – the genetic errors and inefficiencies accumulated over evolutionary time. We now know, however, that many of these sequences are not “junk,” and that in fact they often direct gene activation even though the nearest gene may be far away. So why were these sequences ever referred to as “Junk DNA”? It is as if we viewed ourselves as broken people with baggage – even at the biological level.

A Code Above Our DNA

Although Christians know that we were “fearfully and wonderfully made,” we also often relegate that fact to a past event located in our mother’s womb for which we are not responsible. Having no hand in our own construction would push the responsibility of who we are to our parents and ultimately to God. But what if my construction, my biological development, were not complete? What if my genomic fate were yet to be fully determined, and the “genomic concrete” were still wet and malleable? If our DNA were like this, we would find ourselves subject to another set of rules that aim to influence who we will become.

Life is full of examples that suggest we are more than just our base DNA sequence. Studies with monozygotic twins (a.k.a., identical twins) have identified discordance with various disease states.1 While one twin develops Alzheimer’s disease, the other does not. Even though one twin seems perfectly healthy, the other undergoes chemotherapy as a part of their cancer treatment. Since identical twins have the same DNA sequence, something else must be responsible for the apparent discrepancy in their health. Identical DNA sequences do not necessarily produce equal identities.

Since identical twins have the same DNA sequence, something else must be responsible for the apparent discrepancy in their health. Identical DNA sequences do not necessarily produce equal identities.

Even within a single individual, the same DNA sequence can produce multiple outcomes depending on how it is influenced by the environment. For instance, cellular differentiation is the process by which primordial cells develop into the specialized cells that form our organs and tissues. All the cells of the human body contain the same DNA sequence, yet they use that information differently. Chemical marks, such as DNA methylation, are imprinted on the DNA and direct the cell to turn on certain genes or turn off others. The local external environment of the cell acts as the stimulus to initiate these different marks – making the environment a major contributor to the identity of each individual cell. The term “epigenetics” refers to this chemical code which acts above the normal code of our DNA sequence. If the genome were compared to the cell’s library of information, then epigenetics refers to the availability of various books and journals within that library. If we want to describe the identity of a cell, we cannot look simply at the contents of the library (the DNA sequence) but rather the portions of the library that are used.

Affecting the Present

So we see that our genetic identity is framed by several variables. One of these is the contents of our library, established for the most part by the contributions from our parents at conception. The other is the environmental influence (through epigenetics) which can alter the accessibility of these contributions and even modulate the use of individual genes. Together, these mechanisms contribute to our genetic identity. The question remains though, “Can we contribute to the identity of others?” The answer is a resounding “Yes!” We ourselves are part of the environment; we do not operate on an island but as part of a community. Genetically speaking, our actions and environment not only alter our own development, they also can contribute to the development of others.

One of the best examples of how the epigenetic influence of one person can affect another is from a study published in 2005 on the mother-infant relationship in rats.2 The study centered around two types of mothers – those that took good care of their young by licking and grooming them, and those that took a laid-back approach to their parental responsibilities. Initial observations of the offspring from these two cohorts revealed that pups with “low-licking mothers” had severe difficulty dealing with stress. They would bite caretakers when handled and scream when people entered their cage room. Medical tests also revealed a significant elevation in their blood pressure and stress hormones during times of stress.

These responses were not caused by a mutation passed down through the maternal or paternal line as the effects were negated when the new-born mice were switched at birth (a process known as cross-fostering). Pups born to “low-licking mothers” developed normally if raised by “high-licking” mothers. Conversely, pups born to “high-licking mothers” had difficulty dealing with stress if raised by “low licking” mothers. This study opened the door to the concept that we are not only responsible for our own genome (both genetic and epigenetic), we are also responsible for the influence we have on the world around us.

Affecting the Future: A Transgenerational Response

If we view ourselves as ‘this is all I am’ then the thought ‘this is all I can do’ is not far behind.

This influence may be deeper than any of us realize, as several studies have demonstrated that epigenetic identity developed in one generation could be passed down to the next. Research from Dr. Michael Skinner’s lab determined genetic differences in rats that resulted to maternal pesticide exposure three generations earlier.3 The experiences of one generation were preserved as a chemical signature on the DNA and passed down to subsequent progeny. This phenomenon is not unique to animals, as human history has recorded world events now known to have caused a transgenerational response. Century-old public health records from a small town in Överkalix, Sweden, have been used to correlate the nutrition of grandparents to the health of their grandchildren noting that some ancestral environments can produce positive or negative outcomes in subsequent generations.4 In 1945, the events of World War II set the scene for the Dutch Famine, which reduced the caloric intake of pregnant mothers along with the rest of the urban west of the Netherlands. An examination of the children born or conceived during that time suggests that the mother’s nutrition before pregnancy plays a role later in the disease susceptibility of their offspring.5 Together, these studies paint a clear picture of the biological influence we can have on those that come after us.

Concluding Thoughts: Identity and Culture

Based on our understanding of epigenetics, how should we define our identity and our role in society? I believe this can be answered with one word, “stewardship.” As created beings we were formed in our mother’s womb, but we are also being made in the likeness of Christ, and we are challenged to make disciples. We are creatures dependent on our maker. And yet, we are still being re-made to shape the world around us (Gen. 1:26-28; Matthew 28:28-20). The call to be “in the world and not of it” is a challenge towards fulfilling the cultural mandate – to leave a positive mark on the world (not unlike the chemical marks on top of our genetic code). Our mission is not to uproot the culture and destroy its base, but rather, to influence it through our faithful presence in all the communities we find ourselves in. We are thus stewards of who we become and who we enable others to be. Our Lord, after all, has given us dominion as his image bearers. If we dismiss ourselves with statements such as “this is all I am,” then the thought “this is all I can do” is not far behind. Using a model of epigenetics, if we view each other as impressionable people who are easily influenced by our environments, we will realize the importance of forming intentional counter-cultural Gospel communities for the sake of those around us and those yet to come.


1. Diego Mastroeni, Ann McKee, Andrew Grover, Joseph Rogers, and Paul D. Coleman, “Epigenetic Differences in Cortical Neurons from a Pair of Monozygotic Twins Discordant for Alzheimer’s Disease,” PLOS One, August 12, 2009, accessed October 17, 2016, https://journals.plos.org/plosone/article?id=10.1371/ journal.pone.0006617; Jaun E. Castillo-Fernandez, Tim D. Spector, and Jordan T. Bell, “Epigenetics of Discordant Monozygotic Twins: Implications for Disease,” Genome Medicine, July 31, 2014, accessed October 17, 2016, https://genomemedicine.biomedcentral.com/articles/10.1186/s13073-014-0060-z.

2. Moshe Szyf, Ian C. G. Weaver, Francis A. Champagne, Jose Diorio, and Michael J. Meaney, “Maternal Programming of Steroid Receptor Expression and Phenotype through DNA Methylation in the Rat.” Frontiers in Neuroendocrinology 26, no. 3-4 (October-December 2005): 139-162, accessed October 17, 2016, https://www.sciencedirect.com/science/article/pii/ S0091302205000476.

3. David Crews, Ross Gillette, Samuel V. Scarpino, Mohan Manikkam, Marina I. Savenkova, and Michael K. Skinner, “Epigenetic Transgenerational Inheritance of Altered Stress Responses,” PNAS, April 18, 2012, accessed October 18, 2016, https://www.pnas.org/content/109/23/9143.full.

4. Marcus Pembrey, Richard Saffery, Lars Olov Bygren, and Network in Epigenetic Epidemiology, “Human Transgenerational Responses to Early-life Experience: Potential Impact on Development, Health and Biomedical Research.” NCBI, July 25, 2014, accessed October 18, 2016, https://www.ncbi.nlm.nih.gov/pmc/articles/ PMC4157403/.

5. Tessa Roseboom, Susanne de Rooij, Rebecca Painter, “The Dutch Famine and its Long-Term Consequences for Adult Health.” Early Human Development 82, no. 8 (August 2006): 485-491, accessed October 18, 2016, https://www.sciencedirect.com/science/article/pii/S0378378206001848.