Epigenetics: The Effects of Nature & Nurture on Mental Health
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The phrase “nature versus nurture” is usually attributed to Francis Galton (1822-1911), who was also Charles Darwin’s cousin. Galton was pursuing a question that had elicited lively discussion from philosophers and scientists for years—what is the basis of knowledge?
On the nurture side, the British empiricists with their “blank slate” approach pushed back vigorously against inherited privilege. People shouldn’t be respected because of their birth, they said, but rather by what their experience had taught them. On the nature side, Galton and like-minded others were comfortable extrapolating from agricultural knowledge about breeding animals to human traits like intelligence, which Galton believed was largely due to inheritance. Over time, the pendulum of psychological thinking swung from side to side, but nurture was generally more favored than nature.
With the recent explosion of knowledge in the area of genetics, we can hopefully put this dispute to bed. As is true of so many issues, taking an either-or position is likely to be wrong. Truth is usually found somewhere in the middle. In the case of nature and nurture, we now understand that our genetic heritage interacts so intimately with our experience that it is no longer meaningful to pull these apart.
The nail in the coffin for the nature-nurture dichotomy quite possibly could be epigenetics. Epi means “above” or “around,” so epigenetics refers to changes in the way genes perform—not changes in their underlying DNA. Because many aspects of experience, such as choosing to smoke or drink alcohol, can change the performance of genes, viewing nature and nurture as isolated and separate makes no sense.
What is Epigenetics?
What does it mean to change the ways genes perform? Biologists have known for decades that genes can be turned on or off. If a gene is turned on, it is “expressed,” or able to produce the protein that it encodes. If a gene is turned off, it is not expressed, and its protein is not produced.
The most obvious and possibly best understood example of epigenetics occurs in early development. Each cell in a zygote typically contains the full complement of 23 chromosome pairs. As development and differentiation proceed, however, not all of the genes on those chromosomes will be expressed in every cell. A skin cell requires a different set of protein building blocks than a neuron or a muscle cell does. Something must tell the right set of genes to build their proteins at exactly the right time.
What happens when a gene turns on when it should not do so? Randy Jirtle and his colleagues published a dramatic example of this in 2007. They demonstrated that a mother mouse’s diet could have epigenetic effects on the phenotype, or outward characteristics, of her babies. When the mother mouse was fed a diet containing the plastic contaminant BPA, her babies were obese and had yellow fur. Fortunately, when the mother mouse was fed other nutrients, including folic acid, the disruption caused by BPA was prevented.
How are BPA and folic acid producing these outcomes? Several processes make a gene more or less likely to be read or expressed. Among these processes are modifications of the histone scaffolding supporting DNA. Another important mechanism is methylation, in which a methyl group is attached to the relevant segment of DNA. Genes that are methylated cannot be read, similar to stapling a few pages in a book.
Similarly, substances like BPA can remove methyl groups, allowing a gene to be read that wasn’t supposed to be. This is the likely mechanism behind the birth of the obese, yellow baby mice. The mother’s BPA intake had demethylated the Agouti gene responsible for these traits. Folic acid, in contrast, is capable of donating methyl groups and thus promotes methylation. The folic acid in the mother mouse’s diet canceled out the effects of BPA.
We can’t make a simplistic “methylated-good; demethylated-bad” heuristic or vice versa. One factor contributing to cancer is the methylation of tumor suppression genes. If these can’t be read, the processes to which they contribute will not happen. The important thing is that the methylated status of a gene is “right” for that particular cell at that particular point in time.
What Factors Can Produce Epigenetic Change?
We have only scratched the surface in efforts to identify epigenetic factors in the environment.
Psychologists have understood for many years that early childhood experiences seem to have more than their fair share of influence on adult outcomes. Child maltreatment is associated with a whole host of negative outcomes later in life, both medical and psychological.
Michael Meany and his colleagues demonstrated that one aspect of maternal nurture could strongly influence the adult reaction to stress by the offspring. In rodents, maternal nurture consists of licking and grooming the pups. The researchers found that the pups receiving more nurture were more resistant to stress later in life, as measured by how long they would stay in the open field. This, in turn, was associated with gene expression in the pups’ brains, affecting the number of receptors they produced for the stress hormone cortisol.
In other words, the nurture provided by the mother rodent had epigenetic effects on the genes making the protein structure of the receptor. We assume that many similar things could be happening in human children exposed to varying levels of nurture.
In addition to child maltreatment and maternal care, the list of known epigenetic factors is long. Diet, including the folic acid mentioned previously, and especially the maternal diet, can have significant epigenetic effects. Exposure to alcohol, tobacco, physical activity levels, environmental pollutants, and the levels of stress a person experiences can also produce epigenetic change.
What Does Epigenetics Have to Do With Psychology?
In addition to helping us reframe questions of nature and nurture, epigenetics helps us understand several previously puzzling situations.
You might know a pair or two of identical twins. Identical twins have identical DNA, yet over time, they might experience divergent outcomes. One is diagnosed with schizophrenia and the other is not. Although genetics is considered a strong risk factor for schizophrenia, the concordance rate (or rate of agreement) in identical twins is only 50 percent. That means that if one twin is diagnosed with schizophrenia, the other has about a 50 percent lifetime risk of also being diagnosed with the disorder. What accounts for the other 50 percent of risk?
Behavioral geneticists note that in addition to genetics, identical twins are exposed to both shared and unshared experiences that interact with their genetic inheritance. Shared experiences are things they do together, such as having holiday meals with their extended family. Unshared experiences are things they do differently, such as one twin taking up smoking or playing soccer while the other does not. The differences between these experiences and their effects can help us better understand risk factors unrelated to genetics.
Interactions between genetics and experience can also be illuminating. Autism spectrum disorder (ASD) has strong genetic roots, yet parents of children with ASD usually have one or more children who do not have the disorder as well. Combining a genetic vulnerability with exposure to certain environmental events, such as the mother’s contracting an infectious disease, could lead to ASD in a particular child.
Also, children born to malnourished mothers in the Netherlands at the close of World War II (the “Dutch Hunger Winter”) have significantly higher rates of schizophrenia and depression. It is likely that the experience of prenatal malnourishment and the effects of maternal stress interacted with a genetic predisposition for a psychological disorder.
Applying Epigenetics to Counseling
Although many epigenetic changes early in life are persistent, there is also the possibility of change. Counseling interventions, including cognitive behavioral therapy, exercise, and mindfulness training, have the potential to serve as epigenetic factors themselves to initiate positive and lasting change.
The experience of stress is often a factor in biopsychosocial models of the development of psychological disorders. By itself, stress is not capable of initiating disorders, but coupled with additional risk factors, its contribution is significant. Early stress, in particular, is associated with negative outcomes later in life. Epigenetics contributes to our understanding of this phenomenon. Early stress impacts the methylation of numerous genes, leading to changes in the hypothalamic-pituitary-adrenal (HPA) axis that controls our response to stressors.
Child maltreatment changed patterns of methylation in a meta-analysis conducted by Parade et al. (2021). The genes with altered function were consistent with those we would expect based on their involvement with the negative outcomes of child maltreatment. Genes influencing the HPA axis, oxytocin, serotonin, opioids, inflammation, and cell proliferation performed differently in those who were and were not subjected to maltreatment. The systems affected by these altered genes included the HPA axis, endocrine system, neurotransmitter systems, early neural development, neural signaling, apoptosis (programmed cell death), cancer, and metabolic functions.
Major depressive disorder and schizophrenia have also been linked to epigenetic change. Addictions of many types are likely to be associated with epigenetic changes, which provides some understanding of why long periods of abstention do not guarantee continued freedom from the addiction. In particular, epigenetic changes related to the functions of dopamine could support long-term distortions in the processing of reward.
One of the main takeaways of the contributions of epigenetics to counseling is that change can happen. The earlier approach to nature and genetics was somewhat deterministic and static. Understanding epigenetics provides confidence in the ability of interventions to succeed.
Secondly, epigenetics points to the value of early interventions. Although epigenetic change occurs throughout the lifespan, there are periods when the system is more plastic than others. Our understanding of epigenetics should energize us to advocate for prevention and remediation as early in life as possible.
This discussion might make some counselors or counseling students feel underprepared to deal with the directions the field is taking. While we strongly support the inclusion of genetics in the academic preparation of counselors, that might take time to implement.
In the meantime, counselors are encouraged to reach out to colleagues in other fields, including behavioral neuroscience and genetics, to compare notes. A great way to do this is to attend relevant conferences. Researchers need to know what tools practitioners require and practitioners need the latest and most accurate research news to carry out evidence-based practice.
Laura Freberg, PhD
Writer & Contributing ExpertLaura Freberg serves as professor of psychology at Cal Poly, San Luis Obispo, where she teaches introductory psychology and behavioral neuroscience.
Dr. Freberg is the author or co-author of several textbooks, including Discovering Psychology: The Science of Mind, Discovering Behavioral Neuroscience, Applied Behavioral Neuroscience, and Research Methods in Psychological Science. She served as President of the Western Psychological Association (WPA) in 2018-2019.