A Revolution in Evolution! Evolution without Changes in Genes

This is the fourth article of a series on “The New Epigenetics”.  The epigenetic perspective in biology and psychology provides a solution to the clunky, age-old nature-nurture issue.  It says that the old view that pits nature against nurture (genes against environment) as rival explanations for how development happens is flawed.  Genes and environments are partners in development; they can’t work without each other.  This has radical implications for how we understand biology, development, and human nature.  Because different political ideologies are build largely around different conceptions of human nature, it has deep implications for political life as well.  

We were all taught that for evolution to occur, there must be some change in the genes.  For example, genes must mutate for new physical structures or behavioral dispositions to evolve.  We now know that there is more to evolution than mere genetic transmission.  Developmental changes in the life of individual organisms – including humans – can result in the passing on of epigenetic markers to offspring – codes that “turn on” or “turn off” genes at different point in an offspring’s development or in result of environmental events.   Evolution can occur in the absence of changes in genetics (Osborne, 2017).  This is a revolutionary finding.

For example, the human body regulates stress through the activity of something called the HPA axis.  Stress reactions tend to involve three stages: alarm, resistance, and finally stress management. In the first step of the process, the hormone cortisol is released by the body. The presence of cortisol signals the beginning of the “fight or flight” response to stress. This process helps us to react to everyday stressful events such as deadlines or accident.  However, when someone is exposed to chronic stress, a person may experience chronically elevated levels of cortisol.  Such chronic levels can arise as a result of emotionally traumatic events such as war, sexual assault, natural disasters. They can also result from arguably less traumatic experiences such as a difficult divorce, ineffective or hostile caregiving, or a stressful work environments (Matosin, et al. 2017).  Such events can lead to conditions known as post-traumatic stress disorder (PTSD) .  Physical ramifications of chronic stress can result in epigenetic changes that can lead to obesity, diabetes, weight gain, heart conditions, high blood pressure, and a suppressed immune system (Smith & Vale, 2006). Other ramifications include increased susceptibility to depression, anxiety, cognitive impacts, and misdiagnosis of cognitive impacts as ADHD leading to less effective treatment strategies (Cecil & Nigg, 2022; Nestler, 2014).

Research has shown that chronically elevated levels of stress-induced cortisol can produce physical changes in a person that can be epigenetically transmitted to the affected person’s offspring in the absence of genetic changes in the DNA.  Neither the parent’s nor the child’s DNA is modified by the chronic stress of the parent.  Instead, chronically high levels of cortisol produce “epigenetic markers” that are passed on to children.  These epigenetic markers affect the biological development of children in ways that “turn on” or “turn off” sequences of DNA (genes) that influence (but do not autonomously determine) the development of a child’s disposition to respond to stress.

These are fascinating sets of findings.   Although epigenetics does not permanently alter the structure of DNA, the epigenetic changes that occur in individuals with chronic stress can be inherited and result in intergenerational trauma even if the offspring of that person never experienced the stressful events themselves. These findings show that environmental events that occur in parents can affect the expression of genes passed on to children without actually altering the genes themselves.  Evolution doesn’t occur simply as a product of mutation of genes; it also occurs as offspring inherent epigenetic markers acquired over the course of a parent’s development.

Epigenetic markers that lead to advantageous development can also be inherited. Fetal programming is a term used to describe the communication that occurs between the mother and fetus’ HPA axis during pregnancy which causes fetal epigenetic changes so the baby will be better equipped to survive after birth. An example of fetal programming can be observed in the children born after the Dutch Hunger Winter of 1944-1945. The Dutch Hunger Winter occurred during World War II when the Nazis blocked off the only road in the Netherlands that had access to incoming food or supplies (Konkel, 2016). A study conducted by Heijmans et al. (2008) found that periconceptional exposure to famine resulted in epigenetic changes that correlated with lower weight at birth. The babies born during this time period were also able to survive on the lower ration portions that were provided, while the caloric restrictions were much more difficult for all others to endure. Further, the individuals exposed to famine at later stages of birth did not exhibit as much of a change in average birth weight signifying that the epigenetic change was a direct result of the reduced food intake during the pregnancy. A follow-up study found that in addition to low birth weight, individuals with prenatal famine exposure also had issues with obesity and heart disease since the environment they were epigenetically programmed to survive in was different from the environment they experienced outside of the womb (Tobi, 2013).

Other studies found evidence of fetal programming in response to stress. If a mother experienced elevated levels of stress during the pregnancy, the baby was likely to have an altered HPA Axis and be prepared to enter into a world that has higher levels of stress. This included having measurably lower levels of cortisol in response to stressful events than control subjects. Behavioral and physical exhibits of activated HPA have also been reported including hyperactivity, cardiovascular disease, mood disorders, Type 2 diabetes, obesity, and cognitive decline (Brunton, 2010).

The study of epigenetics is altering our conceptions of evolution.  We now have an alternative to the idea that evolution occurs merely through chance mutations.  Instead, we can see that epigenetic changes that occur the life on individual organisms can produce biological markers that can be passed on and affect the development of offspring.  All of this can occur without a modification of genes.  This makes the long and complex process of evolution make sense.  We now understand how adaptations acquired over the course of an individual organism’s life can affect the biological development of offspring. In this way, the study of epigenetics is taking us to a place where it is much easier to understand how the complexity of organisms can evolve over time.


​​Brunton, P. J. (2010). Resetting the dynamic range of hypothalamic‐pituitary‐adrenal axis stress responses through pregnancy. Journal of neuroendocrinology, 22(11), 1198-1213.

Cecil, C. A., & Nigg, J. T. (2022). Epigenetics and ADHD: Reflections on current knowledge, research priorities and translational potential. Molecular diagnosis & therapy, 26(6), 581-606.

Heijmans, B. T., Tobi, E. W., Stein, A. D., Putter, H., Blauw, G. J., Susser, E. S., … & Lumey, L. H. (2008). Persistent epigenetic differences associated with prenatal exposure to famine in humans. Proceedings of the National Academy of Sciences, 105(44), 17046-17049.

Konkel, L. (2016). Lasting impact of an ephemeral organ: the role of the placenta in fetal programming.

Matosin, N., Cruceanu, C., & Binder, E. B. (2017). Preclinical and clinical evidence of DNA methylation changes in response to trauma and chronic stress. Chronic Stress, 1, 2470547017710764.

Nestler, E. J. (2014). Epigenetic mechanisms of depression. JAMA psychiatry, 71(4), 454-456.

Osborne, A. (2017). The role of epigenetics in human evolution. Bioscience Horizons: The International Journal of Student Research, 10.

Smith, S. M., & Vale, W. W. (2006). The role of the hypothalamic-pituitary-adrenal axis in neuroendocrine responses to stress. Dialogues in clinical neuroscience, 8(4), 383–395. https://doi.org/10.31887/DCNS.2006.8.4/ssmith

Tobi, E. W. (2013). Epigenetic differences after prenatal adversity: the Dutch hunger winter (Doctoral dissertation, Leiden University).

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