Are genetics fixed? How our environment can change how our DNA works
- Rosie Jephson
- 7 minutes ago
- 6 min read
There are countless approaches to try to explain why people think and behave in the ways that they do, and like many Inspire the Mind readers, I have always been interested in this question.
As a teenager, I had heard about the ‘nature vs nurture’ debate, where scientists disagree over how much our traits and behaviours are determined by our genes, and how much they are shaped by the environment around us. Of course, the general answer tends to be: it’s a bit of both.
But one Thursday morning, sitting in my A level biology class, I learned something that blew my mind. Not only can nature and nurture interact, but how our DNA works can actually be changed as a result of our experiences, via a very clever process called epigenetic modification.
This idea fascinated me (and still does!) and discovering it is partly what confirmed to me that I wanted to study psychology; so here I am, having finished my Batchelor’s degree at Oxford University, now doing a Master’s degree in Psychology and Neuroscience of Mind Body Interface at King’s College London.
What is epigenetics?
This can be a complicated topic, so let’s start with a few definitions. DNA (deoxyribonucleic acid) is the “molecule that carries genetic information for the development and functioning of an organism”, whilst a gene is a section of DNA that provides specific instructions, for example about how to build a particular protein.
The field of research that investigates how our behaviours and environment can affect the way our genes work is called epigenetics. Taking a closer look at this word, we can see that ‘epi-’ comes from Greek and means ‘upon’ or ‘near’, whilst ‘genetics’ of course refers to the study of DNA and genes, and how these are passed down to offspring. This breakdown provides a clue as to what we mean when discussing epigenetics: within a cell, our DNA interacts with smaller chemicals that are ‘upon’ or ‘near’ the DNA itself. It is these smaller chemicals, that are key for understanding gene-environment interactions.
How does it work?
So what is actually going on? What do we mean when we say that environmental factors are changing the way our DNA is working? Let me be clear, the content of the DNA itself is not being altered here; the sequence of units that make up our strands of DNA stays the same. (Note: When this sequence is changed, through damage or random error, it is not an epigenetic process but a genetic mutation, and these changes tend to be permanent). In epigenetic modification, it is the (generally reversible) labelling of the DNA that is altered, which determines whether genes are switched 'on' or 'off'

Let’s say that our DNA is an instruction manual, and the genes that it is made up of are paragraphs detailing each of the many things that the cell could potentially build. All of our cells have the same whole instruction manual, but they only need to pay attention to the paragraphs that are relevant to their particular function. For example, cells in the pancreas may need to read the paragraph on how to build the protein insulin, but cells in the skin can (and should) ignore this paragraph, as producing insulin is not their job. The way that these cells know which paragraphs to read, and which to ignore, is through a labelling process. Essentially, an instruction paragraph (i.e. a gene) can be labelled with a sticky marker that indicates whether it should be read, and this helps different cells to perform their different functions.
There are a number of ways that genes can be labelled. One way is by adding a chemical called a methyl group, a process which is called DNA methylation (or demethylation when a methyl group is removed). This type of label essentially tells the cell’s machinery to ignore the methylated gene, i.e. to stop reading the instructions for the particular protein which that gene is responsible for building, and therefore less of that protein gets produced.

What environmental factors can affect this process?
Our epigenome – the collection of chemical labels determining how our genes are processed – changes massively through adolescence and across our lifespan as a feature of normal ageing. But it can also be affected by exposure to things in our environment both in the womb and throughout life. This is a huge topic, and these environmental influences span from nutrition and chemical exposure to mental illness, stress and many others.
For example, offspring of mothers who were subjected to famine during their pregnancy show epigenetic changes at several genes with many potential health implications. One of the most affected genes, IL10 (interleukin-10), has been linked to schizophrenia risk, which is consistent with the finding of significantly higher rates of schizophrenia in children conceived at the height of the Dutch 1944/1945 famine.
Pre-natal exposure to cigarette smoke has also been linked to epigenetic changes: adolescents whose mothers smoked during pregnancy who had more DNA methylation at a section of DNA that is part of the BDNF gene (brain-derived neurotrophic factor gene). This is important as epigenetic changes to this gene are proposed as a potential biomarker for Major Depressive Disorder (MDD).
Another well-studied example of how a foetus’ environment in pregnancy can alter their epigenome relates to maternal mental health during pregnancy. Infants of depressed or anxious mothers reliably show epigenetic changes in genes that are important for dealing with stress, neurotransmission and neuroplasticity, and thereby increasing vulnerability to psychopathology.
What environmental factors can affect this process?
Our epigenome – the collection of chemical labels determining how our genes are processed – changes massively through adolescence and across our lifespan as a feature of normal ageing. But it can also be affected by exposure to things in our environment both in the womb and throughout life. This is a huge topic, and these environmental influences span from nutrition and chemical exposure to mental illness, stress and many others.
For example, offspring of mothers who were subjected to famine during their pregnancy show epigenetic changes at several genes with many potential health implications. One of the most affected genes, IL10 (interleukin-10), has been linked to schizophrenia risk, which is consistent with the finding of significantly higher rates of schizophrenia in children conceived at the height of the Dutch 1944/1945 famine.
Pre-natal exposure to cigarette smoke has also been linked to epigenetic changes: adolescents whose mothers smoked during pregnancy who had more DNA methylation at a section of DNA that is part of the BDNF gene (brain-derived neurotrophic factor gene). This is important as epigenetic changes to this gene are proposed as a potential biomarker for Major Depressive Disorder (MDD).
Another well-studied example of how a foetus’ environment in pregnancy can alter their epigenome relates to maternal mental health during pregnancy. Infants of depressed or anxious mothers reliably show epigenetic changes in genes that are important for dealing with stress, neurotransmission and neuroplasticity, and thereby increasing vulnerability to psychopathology.

However, even in the absence of a mental health disorder, our mood and stress levels can shape our epigenome. One example of this relates to the neurotransmitter serotonin, which is implicated in depression. It has been long established that variations in the serotonin transporter gene can make some people more vulnerable to developing depression following stressful life events. More recent research recognises the crucial role of epigenetic mechanisms (e.g. methylation of the serotonin transporter gene) in this process.
Similarly, some researchers have found that chronic stress is linked to epigenetic changes that reduce the expression of the BDNF gene (mentioned above as being associated with depression risk and sensitive to tobacco smoke, among other environmental factors). This stress-related epigenetic down-regulation of the BDNF gene can persist well into adulthood. However these changes are not necessarily permanent, as shown by the fact that antidepressant medications can act via epigenetic mechanisms to re-establish normal BDNF expression levels following chronic stress.
This last point helps to demonstrate why understanding these relationships between our environment, genetics and mental health is so key: these processes can be modifiable and may offer promising targets for therapeutic approaches. However, it is important to emphasise that it is not as simple as identifying and targeting any single gene, epigenetic mechanism, or environmental factor; the interactions between our biology, psychology and the world around us are incredibly complex. Nonetheless, investigating epigenetic mechanisms is one way to get a deeper understanding of how it all ties together to make us who we are.


