On Identical Twins, Genetics, and Free Will


Monozygotic or identical twins are commonly known for being perfectly identical at the genetic level, and any differences between them are usually attributed to the environment. But advances in genetics over the last two decades have challenged this idea. What does that mean and why does it matter? Join us in this post to find out.

Monozygotic twins are not only virtually identical in terms of physical aspect, but for a long time, they were believed to be perfectly identical at the genetic level. An implication of this belief was that any differences appearing between the twins would be caused exclusively by differences in their environment and their life experiences.

As such, studies looking to estimate how much of a trait or a disorder is genetically vs. environmentally determined found ideal candidates in twins. Otherwise known as classical twin studies, they followed a relatively simple structure:

  1. take pairs of monozygotic, i.e. identical twins, and pairs of dizygotic, i.e. fraternal twins;
  2. check whether the trait/disorder of interest is more similar in identical twins compared to fraternal ones;
  3. if so, conclude that the trait/disorder of interest has a significant genetic component.

In practice, the results were summarized through a statistical measure called heritability: the fraction of phenotype variability which can be attributed to genetic variability. This was applied to a wide range of disorders, including cancer, asthma, and of course, psychiatric disorders. In particular for the latter, heritability estimates formed the basis of a lot of research aimed at identifying the causes of various psychiatric disorders. But again, an accurate estimate of heritability in this case is based on the assumption that monozygotic twins share 100% of their genes, while dizygotic twins only share 50%.

And the fascination with monozygotic twins extended well beyond this. Philosophers turned towards them hoping to find an answer to one of philosophy’s greatest debates: free will. Interestingly, arguments based on twin studies have been made in any direction you can imagine. The starting point was the questionable premise that monozygotic twins are genetically identical. The details were added by cherry-picking the data that best fit the desired hypothesis. Those looking to claim that free will exists have looked at monozygotic twins raised together, who still ended up making significantly different decisions. On the other hand, those looking to claim that free will does not exist have looked at twins adopted by different families, who still ended up in very similar life situations.

And now, as you would expect, we come to the part where I tell you that this premise is flawed. Although monozygotic twins share a lot of genetic material, it’s not 100%. What’s more, even if a big part of the genetic material is the same, genes do not map 1:1 on behaviour or phenotype. It’s not enough to have a certain gene present, this also needs to be expressed. In fact, your genes merely set the constraints within which you can develop, but there are still many paths to choose from within those constraints. This is something that advances in genetics have already made known for decades, but the origin and extent of those differences are still an incredibly active topic of research.

In what follows, we will take a look at some of these sources of variation, but please keep in mind that the same mechanisms which lead to individuality in monozygotic twins also lead to individuality for every single one of us. Afterwards, we will outline what the implications are both for psychiatry, as well as on the topic of free will.

Before birth

Usually, when a sperm fertilizes an egg, a cell called zygote is formed. This zygote divides into two identical cells, which will each divide into another two and so on. At some point, the dividing cells begin to specialize or differentiate, and in the end a baby is born.

But in the case of monozygotic twins, at some point in the zygotic stage, the cells that should stick and grow together into a single baby separate and end up giving rise to two babies. Scientists are still trying to understand why exactly that happens, but most recent evidence points to changes affecting the proteins that should hold the cells together before they attach to the uterine wall.

Genetic effects

Chromosomal aberrations

Regardless of why that happens, this split gives us the first and easiest clue with respect to differences in monozygotic twins. If you remember from your biology class, when a cell undergoes division, it first doubles its number of chromosomes, then each new cell gets a copy of each chromosome. But, although rare, problems can appear in the distribution of chromosomes or mutations can spontaneously occur. The earlier the chromosomal aberration appears, the more severe it usually is, because all subsequent descendants of the affected cell/s will also be affected. If the chromosomal aberration affects the sex chromosomes, it can even result in monozygotic twins with different sexes. The figures below illustrate a couple of examples of chromosomal aberrations.

When the chromosomal aberration occurs before the twinning effect, both monozygotic twins will be affected.
When the chromosomal aberration occurs early in the development of one monozygotic twin, only that twin will be affected.
When the mutation occurs later in the development of one monozygotic twin, only that twin will be affected, but the later the problem occurs, the less severe will the effect be. In all three cases, the monozygotic twins will not be identical.

Mitochondrial DNA

In addition to the chromosomal DNA contained in the cell nucleus, each of us also has a small amount of DNA in mitochondria. And while it really isn’t much, this DNA contains a number of genes important for proper cell function. Unfortunately, unlike the nuclear DNA, mitochondrial DNA lacks a lot of the mechanisms protecting it against mutations. In fact, it is estimated that mitochondrial DNA is 10-20 times more likely to become mutated than chromosomal DNA. And in monozygotic twins, this means that they are likely to accumulate different mutations over time, which contribute to further differences between them.


If so far things were relatively straightforward, this is where they start becoming…a bit weird. Broadly speaking, transposons are defined as pieces of DNA which can “cut” themselves from their original place in the genome and “paste” themselves somewhere else – they become transposed, hence the name. Retrotransposons are even cooler: instead of leaving their original place, they copy themselves into RNA. This RNA is then reverse-transcribed into DNA and inserted somewhere else in the genome. Basically, retrotransposons add new genetic material into the genome, and in theory, they can copy themselves indefinitely.

As you can imagine, this sort of instability isn’t all that great for the genome: new DNA elements randomly inserted all throughout the genome can alter or completely shut off normal genes. So to protect against that, retrotransposons are usually silenced through some fancy mechanisms. But in recent years, scientists have discovered that retrotransposons are actually much more active than it was initially believed.

And from a brain-centric perspective, the most interesting part about retrotransposons is that they are highly active in the brain, in particular in the hippocampus (a main area for memory consolidation and one of the two places in the adult human brain where new neurons are still formed). Unfortunately, it’s currently unclear why hippocampal neurons have so many retrotransposition events, but one hypothesis is that it has something to do with learning and memory consolidation.

More generally, given that retrotransposition happens randomly, the cells of one individual end up with different genomes. Similarly, even if they were to start out with perfectly identical genes, retrotransposition is one of the mechanisms which causes monozygotic twins to end up drifting over time.

Epigenetic effects

There are, however, more common mechanisms which cause differences in virtually all monozygotic twins. And they have to do with something that’s already a buzzword: epigenetics.

To put this in simple terms, imagine your genetic code like a huge library. There are millions of books in there, but that doesn’t mean that you will read all of them. Many factors can influence what you pick, such as whether you can reach them on the shelves, or whether they have cool covers. In your genetic code, epigenetic changes are the factors influencing whether these genes will be read or not. And just as you don’t read the same books over and over again, but instead you put some back on the shelf and choose other ones, your body doesn’t always read the same genes. Some of them become inactivated over time, while others can be activated instead. And a gene which is not read basically doesn’t matter.

In general, inactivating a gene means binding the DNA to certain proteins such that it cannot be read anymore. But there are several mechanisms which influence the activation and inactivation of various genes throughout the lifetime, and below we will detail some of them.

Skewed X-inactivation

This first mechanism only affects monozygotic female twins. We all know that females have two copies of the X chromosome, while males have one. Additionally, the X chromosome is much larger and contains many more important genes compared to the Y chromosome. Because gene expression is additive (two expressed copies will have a stronger effect than a single one), and because the organism needs balance, one X chromosome is inactivated during development. This happens early in development, close to the uterine implantation moment, and it’s a random process for every cell. The descendant cells then inherit this specific methylated chromosome.

As the inactivation is random, like a coin flip, we would expect a ratio of approximately 50:50 in terms of mother/father-inherited X inactivation. In other words, in half the cells the inactivated X chromosome should be the one inherited from the mother, and in the other half, from the father. But that is not always the case. In fact, this ratio can be skewed up to 90:10. A simple reason is that the number of cells at the moment of inactivation is quite small. (If you flip a coin 16 times, it’s quite unlikely that you will get a relatively even split between heads or tails.)

Regardless of the reason behind it, skewed X-inactivation leads to small, but quantifiable differences in monozygotic female twins. If you want to see it in action, just look at calico cats. Because the gene controlling fur color is located on the X chromosome, female calico cats are the only ones who can develop the characteristic patterned look.

Genomic imprinting

Similar to the inactivation of the X chromosome, genomic imprinting refers to the inactivation of a copy of a gene. But in the case of genomic imprinting, this inactivation happens before the zygote is formed. In fact, it happens already during gametogenesis, the process through which sperm and eggs are formed. A small number of genes are preferentially inactivated depending on whether they originated from the mother or the father.

As this happens way before the twinning event, monozygotic twins should, in theory, inherit the same pattern of inactivation for such genes. But scientists have uncovered differences here too. For example, identical twins in which only one suffers from a rare disease such as the Beckwith–Wiedemann syndrome (a disorder which increases the risk of childhood cancer) show differences in imprinting. However, a lot more work is necessary to determine why monozygotic twins show imprinting differences and whether imprinted genes and differences thereof are related to more common disorders too, in particular to psychiatric ones.

Environment and randomness

Finally, the most common epigenetic changes occur during the lifetime of an organism. Some of them involve switching genes on and off in response to environmental influences. In this case, we can imagine that monozygotic twins undergo very similar epigenetic changes as long as they share a similar environment, but their expressed genes start diverging if exposed to drastically different conditions.

But other changes are simply random. There is no sense or reason when it comes to it (at least none that we could identify yet): some genes spontaneousy switch on or off. Scientists have named these random epigenetic changes “epigenetic drift”. And this seems to be the main driver for the divergence of identical twins’ genomes throughout the lifespan.

Implications for psychiatry

Ok, so we’ve learned that monozygotic twins don’t have identical genomes. This could be due to chromosomal aberrations (rare), mutations in mitochondrial DNA (more common), and retrotransposons (very common). More than that, all of these factors imply that not even all of the cells of one individual have the same genome.

At the same time, even the identical genes of monozygotic twins can be expressed differently due to mechanisms such as skewed X-inactivation, genomic imprinting, and more commonly, random or environmentally-influenced epigenetics. And of course, these differences are accumulated not just between individuals, but also between the cells of a single organism. So where does that leave us when it comes to psychiatric disorders?

To put it simply, it makes things more complicated. The picture that is beginning to emerge is that of phenotype as the product of a dynamic interaction between genetic, epigenetic, and environmental mechanisms. In this context, it seems more likely that scientists can only identify risk factors for psychiatric disorders up to a certain extent. Of course, that can still be incredibly useful for guiding preventative, therapeutic, and research approaches. But an added layer of complexity could naturally slow things down in what is already a field in need of a boost.

At the same time, just because monozygotic twins are not perfectly identical does not mean that such studies are now useless. New advances in genetics can help uncover previously hidden differences and contribute to a clearer picture regarding genetic influences in psychiatric disorders. And expanding knowledge of epigenetic mechanisms could help us gain a more general understanding of susceptibility to psychiatric disorders. The entire nature versus nurture debate is slowly being recast as a nature and nurture collaboration, with epigenetics and randomness acting as the mediators.

Implications for free will

Finally, we come to the murkier topic for which the presumed genetic identity between monozygotic twins has been used for speculation: free will. As we’ve already seen in the introduction, the arguments went like this: if monozygotic twins are genetically identical and grow up in virtually the same environment, then it means that when they make different decisions, it’s because they have the free will to do so, no? And if they are genetically identical and grow in completely different environments, then it means that when they make similar decisions, it’s because free will doesn’t exist and their genetic code maps out their entire life trajectory, right?…

By now we know that the entire premise here is flawed: they are not genetically identical. And due to environmental effects and pure chance, they also become more dissimilar as time goes on. From my perspective, this means that we simply cannot derive any meaningful information with respect to the existence of free will by simply comparing life trajectories of monozygotic twins.

Still, some of the concepts outlined above give rise to an interesting question: between fixed genetics, randomness, environmental influences on genes through epigenetic mechanisms, and even environmental influences on one’s thought patterns and behaviour, is there any room left for free will? So far, of course, there is no clear answer to that. And beyond the “empirical” truth, it depends on how you define your terms, what your socio-educational background is, and maybe even how convincing the latest read philosophy paper on free will was.

Personally, I don’t think that we currently have the methods necessary to answer this question. It’s unclear if we ever will. But for the time being, I choose to enjoy my potentially illusory free will by ending this post here and pondering the mysteries of life over a nice cup of coffee instead. As for you, you’re free to do as you will.

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Further reading

Calude, C., Kroon, F., & Poznanovic, N. (2016). Free will is compatible with randomness. Philosophical Inquiries4(2), 37-52.

Castellani, C. A., Laufer, B. I., Melka, M. G., Diehl, E. J., O’Reilly, R. L., & Singh, S. M. (2015). DNA methylation differences in monozygotic twin pairs discordant for schizophrenia identifies psychosis related genes and networks. BMC Medical Genomics8(1), 1-12.

Charney, E. (2012). Behavior genetics and postgenomics. Behavioral and brain sciences35(5), 331-358.

Gericke, N., Carver, R., Castéra, J., Evangelista, N. A. M., Marre, C. C., & El-Hani, C. N. (2017). Exploring relationships among belief in genetic determinism, genetics knowledge, and social factors. Science & Education26(10), 1223-1259.

Gribnau, J., & Barakat, T. S. (2017). X-chromosome inactivation and its implications for human disease. bioRxiv, 076950.

Haque, F. N., Gottesman, I. I., & Wong, A. H. (2009). Not really identical: epigenetic differences in monozygotic twins and implications for twin studies in psychiatry. In American Journal of Medical Genetics Part C: Seminars in Medical Genetics (Vol. 151, No. 2, pp. 136-141).

Joober, R., & Karama, S. (2021). Randomness and nondeterminism: from genes to free will with implications for psychiatry. Journal of Psychiatry & Neuroscience: JPN46(4), E500.

Oh, E. S., & Petronis, A. (2021). Origins of human disease: the chrono-epigenetic perspective. Nature Reviews Genetics22(8), 533-546.

Roseman, C. C., & Kaplan, J. M. (2022). Reliability is No Vice: Environmental Variance and Human Agency. Biological Theory, 1-17.

Thomsen, S. F. (2015). The contribution of twin studies to the understanding of the aetiology of asthma and atopic diseases. European Clinical Respiratory Journal2(1), 27803.

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