Do your genes make you, you?

We often talk about "genes for" traits such as depression, and anxiety but what is it for a gene to cause something? Is genetic causation as simple as it is frequently made out to be? In this episode we explore this question asking are your genes who you are? 

Use of AI disclosure: GenAI was used in drafting the script for this podcast episode to get feedback and suggestions on podcast style aimed at improving audience engagement.  

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Hello and welcome to the P-Value, a podcast about science, philosophy, and everything in between. The P-Value is an initiative of the Centre for Philosophy of the Sciences at the Australian National University. It's tempting to think of your genes as a blueprint for building you, like a recipe for a cake or a set of instructions for a Lego kit. But the role of genes in making you you is far more complicated than that. I'm your host, Associate Professor Rachel Brown, and in this episode of the P-Value, we delve into the question, do your genes make you who you are? Before we continue with the episode, please note that we will touch on some sensitive topics here eugenics, racism, sexism, and forced sterilization. Please take care as you listen further. Some of the most disturbing political movements of human history, from slavery to Nazism to contemporary white supremacy, have relied on the idea that our genes determine who we are in an overwhelming and immutable way. This kind of essentialism about genetics was prominent in the early 20th century and underwrites much of the eugenics movement. Eugenicists believe society could be improved by encouraging the reproduction of people considered genetically fit or preventing those labelled undesirable from reproducing. And this wasn't just fringe thinking. In Australia, eugenic ideas were influential well into the 20th century. There are documented cases of medically and government sanctioned forced sterilization of people deemed mentally ill or intellectually disabled. These policies were justified using the language of genetics. One prominent example comes from American political scientist Charles Murray, author of the infamous Bell Curve and Human Diversity. He argued that progressive social policies encourage poorer women, who he claims are disproportionately at the lower end of the intelligence distribution, to have more children, while discouraging wealthier women with supposedly higher IQs from doing the same. A curse research of the literature on IQ and genetics reveals others expressing similar sentiments. And so it's perhaps not surprising that this work has become popular amongst white supremacists today. Now you might think the obvious response to arguments like this is simply moral outrage. And certainly there are powerful moral reasons to reject them. But many scientists and philosophers have argued that there's also a scientific mistake at the heart of these sorts of movements. They rely on a picture of genes as simple, powerful determinants of who we are, almost like instructions that directly produce our traits. And that picture turns out to be misleading. One of the main criticisms of these arguments is that they rely on a very simplistic picture of genetic causation, often verging on what we would call genetic essentialism. And that's what we're going to unpack today. Most commonly when genes are described as being four particular traits, for depression or for autism. I suspect this talk has its origins in the sort of simple Mendelian genetics that are taught in science classes, you know, sort of the inheritance of blue eyes and brown eyes and dominance and recessive genes. It's also partly in the sort of disorders and diseases which we've been able to genetically test for for a long time, such as cystic fibrosis. These types of diseases tend to have relatively simple inheritance patterns. But what our best science tells us is that while it's true that your genes play an important role in producing you, the causal role they play is typically far from simple. Amongst other things, our genes carry the code for making proteins, one of the essential molecular building blocks of our bodies. But there are only one causal contributor to who we are. Our environment, our culture, the food we eat, the planet we live in, etc., all contributes to who we are. A person's height, for example, is due to both their genes and their diet. Since the Industrial Revolution, there's been a general trend for people to be taller, but this is not thought to be due to genetic changes in populations, but because of the mass availability of better nutrition. Similarly, the obesity epidemic is not due to a shift in our genes, but due to a shift in our diets, towards processed food and a more sedentary lifestyle. Perhaps less obviously, the expression of all sorts of traits, from language to our capacity to think about the mental states of others, is dependent on culturally inherited inputs from your environment. Let's take language for an example. It is given a boost in some cultures by the use of mother-ese or baby talk by caregivers. The language we learn more broadly is a product of our cultural context. In this sense, while our genes do contribute to who we are, they are by no means the only contributor. Because of this, we can't simply read off someone's genome the traits that they will be likely to have, like we might read off a set of instructions. While the instruction analogy doesn't completely work, we might still ask, though, whether we can define the relative causal contribution of genes versus the environment and other factors in who we are. So rather than asking, do your genes make you, we might ask how much of who we are is caused by our genes. Answering the question of how much of who we are is caused by our genes is far from simple. In part, this is because our genes shape our environment and our environments shape our gene expression. Consider, for example, babies and how they're innately drawn to faces. When they look at their caregivers, their caregivers give them positive feedback for that gaze, and this sets up a feedback loop, which reinforces the parental bond. Now one might say that the parental bond then is kind of innate. It goes back to this innate attraction to faces. But in many ways, a genetic disposition to kick it is a genetic disposition to kick off a complicated set of feedback loops involving lots of causal factors. And it's this kind of feedback loops that make determining what is the product of nature and what is the product of nurture extremely difficult. Because our environment and our genes are both causally responsible for who we are, and they're not independent causes, it's hard, some say impossible, to think about their relative contribution. A simple case is illustrative here. PKU or phenylketinuria is a disease many of you will have heard of either through a biology class, it's a classic example of a genetically inherited disease, or perhaps because of the ubiquity of newborn screening for it in Australia at least. Children with PKU can't break down the amino acid phenylalanine, a common protein building block found in foods such as meats, eggs, nuts, and milk. Without treatment, the high levels of phenylalanine in their bodies is toxic, leading to seizures, brain damage, and other serious health problems. Now PKU is caused by mutations to the PAH gene. The PAH gene is one of the key of key is a gene of key importance in the production of the enzyme that would normally break down phenylalanine. It is, you might therefore think, a straightforward case of pure genetic causation. Indeed, it's commonly described as having a heritability of one, or close to it, meaning that variation within the population is due to variation in the PAH gene alone. But once we scratch the surface, we see that even this simple case becomes complicated. The treatment for PKU is dietary. Those identified during newborn screening as having PKU are placed on a low phenylalanine diet and they don't end up exhibiting the adverse impacts of high phenylalanine on their bodies. In some sense, then, says philosopher of biology Evelyn Fox Keller, whilst in a population of untreated individuals we might say the heritability of the pathological PKU phenotype is high, in a population of individuals on a low phenylalanine diet, the pathological phenotype vanishes. And then it seems odd to say that heritability of PKU is high. Variation in the PAH gene no longer closely tracks phenotypic variation at all. Pulling out the genes alone in any given case appears to be misleading. The idea that we can do it is an illusion brought about by holding the environment fixed as a background condition when it never really is such a thing. This is often called the interactionist consensus. Genes interact with other genes. Genes interact with environments. Environments influence gene expression. Genes influence the environments we create and select. And pulling this not apart is nigh impossible. Now this is all well and good, you might say, but what about genetic testing? How can that work so well if these kinds of critiques are right? Stay tuned to the p-value to find out. Philosopher of biology Ken Waters offers a useful distinction. He suggests we distinguish between causes of a phenomenon and the cause that made the difference or the difference maker. Imagine someone says, Mary striking the match caused the match to light. Well, oxygen is required for the match to light, but we rarely mention oxygen as the cause, because it's a stable background condition is something we expect to be hold true for all instances of match lighting. Mary striking the match is a difference maker. Without Mary, the match wouldn't be lit. Now Waters suggests that when scientists talk about the gene for something, they often mean that variation in that gene is the difference maker within a particular population and environment, within a particular set of background conditions. So, in a population eating a normal diet, mutations in the PAH gene are a difference maker for PKU. But in a population following the strict PKU diet, the mutation stops being a difference maker. Diet becomes the difference maker instead. In this sense, says Waters, genetic explanations are going to always be context dependent. They depend on the background conditions in which the gene is present or absent. Most human traits are far more complicated than PKU though. Traits like intelligence, personality, and educational attainment are polygenic. They're influenced by thousands of genetic variants, each contributing tiny effects, which are interactive and also a contingent on the environment. To study these traits, researchers rely on statistical tools such as heritability estimates and genome-wide association studies, or GWAS. But these measures are often misunderstood. Heritability estimate, for example, of 0.7 doesn't mean a trait is 70% genetic. It means that 70% of the variation in that trait within a particular population environment is statistically associated with genetic variation. Change the environment and heritability can change too. Change the population, again, heritability can change too. And this is because it changes the background reference within which the genes are acting. GWAS studies, in contrast, identify thousands of variants associated with complex traits, each with very, very small effects. Many see this as opening the door to personalized education or medicine, but others worry it risks reintroducing genetic essentialism through the back door. And more importantly, many of the most powerful interventions we already know about education, nutrition, healthcare, and social support, are environmental. So where does this leave us? Why are we the way that we are? The honest answer is it's complicated. In a few cases like PKU, we can identify clear genetic difference makers under specific environment conditions. For most traits, what we find are statistical associations between genetic variation and trait variation within particular populations. What this means is that genes matter, but also so do environments. And these different causal factors interact in dynamic, context-dependent ways. The danger lies in oversimplifying that story, especially in treating genes as destiny. The promise lies in understanding causal relationships more carefully, without slipping into genetic essentialism. So perhaps the most responsible answer to the question to do your genes make you who you are is this. Your genes are just part of the causal story of you. Sometimes they're the difference makers. Often they're just one contributor amongst many, and they're never your essence. And how we talk about them matters, scientifically, politically, and morally, because the stories we tell about genes shelp shape how we understand our ourselves and how we treat each other. You've been listening to the P Value. I'm your host, Dr. Rachel Brown. See you next time.