A controversial new book suggests that our success or failure in life is hard-coded in our genes at conception. By Danyl McLauchlan.
It's deeply unfair. Shortly after we're conceived, our genetic material long sequences of chemical codes arranged in a double-helical structure called DNA, tightly bundled into dense thread-like structures called chromosomes is uncoiled and scanned by complex factories of molecular machinery.
These factories use our genes as blueprints for turning a tiny, fertilised egg into a fully grown human, assembling proteins into cells, cells into organs, organs into anatomical systems digestive, muscular, cardiovascular, nervous that allow us to eat, walk, breathe and think. But we have no control over which genes we get, or the type of person they turn us into.
Each of us is genetically unique. We inherit our DNA from our parents, but in each sperm or egg the genetic sequences are recombined, shuffled around, mixed up. Which is why each of us resembles the other members of our family, but none of us is identical to them (even identical twins have minor genetic differences). If two people were able to produce kids carrying every possible combination of their genotypes, they'd have 70 trillion children.
We like to tell ourselves that we're all equal, despite our vast, randomly generated genetic diversity that life is about the choices we make or the world we're born into. These assumptions carry over into our politics. On the right, success or failure is considered meritocratic: people should have equality of opportunity but then take personal responsibility for themselves and work hard to get ahead. Left-wing politics focuses on social or economic injustice: income inequality, exploitation, discrimination. But in the first decades of the 21st century, new findings in the field of behavioural genetics call the premises behind both political projects into question.
Kathryn Paige Harden is a psychologist and behavioural geneticist at the University of Texas. In 2021, she became one of the most controversial scientists in the world when she published her first book, The Genetic Lottery. In it, Harden argues that genes matter. A lot. Social scientists have long known that family income is a strong predictor of educational attainment: if you grow up in a wealthy household, you're more likely to get a degree and a well-paid job. But what Harden is saying is that genetics are just as decisive that an important part of our success or failure is hard-coded at birth.
The sum total of all your DNA across all of your chromosomes is known as your genome. The first human genome was sequenced back in 2003, a 13-year project that cost more than a billion dollars. Today, a whole genome sequence costs about $1000 and takes 24 hours to produce. However, most labs doing behavioural research use a cheaper technique that looks for a known collection of genetic markers. This costs about $100.
There's a gene on your fourth-largest chromosome, called the huntingtin gene. It tells your cells how to create a protein that plays a role in building subcellular structures, especially in the brain. If you have a specific mutation in this gene, you're doomed to develop Huntington's chorea, a terrible neurodegenerative condition that strikes in adulthood. (When biology and medical students first learn about the gene, they worry that they might have this mutation, but if you're a member of one of the rare families that are stricken by the disease, you'll already be very aware of it.)
For a long time, genetics researchers thought that all genes worked like the huntingtin gene, in the sense that it coded for a specific protein, and a mutation caused a specific disorder. So they went in search of other monocausal genes; they looked for drug-addiction genes, depression genes, height genes, cancer genes, gay genes, criminal genes, and schizophrenia genes. Rather embarrassingly, they often announced that they'd found them.
But in 2007, the first large-scale genome-wide association study (GWAS) was published, and it revealed that most genes and gene variants were totally unlike the huntingtin model, and that none of these "depression genes" or "criminal genes" had any scientific validity.
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GWAS is a suite of statistical tools: it works by comparing huge numbers of individual genomes the first studies used 10,000 people, now they're into the millions to look for differences in life outcomes. Which individuals have heart disease or cancer? How tall are they? What's their highest educational qualification? What's their household income? Researchers then use high-performance computers and sophisticated algorithms to find genes that correlate with those outcomes.
The results show us that most gene effects are tiny a variation in a single gene usually has a minimal impact, and almost all genetic effects are "polygenic", meaning they're the combination of many genes working together.
Instead of a single gene for height, there are about 700 gene variants involved, influencing everything from growth hormones to bone length. GWAS reveals that most genetic diseases or inherited traits are staggeringly complex. Even something as seemingly simple as hair colour is influenced by more than 100 different genes interacting with each other.
Because GWAS is such a powerful technique, it has been taken up by researchers across the life and social sciences. And they're uncovering the genetic origins of thousands of diseases and conditions.
You can look at the health outcomes, hair colour or height of the people in your study and correlate them to which variants they have. And you can calculate a polygenic score in which you add up all the effects of all the gene variants and estimate the likelihood that an individual will have the trait you're investigating that they'll be short or tall, have red hair or be prone to heart disease.
At the heart of Harden's argument in The Genetic Lottery is the claim that academic success in modern educational systems is innate that it's less to do with determination or grit and more like tallness or hair colour. "There are specific types of cognitive skills that are richly rewarded in modern educational systems: the verbal and visuospatial reasoning abilities that are tested by standardised cognitive tests," says Harden. And gene variations and combinations that correlate to those abilities show up in the GWAS results. "Beyond that, we see genes associated with personality traits, such as delay of gratification and openness to new experience, are also associated with going further in school."
When Harden was 22, her boyfriend at the time was a history PhD student, and for her birthday he gave her a copy of Daniel Kevles' horrifying historical study, In the Name of Eugenics. "Not the most romantic present I've ever gotten," she admits, "but certainly one of the most durably influential." So, she gets why people are so sensitive to this conversation: statistics and genetics share a very sinister past. People are right to be apprehensive.
But first, she counters, the way eugenicists and white supremacists talk about race is scientifically incoherent. Humans are a very promiscuous species; none of us are descended from one single group of people. Recent research estimates that the most recent common ancestor of every person currently alive probably lived in East Asia a few thousand years ago. We have superficial differences facial features such as the colour of our skin, eyes and hair based on where the majority of our recent ancestors are from, but we're all fairly recent relatives. "Ironically," Harden says, "genetic data help us see why modern 'race science' is actually pseudoscience."
Second, it's very hard to make racial comparisons with GWAS. This is partly because the biological markers don't line up properly across different ethnic groups and these mismatches confound the analysis. But it's also because the genomes currently available for GWAS analysis are mostly from white people. "I think it's helpful to step back and think about where the data in large-scale genetic studies of education are coming from," says Harden. "The biggest sources are European-ancestry participants from [genetic testing company] 23andMe and the UK Biobank. This is a very particular segment of the American and British populations people who are likely to be racially identified as white and who went to school in the UK and the US in the latter half of the 20th century. The genetic data does give us some clues about what sorts of traits are rewarded by the educational system for this segment of the population."
Third, Harden asks, if there's a cluster of genes that reward educational attainment, at least among people with recent European ancestry, and those people get good qualifications and access to well-paid high-status jobs how is that fair? None of us choose the genes we're born with. It is, quite literally, a lottery. "There is no measure of so-called 'merit' that is somehow free of genetic influence or untethered from biology," she says.
Instead of accepting the outcome of genetic meritocracy, she challenges us in the book with the assumption that a meritocratic society is moral. Shouldn't we be asking ourselves why our education system and labour markets allocate success and status to such a narrow set of attributes and punish others?
When it comes to genetic discrimination and how to address it, Harden says two things that school systems seem to be selecting against are ADHD symptoms and early fertility. "Making schools more inclusive and supportive of children who feel the need to move their body constantly, and of teenagers and young adults who have care responsibilities, would change the pattern of what genes are associated with getting more education."
In 1973, psychologists at the University of Otago began studying the lives of 1037 babies born between April 1, 1972 and March 31, 1973 at Dunedin's Queen Mary Maternity Hospital. In what is known as the Dunedin Study, researchers survey the participants at regular intervals, conducting interviews, physical tests, blood tests and even dental examinations. The Dunedin Study has been running for nearly 50 years and is one of the most respected longitudinal studies in the world.
In 2016, the journal Psychological Science published a paper in which the genomes of 918 non-Mori Dunedin Study participants were subjected to GWAS analysis for educational attainment. And they reported a number of key findings: educational attainment polygenic scores also predicted adult economic outcomes, such as how wealthy the subjects became; genes and environments were correlated in that children with higher polygenic scores were born into better-off homes; children with higher polygenic scores were more upwardly mobile than children with lower scores; polygenic scores predicted behaviour across the life course, from early acquisition of speech and reading skills through to geographic mobility and mate choice and on to financial planning for retirement; polygenic-score associations were mediated by psychological characteristics, including intelligence, self-control and interpersonal skill.
What they found was that children with gene-variant combinations that correlated with educational attainment were more likely to say their first words at younger ages, learn to read at younger ages and have higher aspirations as high school students. All of which sounds like a massive validation of Harden's thesis. But Professor Richie Poulton, a co-author of the paper and director of the Dunedin Study since 2000, cautions strongly against linking these findings to Harden's conclusions.
"A key point, often missed," he says, "is the genetic effects were small. A lot of hot air has been expended without acknowledging this very critical and basic fact. [Genes] are not huge influences by themselves: it's nature-nurture interplay that accounts for the most important outcomes. That's where the real gold (versus fool's gold) lies in understanding how people's lives turn out."
The same point is made by the University of Auckland's Sir Peter Gluckman, an internationally recognised expert in child development. For him, the problem with Harden's approach is that "there's no discussion of developmental plasticity. There's no doubt that genes influence behaviour. We know that genetic associations with educational achievement are very real.
"But we also know a lot of those mechanisms are very indirect. And we know that environmental influences, starting from before birth and acting right through childhood have the biggest outcomes. Take the famous experiment on the cat."
Gluckman is referring to the Harvard "pirate kitten experiment", an influential experiment in the 1960s that biology lecturers still like to shock their undergraduate students with. It involved suturing a kitten's eye closed for the first three months of its life. When the sutures were removed, the kitten was blind in that eye because the animal's brain didn't develop the ability to process data from it. "Yes, we have genes that determine eye growth," says Gluckman, "but if we don't use the eye properly in the first few months after birth, then those genes don't work properly. And at the end of the day, what we can affect is the environment."
Poulton agrees that it's far too early to talk about policy solutions based on behavioural genetics. "The understanding of how you would do this and what you would focus on is far too primitive. But you can focus on some of the 'environmental' factors that mediate the genetic effects Self-regulation abilities play a role here, and trying to strengthen those skills among all young people would have benefits."
Harden acknowledges that environmental factors are hugely important. And she believes that the effect sizes for educational attainment polygenic scores will only increase as the datasets grow and the genomic information becomes more fine-grained. But she doesn't believe you can talk about proper educational intervention without discussing genetics. She points out that most current educational interventions have almost no effect on student outcomes, no matter how well funded they are. "Not talking about genetics means sticking with the status quo," she says.
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