Notes on Kathryn Paige Harden's book The Genetic Lottery: Why DNA Matters for Social Equality. Posted by Jacob Williams on 2022-04-26. Send feedback to

1. Key points

2. Definitions

Your polygenic index is calculated by taking the number of alleles you have which are associated with the trait, weighted by how strongly the SNP is correlated with the trait.

3. Two types of gene study

Candidate gene study: an older type of study in which scientists check to see if a particular gene is present in test subjects who have particular traits. Harden indicates that in the past, these often reached completely incorrect conclusions due to inadequate sample sizes and failure to recognize how many different genes are involved in a given trait:

Depression, body size, graduating from college, impulsivity, even height—these are all complex traits ... They aren't caused by a single gene. They are influenced by thousands upon thousands of genetic variants, each of which has a minuscule effect. And because the effects are so minuscule, you need to study many, many, many more people than were included in any of the early candidate gene studies.

Genome-wide association study (GWAS): looks at a large number of people and a large number of SNPs to find correlations. These provide the data that are used to calculate a person's polygenic index. Harden presents these in a positive light, but wants to make sure you understand the caveats, including:

...the correlations that a GWAS detects are very, very, very, very small. ... Each SNP associated with educational attainment is worth, at most, only a few extra weeks of schooling, and most SNPs are worth much less.

4. Causation

A claim that genes "cause" anything might seem problematic if we're not clear on exactly what it means - it's not like there's a gene that forces you to graduate from Harvard, say. Harden spends chapter 5 explaining exactly what she means.

As a social scientist, when I say that genes cause behavior, I’m making a probabilistic statement about a counterfactual—if your genes had been different, then there is a non-zero probability that your life would have been different. I am not claiming that any particular DNA sequence is a necessary or sufficient cause of one’s life outcomes, that DNA determines anything about your life, that this counterfactual is perfectly portable across time and place, that I can retroactively infer that the capital-C Cause of your life is your genes, or that I even know how any stretch of DNA works.

The important thing is that, for a given set of circumstances, your genes affect your odds of achieving a particular outcome in those circumstances. So if we care about outcomes, we shouldn't ignore genetics.

5. Genetic roots of educational attainment

For education, there remains some uncertainty whether genes cause 40 percent of the variation in people’s outcomes, or something closer to 17 percent. But by comparison, recall that family income accounts for just 11 percent of the variation in educational attainment among White-identifying people in the United States.

Harden says that general executive function "is nearly 100% heritable", and that so-called non-cognitive skills like grit (which are also associated with educational achievement) are "moderately heritable" too. But:

The SNPs correlated with non-cognitive skills were correlated with higher risk for several mental disorders, including schizophrenia, bipolar disorder, anorexia nervosa, and obsessive-compulsive disorder. This result warns us against viewing the genetic variants that are associated with going further in current systems of formal education as being inherently "good" things.

6. Race

Suppose a GWAS somehow proved that certain alleles are associated with higher intelligence. If we also knew that those alleles were more prevalent in some racial groups than others, that would mean we know that those racial groups are (on average) genetically predisposed to be more intelligent, right?

Wrong, because:

Why isn't the research portable?

The non-portability of the research has been checked empirically:

When researchers have used an educational attainment GWAS to construct a polygenic index in White-identified, European-ancestry samples from the UK or Wisconsin or New Zealand, then the score “worked”—it captured more than 10 percent of the variance in educational attainment in those samples. But when researchers tested the polygenic index in a sample of African Americans, who are all expected to have at least some African ancestry, it was much less strongly associated with educational attainment.

7. Antieugenics

Genetics research has often been misinterpreted and abused to support racist beliefs and policies: bad outcomes are blamed on bad genes, with the implication that there's nothing we can do about those outcomes (or, worse, that the thing to do is to eliminate those genes from the gene pool). Progressives have often reacted against this by viewing any genetics research on things related to intelligence as inherently dangerous and bogus.

Harden is arguing for a third path, in which we use our knowledge of genetics not to rank and judge people and explain away inequality, but to identify people's needs so that we can meet those needs.

...we must dismantle the false distinction between "inequalities that society is responsible for addressing" and "inequalities that are caused by differences in biology."

I particularly like this example, which Harden credits to psychologist Leon Kamin:

His example was phenylketonuria (PKU), a rare disorder caused by a single-gene mutation.... Untreated, PKU causes intellectual disability. But high-income countries now routinely screen newborns for PKU, which is treated with a restricted diet low in phenylalanine.

The treatment of PKU with diet, just like the treatment of myopia with eyeglasses, reminds us ... genetic causes can have environmental solutions.