Author: Callie Burt

Still Searching for a Justification: More Thoughts on Harden’s The Genetic Lottery

/ Callie Burt / 1 Comment

In addition to the usual disclaimers (i.e., this is an unpolished blog, written perhaps a bit more stream of consciousness and repetitive than some (all?) readers would like because this is a free time activity to which I am not devoting time to edit because I have football to watch), I will add one more. This turned out longer than usual. Brevity has never been my strong suit. Warning: unpolished and meandering.

At this point, I would guess that Harden’s book The Genetic Lottery, a rapid review of which was the focus of my last blog post, has been a success in terms of sales and stimulating thought and attention. I’m not a fan at all, and I’m still thinking about it. Yet, in terms of its actual contribution–in its logic and argumentation–I remain utterly perplexed by the plaudits the book has received. I have been thinking (and now writing) more about the issue I raised in my previous review about Harden’s claim that incorporating genetics has much to offer social science and policy, so much so that it is not just helpful but necessary to include genetics in social science models. I noted toward the end of my rapid review: “Given that Harden agrees that genetic engineering is unwise, what, exactly, does she think this [the incorporation of genetics into policy] offers us? She doesn’t tell us in this book.”

The (lack of) answer to this question has continued to nag me, and so too for the value for (social) science understanding. Thus, I re-read—well, more like skimmed–the book and reviewed some other relevant works to try to smack myself in the face with their arguments for ‘why this is valuable’, so valuable, to remind the reader, that Harden avers that ignoring genetics in social science research and models is the moral equivalent of bank robbery [again, I think that she meant to use a burglary as an example, but still].

Here, I wanted to quickly outline what I understand to be their arguments for the value-added, even necessity, of incorporating genetics into research on human social behaviors/social science. In so doing, I aim to clarify what I see as the problems with her/their logic. First, I discuss social science and then policy.

Why incorporating genetics into social science models is valuable, even necessary: Harden and colleagues’ justification; (reader please note this my summarizing what I understand to be their arguments):

(1) All complex social behaviors are heritable. As Harden (2021) notes, twin studies have demonstrated for decades that for all complex social behaviors of interest to social scientists, heritability is substantial (an average of 50% heritability).

(2) Heritability estimates indicate causal effects of genetic differences on individual differences in traits. [Again, this is a contested viewpoint, but this is her view.]

(3) Ergo, individual differences in all complex social traits are partially caused by genetic differences, and, as Harden (2021) notes, we have known this for years. [At least twin studies showing non-trivial heritability of complex social traits have existed for years.]

(4) When examining the influence on social forces on complex social outcomes and behaviors (e.g., educational attainment, crime), leaving out genetic differences is a problem of omitted variable bias. That is, if we do not incorporate genetic differences, which may partly cause—only partly because it should be remembered for most outcomes the twin study heritability is <70% and for many reasons this is a high end estimate—putative environmental causes, these uncontrolled genetic influences can and will masquerade as causal environmental effects.

(5) Consequently, the estimate of the environmental effect will be less precise (and potentially inflated in some cases) by not parsing out genetic influences.

(6) Therefore, to get more precise point estimates of environmental influences, we must incorporate genetic influences.

(7) Harden et al. recognize that methods that can provide (roughly) genetically unconfounded estimates exist as instrumental variable methods and fixed effects models where individual differences are held constant to assess change over time in response to changing circumstances, but these require expensive panel data.

For the non-quantitatively oriented science reader, I will note a few things. First, to point #7, federally funded rich panel data already exist, and using such data, numerous fixed effects models have shown that changes in environments produce changes in the things that we care about. Second, and more importantly, precise point estimates are generally not of major interest to social scientists. Nearly all of our measures, including our outcome measures, are noisy, (contain error), even biased. In general, what we want to know is whether more of something (education, parental support) is associated with more (or less) of something else (income, education) that we care about, ideally with some theoretical orientation. Frequently the scale used to measure social influences is somewhat arbitrary anyway, such that the precise point estimate (e.g., weeks of schooling) associated with 1 point increase in the ‘social support scale’ is inherently vague. 

Third, for reasons that are out of scope, genetic measures (as PGS scores) are always noisy and biased as well, due to the measurement of only some of genetic variants we possess, imputation (informed guessing) for some of the unmeasured variants, and the presence of environmental confounding, known as population stratification, which can be understood more simply as the effects of shared culture or social structures in the form of distant relatedness. That is, people who live in geographically proximate areas and thus share more similar physical and social environments also tend to mate with each other creating greater genetic similarity in groups which also share more similar social and physical environments. Controls for population structure are included, but except in the case of sibling different studies, these are inadequate. 

PGSs created from the estimates from sibling studies are the rare exception, such that most PGSs are tainted with population confounding (i.e., pick up sociocultural and physical environmental differences). Therefore, PGSs capture both ‘genetic’ differences that influence the trait through biological mechanisms (usually distantly) and sociocultural differences that are associated with allele (genetic variant) frequency differences across subgroups. For a quick example, due to the greater UV rates at lower latitudes, if we were to do a GWAS of the Eastern US population for skin cancer, we would likely pick up, in addition to any genetic predispositions to skin cancer (e.g., genes involved in cellular repair) genetic variant (allele) frequency differences among those in the US South and those in the Northeast due to the fact that people in the South have tended to mate with each other and are more closely related and so too for the North. Some unknown number of these genetic differences, however, will have nothing to do with the biology of skin cancer and everything to do with being randomly differentially distributed between the South and North, the former which is exposed to higher UV rays and more sun. (These random differences that develop over time are known as genetic drift through assortative mating based on sociocultural and physical environmental proximity.) In short, some of the genetic variants identified will be a function of random genetic differences and associated with the outcome for purely environmental reasons that have nothing (biologically) to do with the outcome.

For all of these reasons, the ‘greater precision in estimates of the environment’, at the current moment, is debatable. Perhaps we’ll see a little greater precision in some environments, but a very meager and not very useful benefit. Thus, leaving out genetics is, in my view, akin to jaywalking (at worst) not bank robbery.

Why incorporating genetics into social science models is important for policy—Harden et al.’s view:

I must first admit I found this even less clearly articulated in Harden’s book, which is why I wrote that ‘she doesn’t tell us why in this book’. I don’t think she does, clearly. However, if one looks at some of her other co-authored work, especially with Koellinger (who she references as a high-quality cook in her book), one can see more clearly their ‘logic’. 

For example, in a paper called, “Genetic Fortune: Winning or Losing Education, Income, and Health”—similar to the ‘lottery’ with a somewhat awkward subheading (what does ‘losing education mean’?) a study/paper designed and overseen by Koellinger and co-authored by Harden and published online in November 2020 (though I have the updated December 2020 version), spells out why they believe this work is important to policy. I disagree with this reasoning, as you can imagine. Notably all of the below are quotes from Kweon, Burik, Linnér, Vlaming, Okbay, Martshenko, Harden, DiPrete, and Koellinger (2020), unless otherwise noted.[1]

(1) “The origins, extent and consequences of income inequalities” differ across contexts,”

(2) “a universal fact is that parents influence the starting-points of their children by providing them with family-specific environments and by passing down a part of their genes [1 of each chromosome from each parent, plus an X from mom and an X/Y from dad, all going well]. This phenomenon creates individual-specific social and genetic endowments that are due to luck in the sense that they are exogenously given rather than the result of one’s own actions [here we can see the luck language].”

(3) “Thus inequalities of opportunity can partly arise from the outcomes of two family specific “lotteries” that take place during conception—a “social lottery” that determines who are parents are [?social status], and a “genetic lottery” that determines which part of their genomes our parents pass on to us.”

(4) “Inequalities in opportunity restrict the extent of intergenerational social mobility and limit how much credit people can claim for achievements such as their education or income.” [Okay, inequalities in opportunity affect a lot of things, curious that these are the two accentuated here.”]

(5) **Key** “The relative importance of social and genetic luck has policy relevance because the extent to which people are willing to tolerate or endorse inequality partially depends on whether they perceive that disparity originates from differences in effort and choice (e.g., working hard) or from differences in circumstances that are outside of one’s control (e.g., luck in the social or genetic lotteries). The empirical results suggest that inequality that can ultimately be traced back to luck may be perceived as unfair and people may favor redistributive polices more strongly *if* inequality is the result of luck rather than agency” (bold and asterisk emphasis added).

Phrased alternatively, their argument here is that the more people perceive that disparate outcomes/inequalities are due more to luck than to personal agency/hard work, they may be more inclined to favor redistributive policies. (The word perception jumps out at me here; I will return to that later.)

(6) “*If* the outcomes of the genetic or social lottery influence economic outcomes, it [confusing pronoun usage] can challenge common intuitions about the relative importance of luck and agency” (asterisk emphasis added).

(7) “It is important for science and policy to understand the extent to which genetic and social fortune[s] contribute to inequality, the mechanisms that are at work, and whether and how the consequences of exogenously given endowments can be altered.”

This argument pulls in some new facets and combines them with the ongoing logic. Understanding “the extent to which genes and social fortune contribute to inequality” is important, they argue, because presumably that shapes people’s perceptions about the importance of such factors and therefore their willingness to support redistributive policies. Here they also add in a focus on mechanisms and changeability, presumably due to their obvious policy relevance-but genetics isn’t needed to examine changeability.

Therefore, the Kweon et al. (2020) paper “makes progress in this regard by using large-scale molecular genetic and family data to test the influence of genetic and family-specific endowments on income inequality and its consequences for health.” Health, you say; where did that come from? I agree; (for those not in the know, the funding for health outcomes in the USA from NIH is high, less so for non-health social outcomes.)

   A few points, of course.

 First, I must make note of the importance of the perceptions bit. Of course, facts and empirical patterns don’t determine action. Whether such facts are known and how they are interpreted/given meaning shapes action. Again, Harden and colleagues note that to the extent that people perceive that inequalities are the result of luck (genetic or social), the more inclined they tend to be to support redistributive policies. This makes sense. 

However, I have a few issues. First, the extent to which people’s perceptions of the sources of inequality are reflected by empirical evidence/facts is not entirely clear. Indeed, I am sure that a twin heritability study would likely reveal that a non-trivial portion of the variance in perceptions of sources of inequality would be found to be heritable. To be clear, from that finding, I do not personally conclude that this means that this same portion of variance across individuals is caused by genetic differences, given the inflationary biases of twin study heritability estimates. My point is, by their own logic, much of this variance in perception in the source of inequality is due to, even caused by, genetic differences. There is, in a sense, an infinite regress or circle in behavior genetic models when everything is ~50% heritable—perceptions, beliefs, attitudes, traits, and behaviors; every non-randomly assigned allegedly ‘environment exposure’ is approximately half caused by genetics, on this view, which makes everything a bit awkward.

Second, and more importantly, we already know both from common sense and a wealth of social research that both one’s family-specific environment (income, wealth, status, race/ethnicity, religion, beliefs) and genetic endowment shape one’s life trajectory, including social outcomes like educational attainment and income. We know this from a wealth of social science and behavioral genetic research and basic observation of reality. Harden tells us this repeatedly in her book and Kweon et al (2020) mention it in their paper.[2] WE KNOW THIS. Thus, there repeating the *if* this matters, then so and so, is a misrepresentation of the literature. We already know these matter. We do not need yet another study to show that these things matter, and it is somewhat disingenuous to highlight that these things matter, you all, so much so that if you exclude them from your models you are the moral equivalent of a bank robber, while turning around and publishing papers questioning whether these things matter. At least, that’s my opinion.

Third, social and genetic endowments are inextricable. We also know this. We are not going to be able to parse them out because human development and behaviors emerge from a biological system that always operates in with responses to social environments. Humans are organisms, which are processes in constant flux in response to internal and external input. Environments up and down regulate genes; initiate cascades of action and reaction; shape our motivations, desires, and behaviors, among other things. Likewise, our genetic differences can shape both the amount and the nature of protein products produced and other gene products in a manner that can and does affect how we look, perceive the world, and react to it. 

All of this is why the results of their study: “We show that the well-known gradient between sociogenomics status and health is partly rooted in exogenously given genetic and social endowments. Furthermore, we demonstrate that a substantial part of genetic luck for income and its link with health appears to operate via educational attainment and its accompaniments, i.e., environmental factors that are in principle malleable through policy interventions” can be met with a “duh”. Of course, this is the case. How this advances policy relevant knowledge one iota I cannot say (because I do not think it does).

Heritability says nothing about malleability, as Harden and Kweon et al. remind us on multiple occasions, and a wealth of social scientific evidence on traits that have been found to be substantially heritable has already shown that highly heritability says nothing about responsivity to social influences. Indeed, that is part of their argument—that genetic causes operate through malleable environmental pathways. But here, they throw “does it matter” as unknown and then answer it as if they are offering something new. That’s double dipping, which is kind of like jaywalking but dirtier.

Broadening our lens, and thinking about the well-known fact (again repeated by Harden in her book several times) that high heritability, interpreted by her to mean and thus include ‘genetic causes’, of differences in social outcomes say nothing about malleability to policy influences, brings to stark relief the question of why then do we care about the extent to which these differences may be partially—as again even the upward bounds of heritability are almost always less than 70%–rooted in genetic differences between people? Given that this is not relevant to changeability, I am left to believe that this is meant to go back to “perceptions”, and with it that is intended as the policy-relevant import of this work, in Harden’s view, and indeed, perhaps the purpose of her book.

Phrased more clearly, this would make the aim of Harden’s book, in my view to try to change people’s perceptions about the causes of inequalities from personal responsibility and hard work to ‘luck’, with an emphasis on genetics. Doing so, in her mind, will perhaps promote the redistributive policies she clearly publicly supports. 

This angle is also how she distances herself from the ‘bad’ (according to Harden: eugenic, racist) arguments of infamous hereditarian scholars before her—the Bell Curve types who, it might be noted, focus less on genetic differences, in general, and more on IQ, which they view as largely genetic and, crucially, mostly fixed, if not at birth, then certainly after childhood. Harden, for her part, recognizes that genetic differences do not imply fixity (although she has used the language of ‘genetic predisposition’, so this is in some ways a difference in degree rather than kind, but a notable one nonetheless). However, that recognition does not, as Harden argues, somehow make a consideration of genetics useful for social science or policy. From the fact that genetic differences do matter for development and individual social behaviors, it does not follow that incorporating (noisy, environmentally confounded) measures of genetic differences will advance social science models or policy since, as we have noted ad nauseam, heritable or genetic does not mean unchangeable. Whether I’m naturally a bad singer or fail to get the proper socialization about singing from my parents is irrelevant to the question of whether or not singing lessons (or parenting lessons for singing support) can make me a better singer. If they can work for me, we do not need to know the extent to which genetic and social endowments shape the extent to which I am a bad singer. That is, if we can teach or support parenting skills to make me a better singer, who cares about the why especially given that we cannot really answer this question anyway given gene-environment inextricability and context-specificity (though replace singer with student, since we don’t care about my singing…well, you might if you had to listen to it. I’m serious.)

In addition to being irrelevant to policy, there remains a potential dark side to even benign, explicitly anti-eugenic work and not only if these results are used by those with whom we disagree (e.g., the billionaire insurance person with whom Harden and colleagues had dinner with at the fancy French restaurant). Indeed, even work with ‘good intentions’ from Harden and colleagues to understand the sources of inequalities can reveal the potential harmful effects of genetically-informed policies.

Specifically, in co-authored work, Harden focuses using PGSs as a molecular tracer in school achievement. Although more detail is out of scope, for reasons abovementioned, including but not limited to their environmental confounding, PGSs do not measure genetic potential for educational attainment—they capture the differences in those who receive educational attainment under current systems. And again, potential for educational attainment does not reside in our genomes, but emerges from a complex biosocial system in which genes are important resources but not the drivers of development. Yet, that is often missed or ignored despite the professed environmental awareness of those conducting this work. 

Additionally, Harden et al recognize that PGSs are not useful for individual prediction but that they are useful for aggregate prediction and can be used, for example, to assess school performances. They suggest that we might, for example, control for the average PGS of schools when comparing their performances, and/or devote extra resources to schools with more students with lower ‘education-related genetic variants’. However, this quite clearly, in my view, begins to solidify this view of these PGSs/measures of ‘education related genetic differences’ as “education potential”, which is problematic. And while the outcome might be positive in some cases, even if misguided, e.g., by directing resources at the lower SES schools, given the environmental confounding, there are other potential negatives, including labeling and lower expectations. 

Equally important, why in the world would we use noisy, problematic measure of ‘genetic potentials’ to direct resources and evaluate schools, rather than more easily measurable and more accurately predictive measures of past achievement, SES, and even standardized test scores? As others have noted, a much better predictor of future school performance is past and current performance (see Morris et al. 2020). We can easily see which students struggle and ascertain which students are getting support and extra help in the home and which students aren’t and respond accordingly with more sensitivity and specificity. No need for genetics whatsoever.

Genetic measures are not only less accurate predictors but also potentially a source of differential treatment. Sure, Harden wants this information to be used to good ends, but why in the world do we think that it will be? Best intentions gone awry is perhaps the most obvious lesson from all of history, and there is no reason to think that many actors agree with us on the proper courses of action. Other potential implications could be lowering expectations and standards for schools/individuals with lower ‘education-related genetics’ (estimates). One could easily see how we could treat such measures as potential, think this is the best we can get from individuals, and set the bar low for them, despite the fact that, to repeat ad nausem, even if educational attainment is strongly genetically influenced, it is strongly socially influenced and–both genetic and social influences are potentially malleable. 

In sum, the policy value of this work for education systems is, in my view, minimal to nonexistent and potentially harmful to students and society. I might also note that almost all of the samples used to create these large-scale education-related (and, income-associated) “genetic propensities” use older samples, who grew up in the pre-internet era. One of the younger samples is the Add Health sample, which includes my age category (I’m 42), when google, youtube, and other concomitants of the growth of non-dial-up internet access were not prevalent (at least not until I was in graduate school). Today’s students grow up in a connected world of easily accessible information online. These technological innovations have transformed the learning environment in non-trivial ways, further altered by the pandemic. Does anyone want to argue that the individual characteristics shaping educational achievement and income are the same today as they were for children born in the 1970s and early 80s, much less the 1940s-1960s? I don’t; (even as I would agree many are the same). Distractibility working on a computer is, in my view, exponentially greater than that in pre-internet times when we worked with pen and papers and with books (hard copies of). 

In sum, for real this time, even if genetic differences have a substantial influence on educational attainment, income, and via those pathways, health outcomes, given that these social influences are malleable regardless of their origin, there is no obvious policy-relevant value added to incorporating genetic differences given our measurement and knowledge limitations. If genetic meant unchangeable, then a case could be made; but it doesn’t. There are potential harms. For all these reasons, I find these arguments to be flimsy at best, with some of the recent framing about uncertainties (*if* this is shaped by social and genetic endowments), which have been well established, as unknowns, almost disingenuous. 

One can believe that genetic differences exist and shape differences in complex human social outcomes without being a eugenicist or racist or sexist, etc. But it does not follow that study of the effect of genetic differences on these social outcomes from an anti-eugenicist or anti-racist perspective is thereby useful and important (or that it can’t then be used to support racist or eugenics ideologies and policies, to be fair, a fact recognized by Harden and others on multiple occasions very clearly. Clearly recognizing a danger and acting to prevent it, are, however, two different things, which is how I once broke both my hands.).

If you made it this far, bless you, ha. Before closing, I want to reiterate what this long-winded verbosity was and wasn’t about. I am *not* arguing that perceptions about the sources of inequality do not matter for how we address (or whether we tolerate) inequality. I agree that perceptions about the sources of inequalities shape individuals’ views about whether and how to address inequalities. I am saying that we have a wealth of research over decades that shows that genetic and social endowments at birth profoundly shape our economic and social outcomes. We do not need more data showing this if the aim is to change perceptions; we do not need genetic data, for example, to show more clearly that environments matter for our life trajectories. Doing more research to compile yet more facts that this matters is not, in my view, necessary or efficient to change perceptions, in other words, if that is the goal.

To summarize too my thoughts on policy-relevance, my argument is not that genetics don’t matter or that genetic data can’t tell us anything. To use again Harden’s example about controlling for average student PGSs for educational attainment in schools to assess school performance while controlling for individual differences, this is both unnecessary and limiting. Net of environmental and shared family environments, the educational attainment PGS explains not quite 3% of the variance in education. And without controlling for such confounding these PGSs explain 12-14% of the variance in educational attainment. Why would we control for a noisy measure that explains less than 15% of the variance, when we could use already available standardized test scores from previous years or past school performance–scores already available–that would explain more than 50% of the variance in student performance. The only reason that I can think we would do that is if we assume that the genetics measure is actually a measure of ‘genetic potential’ or ‘ability’, an assumption which Harden et al. disavow. This doesn’t mean genetic differences don’t matter. It’s like bringing pliers for a wall nailing job; sure you can do it, but why would you when you could bring and use a hammer.

Perhaps I’ll read the book one more time in my “for fun” time to make sure I haven’t missed anything. Feel free to add your thoughts; if I’ve missed something important, I’d particularly like to hear about it.

[1] Citing from Harden’s book required much more words as she sprinkled arguments in larger discussions with examples and personal stories, which is good for a trade book, but makes for more difficult quoting. However, she makes similar claims. For example, Harden (2021, pp.181-182) makes: “First, environmental experiences—whether it be having a sexual relationship at a certain point in one’s adolescence or receiving a certain type of parenting or living in a certain type of neighborhood—can be correlated with life outcomes but not be causes of them. Second, policies that are built on a flawed understanding of which environments are truly causal are wasteful and potentially harmful [why–since malleability is not related to heritability?]…. Third, genetic data—whether it be comparisons of identical twins or comparisons of people with similar polygenic indices— help researchers solve the first problem and, in so doing, avoid the second problem. Genetic data gets one source of human differences out of the way, so that the environment is easier to see.” 

[2] Curiously, in what is likely a common instantiation of our arbitrary citing practices and unclear protocols and expectations, Kweon et al. (2020) cite Rietveld et al. (2013) twice in one paragraph on the bottom of p.5 cite after a statement about what twin studies show. Yet, Rietveld et al. (2013) is a GWAS study–known as EA1 (educational attainment GWAS 1). I’m not sure if they cite Rietveld et al. because Rietveld et al. also noted what twin studies show, but that is confusing, in my view. When someone (perhaps most commonly the author in their prior work) make a similar statement about existing research, this does not not warrant citing the prior research for making that not-so-unique claim. If wanting to point to a similar paper–in this case no idea why the Rietveld et al. was chosen, I think more helpful to say “see summary in xx”. Just me, perhaps.

Genetic Promissory Note with a Moral Twist

/ Callie Burt / Leave a comment

A Rapid Book Review[1] of The Genetic Lottery by Kathryn Paige Harden (Princeton University Press)

We all know that our DNA makes us different and unique. To what extent, how, and whether we can understand how our genetic differences shape differences in social and behavioral outcomes has long been debated. [Post posting read–that is a terrible sentence.] The field known as behavior genetics has used family, twin, and adoption studies, and more recently measured genetic differences, to show that our genetic differences are correlated with social and behavioral outcomes that matter to us. The idea that ‘our genes’ shape our social and behavioral outcomes, including educational attainment, dates back at least 50 years.

In her forthcoming work, K. Paige Harden, a now-renowned behavior geneticist at the University of Texas at Austin, draws on these findings to a make a stronger (more controversial) case. Skirting important methodological issues, Harden argues that these studies identify genetic causes of our life outcomes, such as educational attainment, income, wealth, and ‘externalizing’ behaviors (crime, substance use, risky sex). Further, she claims that social science research and policy must incorporate a consideration of genetic differences into our theories, models, and policies if we are to truly understand inequality and reduce it. By positioning herself as distinct from those who are infamous for promoting genetic determinist claims, especially with direct or indirect implications for genetic racial differences in outcomes like IQ, Harden frames herself as a scientific realist with progressive aims. Yet, as I will quickly argue here, the reasonable, progressive story she presents only works by ignoring or downplaying important scientific details. 

Having just finished reading her book, I feel compelled to write something in response, in part because Harden’s writing is engaging, disarming, and persuasive and likely appeals to the segment of the public who hear of the irrational academics who deny biology (e.g., recognition of the reality of biological sex in gender studies) along with those who wish to position themselves against those Galtonian types and Bell Curve supporters of the world, whose works are fodder for white supremacist groups, according to Harden. (She makes several claims that white supremacists are avid consumers of the scientific products of these scholars; I have no idea if that is true). In large part, Harden’s book continues her (and others’) appeal to use genetics because those other (‘bad’) guys will use it anyway and not to good ends. Yet, Harden’s clear prose and ostensibly lucid arguments obscure substantial scientific complexities and unknowns, and contains some leaps in logic and reasoning. With few minutes I have, here are my thoughts hastily written. 

If you are looking for a detailed overview or a description of the biological and methods of contemporary social science genomics (sociogenomics) work, including GWAS, polygenic score studies, sibling difference studies, and the like, look elsewhere. Introducing readers to the science of sociogenomics is not the aim of this book. Indeed, for readers like myself with extensive familiarity with sociogenomics, including Harden’s prior works, this book’s primary new contribution is its (a) depiction of her conception of causality, and (b) a glimpse into her personal life through stories. For those not reading her recent work in which she pitches many of these same arguments (including a 2021 Annual Review of Psychology piece, for the interested reader with less time), Harden does flesh out the arguments that she presents in recent work elsewhere, captured in the summary of the primary aim of her book:

“I am going to argue that [the data showing the] relationship between measured genes and educational outcomes, is also critically important, both empirically and morally, to understanding social inequality. Like being born to a rich or poor family, being born with a certain set of genetic variants is a lottery of birth…. And, like social class, the outcome of the genetic lottery is a systemic force that matters for who gets more, and who gets less, of nearly everything we care about in society” (14-15). 

Harden argues, incorrectly in my view, that the genetic influences on social outcomes, like educational attainment, are not given due attention in social science and policies in part due to our sordid legacy of eugenics, which she immediately addresses head on and from which she distances herself. As a result of this history, in Harden’s view, mainstream social science is ‘biophobic left’, such that it theorizes ‘genetic sameness’ out of fear of what studying genetics might reveal about ourselves and how this may be put to use (in the service of bolstering the status quo and social hierarchies). I will note, and do so more below, I do not think this is a proper characterization of the position of most who critique behavior genetics.

On the other side, Harden argues that there are others who support genetics research on social outcomes, include a eugenics right, which has and will put this to use in the service of inferiorizing racial/ethnic and other disadvantaged groups. Harden positions herself as occupying the rational (ostensibly non-ideological) middle: In contrast to this ‘eugenics view’, Harden states that “[w]hat I am aiming to do in this book is to re-envision the relationship between genetic science and equality.” She asks, “[c]an we peel apart human behavioral genetics … from the racist, classist, and eugenicist ideologies it has been entwined with for decades? Can we imagine a new synthesis? And can this synthesis broaden our understanding of what equality looks like and how to achieve it?” (p18-9).

To this she answers not just ‘yes we can’, but ‘we must’. Indeed, in a surprisingly aggressive section of the book, which departs someone from her tone elsewhere, she argues that to do social research without considering genetic differences between individuals is the moral equivalent not of jaywalking but bank robbery(!!). Specifically, Harden writes about an asserted (but not demonstrated) “tacit collusion in social science to ignore genetic differences between people.” She states such ‘tacit collusion’ (which I dispute exists, more on that below), “is not wrong in the way that jaywalking is wrong…. It’s wrong in the way that robbing banks is wrong. It’s stealing.” 

Yikes. For the non-criminology readers, robbery isn’t ‘stealing’. Robbery is the use of force or threat of the use of force to take something from others; in bank robbery, this would be money. Perhaps if she mentioned this offhand or in a talk, I may let it go, but in a book this was clearly a thoughtful, albeit absurd and unjustified in my view, moral comparison. How does she get here? And, are her arguments sound? [Foreshadowing: no idea and no.]

The journey is interesting, especially with the relatable personal examples, but the logic and evidence presented is partial and tendentious. Harden battles with straw men, overlooks nuance and contrary or complicating evidence, and deftly avoids several of the longstanding critiques of behavior genetics, which now apply to sociogenomics: these include the population specificity and, therefore, incomparability of heritability studies across groups (defined, for example, by social class), the social construction of the outcomes, and downward causation, as well as a host of methodological issues, including assumptions and limitations, in current GWAS and other sociogenomics studies.

 I do think there is much to discuss on these issues (in fact, I’m writing a book about it myself), but charitable engagement with different views and thorough engagement with existing scientific evidence and theory is not found in this book, in my reading. She’s selling a view, in part by curiously denigrating her opponents while ignoring their critiques. I’ll briefly break down the arguments into their two parts to reveal the shortcomings. 

First, Harden’s portrayal of the genetic-resistant, even biophobic, mainstream social science is misguided, in my view. Few to zero social scientists believe endorse a ‘genetic sameness’ or ‘blank slatist’ view of the world, where individuals are genetically the same, and no scholar I’ve ever met. While her book is thin on citations, for a university press book, these sections are particularly sparse in terms of actual references. Rather than scholars, Harden references speeches and claims made by non-scientist, then president Bill Clinton on the Human Genome Project in support of her arguments for the mainstream social scientist view of ‘genetic sameness’. This straw man depiction allows Harden to dismiss social scientific critiques as being ideological rather than scientific—and no doubt some are ideological. But others are scientific. These are curiously ignored or quickly dismissed without engagement. 

Harden also repeats the longstanding argument that social science genomics continues to be relegated to the margins of academia and ignored by social scientists. Yet, here too, the evidence is missing, and I disagree. Harden has received considerable public and private funding, including prestigious fellowship, like several of her sociogenomics and behavior genetic colleagues. She, like those colleagues, publishes in high prestige general science outlets and social science outlets. Sociogenomics work receives public and media fanfare that I would argue is significantly greater than that of most social scientific work. The claim that the public and academics are tacitly colluding to ignore genetics is surely questionable (and requires supportive evidence) given that Harden herself has graced the pages of the NYT and New Yorker, as well as the Guardian, the Atlantic, and others, with these same arguments—with much fanfare–in addition to publishing these ideas in prestigious social science journals. Given sociogenomicists’ success in funding, publication, awards, and popularity—where exactly is the ‘tacit collusion’ to ignore this work? As Aaron Panofsky has argued, this claim that behavior genetics scholars scholars are outsiders fighting a reality-resistant academia is central to the identity of this field. Yet, at present, I keep coming back to ‘who does she think believes ‘genes don’t matter” because she doesn’t cite these people; (some personal correspondences where no one says ‘genes don’t matter’ are discussed). I think Harden’s creating an oversimplified, inaccurate portrait of critics on the political left is a result of her misunderstanding our critiques (which I turn to next).

Harden takes great pains to distance herself from the ‘eugenics’ or ‘Galtonian’ scholars, such as Robert Plomin, and the late Herrnstein as well as Charles Murray (of the Bell Curve infamy). Although at times I found myself concerned that she was exaggerating their differences, it seems clear that Harden truly believes that studying social science genetics is not just consistent with supporting egalitarianism, but it is necessary to creating a better society. Yet, why this is the case is never clearly articulated, in my reading. Importantly, in making this case for its importance (and the moral imperative that social scientists include genetics), Harden skips over some important methodological details and less supportive studies that would cast some doubt about her claims. 

For example, Harden notes that education polygenic scores explain from 10-14% in educational attainment (without noting this is basically net of only age and sex and 10 or so ancestry PCs). While mentioning that these findings ‘hold up’ when using sibling studies, which control for the potential environmental confounding variables by examining differences between siblings who share such environments, she never acknowledge that the variance explained/effect size drops in these sibling studies from 10-14% to <3%. Nor does she note that the variance explain dives when well-known, easily measurable variables like parental income and educational attainment, are included. Throughout she grapples with ‘genetics of educational attainment’ which, she claims, causally explains more than 10% of differences in educational attainment rather than the more realistic (net of relevant controls) relatively <3%.

This matters for her thesis. Given that ‘genetics’ explains less than 3% of the variance in educational attainment net of environmental confounds, it is (a) unlikely that it will explain away *larger* social environmental influences, such that we are being morally bankrupt (or rather bank robbers) for not included genetic measures in social scientific models, and (b) unlikely to significantly shape public policies in a way that would radically change things. That is not to say it can’t; some social scientific variables that are considered important explain less than 3% of the variance in outcomes. Yet, we have some idea what these variables are and what they do. This is not the case with current sociogenomics studies.

Harden also ignores concerns about what these GWAS results indicate. She barely mentions, more as a quick aside, that GWASs do not measure genes or causal variants, and that efforts at biological annotation (i.e., linking these measured genetic variants with genes, much less causal variants) remains an exercise in educated guesswork. She asserts that, for example, the ‘genes relevant to educational attainment are found in the brain’, while also recognizing elsewhere that because we, for example, treat taller, more attractive people better, they have advantages in educational and labor market outcomes which would, in her view, be appropriately deemed a genetic cause. That we still don’t know what most genes do is fully ignored in this book. The charge that scholars that fail to consider genetic influences are morally equivalent to bank robbers against this backdrop seems silly at best.

Ignoring Downward Causation

Harden devotes a section to causation to bolster her (quite controversial) claim that heritability studies identify genetic causes of individual differences. Curiously, she does not sufficiently engage with the work of her mentor who has written several pieces articulating why heritability studies are not about cause, (personally, I agree with her mentor Turkheimer on this one). Even more surprisingly, she uses the hypothetical from Sandy Jencks explaining how putative genetic causes reflect social causation and thus heritability studies cannot be used to inform us about biological causes. In Jencks’ well-known hypothetical, under an arbitrary social policy that banned red-haired people from getting an education, genetic differences related to (causing) red hair would appear as genetic causes of educational attainment, despite the cause actually being the social policy proscribing education for those individuals. This is really important to understand, as I believe this is a key source of differences in approach between scholars such as Harden and myself, and why behavior geneticists like Harden are speaking at not with behavior genetic critics.

The red hair example seems, on the one hand, preposterous because we obviously would never exclude people based on their hair color….but then you remember we excluded people on the basis of skin color and sex not very long ago. But, today, you say, this wouldn’t happen in western industrialized countries, even if in other parts of the world some biological characteristics (e.g., sex) do restrict people from education. What I and others have argued, and Harden does not fully account for, is the fact that our genes, and thus the effects of our genetic differences, always operate in context, and an unequal one at that. And, genetic studies—even sibling difference studies—do not control fully for context. As Harden recognizes, people who are more attractive tend to be treated better in a variety of social environments, including educational ones. But does anyone—besides Harden—really think we want to focus on genetic differences related to greater attractiveness as causing higher education? Whether or not this is properly treated as a ‘cause’ of educational attainment, how in the world is this useful to help (a) advance knowledge or (b) ameliorate inequality in a world where we can easily see who is more conventionally attractive and measure any privileges they may experience from it (see Monk, Esposito, & Lee 2021). Second, again, we do not know what most genes do (and, as Harden doesn’t really explain well, we don’t measure genes in GWASs, we measure variants). 

I, and others, have a serious problem with studies of the ‘genetic potential for educational attainment’ because they confuse downward causation with upward causation by viewing genes as the primary cause of action. The effect will be—as Harden admits openly—that social policies that give meaning to genetic differences that are otherwise not involved in the biology of educational attainment, will be conceptualized as ‘genetics of potential’ or ‘innate differences’, when they may result from social and physical arrangements. To use but one real world (non-red haired exclusion policy) example, many kids have a lot of energy and struggle with the artificial nature of the classrooms that require us to stay still and be quiet, much more so than the careers that we may choose and the lives we craft around them (e.g., use lunch break to go on a run)–because everyone must go to school, usually not of their choosing, but we have agency in the choice of our jobs (within huge constraints, of course). Yet, in a school district where recess and exercise is shortened or not daily (as I experienced in my third grade class when I struggled to ‘not talk so much’, where we had recess only on Mondays and I ended up in the principle’s office for talking too much), or in all schools where physical activity and movement breaks are arbitrarily restricted, those kids who have a higher metabolism or more energy—in many ways and contexts a positive trait—will be penalized, stigmatized (maybe as ADHD, when they just need to move more), and struggle. Do these kids have a lesser ‘genetic potential for educational attainment’? I would say no. Harden’s view would say yes. 

Aha, but you may argue, Harden thinks we need to understand these differences, identify these ‘high energy genes’, and accommodate those individuals!! That all sounds well and good, but a closer look suggests otherwise. Talk to a first-grade teacher (such as my sister), and you will find that within the first few days of class she can often readily identify the students who have excess energy and could benefit from (my words) ‘a good running’ (such as my own son). Second, recall the effects of these genetic variants are MINISCULE. There is no ‘high energy gene’ that we can find and figure out what it does, and again, we can usually already identify the high energy kids with ease by watching them for a day or two.

What Harden fails to acknowledge and grapple with is the fact that most teachers can readily identify students who struggle, and many teachers can understand the source of their struggles (focus versus logic, versus application of concepts, versus problem solving). In a recent piece, Morris et al. (2020) examined whether ‘education-related genetics’ could actually provide more useful information than well-established, easily measurable variables such as prior GPA, parental educational, current performance in shaping policies or programs to enhance educational attainment. They concluded, quite clearly, that genetics does not really move us forward in policy or programs or understanding.

Harden suggests that by incorporating genetics, we will have better interventions and waste less money, but how is that supposed to work? We have already identified low hanging fruit, in terms of large effect size genes for monogenic disorders. The genetic influences on educational attainment are nothing like that, instead characterized by thousands of variants associated with educational attainment for reasons we do not know and probably, for most, will never really understand (at least in the next several decades, if ever). Given that Harden agrees that genetic engineering is unwise, what, exactly, does she think this offers us? She doesn’t tell us in this book.

In sum, because my time is running out, Harden’s book is interesting, if oversimplified and unsatisfying. She exhorts us to incorporate genetics for a more egalitarian society, but does not tell us how this would enhance understanding or make society more equal. And, she rightly notes that resources are not unlimited, which is why I question our application of millions of public funding to the understanding of genetic influences on educational attainment when the payoff is unspecified.

Harden thinks the worst-case scenario is that we are going to find that some people are just ‘better at educational attainment’ which could be used to justify the status quo, which is why we have to study it with an egalitarian approach. I disagree. We already know some people are better at educational attainment, just like some people are better at golf, playing musical instruments, learning foreign languages, and dancing (not me). We aren’t all the same. However, education is not like height or deafness, two examples she uses frequently as analogies. Educational attainment is not a ‘biological trait’, except in the banal sense that everything we do is biological because we are biological creatures. Given the state of knowledge, we already know that genetic effects are far too complicated to link to such a distant, complex, socially constructed outcome like educational attainment. Instead, in my view, the realistic worst-case, is, as we have seen for the candidate gene era and candidate gene interaction era before it, that we throw tens of millions of dollars and hundreds of thousands of scientists hours chasing a chimera of actionable or useful genetic influences for social disparities. I’d rather throw that money at social interventions that may not work well, but they might help a few. Harden disagrees, which she is free to do, but I won’t call her a bank robber [the moral equivalent of] for thinking differently.

Back Cover Description of ‘The Genetic Lottery’

A provocative and timely case for how the science of genetics can help create a more just and equal society

In recent years, scientists like Kathryn Paige Harden have shown that DNA makes us different, in our personalities and in our health—and in ways that matter for educational and economic success in our current society.

In The Genetic Lottery, Harden introduces readers to the latest genetic science, dismantling dangerous ideas about racial superiority and challenging us to grapple with what equality really means in a world where people are born different. Weaving together personal stories with scientific evidence, Harden shows why our refusal to recognize the power of DNA perpetuates the myth of meritocracy, and argues that we must acknowledge the role of genetic luck if we are ever to create a fair society.

Reclaiming genetic science from the legacy of eugenics, this groundbreaking book offers a bold new vision of society where everyone thrives, regardless of how one fares in the genetic lottery.

[1] Because I’m busy, like everyone else, but I also have things I want to say about things, I allow myself ‘fun writing’ on topics that I feel compelled to write about, without encroaching upon my family/leisure time and/or my work time. So, I am giving myself 30 minutes write this review. These are quick thoughts written hastily because I want to and I can. I ran out of time to think of a catchy title, so this one, which is disappointing, will have to do.

This Again? Homogenizing Racism, Dismissing Structure, and Adding Biology: A Response to Walsh & Yun (2017)

/ Callie Burt / 11 Comments

This, my second, blog post is my response to the recent Walsh and Yun (2017) paper “Examining the race, poverty, and crime nexus adding Asian Americans and biosocial processes” forthcoming in the Journal of Criminal Justice. No one asked me to write this, but I have things I want to say in response to this piece, which is, in my view, misguided and disjointed at best. In their article, WY repeat the tired, familiar trope of Asian Americans as the “model minority” to undergird their argument that African American cultural deficiencies and lifestyle choices are the source of elevated rates of black poverty and crime. In addition to dismissing significant differences in the historical experiences of Asian Americans and African Americans, WY sweepingly discount, if not dismiss, the existence of contemporary anti-black racism in the USA with feeble assertions about the success of some black Americans (we had a black president elected twice!; we have a holiday for MLK, Jr. “the only individual of any race so honored”!), as sufficient evidence to prove that we live in a post-racial world. In the second half of their paper, WY point to biosocial science (as others have done before) as a more scientific approach offering way out of this murky, biased social scientific haze. This section, which echoes many calls made by other ‘biosocial criminologists’, largely summarizes research on various biological pathways, seemingly oblivious to the contextual nature of the familial “abuses” they identify as causal triggers.

Despite the problems of this article, and there are many, this effort, which “[ignores] criminological orthodoxy” in attempt to “spoil the politically correct mantra that black crime results from white racism,” can be a useful reminder that the established, empirically supported models that frame scholarship on race and crime are neither universally accepted or understood, even among criminologists. Responding to pieces that challenge the orthodoxy (albeit while ignoring key facts and important scholarship) provides an opportunity for clarification. As a scholar of race and crime, this is my contribution to such a clarification. As a busy and important person, (okay, just busy), I am allowing myself 3 hours to devote to this response (so if anyone actually reads this, judge it on its terms) because I want to and I can. In this case, I believe a hasty response is better than no response at all.

This post is organized as follows (and, as usual with my writing will probably be longer than necessary to make the point). First, I will summarize my interpretation of the Walsh and Yun (2017; hereafter WY) piece. This is followed by a more detailed, critical look at some of the points WY make to support their claims, particularly those that I believe are essential to their claims and/or are deficient in particularly significant ways. Finally, I conclude as briefly as my writing allows.

I. Summarizing WY’s piece:

In my interpretation, WY seek two ends in this paper: a) debunking the notion that “[elevated] black crime [compared to whites] results from white racism,” pointing instead to culture and individual choices, and b) then (curiously) suggesting that the biosocial approach offers a way forward. If you find yourself perplexed at the two different aims and how they work together (agency and biological forces?), you are not alone. I found both the logic and flow of the arguments in this paper to be a bit disjointed and, in some cases, contradictory, especially the linkages between the sections of the paper. I discuss each in turn.

Part 1: It can’t be racism:

1) Mainstream explanations for African American crime—don’t forget choice!!: In this first section, WY make several critical claims about mainstream explanations for black-white racial disparities in crime, narrowly emphasizing Unnever and Gabbidon’s (2011) theory of African American offending (as if it is the only theoretical explanation of racism and crime). Reinterpreting Unnever & Gabbidon’s theory “through a different lens,” WY argue that the “criminalblackman” stereotype is grounded in the reality of higher “violence” among African Americans (pointing to racial disparities in homicide). They maintain that the allegedly causal linkages between experiencing racial discrimination and higher rates of offending are instead the result of African American’s “stultifying surrender to the cult of victimhood that sabotages self-reliance and excuses failure” (citing McWhorter 2000). Next, and without transition, WY link the “criminalblackman label” (Russell’s (2009/1998) theoretical concept) to the idea that being a “bad-ass” is actually valued by inner city young men (citing Anderson 1999), implicating culture.

WY conclude this section a bit abruptly, in my view, but here is what I think they are trying to say: scholarship shies away from cultural arguments because such explanations are a seen as “blaming the victim.” Instead, structural arguments are proffered, but such explanations “do not explain why these behaviors [crime] are structural rather than the products of human choice” (p.2). Uniquely citing Robert Sampson as “the dean of social ecology theory,” WY emphasize that we should not ignore human agency and individual choice, citing one of Sampson’s[i] statements that culture and structure are mutual creations. WY maintain culture and structure create each other, and human agency cannot be ignored, thus structure cannot determine culture (and crime) because we are free agents who make choices. How this all works together isn’t particularly clear, but as we shall see later, that is fine because the agency argument is inconsistent with the biosocial one.

2) The lower rate of offending among Asian Americans debunks the racial discrimination—higher crime thesis (this is presented as if this was a new idea![ii] or perhaps one that had not been given enough attention. Neither are true.). According to WY, Asian Americans have experienced discrimination, negative stereotypes, and hyper-ghettoization and have lower rates of crime than whites. Their misguided homogenization of the oppressive experiences of Asian and African Americans (themselves composed of groups and individuals with a multitude of diverse experiences) is used to minimize the role that racism plays in life chances, and, thus, falsify theories that link racial discrimination to increased offending and/or hyper-ghettoization to increased offending.

3) Racism is pretty much a thing of the past. Seriously, that is the point of this section, with powerful (sarcasm) statements such as: “Of course, anti-black racism is by no means dead, but we have a national holiday celebrating Martin Luther King, the only individual of any race so honored, and blacks win mayoral races across the U.S. in cities where they are a minority of candidates (Thernstrom & Thernstrom 2009)” (emphasis added). WY plainly argue that anti-black racism is (basically) a relic of an earlier age, and they dismiss scholarship documenting ongoing racism as output from “those with a vested interest in keeping racism alive.”

Following several paragraphs that can be ignored without missing a beat, WY conclude by arguing that based on the interracial official crime statistics for rape, robbery, homicide, and assault, Feagin’s oft-quoted statement about the prevalence of anti-black actions should be changed to the following:

“Being white in U.S. society means always having to be prepared for antiwhite actions by blacks” (p.3).

And, there you have it folks. Their “different lens.” I don’t think anything needs to be added to that. They conclude this section writing: “We cannot soberly and honestly assess racial crime differences as long as academics continue to make patently false, wildly exaggerated, and incendiary statements.” I concur; the irony is astounding.

4) It’s not poverty, its culture: Here WY argue, again falsely conflating anti-Asian racism with anti-black racism, it’s not poverty causing crime, it’s culture because Asians also experience discrimination, and they aren’t poor. Using impeccable logic, WY assert that if discrimination caused differences in poverty levels, then we would have to conclude that whites favor Asians, “which of course no one would believe” (p.3-4).[iii] So, WY deduce: it’s black culture and lifestyle choices that cause black poverty and black crime.

5) Education and poverty: WY dogmatically assert that black culture devalues education (selectively citing passages from prominent African American scholars Elijah Anderson and Orlando Patterson in decontextualized ways), and this cultural devaluation produces lower/worse educational outcomes among black Americans compared to whites. Conversely, Asian Americans value education highly and have better STEM outcomes that whites.

No effort is made to link this to any explanation of crime; rather, this section was just to further cement the notion of a deficient black culture with decontextualized facts and citations. WY thus further blame blacks for their position in society by juxtaposing black educational outcomes with those of Asian Americans, as if all else was equal.

Part 2: “Biosocial Lens”

6) In a quite disjointed fashion, WY shift to a biosocial lens arguing: “Theories that rely on social class and poverty to explain crime cannot explain variance in criminal behavior within social class” (p.4)—as if no theories have been offered to explain within-class variations in offending. They continue by noting that structural and cultural effects are not invariant; therefore: “Clearly, we have to go beyond raw demographics to explain why some people become criminal while other demographically similarly situated people do not.” WY fully ignore social theories of within-group differences in offending that seek to explain individual differences (e.g., Burt et al. 2012; Kaufman et al. 2008; Simons et al. 2003; Simons & Burt 2011; Unnever et al. 2009; Unnever & Gabbidon 2011) because why spoil a politically incorrect story?

In this section, WY continue a biosocial criminology tradition of highlighting “the” biosocial approach’s gift to the social sciences: the techniques of the “more robust natural science.” Notably, in this half of the paper, the emphasis on human agency disappears. Human choice is apparently only relevant when talking about structural effects. This is replaced with compilations (largely summaries, but informative ones) of research pointing to potential or recently empirically-validated biological pathways from exposure to childhood abuse, neglect, toxic exposures to various outcomes (some related to crime). WY aver: “Growing up in our inner cities often exposes black children to single parenthood, violence, parental abuse, neglect, and substance abuse. These children bear no blame for the conditions in which they find themselves, but as a result of cultural transmission and biological changes to the HPA axis and the ANS wrought by these conditions, grow up to perpetuate them” (emphasis added). Unfortunately, WY previously dismissed social-structural theories of these “tangle of pathologies” that explain how and why social arrangements shape contexts and pressures that increase the risk of black children’s exposure to these adverse conditions and experiences. Given this, they leave themselves in a peculiar position of pointing to culture and human agency as causes of (deterministic) biological processes. That is a first, I think.

Although, I should note that if their second section on biological processes is reframed as an explication of how structural-cultural processes get under the skin to have lasting effects on development, including criminal behaviors, elucidating how “human agency” and “lifestyle choices” are misguided explanations for racial disparities in social behavior and demographic outcomes, then this section, as a summary of what is out there (albeit a bit oversimplified), might be valuable. Obviously, such was not the intent of WY.

II. My Specific Critiques of WY paper

As should be manifest by now, even though I have done little but summary, I think this paper suffers from a host of problems in the way of evidence and logic. Rather than quibble with every point, which I want to but that would not be efficient or effective, I highlight four main ways this paper nosedives, which were suggested in the above.

1. Racial discrimination persists. I honestly cannot believe that in this day, post-Trump election, that a serious scholar could question the existence of anti-black racism in American today. One might conclude that either they are not serious scholars, or they are not serious. (Are we being punk’d?) To argue that racism is a relic of the past, WY dismiss a wealth of diverse sociological research on the topic of “white racism,” at both the interpersonal and the structural level (as a racialized social system; Bonilla-Silva 1996). WY downplay (really basically ignore) the significance of the structured nature of white advantages rooted in historical (material and ideological) struggles. Their broad brush depiction of white racism as practice of the past, with contemporary forms as being invented by “those with a vested interest in keeping racism talk alive,” is not only ignorant and fallacious, but offensive. This section is basically a farce and becomes even more so in the end when WY reverse Feagin’s claim about the prevalence of antiblack actions by whites. I don’t have the time to say more, but for some (of many) excellent discussions of racism and our racialized social system see: Bonilla-Silva 2001; 2017; Essed 1991; Feagin 1991; 2014; Omi & Winant 1986.

2. Racial discrimination/racism is not uniform across racial-ethnic minority groups. Despite WY’s claims (echoing others over the years), racism against Asian Americans is not tantamount to that against African Americans. To be fair, WY mention that “unlike blacks the Chinese came to the United States voluntarily,” but summarily downplay that stark difference by noting that the employment conditions of the Chinese “often amounted to what Kitano and Daniels (1995:22) called a ‘new system of slavery.’”

The repeated false conflation of the Asian and African American experience of oppression, which includes the overworn trope of the “model minority” in contradistinction to black Americans, is neither novel nor productive, and WY’s brief discussion of this is banefully ignorant of social scientific scholarship in this area. As Wu documents in her (excellent) book The Color of Success (2014) before the 1940s and 1950s, whites considered Asian Americans as unfit for citizenship and unassimilable, “marking them as definitively not-white, and systematically shutting them out of civic participation…” (p.2; emphasis in original). However, Wu documents how, in seemingly an astonishing public transformation, the “model minority” narrative was invented in response to geopolitical dilemmas, among them the Cold War and civil rights movement:

“A host of stakeholders resolved this dilemma by the mid-1960s with the invention of a new stereotype of Asian Americans as the model minority—a racial group distinct from the white majority, but lauded as well assimilated, upwardly mobile, politically non-threatening, and definitively not-black.” (p.2, emphasis in original).

To be sure, like Wu, I do not wish to diminish the efforts of Asian Americans, but focusing narrowly on their actions is but one (and some argue small) piece of their story of upward mobility. Instead of a shift in “lifestyle choices,” socio-historical scholarship suggests that it was a transformation in the public image of Asian Americans from disgusting and unassimilable (not white) to law-abiding, hard-working, compliant, and the like (not black) that opened doors for Asian Americans to climb the social ladder. Thus, while WY credit this shift to hard work and a cultural emphasis on education among Asian Americans, research suggests that the upward mobility observed among Asian Americans between 1950 to the 1970s was due to this shift in treatment that this change in public image fostered: a decline in racism against Asian Americans (Hilger 2016).

To be sure, this social scholarship was available to WY, but it didn’t fit their politically and (factually) incorrect story that the experiences of Asian and African Americans are, for all intents and purposes, tantamount. This undergirds “their alternative view” that at the root of racial disparities in offending is not white racism/structure but black culture and poor lifestyle choices.

Futhermore, clearly misunderstanding (or forgetting) the tenets of labeling theory and excellent criminological and historical work on the criminalization of blackness, as a means of racial control,  and the roots of the “criminalblackman” stereotype in white racism (e.g., Alexander 2010; Russell-Brown 2009; Muhammad 2010), WY note: “Despite these hardships and negative stereotypes, the Chinese have never had a reputation for being criminally inclined” (p.2). That is, in part, exactly the point. Labeling theory, generally, and research on racial threat and criminal justice control, which focuses on the criminalization of blackness and the equating of blackness with criminality, specifically, theorize that this criminalblackman stereotype will increase crime and criminality, all else equal, and distort official rates of offending, due to the increased surveillance and greater punishment accorded to black law violators as a result of the belief that they pose a greater danger to society (Tonry 1995; Spohn 2015). There is so much to discuss here but so little time, so I will move on. Ultimately, and unfortunately, social scholarship documenting the ways in which powerful individuals/stakeholders can project various political agendas onto a socially-constructed cultural narratives is ignored, like much other relevant scholarship.

Additionally, WY attempt to debunk prominent macro-level theories that focus on the hyper-ghettoization of African Americans as a causal factor in elevated rates of offending, by noting that the hyper-ghettoization of Asian Americans has been used to explain their lower crime rates. Therefore, according to WY, hyper-ghettoization cannot explain crime. Viewed in isolation, that argument might be reasonable or persuasive, but only if it is removed from the entire theoretical apparatus in which it is situated, including historical and current struggles (such as the deterioration of community bonds to the high rates of incarceration of African American males and so on). These various issues/influences are all intertwined in complex ways, and the idea that voluminous amounts of social scientific research on race, racism, and crime can be swiftly dismissed by a cursory comparison of Asian Americans and African Americans is astonishing. WY must adhere to that same worldview as Wright and Morgan (2014) that most social scientists are so blinded by their liberal worldviews, hampered by their allegiance to the methods and assumptions of that inferior branch of social “science,” and fettered by their fear of being labeled racist, that the biased, “politically correct” knowledge they create can be dismissed with quick and weak arguments. Such sweeping dismissals of the “standard social science model” as well as dogmatic overreactions to findings ostensibly contradicting theoretical explanations is rather unproductive, and in this case, quite preposterous.

To be sure, I am not suggesting that the Asian American experience (historically or at present) has not involved considerable oppression and discrimination. It has, and that is not up for debate. Rather, I am stating clearly (following many others) that the Asian American experience and the African American experience are not interchangeable but are quite different in many significant ways due numerous factors, including the legacy of slavery, Jim Crow, and the criminalization of black Americans, all of which shape structure, culture, and social behavior in profound and complex ways that must be considered when theorizing about criminal behavior.

3. “Biosocial Approach”: In the second half of the paper, as noted, WY present a “biosocial approach” as an alternative to mainstream social scientific criminology, one which “can lead to a criminology that is rooted more in science and empirical observations” and which can aid our understanding of within-class differences in criminal outcomes. In making their case, WY state: “Clearly, we have to go beyond raw demographics to explain why some people become criminal while other demographically similarly situated people do not” (p.4). No problem, here, but recourse to biological mechanisms is not necessary to explain differences in offending within various groups; many micro-level theories, some cited above, (especially combined with theories including resilience processes) explicate within-group differences in “positive” or “negative” outcomes.

Next WY state: “Too many black children are born into fatherless homes in neighborhoods riddled with violence and poverty for which the children bear no responsibility.” I concur, too many black children (and children of all races and ethnicities) are born into harsh, unpredictable conditions not of their own making that impede their health and life chances. (Although I will quibble that good evidence suggests that rather than needing a mother and father, children need a loving family (regardless of gender) who have the time, energy, and resources to provide warmth, nurturance, and predictability for healthy development, but that is just a queer digression.) Finally, WY conclude, more debatably, “and the conditions in which these children grow up require a biosocial analysis of how the environment penetrates the person down to the molecular level.” I don’t know about you, but I don’t follow their logic. To be sure, analyzing the biological mechanisms through which environmental exposures is one level of analysis that, in my view, has value. But, incorporating biological pathways at the current state of knowledge (and likely ever) is neither necessary nor sufficient to understand within-class differences in outcomes (or within-race differences). Rather it is one layer of information, but one that is certainly not more valuable than the socio-environmental layers. That a biosocial analysis (which focuses on biological pathways) is necessary to understand racial disparities (or more valuable than social explanations) seems particularly misguided, in my view, given the fact that social interventions to prevent or reduce minority groups’ exposures to harsh, noxious, and unpredictable environments seem preferable than pharmacological interventions (if possible at some future date) to undo or offset biological adaptations to such conditions. But, I am getting ahead of myself. I shall quickly look at a few ideas WY consider:

Epigenetic processes: WY focus on DNA methylation, which is the most well-understood and well-researched form of epigenetic regulation. As WY note, research reveals that the effect of methylation, especially when it occurs in the promoter region of a gene, is typically to reduce gene expression. In other words, DNA methylation serves as a dimmer switch for genes (by blocking DNA transcription enzymes; Ng & Bird 1999). Importantly, research suggests that DNA methylation patterns are dynamic and responsive to the environment, especially during sensitive periods, and can have long-term impacts on development (Meaney 2010; Slavich & Cole 2013). In other words, research suggests that DNA methylation is a key biological (genomic) mechanism mediating the effects of social conditions on development (e.g., Feinberg 2007; Hochberg et al. 2011).

Just to repeat clearly, because I am fond of repetition, DNA methylation has been identified as a key mechanism through which socio-environmental forces have enduring effects on development (McGowan & Roth 2015; Syzf & Bick 2013). In recent years, researchers have generated a small but steadily growing body of evidence connecting social adversity to DNA methylation patterns and adverse health outcomes, including depression, antisocial behavior, and the like (e.g., Beach et al. 2016; Essex et al. 2013; van der Knaap et al. 2015). Moreover research has also identified epigenetic markers of exposure to social disadvantage, including SES and racial discrimination (Essex et al. 2013; Simons et al. 2016).

Evidence over the past decade suggests that a social epigenetic approach will provide a new layer of information, not an alternative explanation to that offered by social theories. Importantly, some epigenetic marks appear to be intergenerationally transmitted (see Kuzawa and Sweet 2009 for a discussion involving race and health disparities), meaning that, for example, stressful experiences including those accompanying slavery, Jim Crow, lynchings, and ongoing racial discrimination may induce epigenetic changes (adaptations) that are transferred to future generations, in ways that may influence biopsychosocial development.  Among humans, Kuzawa and Sweet (2009: 7) note:

   “Indirect evidence for maternal-fetal transfer of epigenetically based alterations in stress (HPA) reactivity has been documented in humans. In holocaust survivors, severity of post traumatic stress disorder (PTSD) symptoms—which influences maternal cortisol production during pregnancy—predict levels of cortisol excretion in postnatal offspring, and Manhattan women who were pregnant during the 9/11 attacks gave birth to offspring who show evidence for alterations in HPA activity in childhood (Yehuda and Bierer, 2008).”

Recent evidence accumulating over the past several years suggests that it is hardly a stretch expect that historical and contemporary traumatic racialized experiences, including ongoing vicariously experienced incidents involving police (and citizen) shootings of unarmed black men (Trayvon Martin and so many others), influence epigenetic alterations or patterns that influence development, such that at the present day individuals are “marked” (in potentially insignificant, but also potentially significant ways) by experiences of racial oppression (in the same manner that impoverished individuals may be shaped by harsh conditions accompanying low SES in the USA). Of course, this area of research is incredibly new and there is so much we still do not know[iv]; yet, all the new evidence emerging further underscores the fallacy of the (long dead in most circles) independent “culture of poverty and crime” explanations for racial disparities in social outcomes.[v]

Perhaps more importantly, across all of the biosocial factors WY examine, there is a need for social scientific models to elucidate the social factors that shape biological adaptations, such as DNA methylation. This is why recent calls from NIH and other scientific bodies have highlighted the need for social and genomic scientists to work together to develop holistic models linking various levels.

Summarizing the point of the above, WY’s focus on epigenetics, allostasis, telomere length, cortisol, sex hormones, and the like is both curious and explanatorily evasive because research on each of these points to the central role of environmental (including social, structural) influences. Rather than replacing a social scientific model linking our racialized social system to social behavior, a focus on such biological processes are more likely to provide evidence supporting it, including by identifying “hard” (biological) pathways for racism’s enduring effects. The more we learn, the more we see that human psychophysiological development is profoundly shaped by the social-environmental conditions of experience, and given the role of structural arrangements in shaping exposures to stressful, oppressive, and noxious conditions, the unique oppressive experiences of African Americans undoubtedly influence life chances through biological adaptations in a manifold of ways.

 4) Crime is a social construct: In discussions of race and demographic outcomes, scholarship invariably notes that race is a social construct (WY is an exception in this paper, but they have discussed this in earlier pieces). Yet, crime, including violence, is a social construction that involves not only arbitrariness and vagueness but also is, as we all know, itself shaped by structure (including racism) and historical context. I will make three points, none novel, but all worthy of remembering:

i) Crime is racialized; race (especially blackness) is criminalized. Approaching the race and crime question without serious consideration of this reality will distort any explanation.

ii) Crime is not a biologically-given construct. Any biosocial explanation of “crime” must recognize that what counts as “crime” or even “violence” is not given in nature. Physically and psychologically injurious acts (“violence”) can be lauded (in war, on football fields, in the boardroom), can be excused (“justified” killings by self-defense or official agents of government), or can be punished. There is no inner biological reflection or any clear phenotype of “illegal violence” or “crime” that does not rely on historical, situational, individual and other social influences. Hence, any “bio” explanation of “crime” must inherently be incomplete because crime is not bio; crime and illegal violence are not given in nature.

iii) Crime is invariably measured/theorized as “street crime” not the universe of illegal acts. Should we capture that universe (corporate crime, governmental crime), and the harm entailed, race and crime statistics probably look quite different.

Conclusion: The criminological study of race and crime over the past several decades has moved from an uneasy state of “controversy and silence” to a fertile terrain for new developments and considerable knowledge growth. Although much remains to be learned and much more (most) remains to be done, a complex, diverse set of studies has evidenced the manifold ways that white racism—from the structural level to its interpersonal instantiations—increases the risk of African American offending, in large part, through its associations with life chances (education, employment, health, and the like) and worldviews, including individual schemas and shared cognitive landscapes. Moreover, more recent years have seen the potential, and in some areas hard evidence, for biological pathways through which racism influences development, including physiological and psychosocial outcomes. We have also witnessed enhanced recognition amongst many social scholars of the potential for biopsychosocial work to advance knowledge on the lasting effects of living and developing in a racialized social system such as ours. Thus, at the present time with the current knowledge base, it is rather astonishing that a paper such as this would make its way to publication. On the other hand, as we all know science (and publication) does not exist a part from social context and political agendas but is itself part and parcel of this racialized social system.

(Really, I am concluding this, promise.) In this post, I have tried to make sense of WY’s paper, attempting to avoid the trappings of their one-sided agenda and dogmatic rejections of a diverse body of research documenting the complex relationship between race/ethnicity and crime, while resisting the almost paralyzing recourse to the “hard sciences” as a way out of a “period of controversy and silence” long past. Now, more than ever, we have the evidence, tools, and motivation to further explore the nuances of living in our racialized social system and, especially, the deleterious effects on oppressed groups. I will end by fully endorse WY’s concluding remarks with a few corrections:

“We agree with LaFree and Russell (1993. p. 279) who argue that the crime/race connection should be studied honestly and courageously because ‘no group has suffered more than African-Americans by our failure to understand and control street crime.’ The corollary of this is that no other group can benefit more from a candid examination of race and crime. This will not, and cannot begin to happen, until we stop misidentifying causes,” [exhuming long-buried arguments, such as the “culture of poverty” thesis and reiterating misguided notions about the “model minority”.]

Anti-black racism persists, and scientists are not immune.

 

References (not cited in WY’s article):

Alexander, Michelle.  2010. The New Jim Crow: Mass Incarceration in the Age of Colorblindness. The New Press.

Beach, SRH, M-K Lei, GH Brody, S Kim, AW Barton, MV Dogan, & RA Philibert. 2016. Parenting, socioeconomic status risk, and later young adult health: Exploration of opposing indirect effects via DNA methylation. Child Development 87: 111-21.

Bonilla-Silva, Eduardo. 2001. White Supremacy and Racism in the Post-Civil Rights Era. Lynne Rienner Publishers.

Bonilla-Silva, Eduardo. 2017. Racism Without Racists: Color-blind Racism and the Persistence of Racial Inequality in America. Rowman & Littlefield.

Brody, Gene H., Yi-Fu Chen, Velma Murry, Xiaojia Ge, Ronald Simons, Frederick Gibbons, Meg Gerrard, and Carolyn Cutrona. 2006. Perceived Discrimination and the Adjustment of African American Youths: A Five-Year Longitudinal Analysis with Contextual Moderation Effects. Child Development 77:1170–89.

Burt, Callie H., Ronald L. Simons, and Frederick X. Gibbons. 2012. Racial Discrimination, Ethnic-Racial Socialization, and Crime: A Micro-Sociological Model of Risk and Resilience. American Sociological Review 77:648-677.

Essed, Philomena. 1991. Understanding Everyday Racism: An Interdisciplinary Theory. Sage.

Essex, MJ, WT Boyce, C Hertzman, LL Lam, JM Armstrong, S Neumann, & MS Kobor. 2013. Epigenetic vestiges of early developmental adversity: Childhood stress exposure and DNA methylation in adolescence. Child Development 84: 58–75.

Feagin, Joe R. 1991. The continuing significance of race: Antiblack discrimination in public places.” American Sociological Review 56: 101-116.

Feagin, Joe R. 2014. Racist America: Roots, Current Realities, and Future Reparations. Routledge.

Feinberg, AP. 2007. Phenotype plasticity and the epigenetics of human disease. Nature 447: 433-40.

Hilger, Nathaniel G. 2016. Upward Mobility and Discrimination: The Case of Asian Americans.  No. w22748. National Bureau of Economic Research, 2016.

Hochberg, Z, R Feil, M Constancia, M Fraga, C Junien, J-C Carel, et al. 2011. Child health, developmental plasticity, and epigenetic programming. Endocrine Reviews 32: 1-66.

Kaufman, Joanne M., Cesar J. Rebellon, Sherod Thaxton, and Robert Agnew. 2008. A General Strain Theory of Racial Differences in Criminal Offending. Australian and New Zealand Journal of Criminology 41: 421-37.

Kuzawa, Christopher W., & Elizabeth Sweet. 2009. Epigenetics and the Embodiment of Race: Developmental Origins of US Racial Disparities in Cardiovascular Health. American Journal of Human Biology 21:2-15.

McGowan, PO, & TL Roth. 2015. Epigenetic pathways through which experience becomes linked with biology. Development and Psychopathology 27: 637-48.

Meaney, MJ. 2010. Epigenetics and the biological definition of gene x environment interactions. Child Development 81: 41-79.

Muhammad, Khalil Gibran. 2010. The Condemnation of Blackness: Race, Crime, and the Making of Modern Urban America. Harvard University Press.

Ng, HH, & A Bird. 1999. DNA methylation and chromatin modification. Current Opinion in Genetics & Development 9: 158-63.

Omi, Michael, & Howard Winant. 2014. Racial Formation in the United States. Routledge.

Russell-Brown, Katheryn. 2009. The Color of Crime, 2nd Ed. New York University Press.

Simons, Ronald L. and Callie Harbin Burt. 2011. Learning to Be Bad: Adverse Social Conditions, Social Schemas, and Crime. Criminology 49:553–98.

Simons, Ronald L., Yi-Fu Chen, Eric Stewart, and Gene Brody. 2003. Incidents of Discrimination and Risk for Delinquency: A Longitudinal Test of Strain Theory with an African American Sample. Justice Quarterly 20:827–54.

Simons, RL, MK Lei, SRH Beach, CE Cutrona, RA Philibert. 2016. Methylation of the oxytocin receptor gene mediates the effect of adversity on negative schemas and depression. Developmental Psychopathology, Advance online publication.

Slavich, GM, & SW Cole. 2013. The emerging field of human social genomics. Clinical Psychological Science 1:331-48.

Spohn, Cassia. 2015. Race, Crime, and Punishment in the Twentieth and Twenty-first Centuries. Crime and Justice 44: 49-77.

Szyf, M., & J. Bick. 2013. DNA methylation: A mechanism for embedding early life experiences in the genome. Child Development 84: 49-57.

Tonry, Michael. 1995. Malign Neglect: Race, Crime, and Punishment in America. New York: Oxford University Press.

Unnever, James, Francis Cullen, Scott Mathers, Timothy McClure, and Marisa Allison. 2009. Racial Discrimination and Hirschi’s Criminological Classic: A Chapter in the Sociology of Knowledge. Justice Quarterly 26:377–409.

van der Knaap, LJ, JM Schaefer, IHA Franken, FC Verhulst, FVA van Oort, & H Riese. 2014. Catechol-O-methyltransferase gene methylation and substance use in adolescents: The TRAILS study. Genes, Brain, and Behavior 13: 618-625.

Walsh, Anthony, & Ilhong Yun. 2017. Examining the race, poverty, and crime nexus adding Asian Americans and biosocial processes. Journal of Criminal Justice: advance online publication.

Wu, Ellen D. 2014. The Color of Success: Asian Americans and the Origins of the Model Minority. Princeton University Press.

Young, Vernetta. 2006. Demythologizing the ‘Criminalblackman’: The Carnival Mirror. Pp.54-66 in The Many Colors of Crime, edited by R.D. Peterson, L.J. Krivo, & J. Hagan. New York: New York University Press.

 

Notes:

[i] Pointing to Sampson to support their claim about missing agency in the structural-cultural arguments about race and crime is super ironic (or ignorant) given that Sampson & Wilson (who they cited earlier) provided one of the seminal pieces linking racial stratification (structure) to cultural adaptations shaping black-white disparities in crime, often viewed as the piece that ended the “period of controversy and silence” around race and crime.

[ii] Notably, WY did not cite William Petersen, a UC Berkeley sociologists whose 1966 NYT piece encouraged comparisons between Japanese-Americans and African Americans and strengthened stereotypes of Asian Americans as the model minority in contrast to African Americans, nor any of the numerous responses to this comparison that have unmasked the hollowness of such comparisons in the more than 50 years since Petersen popularized this juxtaposition.

[iii] WY assert: “To be consistent with structural arguments for black crime, proponents of such views would have to attribute Asian successes to pro-Asian bias on the part of whites to their own detriment, or to return to cultural or genetic arguments to explain Asian advantage vis-a-vis whites and blacks. They are not likely to do so because that would entail group comparisons along these lines, which they find invidious.”

[iv] As WY note, the potential of the epigenetics field has not yet been matched by the reality of research given its complexities; yet, that is not reason to deny that epigenetic research provides a plausible biological mechanism linking racist and other social experiences to development in lasting and potentially reversible ways (with supportive preliminary evidence).

[v] To be clear, WY are not completely silent about the social inputs into the biological pathways on which they address. Rather, WY focus on parental abuse and neglect and its lasting effects. Given their earlier arguments, they seem to imply that such parental treatment—no fault of the child—they assure, is due to not only to culture and structure but to human agency. However, the very first epigenetic example they provide reveals, at least among rodents who clearly have less complex lives especially in the social realm, that female rat pups who were licked and groomed in early life go on to become licking and grooming mothers. As noted, cross-fostering studies show that this is not learned or genetically transmitted, rather the experience of licking and grooming in the early life of rat pups produces a cascade of epigenetic changes which shape development and later parenting, presumably for adaptive reasons. This implies, at least extrapolating from the simpler life of the rat pups, that parenting practices are powerfully shaped by familial experiences, and likely among humans, ongoing experiences in development that provide cues about the nature of the world and the people in it. This example completely undermines their arguments about culture and agency.

Overgeneralizations and Obfuscations: A Response to Turkheimer(‘s blog)

/ Callie Burt / 6 Comments

Recently, Eric Turkheimer, a foremost behavioral geneticist, wrote a blog about the debate in Criminology around heritability studies, primarily focusing on arguments in our original article (see here and our rejoinder). While I am under no illusion that people will actually read this response/blog, I wanted to respond to Turkheimer’s critique because, like other (pro-BG) responses to our critique, it is grounded in a misunderstanding or mischaracterization of our argument.[a] Like Barnes et al., Wright et al., and Moffitt and Beckley before him, Turkheimer seems unwilling to engage with the substance (explicit focus) of our critique, but rather chooses to interpret it (wrongly) as anti-genetic and “anti-BG.”[b] I feel compelled to address these misguided responses to (critiques of) our critique.

To foreshadow the discussion below, drawing on Turkheimer’s quotes, including his critique, I maintain that Turkheimer agrees with the substance of our critique, with discord only appearing if our arguments are mischaracterized (overgeneralized to topics that they were avowedly not addressing, e.g., the broader field of behavior genetics, the use of twin and adoption studies for non-heritability purposes), and that we cited him correctly.

I respond to each of Turkheimer’s points below. The responses are numbered to correspond to the numbered points he raised in his blog.

(1) Like Wright et al. and Barnes et al., Turkheimer balks at our call for an end to heritability studies as (“sounding a lot like”) scientific censorship. This is both unnecessarily polemical and a rather weak response to a scientific argument, given that this is the way science proceeds when advances uproot the flaws (or lack of utility) of certain scientific practices. This is a gradual process whereby (some) scientists begin to realize the flaws of a paradigm or practice (e.g., the geocentric theory of the universe or phrenology) and bring it to attention and the topic of debate. Ours was an attempt to inform criminologists, who have neither the background in biology nor the time or interest to keep pace with the incredible advances in the life sciences in recent years, about the flaws of the heritability study and to make a case for superannuating (or hastening the decline of) the practice of estimating h2 as well as recognizing the flawed nature of its existing estimates. This is in the spirit of advancing science. As Popper (1962) articulated (and we cited this in our paper) “our knowledge grows only through the correction of our mistakes.”

(2) Turkheimer states: “If noting else, the generic citations of Rutter and Turkheimer as a kind of appeal to authority is a lousy way to argue. What did I say, exactly, and why is what I said relevant to the current argument.” We cited Turkheimer and Rutter not as an appeal to authority but as foremost experts in the field. Barnes et al. responded to our initial critique with the intimation that we were merely extreme environmentalists who were uninformed about biology (presumably in contrast to them), and that, as such, our criticisms should be ignored because we did not have expertise in the areas (aka, we didn’t know what we were talking about.)[c] Rather than as an “appeal to authority” as a means of arguing, we cited Rutter and Turkheimer as experts in the area who also thought that heritability studies had little (to nothing) to contribute to science at the present state of knowledge.

But, what did Turkheimer say?[d] In the paper, we pointed the reader to two pages in two articles that contained the discussion supporting our interpretation of his statements indicating that heritability studies, at present, lack utility and should come to the end. Here are the quotes:

Turkheimer (2011: 598)

“Whether this exercise [heritability studies, which he often refers to as variance partitioning because that is what it is] has any scientific content has been the subject of debate for more than a century, and here is a summary of why I think it does not: it is not about cause. Practitioners of the art wanted it to be about cause, in the sense that the relative magnitudes of the various components were supposed to tell us something about the importance of genetic and environmental causes underlying a trait, but they do not…In the real world of humans, in a given context everything is heritable to some extent and environmental to some other extent, but the magnitudes of the proportions are variable from situation to situation, and have nothing whatsoever to do with the causal properties of genes and environment for the trait in question, unless one is interested in the pointless null hypothesis that one of the components is zero….Plomin and Daniels [1987!!] marked the beginning of the end of variance partitioning as a useful endeavor in human developmental science.”

Turkheimer (2014)

“The laws of behavior genetics are not actual laws, and calling them that may have led to some misunderstandings of what was originally intended. In particular, although the First Law of Behavior Genetics has sometimes been considered an endorsement of a hereditarian view of behavior (e.g., Pinker 2003), the universality of heritability is best interpreted as a reductio ad absurdum of these very distinctions—as a way of observing that the endeavor of figuring out how genetic or environmental a trait is, let alone declaring that it is exclusively one or the other, is pointless. (p.532; emphases added).

And,

“The prospect of this outcome has haunted the nature-nurture debate from its inception, as both sides of the old debate were led to a dead end of thinking that the point of the debate was to evaluate the separate effects of genes and environment. It became clear long ago that neither genes nor environment could be discounted for anything important… Genetically informed research designs can partially, imperfectly, control for the genetic and shared environmental confounds that otherwise cloud causal interpretation of associations like these, and they have been extraordinarily successful at doing so. The quantification of heritability itself is unimportant in such analyses…” (p. 535, emphases added).

We could also point to Johnson, Turkheimer, Gottesman, & Bouchard (2009). In the abstract (p. 217): “We see little need for further studies of the heritability of individual traits in behavioral science…”

Furthermore, noting clearly that “heritability studies are no longer important,” Johnson, Turkheimer, Gottesman, & Bouchard (2009) stated: “To understand why heritability estimates are no longer important, it is necessary to understand that they are completely dependent on the specifics of the samples and environmental conditions from which they are taken…This means that little can be gleaned from any particular heritability estimate and there is little need for further twin studies investigating the presence and magnitude of genetic influences on behavior.” (pp. 217-218, emphasis added).

These are some of the things that Turkheimer said that led us to cite him as calling for an end to heritability studies. And, there are more. Although we wish we had the space to include these quotations, we believe that Turkheimer’s words are consistent with our citing him as an insider in the area who also thinks the studies lack utility at the present state of knowledge.

(3) Turkheimer states: “One ongoing problem I have with a lot of recent anti-BG writing is the whole idea of a “heritability study”.  Evan Charney is another person who trades in this idea.  A heritability study isn’t a thing.  A [sic] heritability is a descriptive statistic, an effect size, not a kind of study.  It is kind of like writing a critique of social psychology and railing against “F-ratio studies.”

First, we point out that Turkheimer (like Barnes et al., Wright et al., and Moffitt and Beckley before him) wrongly lumps our study into a body of “anti-BG” writing. We are clear[e] that our critique is narrowly focused on “heritability studies,” and this necessitated and justified our using the term “heritability study” to describe the studies at the focus of our critique.

Second, I wish to clarify what we mean by heritability studies, although I remain rather astonished that this seems to be a point of confusion. What we refer to as heritability studies are those studies whose aims are to come up with a numerical estimate of heritability (h2), which we defined: “Heritability was defined by Wahlsten (1990: 244) as “the proportion of variance in a measure of behaviour or other phenotype in a breeding population that is attributable to genetic variation” and by Plomin et al. (2012: 87) as “the proportion of phenotypic variance that is accounted for by genetic differences among individuals.” (Burt & Simons 2014: 227).

We selected the name “heritability studies” for these studies, following Charney (2012), because we are narrowly focused on studies whose focus is on partitioning variance between “genetics” and “environments”. Heritability studies are not tantamount to twin and adoption studies because studies of twin and adoption samples can be used for other purposes other than to estimate h2. Our critique, as we note in the paper, is not on these other uses of twin (or adoption) studies. (Thus, for example, Moffitt and Beckley’s point that MZ studies of twin discordance can be used to enhance our understanding of criminal behavior is entirely beside the point of our critique. In fact, I think that in some situations MZ studies of twin discordance offer great promise for shedding light on environmental influences on phenotype variance.)

Turkheimer argues that the “heritability study isn’t a thing. A heritability is a descriptive statistic, an effect size, not a kind of study.” Sure it is a kind of study. A heritability study is exactly how we (and Charney) have described above. What’s not to understand? The heritability estimate is a (time, population) specific effect size, and the study that estimates heritability is a heritability study. This is pretty straightforward. Critiquing studies that merely attempt to estimate h2 is not at all like “writing a critique of social psychology and railing against ‘F-ratio studies’. Social psychological studies that use F-statistics do not have the goal of estimating the F-statistic and they do not present the resulting F-statistic in the abstract as the key finding from the study. No, such studies have the goal of examining whether relationships exist, and they certainly don’t report F-statistics as the key finding of the study. If they did, then they could be appropriately called F-statistic studies. Similar to our use of heritability study, scientists refer to studies that assess the dimensionality of various measures as “factor analytic studies.. Heritability studies are absolutely a thing (as Turkheimer notes in his point 4) like factor analytic studies.

(4) But, Turkheimer does in fact understand what we call heritability studies: “What Burt and Simons think they mean by a “heritability study” is a study that has no point other than estimating the heritability of something.  My friend Ron Yeo used to refer to these as h-squared-equals studies. On this point they can cite me, and the 2011 paper they cite is a reasonable source.  The heritability of criminality doesn’t mean that it has somehow turned out to be “biological” and whether the estimated value in some twin study is .3 or .65 makes very little difference and doesn’t tend to replicate anyway”

Yes, what we “think we mean” is, in fact, actually what we mean (thanks).[f] And, with this, we would point out that Turkheimer does acknowledge that heritability studies (h2-equals studies) are, in fact, a thing.

This is exactly how we cited Turkheimer and this is exactly our argument. As we noted, there had been a profusion of heritability studies (Turkheimer’s seemingly preferred appellation, “h-squared equals studies”) in criminology over the past several years, and these were the studies we were calling for an end to.

(5) Turkheimer: “Barnes et al are right: I do twin studies for a living, and it would be mighty hypocritical of me to declare that they are useless in general.  As a BG person who has spent a lot of time criticizing the heritability concept, I have made it a discipline to never suggest that my doubts about numerical heritabilities should lead to a general dismissal of genetic effects on behavior or the behavior genetic enterprise generally.”

With his statements on point 4, it appears that we did cite Turkheimer appropriately, and he does agree that we should stop estimating heritability studies at the present state of knowledge. Yet, like other BG proponents, he wants to overgeneralize our argument rather than conceding his agreement, twisting it into something it is not (or he is just making irrelevant points that genetic effects aren’t zero, something our paper did not question). This critique is not anti-BG, and nowhere do we dismiss either genetic effects or behavior genetics generally. (We repeat this point several times throughout the papers). We are not broadly criticizing quantitative genetics, nor are we endorsing it, we wanted to call an end to these “h-squared-equals studies,” which were being estimated and published on nearly every outcome without an end in sight.

To be clear, studies that employ the twin design for reasons that are not for the purposes of estimating heritability are not the focus of our critique, which, again, is why we employed the term heritability study (not twin studies).

(6) Turkheimer though takes us to task for not doing something that was irrelevant to our paper: “Where in the remainder of their articles is a concession that genetic pathways rule out certain interpretations of the data, an acknowledgement that criminology has to take genetics into account when it is interpreting its findings?  Like every anti-BG paper I have ever read, they spend the rest of their paper finding something to attack in every single genetically oriented paper they can find.  Twin study?  EEA.  Adoption study?  Prenatal effects.  If all of non-experimental social science were held to this standard it would just go away.” Again, this is beside the point. Our goal was squarely on heritability studies, and “finding something to attack in nearly every single genetically-oriented paper we could find”? Weak sauce, as we were focused on criticizing heritability studies and, yes, our focus was identifying their problems. It was simply out of the scope of our paper to concede that genetic pathways rule out certain interpretations of data. We also did not talk about the effects of labeling by the criminal justice system on interpretations of the effects incarceration on the likelihood of recidivism. Both are out of scope.

(7) Turkheimer states that he thinks that studies of twins can be used effectively for purposes other than heritability. Off topic, but good to know. (Such was clear from his papers we cited.)

(8) Turkheimer asks: “Now the question is whether the studies that Burt and Simons list are h2-equals-studies or more interesting genetically informed social science.  I’m not going to take the time to go through them one at a time, but the several I looked at were bivariate “quasi-causal” (as we call them in our lab) studies.”

I can answer this. The studies we identified (per reviewer requests to point to studies) all involved an “h2-equal” as the sole goal if not a primary goal of the paper.

(9) Turkheimer stated: “Moffitt and Beckley wrote a nice reply about epigenetics and I won’t go into depth about it.  I think that people who think that epigenetic explanations of behavioral differences are important should go ahead and do the research and show it.  I doubt very much that a demonstration of meaningful epigenetic effects would meet with any opposition in the behavior genetic community.  Epigenetics of behavior is behavior genetics.  Epigenetics and classical genetics aren’t at odds on a biological level, and there is no reason they should be at odds in social science.”

I have so many thoughts on this point that I’m actually not even sure where to begin, so I shall go in chronological order.

As I noted above, I found Moffitt and Beckley’s response to be both misguided and off topic. For example, they summarized our argument as follows: “In their original article, Burt and Simons (2014) argued that heritability studies should be abandoned because twin and adoption research is a fatally flawed paradigm. They pointed optimistically to epigenetics research as the way forward.” And, later, they summarized our argument as: “recommending…that criminologists should embrace epigenetics and abandon twin studies.” In short, not exactly. For the former, we focused on ending heritability studies because these studies are flawed conceptually and biologically, and we pointed to epigenetics research as demonstrating the biological fallacy of separate G vs. E influences, and how this new paradigm (postgenomic paradigm) might influence future biologically-informed social scientific work on crime. “Twin and adoption research” are not a “fatally flawed paradigm” because they are not a paradigm. Finally, to repeat (perhaps ad nauseam), we at no point called for an end to the use of studies with samples of twins.

Unfortunately, in our view, rather than engage with our critique, Beckley and Moffitt’s response piece was largely off topic to the debate about the utility of heritability studies. (E.g., Burt and Simons (2014) also suggested that the twin design is irreparably flawed. However, one of the most exciting future uses of twin data for criminology is the study of discordant twins…”). We did not discuss the use of twin sample and methods in general, which is why the value of MZ twin discordance studies is irrelevant. They then proceed to discuss the debates and difficulties in engaging in epigenetics research, which I don’t necessarily disagree with, but again irrelevant to our point. Moreover, at points it seems as though they are arguing that the difficulties (and challenges) of doing social scientific research that accords with current biological knowledge justifies or neutralizes studies that are mired in outdated (biological) knowledge. (Would they have us continue develop knowledge based on the model of the earth as flat following scientific evidence overturning this model because of the difficulties and complexities involved in changing paradigms?)

Neither Turkheimer nor Beckley and Moffitt speak to our primary argument about the flawed conceptual (biological) model of heritability studies nor its lack of utility at the present state of knowledge. And, Turkheimer’s point that epigenetics is behavioral genetics is immaterial. Our critique was avowedly not anti-BG. However, Turkheimer’s statement that “Epigenetics and classical genetics aren’t at odds on a biological level,” is simply not correct, see Meloni (2014a; 2014b) and Charney (2012a) clear and detailed refutations of this statement.

I must also register my surprise that a behavioral geneticist is taking social scientists who see epigenetic findings as relevant and promising to task “for not doing the research and showing it.” Missing heritability? And, this from the scholar who states: “Complex human behaviour emerges out of a hyper-complex developmental network into which individual genes and individual environmental events are inputs. The systematic causal effects of any of those inputs are lost in the developmental complexity of the network. Causal explanations of complex differences among humans are therefore not going to be found in individual genes or environments any more than explanations of plate tectonics can be found in the chemical composition of individual rocks” (Turkheimer 2011: 600). But, the nascent field of epigenetics needs to step up and show their results if they want to be in the discussion (?). Even so, there is, in fact, significant evidence demonstrating the effects of epigenetic differences on behavior (see my discussion here, drawing on a number of various sources, e.g., Landecker & Panofsky 2013; Weaver et al. 2006). To be sure, at this point much of this evidence is confined to non-human animals, yet, this is changing. Scholars are doing this work on humans, and evidence is beginning to accrue that “shows it” (the effects of epigenetic variation on behavioral variation).

(10) (Again, the tired tendency to paint us as anti-BG rather than focusing on the substance of our more focused critique). Turkheimer says we are wrong about GCTA studies. We present evidence; where is his? I have yet to come across one GCTA study that even remotely resembles the high heritabilities found in twin studies of complex social phenotypes. That is our argument. I am more than willing to revise my thinking in light of new evidence, but Turkheimer does not provide any (neither did Wright et al. who did not respond to our response to their use of GCTA studies of height as support for the validity of twin studies of social phenotypes).

Turkheimer concludes with the following: “So in conclusion:  if you want to cite me as a critic of some general version of BG, the citation should be limited to the idea that numerical heritabilities aren’t very important per se, and that studies that do nothing other than estimate them are no longer very important.  The next sentence should be something about how I do maintain that nonzero heritability is important methodologically, and that there are many scientifically useful things to do with twins other than just estimating heritabilities.  Better yet, be very specific about what it is I am supposed to have said when you cite me.”

Again, it seems that we are in total agreement. We did not and have not discussed Turkheimer as a general critic of BG, and cited him as indicating that numerical heritabilities are not very important. We were not able due to space limitations to include all the quotes from Turkheimer, but we did point the reader to the sources and pages where his criticisms of heritability studies were found.

After reading Turkheimer’s blog, I cannot seem but feel he wants to have it both ways. He recognizes and publicly states that heritability studies are not useful, and, yet, wants us to refrain from pointing that out because doing so is somehow anti-BG, anti-genetic, and anti-science and is tantamount to indicting all of genetically-informed social science as balderdash (and thus, makes the critique out of touch with scientific reality). Perhaps, before one can criticize heritability studies, one must first establish a record of supporting genetic effects and the BG enterprise (only insiders can criticize the method?)

In sum, Turkheimer’s critique of our critique is not without substance; yet, as with Barnes et al., Wright et. al., and Beckley and Moffitt, Turkheimer creates a general anti-BG argument out of our narrowly constructed heritability study critique. Rather than conceding that we are in agreement, which it does appear we are, Turkheimer makes our argument anti-BG and us anti-genetic. I find this both highly perplexing and frustrating as it seems to muddy the waters unnecessarily and confuse issues and models that are separate and distinct.

[a] I would like to note that I engaged in a series of pleasant emails with Turkheimer after he sent me a link to his blog, and it seemed that we shared some common ground and were both willing to (re)consider our ideas in light of new information.

[b] For example, Wright et al. (2015) stated: “Consider, too, the linguistic gymnastics used by Burt and Simons (2014, 2015) to claim that nothing positive ‘at the present time’ has come out of behavioral genetic research.” Speaking of impressive gymnastics, this entirely twists our argument to try to feebly come up with the value of heritability studies based on “behavioral genetic findings” and “biosocial data”. We stated that at the present state of knowledge heritability studies lack utility. We have yet to see a response (on point) to this critique.

[c] We should note that none of the authors to who responded to our critique in Criminology (JC Barnes, JP Wright, B. Boutwell, J.A. Schwartz, EJ Connolly, JL Nedelec, K.M. Beaver) have any degrees in the biological sciences.

[d] I will note that we had wished to include quotes from both Turkheimer and Rutter, but we were under strict page limitations. We asked if we could have extra space to include quotes from these to scholars, but this was not allowed.

[e] We noted clearly in our rejoinder, for example: “When it suits their purpose, Barnes et al. and Wright et al. wrongly broaden our critique to behavioral genetics and/or biosocial research generally. We have clearly noted throughout that the heritability study method, including its fallacious technical and conceptual assumptions, is the focus of our critique, not behavioral genetics or biosocial work in general.”

[f] Aside, we find our heritability study label much more interpretable and useful than Turkheimer’s seemingly preferred label “h-squared-equals studies” coined by his friend. This slight difference in conceptualization (or non-recognition of our conceptualization) can greatly impair communication and progress. Point of illustration, this occurs on occasion when my son is either trying be difficult so as not to engage with me or refusing to recognize my clear reference to something because I am not employing his (constantly changing) conceptual framework. In response to my request for him to (please) pick up your airplanes and put them away, he continues resting in his chair and responds, “there are no airplanes on the floor.” I point to the ones right in front of him. “Nope, Mommy, those are rocket ships.”

CITED REFERENCES:

Burt, Callie H., & Simons, Ronald L. (2014). Pulling back the curtain on heritability studies: Biosocial criminology in the postgenomic era. Criminology, 52, 223-262.

Burt , Callie H., & Simons, Ronald L. (2015). Heritability studies in the postgenomic era: The ‘fatal flaw’ is conceptual. Criminology 53: 101-112.

Charney, Evan. (2012). Behavior genetics and postgenomics. Behavioral and Brain Sciences 35:331–410.

Johnson, Wendy, Eric Turkheimer, Irving I. Gottesman, & Thomas J. Bouchard. (2009). Beyond heritability: Twin studies in behavioral research. Current Directions in Psychological Science 18: 217-220.

Landecker, Hannah, & Aaron Panofksy. (2013). From social structure to gene regulation and back: A critical introduction to environmental epigenetics and society. Annual Review of Sociology 39:333–57.

Moffitt, Terrie E., & Amber Beckley. (2014). Abandon twin research? Embrace epigenetic research? Premature advice for criminologists. Criminology 53: 121-126.

Turkheimer, Eric. (2011). Commentary: Variation and causation in the environment and genome. International Journal of Epidemiology 40:598–601.

Turkheimer, Eric. (2014). A phenotype null hypothesis for the genetics of personality. Annual Review of Psychology 65: 515-540.

Wright, John Paul, J. C. Barnes, Brian B. Boutwell, Joseph A. Schwartz, Eric J. Connolly, Joseph L. Nedelec, & Kevin M. Beaver. (2015). Mathematical proof is not minutiae and irreducible complexity is not a theory: A final response to Burt and Simons and a call to criminologists. Criminology 53:113–20.