"Why biology is not destiny": an exchange | Kathryn Paige Harden, MW Feldman, Jessica Riskin, et al. (2023)

for the editors:

Marcus Feldman and Jessica Riskin didn't like my book. Or rather, they didn't like a book calledthe genetic lotteryby an author named "Kathryn Paige Harden", but her review [NYR, April 21] distorts my arguments so much that I have the strangest impression that Feldman and Riskin have somehow gotten their hands on an entirely different book, an evil double of mine. Therapists, parents, and unhappily married couples would recognize the feeling I had when I first read your review: It's annoying and confusing when someone argues about something you never said.

As a longtime reader ofDie New York Review of Books, I am surprised and disappointed that this review was published in such a respected magazine. Yes, "we all enjoy overselling syntactically inspired bile," to quote Zadie Smith, and Feldman and Riskin provide the bile. But I assume readers of book reviews not only want to revel in the pettiness, but are also interested in learning what a book is about. Here the Feldman and Riskin test completely fails. This quote from Smith is from his review ofmy pricesby Thomas Bernhard, of whom she wrote: "The gap between what actually happened and how Bernhard writes about it can variously be interpreted as either postmodern hoax or insidious paranoia".the genetic lotterysays and as Feldman and Riskin write about it is really too big, and no playful tone can be found.

Feldman and Riskin set out to slay three dragons: genetic determinism ("why biology is not fate"), genetic essentialism ("you are not your genes"), and genetic reductionism ("all phenomena are "not" linked". reducible"). 🇧🇷 They argue that these three "isms" are not supported by scientific evidence - and I wholeheartedly agree. In fact,the genetic lotterydevotes much space to describing why these three "isms" are false. As I summarized in the last chapter:

Much of this book has been taken up by these arguments. We shouldNointerpret genetic influences as deterministic. We shouldNoRenunciation of the possibility of social policy causing social changes. We shouldNoconfuse an outcome that is socialestimatedwith a human beingof value.

Passages like this, which directly contradict his characterization of the book's supposed determinism, reductionism, and essentialism, are easy to find! But Feldman and Riskin ain't here to do nothingthe genetic lotteryit says. Rather, their aim is to discover what they see as the obscure and repressed meanings of my book, which they feel are being masked by my ignorance and duplicity. Throughout the review, I am portrayed as the ignorant fraud of false consciousness ("behind Harden's protests...") or worse, a liar ("with an admirable poker face, writes Harden..."). The possibility that I'm serious doesn't enter the picture. The hermeneutics of suspicion has its place, I suppose, but as Paul Ricoeur has said, hermeneutics is animated by a "double motivation: willingness to suspect, willingness to listen." You forgot the listening part.

In addition to grossly distorting my book's arguments, Feldman and Riskin also cast their cautious eye on a variety of common scientific concepts. In his narrative, the "normal" distribution, first described decades before Galton by a mathematician who studies errors in astronomical observations, is a "founding axiom of eugenics". They write about measuring personality differences in a conspiratorial tone more associated with Reddit discussions of the Deep State. They dismiss the importance of random assignment of causal inferences as "smoke bubbles". There would be little left of the behavioral and social sciences if everything that Feldman and Riskin considered dubious were removed.

But maybe they want to get rid of all the behavioral and social sciences? We could go back to that more innocent time, when scientists didn't confuse cabbage with royalty, when behavior was understood only as "social practices" and devoid of any reference to biology. You know, the good old days, when autism was blamed on "refrigerator mothers" and homosexuality on rulers, when schizophrenia was the result of familial "double ties", when psychotic patients suffered from late-stage syphilis with no options of treatment.

There's no arguing with anyone dedicated to paranoid reading, and no doubt Feldman and Riskin will respond to this letter with further distortions about how my book should "really" be interpreted. Fortunately, I trust readers. Based on the hundreds of emails and comments I've receivedthe genetic lottery, people are more than capable of appreciating and engaging with the book's arguments. To quote from an (anonymous) reader comment:

As someone with a gene-affected chronic disease (T1D) and the mother of a child with a genetic syndrome and its attendant disabilities, I would like someone to wade into the tricky waters between right-wing eugenics and a refusal to take genes into account. so important to life outcomes on the left. It's impossible to live a life where genes have such an obvious and significant impact without feeling honestly let down on both sides. that, on the one hand, we must accept our inferior status and try not to further contaminate the human race with our filthy genes, or, on the other hand, we have certain access rights defined by physical limitations, but never relate them to genetic causes of as politely as society, or to mention the gaps this refusal creates in our ability to live well.The Genetic Lotteryy … elegantly discuss how the genetic causes of social outcomes can be addressed within a framework of justice and human rights.

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At the end of their review, Feldman and Riskin concede: "It is true that genes shape people and people create social and cultural situations." that genes shape people? What aspects of human beings are shaped by genes? And what should we do with new scientific knowledge about how genes shape people, especially if we are to avoid the evils of eugenics? Exactly these questions arisethe genetic lotteryAdresses. Read it for yourself and decide.


Kathryn Paige Harden
psychology teacher
University of Texas at Austin

for the editors:

In the April 21, 2022 issueThe New York Review, M.W. Feldman and Jessica Riskin Publish a Hostile Review of Kathryn Paige Harden's Latest BookThe genetic lottery: why DNA matters for social equality🇧🇷 The review contains some arguments that don't make sense to me and deserve refutation.

Let's discuss the genetics of educational achievement (AE), defined as the number of years of schooling and measured in adults over 30 years of age. EA occupies a good part of the book and the review. Using genetic data from more than 300,000 people of European descent, it was possible to develop a "score" using the genomes of the people in the study. The details of the score are of minor importance, but it is important to realize that the score is a single number calculated from a genomic sample according to a defined recipe. The score correlates with the EA at an extremely statistically significant level. This result was replicated in an Icelandic study, using completely different people from the first study. Once again, extremely significant results were obtained.

How do Feldman and Riskin explain these results? After a somewhat disjointed diatribe in which they complained that decisions were made on the details of scoring and how exactly the AS phenotype was chosen for study, they concluded that "the researchers [did] do nothing but count their own projections." . How is that reasonable? A prescription is given, verified in another study and the results replicated. (By the way, just this month, a much larger study of over 3 million (!) people was completed and the results were replicated again.) Are we somehow to believe that experimental error in Iceland correlates with the EA of a sample? This is really absurd.

The score has other interesting features. The average has been declining in Iceland since at least 1910, and the score is highly correlated between mating pairs, an effect much stronger than the EA correlation. This argues that the score makes sense without making the meaning clear. Technically, the work on AS is a little different from size genetics studies, and if we were to take Feldman and Riskin's criticisms seriously, it would invalidate a huge chunk of modern genetics, which routinely finds that complex traits are weakly associated with multiples. genetic locations.

Feldman and Riskin also attack Harden for claiming that the score will be distributed normally. The claim that a trait follows a bell-shaped curve is "a founding axiom of eugenics". This is an association guilt plea. The score is a sum of small values ​​that are independent of each other, and any geneticist or statistician would expect the distribution to be approximately normal. In a given study, it is trivial to check the normality of calculated values.

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This classification is confusing. Feldman is a leading mathematical biologist at Stanford who I would assume understood statistical genetics, but if I didn't know who the reviewers were, I would have considered them incompetent or ignorant. Perhaps Feldman and Riskin think that any argument is acceptable as long as it is against outcomes they don't like?

Nick Patterson
Department of Human Evolutionary Biology
Harvard University Cambridge, Massachusetts

To the editors:

MW Feldman and Jessica Riskin rightly point out the many errors and misinterpretations in Kathryn Paige Harden's new book, but seem to dismiss all efforts to identify genetic contributions to complex behavior, going so far as to suggest that studying genetic contributions to life is somehow equivalent to comparing a copy of the Krebs Cycle with a copy of ShakespeareKönig Lear.


How, then, are these experiments of nature to be understood as Williams-Beuren syndrome, a rare congenital genetic disorder caused by a deletion of twenty-six to twenty-eight genes on chromosome 7 and characterized by distinctive facial features, cognitive and cardiovascular dysfunction? , and more interestingly, extreme social friendliness and an engaging extroverted personality? Structural variants of genes identified in the syndrome have also been found to be associated with stereotyped hypersociality in dogs and are implicated in behavioral divergence in dogs and wolves.

Of course, breaking down complex behavioral phenotypes into components that best relate to genetic risk is a difficult task, but it's not crazy and a more nuanced review of the literature would bring more respect to this area.

Victor I. Reus, MD
Dear Professor Emeritus
Department of Psychiatry and Behavioral Sciences
University of California at San Francisco School of Medicine
UCSF Weill Institute for Neuroscience

To the editors:

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MW Feldman and Jessica Riskin in their excellent, well-written and entertaining review ofthe genetic lotteryby Kathryn Harden allude to but do not specify how a person's environment can be functionally and scientifically defined. Such a definition is central to the nature-nurture debate and to any discussion of genetic influences on behavior.

I think Feldman and Riskin, let alone anyone else who talks about the environment, would benefit from a behavioral view.proximityas "all stimuli that affect behavior at a given point in time" rather than the generally accepted and general one which is "the environmental conditions in which a person, animal or plant lives or works".

The behavioral view of the environment has three important implications: 1) the environment is not just our surroundings, but also within us because there are stimuli (pain, proprioception, etc.) that reside in our body and affect our behavior; 2) The environment is in constant flux, as it “comprises all the stimuli that influence an individual’s behaviorany time“, meaning that the environment changes from moment to moment; and 3) no two individuals can ever have the same environment, not even identical twins.

Up until the last point, my mother always asked me how my two brothers and I could be so different despite growing up in the same environment. Now I know she meant same parents, same house, etc. But according to a behavioral view of the environment, we don't grow up in the same environment because a person's environment consists of all the stimuli that influence behavior from moment to moment. And although this environment begins only marginally in the last trimester before birth, the number of responses and stimuli explodes and expands exponentially at birth. Given the incredible number of possible behavioral responses and stimuli with which those responses can interact, any genetic explanation of human behavior in relation to the environment takes a backseat. As Feldman and Riskin wrote, "Living things constantly interact with their environment in ways that transform both at every level."

To the behavioral view of the environment we can add the discovery of how stimuli affect behavior as antecedent events (eg, discriminatory stimuli) and, more importantly, as (reinforcing) consequences, which determine whether and how antecedent stimuli affect behavior. or attenuate). 🇧🇷 This conception of the environment and a selective view of how consequences cause behavior has proven to be a much more productive avenue for research and, perhaps more importantly, for interventions to change behavior in sometimes dramatic ways.

Of course, genetics cannot be ruled out entirely, as the ability of an organism's behavior to be influenced by the environment is a function of the species' evolutionary history and genetic make-up. However, a functional and scientific conception of the environment can largely neutralize any biological or genetic claims of behavioral causality.

Henry D Schlinger Jr.
Institute of Psychology.
California State University, Los Angeles

M. W. Feldman e Jessica Riskinreply:

Kathryn Paige Harden accuses us of selective reading, but she is a careless reader herself. First she writes that we accuse her of “genetic determinism”. But we didn't do that anywhere in our test. We have been as careful to acknowledge her rejection of genetic determinism as she periodically poses it in her book. Although we do not quote the passage she gives in her letter, we quote a similar one that appears on page 46: “A person's genetics may notdetermineYour life accomplishments, but they still involve, among other things, becoming hundreds of thousands of dollars richer at the end of your working life.” not a reductionist, but "; or we might as well have said that his essentialism is of the "I am not an essentialist, but" type. Another example: "Genetic happiness is intertwined with other differences" (page 43), but "Can we really say that the geneswellyou get richer (Short answer: yes)” (page 44).

When she says that we describe the "normal" distribution as "a founding axiom of eugenics", Harden misunderstands us. Indeed, we wrote that the assumption "that there are intrinsic personality and cognitive traits whose distribution in a population follows a bell-shaped curve" was a founding axiom of eugenics - not, of course, the normal distribution itself, which is not an axiom of any kind, eugenic or not.

Harden also misquotes us when he writes that "we recognize that 'it is true, genes shape people and people shape social and cultural situations'". It omits a crucial word. What we wrote was that “GeneHelpTrain people”, hardly an important “confirmation”; neither we nor anyone else would likely deny that.

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Interestingly, Harden says we seem nostalgic for a "more innocent time" in the "good old days". This is surprising: we didn't think our historical sketch of eugenics and scientific racism in the 19th and early 20th centuries could feel nostalgic. At the same time, it is interesting to note that the very diseases and traits she lists that were much more poorly treated in those times - autism, homosexuality, schizophrenia, psychosis and syphilis - seem to be good examples of a principle on which we have made progress in our analysis: Genes don't do everything. We agree that many now see these human phenomena in a better light than before, but this is not due to behavioral genetics or sociogenomics.

Finally, Harden asks whether we reject the psychological and behavioral sciences. We don't: we reject those areas of psychology and behavioral science that claim a false reduction of complex social phenomena to genes. Fortunately, we know that some researchers are following better and less reductionist lines of research in this area. The intrinsic and extrinsic aspects of people in social situations are not fixed and distinct, but are constantly molding and changing, so there is no fact about what causes what. It's not that these situations are too complex for us to figure out how much is intrinsic and how much is extrinsic, but the question itself is meaningless. How much does the California coast owe to the Pacific Ocean and how much to the North American continent?

Overall, Harden's letter confirms what we said in our analysis: while it rejects essentialist, racist, and eugenic notions, it asserts a new version of the old illogic it has long supported.

Nick Patterson's arguments are irrelevant. First, regarding polygenic scores for "educational attainment", he writes that they are calculated "according to a fixed income". OK, but assuming this recipe isn't from the burning bush, it must have been written by someone who made a lot of interpretive decisions, as we said in our review, like which single nucleotide polymorphisms to consider, how to weight and aggregate, and what definition of "educational qualification" " to adopt. Patterson mentions "school years". Dissatisfaction with this parameter has led several institutions, including the US Census Bureau, to replace it with "highest school diploma or highest degree obtained".

These parameters also contain (like all parameters) ambiguities and interpretive assumptions. What kinds of schools, for example? The Census Bureau generally includes “vocational” but not “vocational” training and allows training in chiropractic but not automotive mechanics or aircraft maintenance. The main study cited by Patterson (Okbay et al. 2016) draws on many surveys carried out in different countries, all with different education systems and definitions of "level of education" and uses a UN framework to express the results in "years of Education" . In short, Patterson's "fixed recipe" hides many layers of underlying social theory.

Next, Patterson emphasizes that polygenic risk scores correlate with “education level” to a statistically significant degree; he actually says that these correlations are "extremely significant". Since "huge" is not a technical term, it's hard to guess what he meant by that. “Significant” has a technical meaning in statistics. Just as correlation is not causation, 'significant' does not mean 'important' or even 'relevant'. A "significant" effect is an effect whose p-value - or the probability that it results from pure chance - is less than a specified value. Consequently, it may still be insignificant and/or causally irrelevant.

In fact, data mining can even extract highly "significant" correlations that "explain" a set of randomly generated dependent variables using a set of randomly generated independent variables. The three studies Patterson mentions actually use data mining techniques to develop what he says are polygenic indices of "educational achievement" and establish several weak correlations between the latter and the former. Of course, we never deny that such studies do this; As we said in our review, the field of sociogenomics is devoted to establishing statistical correlations between social outcomes according to different interpretive definitions and aggregates of up to many thousands of single nucleotide polymorphisms. Our point is that there is no reason to believe that these statistical correlations have causal significance.

Patterson writes that our critique "would invalidate a huge chunk of modern genetics". Again, we're not going to question what he means by "enormous," just reassuring readers that our rating ofthe genetic lotteryshould not replace modern genetics. For some physical traits, such as height or body mass index, polygenic scores are associated with a significant fraction of the variance. Even in these cases, the traits are clearly compatible with the environment, and there is no fact about how much of the variation is due to genetic or environmental factors due to the interaction between the two, as demonstrated by Richard Lewontin. Indeed, we would question any claim to show specific genetic causes for such traits based on polygenic scores. Fortunately, such claims make up what we believe to be a less than huge part of the field.

Finally, Patterson doesn't think we're questioning the idea of ​​a polygenic score that follows a bell-shaped curve, writing that "the score is a sum of small values ​​that are largely independent, and any geneticist or statistician would expect the distribution to be approximately normal." .” He says that only someone incompetent or statistically ignorant could dispute that. But our point is ontological, not statistical. The question is not whether a sum of small, independent values ​​is likely to follow a normal distribution. The question is whether there is any reason to believe that such a sum can have a significant relationship with the cognitive, psychological, social or behavioral aspects of people.

Here's an example to illustrate what we mean: We found some letter writers tooThe New York Reviewto be convincing, while others are biased. No doubt, with the right genetic database and using our definitions of persuasive and biased letter writing, we could produce polygenic scores for all, made up of many independent variables. On this basis, a competent statistician could compare the distributions of persuasive and biased letter writers with theDie New York Review of Booksbe bell-shaped. But such punctuation would be an invention without causal significance and would not help the editor to explain the appearance of biased letters.

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Victor Reus invokes the rare disease Williams-Beuren Syndrome, which has a known and relatively simple genetic cause. There is no doubt that even simple genetic abnormalities can have many phenotypic consequences; this is called pleiotropy. But this is a very different situation, even a little opposite to what the authors of polygenic scores claim. In Williams-Beuren and other similar syndromes, differences or deletions in one area of ​​the genome cause many effects throughout the body. On the other hand, the authors of Polygenic Scores claim that clusters of small differences along the genome have specific effects on complex phenotypes.

Polygenic risk scores "do not [break] complex behavioral phenotypes into components." Instead, they associate complex behavioral phenotypes with aggregates of thousands of single nucleotide differences. Furthermore, genomic association studies of social behavior phenomena such as "educational achievement" link only a small fraction of the variation between individuals to single nucleotide differences, and there is no reason to believe that these differences are causal.

Henry Schlinger makes an important point, not just for human behavioral traits, but for evolution in general. Richard Lewontin challenged the neo-Darwinian assumption of a fixed environment, pointing out that organisms constantly construct and change their environment through their own behavior and social interactions. This idea was formalized in a series of articles and a 2003 book.niche construction, by F. John Odling-Smee, Kevin N. Laland and Marcus W. Feldman;Natureit's atAnnals of the Royal Society B🇧🇷 The "extended evolutionary synthesis" framework incorporates this mutual and ongoing transformation of organism and environment into the evolutionary framework.


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