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The "The Dialectical Biologist" account. Structural biology & anti-racism. Loves: birds, proteins, Linux, Lewontin Hates: race science, racists, transphobes

In her new book, The Genetic Lottery, Kathryn Paige Harden, professor of psychology at University of Texas at Austin, attempts the seemingly impossible task of showing that, despite a history of abuse, behavioral genetics is not only scientifically valuable but is an asset to the social justice movement. In this attempt, she fails twice. For the first half of the book, Harden tries to transform the disappointment of behavioral genetics in the years following the Human Genome Project into a success that proves that genes are a major and important cause of social inequality, like educational attainment or income levels. In the second half, she tries to show that this information is not a justification for inequality, rather it is a tool to use in our efforts to make society more equitable and cannot be ignored if we wish to be successful. To say the least, this section too falls short. Harden refuses to engage with the history and trajectory of her field, and ultimately the science fails to uphold the idea that not considering genetic differences hinders our attempts to create a more equitable world.
You must know the parable about the frog that sits in a pot of water being gradually heated, allowing itself to be boiled alive: because the change happens gradually, it never realizes it should leap out. Reading Kathryn Paige Harden’s book The Genetic Lottery: Why DNA Matters for Social Equality is a similar experience, as the author ingenuously points out. “Like a frog being slowly boiled alive,” she observes, readers follow her argument “from an uncontroversial premise to a highly controversial one.” Harden’s “uncontroversial premise” in this case is that siblings raised in the same family share a childhood environment and 50 percent of their DNA randomly assigned at conception, and are therefore like subjects in a controlled study of genetic differences. Ask anyone with a sibling whether their own childhood environment was the same as their sibling’s and you’ll quickly disprove Harden’s claim that her premise is uncontroversial. But putting that objection aside and sitting patiently as Harden increases the heat, we’ll arrive at her “highly controversial” assertion that “if siblings who differ genetically also have corresponding differences in their health or well-being or education, this is evidence that genes are causing these social inequalities.” Harden is a dedicated frog boiler. She introduces many comfortably room-temperature premises: measurement is essential to science; people differ genetically; genes caus
Yet in her effort to convince readers that genes matter, Harden overstates the degree to which they matter. She tells readers that, “in samples of White people living in high-income countries, a polygenic index created from the educational attainment GWAS typically captures about 10–15 percent of the variance in outcomes like years of schooling, performance on standardized academic tests, or intelligence test scores.” She compares this figure to that for household income, which accounts for 11 percent of the variance. What Harden doesn’t tell readers is that much more of the variance is explained by parental education: about 17 percent when only one parent is considered and over 20 percent when both are. The polygenic index for educational attainment therefore captures an underwhelming amount of variance in educational attainment and other socioeconomic outcomes — certainly not enough to justify putting it at the center of policy solutions. Harden expects that, as GWAS samples grow, the polygenic index will become more predictive, but exactly how it predicts educational attainment is not at all straightforward. Consider how Harden chooses to present the 10–15 percent figure, making it account for educational attainment through biological mechanisms. She tells her readers that the genes involved are expressed preferentially in our brains, where they increase the bearer’s intelligence, executive function, grit, and perseverance — the cognitive and non-cognitive skills rewarded in our educational system and labor market. What Harden doesn’t tell us is that these genes are also “expressed” in our environments. People with higher polygenic indices for educational attainment are both more likely to be raised by parents with higher socioeconomic status and to go to well-funded schools. A study of adoptees suggests that about half of the effect of the polygenic index operates through these indirect mechanisms. Harden acknowledges this complex
she does, and moving from ancestry groups to racial labels, she describes a near future in which we will have a polygenic score “that is as strongly related, statistically, to academic achievement in Black students as it is in White students.” [p. 191] (This conflation of an- cestry and race is particularly consequential when considering Black Americans, who vary greatly in their proportions of recent African and European ancestries, in ways that are correlated with both geography and economic opportunity (e.g., Micheletti et al., 2020; Baharian et al., 2016).) Harden warns the reader, however, that such comparisons be- tween Black and White Americans would be “scientifically and ethically wrong” [p. 192]. To explain why comparisons of genetic effects between groups are invalid, and will remain so even when polygenic scores have been constructed for both, she refers to statistical issues that arise from confounders and the lack of environmental homogeneity. But as we outline in our review, similar problems, differing in degree rather than in kind, apply to the move from within-family studies to standard GWAS. Harden interprets our charge that she is trying to have it both ways as somehow related to polygenic scores being “simultaneously meaningful. . . and limited, by virtue of their con- textual dependence and imperfect portability” , adding “As the author Maggie Nelson wrote: ‘There is a lot to be learned from having it both ways’ ”. In reality, we were making the point that she cannot overlook the effects of confounding when interpreting polygenic scores within European-ancestry GWAS individuals–let alone within the racial grouping of “Black Americans"–only to resurrect them when seeking protection against the implications of her claims for between ancestry-group comparisons. The truth is that polygenic scores for ed- ucational attainment are also confounded within ancestry groupings, in ways that greatly complicate interpretatio
In our view, these instances reflect a more general tension in the book, which arises from trying to have it both ways: to argue that PGS for educational attainment provide interpretable and meaningful predictions of inter-individual differences that reflect under- lying genetic causes, yet to claim that they have no validity beyond hypothetical ancestry group boundaries. As we have laid out, we believe instead that current PGS for educational attainment are neither interpretable nor particularly meaningful. GWAS undoubtedly cap- tures some causal genetic effects, i.e., more than confounding alone, and there is interesting science to learn from these initial findings. But we currently understand next to nothing about the causal paths from GWAS findings to educational attainment, notably the extent to which they include analogs of Jencks-style “red hair effects” and the legacy of accumulated indirect effects. That may not matter when PGS for EA are to be employed as a statistical tool in the study of the impact of local social interventions, but it matters greatly when they are used to elucidate, let alone redress, social inequalities. Given these limitations, we do not see what the field of genetics has to add to the conver- sation about redistributive justice, beyond confirming what has long been recognized–that life outcomes differ for all kinds of reasons beyond people’s control–and we very much doubt that overstating our understanding of the genetics of behaviors is going to increase empa- thy. As the author appreciates, there is a history of this kind of practice, invariably with nefarious consequences, yet every generation seems to believe that their technological twist will help them to avoid the same pitfalls. Despite its engaging narrative, the Genetic Lottery therefore leaves us unconvinced, and with the impression of genomics serving as a distraction from much more exigent political conversations
Importantly, in order for polygenic scoring to become a profitable and transformative industry, it doesn’t need to work. That is, these metrics do not need to pick out a class of people with a genuine propensity for virtue or vice, nor does screening an embryo for higher scores need to improve intelligence or law-abidingness. This biotech grift could become the latest trend in conspicuous consumption simply because enough people believe it works. It’s a question of our faith in predestination. An “ethics” industry has grown up around this prospect, focused on the fear that granting limited access to this technology (only to those who can afford it) will create a separate race of tall, athletic, beautiful, brilliant, and virtuous children, who would cordon themselves off from the dysgenic masses. The true function of such alarmism, as with discourses of “AI safety” and “existential risk,” is to reinforce the false inevitability of these technologies’ success. In fact, the stratified society being prophesied already exists—the children of the wealthy already live in a world apart. Everything from their healthcare to their schooling and experiences with the criminal justice system are fundamentally different from the realities of those with fewer resources. At no point in the present or future will maintaining this stratification require the wealthy or their children to be inherently healthier, more intelligent, or more virtuous. Hierarchy is a function of power, amassed within social, historical, and political structures, and resistance requires challenging the belief that social elites are truly the Elect.
Harden’s purported measure of criminality reveals another perennial failing of this scientific method. Respondents were asked if they had ever been arrested, convicted, or incarcerated, and their answers were taken to represent their innate predisposition toward lawbreaking (data for this question came from two US databases, Add Health and COGA). It is inexcusable not to know, or to pretend not to know, that who gets ensnared in the US justice system has little to do with innate tendencies toward violence or lawbreaking. (For excellent critiques of what Harden says—or leaves unsaid—about race, see M. W. Feldman and Jessica Riskin and Anne O’Connor et al.) If the US prison population in the last 50 or so years has grown from less than 100 per 100,000 people to more than 500, that is not because of a change in the population or its genetic makeup. A societal structure, created through a deliberate history of political decisions, determines these “trait values,” and in turn determines who will check yes when a geneticist asks them if they have been incarcerated. Changing this structure or this context would change the “genetics of sin,” which we can therefore see are not a transparent reflection of our nature.
How did they claim to distinguish nature from nurture? Consider just one item from Harden and her co-authors’ laundry list: “age of first sexual encounter.” Their study depends on the notion that the earlier this takes place, the more evidence we have that a person is innately driven toward general risk-taking by an absence of self-control. (A Christian morality pulls the strings behind the scenes of this science: where else does one derive the concept of abstinence as virtue?) Still, they make a noteworthy exception: “[W]e coded all individuals with responses below the age of 12 as missing [i.e., as providing no data on the question], as this could reflect childhood sexual abuse rather than earlier onset of sexual behavior.” One does not need to be a psychologist—in fact, maybe it helps not to be—to spot the shortcomings of this quick fix. Among other things, it is possible to be sexually abused at any age. Harden and her colleagues obviously recognize that they need to filter out this possibility, in order to even pretend their number is a proxy for innate virtue or vice, as opposed to external happenstance, but the data available provides no rigorous way of distinguishing nature from nurture.
Harden would consider herself opposed to all such political projects. Indeed, much of Original Sin consists of anecdotes and asides that check the right boxes to affirm her political leanings as a Good Liberal. Her project, in brief, is to argue that liberals, in order to accomplish progressive goals, must accept the existence of innate genetic predispositions toward scholastic achievement and criminality. This tactic mirrors a broadly adopted political strategy: appealing to liberals to argue that their political aims can only be realized by embracing the current obsessions of conservatives.
Evolutionary Psychology Yields Fascinating and Unexpected Findings. Evolutionary Psychology's Explanatory Powers. Posted June 29, 2009
The revival of the social sciences – inoculation against parasitic ideas and suicidal empathy, and the quest for consilience via the evolutionary lens Gad Saad1 Received: 29 September 2025 / Accepted: 24 November 2025 © The Author(s) 2026 Abstract To maximally flourish, the social sciences must be inoculated against parasitic ideas (e.g., postmodernism) and suicidal empathy (e.g., an epistemology of care), both of which arise when the pursuit of truth is confounded with social justice activism. Furthermore, the social sciences currently exist in disorganized if not incoherent silos of knowledge void of an organizing meta-theory. The evolutionary lens provides such a unifying framework whilst engendering the requisite consilience. Keywords Parasitic ideas · Suicidal empathy · Consilience · Evolution · Social sciences Over the past three decades, the social sciences have promulgated ideas that serve as a blitzkrieg on science, logic, reason, common sense, and the most fundamental fabric of reality. This first became evident in my early attempts to incorporate evolutionary psychology within the business school in general and marketing and consumer behavior in particular (Saad, 2007, 2011a, 2013). Most social scientists resisted the idea that the human mind is shaped by the exact same evolutionary forces that have forged every other species on earth. Apparently, evolutionary theory could be used to explain every single species on earth save one: Homo sapiens. This has been coined the human reticence effect (Ranney & Thanukos, 2011). Some social scientists are willing to concede that evolution might explain the evolution of our respiratory, digestive, and urinary systems but to use evolution to explain the human mind, well, that is pure anti-science quackery.
Fig. 1. Genome assemblies, annotations, and transcriptomes. (A) Species representing the four sugar-consuming groups. [Bird photos (top to bottom): Steven L. Hunter (ML426078561), David J. Southall (ML431374521), Gerald R. Allen (ML633429605), and Charles Davies (ML205719751); photos accessioned into the Cornell Lab of Ornithology | Macaulay Library] (B) Cladogram and diet of the birds included in the study. On the basis of the percentage of dietary nectar and fruit intake, we delineated four groups of core sugar-consuming birds (red font) and core non-sugar controls (blue). Core non-sugar control sets were defined as groups phylogenetically close to sugar-consuming clades and comprising a similar number of species but not taking any nectar in the diet. These were used as direct controls in the downstream analyses. (C) Comparison of genome assembly contiguity. The contig N50 value indicates that 50% of the assembly consists of contigs of at least that size. The nine newly sequenced birds are indicated with a blue circle. (D) Status of 15,133 ancestral bird genes, classified by TOGA as those with an intact reading frame (blue), with gene-inactivating mutations (premature stop codons, frameshifts, splice site disruptions, or deletions of exons or entire genes; orange), or with missing or incomplete coding sequences owing to assembly gaps or fragmentation (gray). (E) Status of 8338 near-universally conserved Aves genes (BUSCO, odb10) in annotations generated in this study (green circles) or NCBI RefSeq annotations. (F) Tissue-specific transcriptomes generated for pairs of sugar-consuming and non-sugar control species. Black arrows specify the direction of DESeq2 analysis (for details, see methods and table S11).
Pinker said that over the years he has regularly offered his linguistic opinions to Dershowitz for use in various cases. “I don’t recall his telling me that the question pertained to the Epstein defense,” Pinker said. “I was not aware of the charges against Epstein at the time. And no, I was not paid for the letter — it’s something that Alan and I do regularly, as colleagues.”
Begin forwarded message: > From: Richard Dawkins < > Date: July 4, 2011 5:42:43 PM EDT > To: John Brockman .‘Z > > Subject: Lawrence > John • > 1. I hope you recovered well from your operation. > 2. There is a rather nasty young woman called Rebecca Watson, who seems to be running some kind of a witch-hunt against Lawrence Krauss because of his defence of Jeffrey Epstein. > http://skepchick.org/2011/04/lawrence-krauss-defends-a-sex-offender-embarrasses-scientists- everywhere/ > There are people on her blog talking about organising a walkout when Lawrence speaks at TAM in Las Vegas. I remember that you told me something of the circumstances of Jeffrey's arrest, and that his case is not as black as painted. Might you possibly remind of it. > Thanks (and greetings from Jackson Hole, Wyoming) > Richard
The research will probably provoke controversy, both for its having been done and for its findings. What is clear is that if Hitler had seen these genes in anyone else, his verdict would have been unequivocal. Professor Turi King, the lead geneticist on this research, said: “If he was to look at his own genetic results, he would have almost certainly have sent himself to the gas chambers.”
The risk of stigma The scientists and documentary-makers are determined to ensure that the revelations are not used to stigmatise people with the conditions that are indicated by Hitler’s genes. While the genome was a factor in the making of Hitler, scientists and historians are clear that it was merely the canvas on which numerous other factors came together. These include abuse suffered in his childhood, trauma from the First World War and, above all, his contemporary context. In short, antisemitism is not genetic or symptomatic of these conditions. That was a societal ill, and in another time he could arguably have been a very different person. People will debate whether his genes were critical to his particular case, but there is little debate that Hitler was in the eye of a perfect storm of factors that led to his rise and his atrocities.
One formative influence was Watson’s making his one and only important scientific discovery when he was only 25. His next act flopped. Although “Watson’s [Harvard] lab was clearly the most exciting place in the world in molecular biology,” geneticist Richard Burgess, one of Watson’s graduate students, told the oral history, he discovered nothing afterward, even as colleagues were cracking the genetic code or deciphering how DNA is translated into the molecules that make cells (and life) work. ‘I really don’t know what happened to Jim’: Friends ask where James Watson’s odious attitudes about race came from “He fell flat on his nose on all these problems,” Harvard’s Ernst Mayr (1904-2005), the eminent evolutionary biologist, told the oral history. “So except for this luck he had with the double helix, he was a total failure!” (Mayr acknowledged the exaggeration.) By the 1990s, even Watson’s accomplishments at Harvard and CSHL were ancient history. Watson nevertheless viewed himself “as the greatest scientist since Newton or Darwin,” a longtime colleague at CSHL told STAT in 2018.
Ed Dutton (aka "The Jolly Heretic"), a white nationalist and race pseudo-scientist, pictured with James Watson.
1.1. Life as thermodynamics: it's disequilibria all the way down In their thermodynamic dimension living systems are staggering and wondrous Taj Mahals of disequilibria—writ in both structure and pro- cess; of intense and dynamic disequilibria in fact, precariously lofted high above the quiet repose of the equilibrium state. This is their essential
@eigenrobot: if H1Bs are supposed to be a means of obtaining Labor not available domestically it's curious they're cheaper than domestic labor. an easy way to ensure that they aren't directly substituting for domestic labor would be to add a $100k surcharge per head
Steven Pinker: Evidence that woke isn't dead, peer review is problematic, and science needs to address deep problems in its culture: A grad student at Harvard conducted the first systematic, data-based study to document & explain the rise in gender dysphoria. His paper was rejected from a leading journal because, among other things, "Throughout the manuscript, the authors use language that is considered prejudicial and outdated (e.g. "natal sex" as opposed to "sex assigned at birth"). It is critical to follow best practice and guidelines surrounding gender inclusive language particularly for research specifically on the topic of gender incongruence, expression, and identity."
A tweet from the official NIH account on X: Today #NIH is terminating more than $250 million in funding—including more than 400 grants—to Columbia University following directives from the Trump Administration’s Joint Task Force to Combat Anti-Semitism. The cancellations are due to Columbia University’s continued inaction in the face of persistent harassment of Jewish students.
Jordan Lasker, AKA ‘Cremieux’ One of the speakers at the conference is billed under a social media alias, Cremieux, but the Guardian has corroborated that the account is apparently run by Jordan Lasker, a long-time proponent of eugenics. The @cremieuxrecueil X account has been boosted or engaged with dozens of times by that platform’s proprietor, Elon Musk, often on the topic of falling birthrates.
Cremieux (a race science fraudster) tweets: DOGE has a very obvious feedback mechanism for its cuts. If DIGE makes a big broad cut against a million programs, people get upset about a few specific, very good ones like PEPFAR, and the program comes back because DOGE's members are, thus, informed it was good.
Arguably, a better use of the Royal Society’s global influence and that of its fellows would be to explain exactly how the measures touted by the US government could damage public health and the environment for decades to come.
My caution stems from something I have been thinking about for years—should science get involved in politics?
a, Schematic representation of the requisites needed to produce a Sierpiński fractal from hexameric blocks and the symmetry-based constraints on oligomeric assembly. Green and blue dots represent active or open interfaces, respectively. b, Cryo-EM density maps of Sierpiński triangles of the zeroth, first and second fractal level. The 6mer (3.1 Å) was derived from the hexameric Δ2–6 SeCS variant. The 18mer (3.9 Å) was derived from the wild-type (WT) SeCS. The 54mer (5.9 Å) was derived from the pH-stabilized variant H369R SeCS.
"Aspartic acid" and "Arginine"
Elon Musk: "can you believe that universities with tens of billions in endowments were siphoning off 60% of research award money for "overhead"? What a rip-off!"
An academic on Twitter/X complaining about scientists moving to Bluesky: "Yes... But, what about the impact on the wider society? If you exclude dissenting opinions and interactions, you starting to live in the Ivory Tower."
Editorial board of Intelligence, volume 107. The last volume before Haier resigned as EiC. https://www.sciencedirect.com/science/article/pii/S0160289624000801
Noah Carl tweeting "Lynn's estimate of the average IQ in Sub-Saharan Africa looks to be about right. This completely undermines the case for "reviewing" all his articles, let alone retracting them"
Logan Roy from Succession: "this is not the end; I'm gonna build something better"
On Exactitude in Science - Jorge Luis Borges
Lorikeet
a, The four types of trimers required to generate pseudosymmetric nanocages with T numbers ≥16, viewed in the context of the GI16-F7 design model. Icosahedral five-fold, two-fold and three-fold symmetry axes are indicated. b, Design models and corresponding building block stoichiometries of GI4-F7, GI9-F7, GI16-F7, GI36-F7 and GI64-F7 nanocages. The stoichiometries listed indicate the number of each kind of trimeric component. c, Graphical depiction of trimer stoichiometry as a function of T number. d, Theoretical nanocage diameters and Z-average hydrodynamic diameters measured by DLS as a function of trimer stoichiometry used during in vitro assembly (indicated by T number). Data are representative of two independent experiments. e, Cryo-electron micrograph of a sample containing GI9-F7 and GI16-F7 nanocages. Scale bar, 100 nm. f, Composition and design model of the GI16-F7 nanocage. g, The 14.9 Å resolution cryo-EM map of GI16-F7. Scale bar, 96 nm.