The following guest post comes from historian of science Gregory Radick, author of the 2023 book Disputed Inheritance: The Battle over Mendel and the Future of Biology, which was nominated for the British Society for the History of Science’s 2024 Pickstone Prize (“awarded every two years to the best scholarly book in the history of science [broadly construed] in English”), and historian of science Sander Gliboff, who reviewed Radick’s book in the Journal of the History of Biology (here). Here Radick responds to Gliboff’s review, followed by a further response from Gliboff.

The Weldonian curriculum and the history of genetics that might have been: An exchange on Disputed Inheritance

Gregory Radick and Sander Gliboff

From Gregory Radick

In Disputed Inheritance: The Battle over Mendel and the Future of Biology (Chicago: University of Chicago Press, 2023), I offer a new history of the early-twentieth-century debate now known as the “biometrician–Mendelian controversy.” On the one side were the Mendelians, led by the Cambridge biologist William Bateson, who championed Gregor Mendel’s 1866 pea-hybrids paper as a scientifically and socially revolutionary basis for understanding heredity. On the other side, the most formidable and far-reaching critique of nascent “Mendelism” came from the Oxford biologist Walter Frank Raphael Weldon, who objected to the Mendelian sidelining of the role of environments, internal and external, in the making and modifying of inherited characters. My thesis is that the Bateson–Weldon confrontation should be regarded as a hinge event in the scientific past, when biology came much closer than previously recognized to taking a consequentially different path than it actually took. On our timeline, of course, Bateson won, with the result that the body of knowledge he renamed “genetics” has come to be organized around the Mendelian entity par excellence, the character-determining gene. Even now, in the era of epigenetics and post-genomics, students begin their studies in heredity by learning that a pea seed is yellow or green, or a child has cystic fibrosis or not, depending only on which gene variants are present at a single locus. Yet this persistently Mendelian organization was not, I suggest, inevitable. On the contrary, it was an accident of history – in particular, Weldon’s dying suddenly from pneumonia in the spring of 1906. Had Weldon instead lived long enough to publish the book on heredity that he was near to completing, his contrasting emphases – on variability beyond the binary, and on the context-dependent interactions which bring about that variability – could well have become the taken-for-granted building blocks of an education in genetics.

Before my book’s publication, I reckoned that the foregoing, in its content (skeptical about a widely cherished intellectual heritage) as well as its form (a what-might-have-been or “counterfactual” argument), would provoke some demurrals – and so it has. I want here to address one of them, in a review of the book in the Journal of the History of Biology from the historian of biology Sander Gliboff.¹ I’ll structure my remarks around the review’s final paragraph, about an experiment in genetics pedagogy that University of Leeds colleagues and I undertook in the autumn of 2013.² Gliboff writes:

In what follows I’ll give Gliboff’s closing question and statements expansive consideration. I hope that in doing so I can usefully throw light on an experiment which has attracted attention within as well as beyond the history and philosophy of science.³ But I also hope to advance discussion more generally on the range of issues that my book raises, and to that end I’m the more grateful to Gliboff for the initial engagement and now for this further exchange.

To start with his question:

But how uniquely Weldonian is that? Gliboff writes about the curriculum experiment as unconnected with my counterfactual thesis except as a loosely tethered afterthought. But, as set out in the book, the whole rationale for the experiment was to put that thesis to empirical test. I hit upon the idea of teaching introductory genetics as if it had emerged from a might-have-been Weldonian past not because I saw a gap in the genetics curriculum market but because I wanted to know whether a science organized around Weldon’s emphases would have been viable. My hunch was that it would have been, and indeed that people educated within it would be less prone to genes-are-destiny exaggerations in their thinking about inheritance than people educated within a start-with-Mendel’s-peas curriculum. To reverse a well-known slogan from the philosopher of science Hasok Chang, the curriculum experiment was an exercise in science as complementary history and philosophy of science.⁴

It’s unfortunate that Gliboff not only omits to mention my reasons for conducting the experiment but misquotes a passage from the book in which I try to convey my excitement about thus enlarging the historian of science’s toolkit. He describes my book’s third and final part as “the ‘non-straightforward’ (as Radick calls it) portion of the book, which deals with what might have been, if only Weldon had lived to publish a finished theory.” In fact what I wrote was that much of the third part, probing the overall significance of the Mendelism debate, is “straightforwardly historical,” and I gave a paragraph full of examples, on everything from Mendel as a hero of American eugenicists to the role of the Cold War in publicizing worries about Mendel’s data. But, I go on, there are “un-straightforwardly historical elements in the mix too,” including my discussion of the curriculum experiment, whose positive results enter into my argument as evidence for the teachability of Weldon’s science.

Why the fuss over Weldon? Not because he was unique in his biological preoccupations (far from it, as I stress), but because, at the very moment and in the very milieu in which emphases on unit-character binaries and exclusively germinal causation got locked in as foundational for “the century of the gene,” as Evelyn Fox Keller famously called it, Weldon supplied not only criticism but an alternative.⁵ Readers can compare Gliboff’s account of my aims in concentrating on the Bateson–Weldon debate (“[Radick] wants a Weldon for our times, too, and real vindication of a scientifically and morally superior, non-gene-centric approach”) with my own account, in a passage directly after the misquoted one:

For all that I aspire to cast the debate over Mendel in a new light, I also want that light to shine on more general themes in the study of human knowledge…. One theme has to do with the organization of a body of knowledge, and the cascading consequences – for everything from individual cognition to scientific advance to social justice – of some items of knowledge coming to be treated as central, exemplary, subordinating and others as peripheral, exceptional, subordinated. Part of what makes the Bateson–Weldon debate worth thinking about historically is the complex way in which Weldon’s emphases have become both thoroughly integrated and thoroughly marginalized. (p. 13)⁶

The Weldonian curriculum came into being, then, as a test of the might-have-been potential of a Weldonian organization for what we now call genetics, and I wrote about the experiment in exactly that spirit in Disputed Inheritance. There’s nevertheless room for disagreement about whether, in line with Gliboff’s doubts, the curriculum deserves the epithet “Weldonian.” Here I think it’s helpful to distinguish two questions. One is whether, for purposes of devising that curriculum, contact with historical Weldoniana is necessary. Yes, I came to the curriculum via that contact, and so, by calling the curriculum “Weldonian,” I gave credit where, autobiographically, it was due. But might not other people, knowing nothing of Weldon, have devised something like the same curriculum? Of course they might have, as my collaborator and co-author Annie Jamieson and I acknowledged in our 2017 paper on the experiment. As we wrote there:

Needless to say, as a matter of principle, no one should need Weldon’s example in order to construct a curriculum along the variability-and-context-emphasizing lines of the Leeds curriculum. A devoted reader of the collected works of Richard Lewontin and Evelyn Fox Keller would be well placed and well motivated to come up with more or less the same thing. Other routes to the same destination run through the small but scorching critical literatures on the defects of “dominance” talk, “gene for” talk and overreliance on monogenic traits in genetics teaching. There is even a growing international body of work exploring the links between persistent genetic determinism and persistently Mendelian ways of teaching, talking and thinking about genetics. Yet in practice Weldon’s example has been indispensable. Perhaps determinist Mendelism is so pervasively a part of what biology has become that the only way truly to escape its grip is to learn from thoughtful, well-informed people who were never in its grip in the first place—from, that is, contemporary critic-witnesses such as Weldon. (It is striking that Fox Keller’s The Century of the Gene, volubly brilliant on why the old gene concepts and language must go, fell silent on what should replace them.)⁷

The other, more substantive question around the term “Weldonian” is whether the tested curriculum is a plausible surrogate for what would now be taught in biology had it taken a Weldonian rather than Mendelian turn in the early twentieth century, especially given Weldon’s allegiance to Francis Galton’s law of ancestral heredity. On Galton’s law, the average hereditary contributions of ancestors to their descendants are expected to halve with each passing generation without ever going to zero. I’ll consider this question under the heading of Gliboff’s next statement.

[Weldon’s] ancestral heredity surely is not part of the program. Behind Gliboff’s sweeping dismissiveness lies, it seems to me, a mistaken view of what happened to the law of ancestral heredity after 1900, in general and in Weldon’s work in particular. As other commentators have noted, ancestral heredity wasn’t so much annihilated by Mendelism as absorbed into it, along exactly the integrate-and-marginalize lines flagged above and elaborated more fully in my book.⁸ So any program with the ambition of inverting center-periphery cognitive relations under Mendelism surely should give serious attention to ancestral heredity. But in a Weldonian version of such a program, that attention won’t result in rigid adherence to the law as Galton formulated it in 1897; for as I show in Disputed Inheritance, from mid-1904, Weldon began to do for Galton’s law what Bateson had previously done for Mendel’s “law valid for Pisum.” In Bateson’s Mendelian publications of 1901‒2, he revised Mendel’s own priorities, promoting Mendel’s physiological explanatory hypothesis about gametic purity as his primary achievement, and demoting the law valid for Pisum, A + 2Aa + a, to secondary, sometimes-it-holds-and-sometimes-it-doesn’t status. Likewise, Weldon in his Theory of Inheritance manuscript and associated lectures took Galton’s now little-remembered views on the context-dependent expression of germinal determinants to be the cornerstone of the Galtonian theory, with the law of ancestral heredity, 1 = ½ + ¼ +…, understood as something that held in canonical form only under specified conditions.⁹

For Weldon, what was most important about the law as a Mendelism-corrective was its making conspicuous the prospect that, with more refined descriptive categories, a time frame extending back many generations, and an inclusive attitude towards the causes impinging on the development of characters, otherwise elusive patterns could be not just identified but explained. Accordingly, this take-home has figured in the genetics lecturing that I’ve been doing recently at Leeds, notably in a segment on “penetrance” and “expressivity” in our first-year module. Textbooks tend to depict the roles of genetic background, environment, and developmental noise as complicating factors which obstruct a dominant gene variant from being completely penetrant and invariably expressed, invoking them in a blanket way to explain why, say, only 65% of people with a mutation “for” polydactyly will show some form of it, and why, within that sub-population, myriad forms get expressed. But – and as the students by this point in the lectures will, I hope, appreciate – complete penetrance and invariable expression don’t much happen outside of textbooks; and when they do, it’s because genomic and extra-genomic contexts are enabling in ways that should inspire our curiosity. Indeed, I suggest, maybe, with help from more fine-grained taxonomies etc., new facts can be discovered as to just why individuals fall on one side or the other of a percentage boundary, why that boundary is where it is, and why a character takes the particular form it does in particular individuals.¹⁰

Of course no one can be absolutely certain that, on the timeline in which Weldon lived to publish his book, an introductory course on heredity given in the 2020s would have included something like the above. But absolute certainty is far too stringent a standard to apply to historical knowledge that bears, as here, not merely on what happened in the past but on why it happened, and so, by the logic of causal explanation, on what might have happened instead.¹¹ We can only judge plausibility, availing ourselves of the best evidence that we can find while keeping alert to the range of benefits that counterfactual reasoning can bring.¹² Last year, after my lecture touching in Weldonian fashion on penetrance and expressivity, a student came up afterwards to say that polydactyly ran in his family, and that its expression was indeed remarkably variable. Without wishing to make too much of it, I was glad that my Weldon-prompted departure from the usual script gave him the plainly novel opportunity to see and hear his condition represented not as a generic “genetic defect” but as something fascinatingly, and instructively, complex.¹³

Modern embryology and developmental genetics have many other sources. Quite so; see above as to why Weldon does and doesn’t matter.¹⁴ Early in his review Gliboff asks: “why does so much depend on the outcomes of this dispute—as if two individuals in one country embodied all the available responses to Mendel, and everyone has to get on either the Bateson train or the Weldon”? But I don’t remotely suggest that Bateson and Weldon’s contemporaries saw themselves as siding with either the one or the other. Rather, their dispute stands out as decisive not when we look forward from their present but when we look back from our present, as inheritors of knowledge still organized along the Mendelian lines that Bateson so pioneeringly and effectively campaigned for – knowledge in which “gene for” binaries are considered basic and phenotypic plasticity a special case.¹⁵ If we want to understand how this situation came about, our inquiries will eventually take us to Britain in the early twentieth century, where Bateson transformed Cambridge into the headquarters of what he early on proclaimed as a revolution. For the most part, when people in Europe, the USA and beyond got interested in Mendelism, they learned about it from Bateson and his group, at secondhand or thirdhand if not at firsthand.

Exactly when the locking-in of the Mendelian organization which Bateson invented and advocated for was completed is hard to say. But I interpret Bateson’s own wobbles in the face of Weldon’s criticisms in 1905–6, as documented in Disputed Inheritance, as a sign that there was still play in the system at that time. And Weldon put those criticisms because, knowing about the latest advances in German experimental embryology, and welcoming their congruence with the Darwinian-Galtonian perspectives on variation, development, and environments that were second nature to Weldon but that Bateson had repudiated, Weldon was singularly scandalized by what Bateson was doing. So if we ask not just how the Mendelian organization of twentieth-century knowledge of heredity came about but why, then we need to know whether an alternative organization was a live option in the relevant time and place – and that leads us to Weldon. In his biological commitments he was mainstream; but no one else in a position to affect the future organization of the science of heredity sought to hammer those commitments into a case for treating patterns like those for spine length in the waterflea Daphnia (dependent jointly on lineage ancestry and water quality) as generally exemplary of inherited characters, with Mendel’s-pea cases – in which almost all ordinary sources of variability are absent – treated as illuminating exceptions.¹⁶ To continue with Gliboff’s metaphor: since the Weldon train never left its station, a ticket to ride on the Bateson train ultimately became the only way in to the science of heredity. Once on that train, passengers could think, say, and do all sorts of things. But they had no choice about their starting point, or about the legacies they carried from that earliest part of the journey – legacies that became most powerfully manifest less in research settings than in pedagogic ones, formal and informal. In Disputed Inheritance, I wrote that, by 1915, a thoughtful Mendelian was indistinguishable from what a thoughtful Weldonian would have been like “until, that is, it was time to teach students, or give a public lecture, or write a popularizing book or article, or provide expert testimonials to judges or legislators seeking to put genetic determinism into eugenic practice. Then, often though not always, the character-maker gene concept, in all its cut-to-the-chase simplicity, came to the fore” (pp. 363–364).

On the whole, Gliboff’s complaints about my book’s counterfactualism seem to me directed at a book in which that statement doesn’t appear. He doubts that chromosomal dynamics could have been fully unpicked under, and then made compatible with, interaction-emphasizing Weldonism. But to the extent that the unpicking depended on crossing with purified breeds, it would have taken place, since that technique would have retained its status as a research tool (without, however, being elevated to the role of window-opener onto heredity, as it was for Bateson); and to the extent that the upshots challenged whatever became of the law of ancestral heredity, the law would have been flexibly reinterpreted (while still helping students to keep their eyes and minds on the long run of a lineage for clues to what’s going on). Gliboff takes me to task for not allowing for the counterfactual possibility of “Weldonians moving in a Mendelian direction;” but under a Weldonian dispensation as conceived in the book, someone anchored educationally on gene-environment interaction patterns going on to specialize in Mendelian patterns would be no more dramatically upsetting of the Established Order than someone educated Mendelianly going on to specialize in spine length in Daphnia. He bats away my discussion of Mendelism in eugenic propaganda as “moralizing” because, he says, the norm-of-reaction concept would have proved just as handy. While I believe that any science can be made consistent with any politics, that’s a long way down from believing that, in sociopolitical terms, it makes no difference at all which science holds sway in a particular society at a given moment. I’m persuaded, for example, that Darwinism made a difference for the worse in Nazi Germany.¹⁷ Gliboff isn’t; and that disagreement now replicates itself in our disagreement over Mendelism.¹⁸ As I put my view in Disputed Inheritance, “Nazi propagandists knew what they were doing. They grasped that to learn that human hereditary traits are like yellowness and greenness in the garden pea is to become the readier to accept the legitimacy of homogenizing categories and the conclusions that seem to follow from reasoning with and from them” (p. 383). If the norm-of-reaction concept had served Nazi purposes better, their propagandists would have used it instead.¹⁹

I don’t see what is accomplished by rehabilitating Weldon’s theory or re-fighting his dispute with Bateson. Finally, Gliboff wonders why, as per convention, I couldn’t be satisfied with treating Weldon as, in Gliboff’s words, “the loyal opposition” – as, that is, someone whose clever criticisms smartened up the Mendelism that went on to take its familiar place in our textbooks. But that story, if brought into the genetics classroom, would serve only to bolster the authority of the traditional curriculum whose replacement Gliboff is cheering on. By contrast, the story I tell in Disputed Inheritance, in which the traditional curriculum turns out to have been written by the winners of a foundational debate that most biology students (and many professionals) have never heard of, but that could have gone differently, fosters critical thinking about genetics and its possibilities, past, present, and future. The reformed curriculum and the counterfactual historiography that inspired it are thus mutually reinforcing.²⁰

From Sander Gliboff

My thanks to Greg for inviting me to post here jointly with him. I will try to explain my reaction to his book.

We have some deep differences about the purpose of history of science, how and why scientific change occurs, and when a historical interpretation is straightforward or not. Considering such differences, I should not have appropriated his term, “non-straightforward,” to describe what is only my own opinion of Part 3 of his book.

I read the book, or at least the first two Parts, as a contribution to the history of genetics and a very successful attempt to recover Weldon’s ideas and arguments from new source material, retell the story of the Bateson-Weldon dispute from the perspective of the participants, and shed new light on the early origins of classical genetics. If Weldon also turned out to be a useful inspiration for a biology curriculum, that was just icing on the cake, not additional support for the historical analysis. So, yes, I did fail to appreciate the centrality of Radick’s pedagogical goals and the extent to which he wanted his book to be received as a contribution to present-day science and science teaching. But it seems to me that Radick is selling his own historical research short if he thinks it has to pay off in contributions to other endeavors. It has value as contextualized history, too, and it is not inappropriate to review it as such.

A more fundamental problem for me is how to account for historical change in science. How central and fateful can single events be, and how indispensable individual scientists? The claim that the entire future of biology hinged upon the outcome of the Bateson-Weldon dispute, or that no one else besides Weldon himself could have kept his approach in play, seems implausible to me, on principle and precedent, but also because many other scientists were engaged with problems of heredity at the same time and were thinking about some of the same issues. Einstein in 1905, maybe, was indispensable, because he had original ideas and was developing them in relative isolation, with no one else well positioned to pick them up where he left off. But Weldon was part of a community of researchers on heredity. The idea that heredity, development, and environment were interdependent was not new to them or difficult for them to grasp, many of them agreed with him on key points of his theory, and there was not yet any genetics establishment that might have been resistant to change. Perhaps the British community was more polarized along Bateson-Weldon lines, but internationally there was a sizable and intellectually diverse community representing a wide range of experimental approaches and agendas, interpretations of Mendel, and possible future directions for the new field of genetics. If they did turn mostly toward Bateson (which I am not so sure they all did), how do you know it was just because Weldon died?

Even granting that Weldon was the crucial historical difference-maker, what exactly was it that would have been enabled by his survival but precluded by his death? Evidently it was not any of the particulars of his theory of ancestral heredity, his conception of the hereditary material, the behavior of his hereditary particles. It was not even the causes of variation, since each side admitted the other’s at least to some extent. For Radick, the difference is in that extent, in the matter of “emphasis” and “center-periphery cognitive relations” between mostly oversimplified gene action and causation one the one hand, and mostly complex interaction of heredity, development, and environment on the other.

The problems I still have with this are the following. First, it minimizes the importance of the more concrete matters that Bateson and Weldon actually argued about and became embittered about in the historical context. Their published exchanges were all about the relative merits of Mendelian segregating factors vs. the finer-grained ancestral germplasm that was halved and re-mixed in every generation, and especially about which theory provided a better, quantifiable, explanation of variation. Neither side aimed for just a general shift in emphasis.

Second, it downplays the ideas and actions of all the other heredity researchers during and after the dispute. Was there really a new emphasis on gene action and determinism just then? Or toward the formation of some kind of Batesonian establishment that would hinder undesired research? And if so, how can you tell it started happening just in 1906 and that the death of Weldon was the cause or trigger?

Third, the concept seems vague and its application arbitrary. How does one gauge an emphasis? It’s fairly clear, I think, when comparing Bateson and Weldon, that the one is more focused on gene action and the other on complex interactions, though there are ways of defending Bateson against the charge of genetic determinism. And even Weldon, looking just at his published critiques of Mendelism, didn’t do much with development and environment. His message to the Mendelians was about complex interactions among the many hereditary determinants. Bateson had nothing against such interactions, as long as they were interactions among the right sorts of hereditary particles. After all, he coined the term “epistasis” and recognized its importance.

But getting back to the problem of emphasis, how does one gauge the emphases of all the other approaches to heredity besides Bateson’s, or of an entire generation of geneticists, up to and including the genetics of today which is claimed to retain Bateson’s emphases? Do developmental genetics, gene regulation, genomics, and epigenetics not suffice as shifts in emphasis, compared to the early days of Mendelism? Maybe a sliding scale would be more informative than an either/or.

The emphasis of classical genetics is likewise problematic. The field was replete with complex gene-gene interactions: polygenic heredity, pleiotropy, linkage, epistasis, modifier genes, genetic background, position effects, dosage effects, of which a Weldonian should probably approve. Maybe there was less work on gene-development and gene-environment interactions, but still early twentieth century genetics gave us sex limitation, penetrance, expressivity, Goldschmidt’s idea of genes controlling biochemical and developmental pathways, Woltereck’s norm of reaction, Kühn’s biochemical genetics. What critical mass do they have to reach before they count as emphases? When people as central as the Morgan group reiterated Weldonian emphases, why does that not count for anything? It seems odd to call any part of The Mechanism of Mendelian Heredity a “rearguard action.”

Fourth, I question the implied constraining power of a field’s emphasis. How does it prevent anyone from going against convention and trying something new? If no one tried to revive Weldonian emphases, or if they tried and were not as influential as we could wish, how do we know that was because of something that happened in 1906? Suppose more people had followed Goldschmidt’s lead in the 1920s, could that not have shifted the emphasis of genetics toward the biochemical and developmental? What was stopping them?

Similarly, in the counterfactual story: how does the emphasis on development and environment prevent a shift back to emphasizing genic effects? Or stop some unscrupulous Weldonian from supporting eugenics? Would a shift in emphasis in 1906 really keep geneticists in line for the next thirty years or more?

One last question that I raised was, what is uniquely Weldonian about the emphasis on complex interactions? Other biologists presumably could have served Radick as models and inspirations as he developed his ideas about how to teach biology. Radick’s answer is that being in just the right place at just the right time made Weldon unique in his importance and potential influence on the future of biology. But of course this presupposes the claim about the uniqueness and fatefulness of 1906, a claim that I don’t think has been well supported and that is unnecessary for a good contextualized analysis of the Bateson-Weldon dispute.

1. https://doi.org/10.1007/s10739-024-09761-z. ↩︎
2. Annie Jamieson and Gregory Radick, “Genetic Determinism in the Genetics Curriculum: An Exploratory Study of the Effects of Mendelian and Weldonian Emphases,” Science and Education 26 (2017): 1261–1290, https://doi.org/10.1007/s11191-017-9900-8. See also Gregory Radick, “Teach Students the Biology of Their Time,” Nature (19 May 2016): 293, https://doi.org/10.1038/533293a, and Annie Jamieson and Gregory Radick, “Putting Mendel in His Place: How Curriculum Reform in Genetics and Counterfactual History of Science Can Work Together,” in The Philosophy of Biology: A Companion for Educators, ed. Kostas Kampourakis (Dordrecht: Springer, 2013), pp. 577–595. The teaching materials from the 2013 course can be downloaded for free at https://geneticspedagogies.leeds.ac.uk/ ↩︎
3. See, e.g., Denis R. Alexander, Are We Slaves to Our Genes? (Cambridge: Cambridge University Press, 2020), p. 12; Rachel A. Sparks et al., “Using Culturally Relevant Pedagogy to Reconsider the Genetics Canon,” Journal of Microbiology and Biology Education 21 (2020), https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7195159/; Ella Whiteley, “The Devil’s in the Framing: Language and Bias,” 8 February 2022, LSE Philosophy Blog,https://www.lse.ac.uk/philosophy/blog/2022/02/08/the-devils-in-the-framing/. ↩︎
4. See Gregory Radick, “Presidential Address: Experimenting with the Scientific Past,” British Journal for the History of Science 49 (2016): 153–172, 171, https://doi.org/10.1017/S0007087416000339. ↩︎
5. Evelyn Fox Keller, The Century of the Gene (Cambridge, MA: Harvard University Press, 2000). ↩︎
6. This concern with historical complexity also informs my handling of my other two main themes, of explanation and its evaluation via counterfactual reasoning. Far from holding that, as Gliboff puts it, there was “[n]o good reason at all” for anyone to become a Mendelian, I expend a large number of pages on an original analysis of the attractions of Mendelism for reasonable people of good will (and in any case, the choice was never between Mendelism and Weldonism, since the latter never appeared in full in Weldon’s lifetime). Nor do I suggest that Weldon’s arguments would “have switched genetics onto a completely different track for decades to come;” on the contrary, I stress over and over how un-radical a Weldonian turn would have been, and relatedly, how much the counterfactual plausibility of that turn depends on the minimal nature of the departure from actual history involved. ↩︎
7. Jamieson and Radick, “Genetic Determinism in the Genetics Curriculum,” 1263–1264, citations removed. On similarities and differences with Michael Dougherty’s near-simultaneous proposal for “inverting the genetics curriculum,” see Disputed Inheritance, pp. 483–484, nn26 & 28. For the Weldonian curriculum described as “applied Kellerism,” see Gregory Radick, “Making Sense of Mendelian Genes,” Interdisciplinary Science Reviews 45 (2020): 299–314, 299, https://doi.org/10.1080/03080188.2020.1794387. I only recently learned from Sonia Sultan that Richard Lewontin briefly managed to begin a major co-authored textbook in genetics with a chapter on the norm of reaction – though even there, the second chapter was on “Mendelism.” See David T. Suzuki, Anthony J. F. Griffiths and Richard C. Lewontin, An Introduction to Genetic Analysis, 2^nd edition (San Francisco: W. H. Freeman, 1981). On other attempts from around the same time to demote Mendelism pedagogically, see Hannah Bapty, “Must Introductory Genetics Start with Mendel? Lessons from Two Unsuccessful Attempts to Revise the Genetics Curriculum,” Science and Education 32 (2022): 1677–1708, https://doi.org/10.1007/s11191-022-00361-z. ↩︎
8. Disputed Inheritance, pp. 278–279, 476n40. ↩︎
9. Disputed Inheritance, pp. 236ff. ↩︎
10. For more on developments on the teaching front, see Gregory Radick, “Alternative Paths for Genetics, Then and Now: Q&A with Gregory Radick about Disputed Inheritance,” Trends in Genetics 40 (2024): 1–14. https://doi.org/10.1016/j.tig.2023.10.005. ↩︎
11. See Gregory Radick, “The Case for Virtual History.” Introduction to a special feature (“What if?”) on counterfactuals in the history of science. New Scientist 187, no. 2513 (20 August 2005): 34-35, 35. ↩︎
12. See Geoffrey Hawthorn, Plausible Worlds: Possibility and Understanding in History and the Social Sciences (Cambridge: Cambridge University Press, 1991). ↩︎
13. I hope in future iterations of the module to deal, under this ancestrian heading, with recent work showing that the famously “high-risk” gene variants BRCA1/2 turn out to have much lower penetrance in people with no first-degree family history of breast cancer; see, e.g., Leigh Jackson et al., “Influence of Family History on Penetrance of Hereditary Cancers in a Population Setting,” eClinical Medicine 64 (2023), https://doi.org/10.1016/j.eclinm.2023.102159. Thanks to Anneke Lucassen for this reference. ↩︎
14. Noting how widespread were interactionist theories of heredity before and around Bateson’s Mendelism, Nathaniel Comfort too has queried whether, in his words, “swapping one English dude for another” is “the best way forward” (FASEB Journal 37, 4 (2023): 1–5, 4, https://doi/epdf/10.1096/fj.202300212). It isn’t if the aim is merely to underline how surprising the post-1900 success of an interaction-marginalizing science of heredity was, given the pre-1900 state of the art. But if, in addition, we want to show that early Mendelism was in fact vigorously contested on precisely those grounds, by someone intellectually and institutionally equipped to win the argument, and that the Mendelians prevailed not because truth inevitably beats error in science but because, like all else human, science is vulnerable to the accidents of history, then the spotlight rightly falls on Weldon. ↩︎
15. For an analysis of historically legitimate presentisms about the scientific past, with especially valuable (and, for purposes of this reply, apposite) discussion of “causal-narrative presentism” and its link with counterfactuals, see Laurent Loison, “Forms of Presentism in the History of Science: Rethinking the Project of Historical Epistemology,” Studies in History and Philosophy of Science 60 (2016): 29–37, 31–32, https://doi.org/10.1016/j.shpsa.2016.09.002. ↩︎
16. For Weldon on Daphnia spine length as exemplifying his dictum that all characters are as much inherited as they are acquired, see Disputed Inheritance, pp. 312–313. ↩︎
17. Gregory Radick, “Darwinism and Social Darwinism,” in The Cambridge History of Modern European Thought, eds Warren Breckman and Peter E. Gordon, 2 vols, vol. 1, The Nineteenth Century (Cambridge: Cambridge University Press, 2019), pp. 279‒300, 299–300. On how the theory of natural selection came both to underwrite and to undermine the case for human rights in the twentieth century, see Gregory Radick, “‘As Man Advances in Civilisation…’: Darwin on the Expanding Circle of Moral Regard, From His Day to Ours,” in Sex, Gender, Ethics and the Darwinian Evolution of Mankind: 150 Years of Darwin’s ‘Descent of Man’, ed. Michel Veuille (London: Routledge, 2024), pp. 209–229.  ↩︎
18. Sander Gliboff, “Darwin on Trial Again,” H-German, H-Net Reviews,Sept. 2004, https://www.h-net.org/reviews/showrev.php?id=9837; see too the response from Richard Weikart, https://www.csustan.edu/history/response-sander-gliboff. ↩︎
19. The environment and its impact on human health and development were major preoccupations in Nazi Germany. For a stimulating counterfactual essay on their “corporate environmentalism” in the event of a Nazi win (or at least non-loss) in WWII, see Steve Fuller, “A Darker Shade of Green,” New Scientist 187, no. 2513 (20 August 2005): 36–37, 37. ↩︎
20. On the social-justice case for bringing the historically contingent settling of the Bateson–Weldon debate into the genetics classroom, see Sparks et al. 2020: 4–5 (op. cit. n3).  In urging the teaching of “the culturally laden history of Mendel, Weldon, and Bateson,” they acknowledge that doing so “may create discomfort in some instructors.” Nevertheless, they go on, “it is entirely appropriate to include this history, as we often teach about the history of scientific knowledge regarding the discovery of the double helix, atomic structure, evolution, and numerous other scientific concepts. Shying away from the impacts of culture on scientific knowledge only serves to reinforce deterministic, essentialist, and racist views of human genetics. It is far more appropriate to embrace the complexity and context-dependent nature of science education and of genetics itself to promote greater learning gains and begin to move toward culturally relevant genetics education.” ↩︎