[Addendum— I’ve only just realized (1005 h) that Jerry posted on this same piece by Carl Zimmer back in 2017. Great minds think alike! But the relevance to today is, I think, even more striking.]
A few days ago I happened to run across an old blog post by the eminent science writer Carl Zimmer, in which he recounts the Lysenko affair and the lessons to be learned from it. Posted in 2017, the lessons he identifies are eerily prescient in light of the U.S. government’s (i.e., Trump’s) response to the coronavirus pandemic:
— A government decided that an important area of research, one that the worldwide scientific community had been working on for decades, was wrong. Instead, they embraced weak evidence to the contrary.
— It ignored its own best scientists and its scientific academies.
— It glamorized someone who opposed that mainstream research based on weak research, turning his meager track record into a virtue.
— It forced scientists to either be political allies or opponents.
— It personally condemned scientists who supported the worldwide consensus and spoke out against the government’s agenda, casting them as bad people hell-bent on harming the nation.
— The damage to the scientific community rippled far, and lasted for years. It showed hostility to scientists from other countries, isolating them from international partnerships. It also created an atmosphere of fear that led to self-censorship.
— And by turning away from the best science, the Trump administration did harm to its country.
It all seems very relevant, and his third item practically screams, “Scott Atlas!” He wrote the piece in 2017 in the context of climate change policy, but the relevance to today must have been evident to Carl, too; the reason I came across the 4-year old post is because he had moved it to near the top of his blog, where I came across it while looking for other things on his website.
The blog post is based on a talk Zimmer gave at a conference on “Science, Journalism, and Democracy: Grappling With A New Reality” at Rockefeller University on how science journalism can deal with the “confusing swirl of reality, misinformation, and so-called fake news” that is “[t]he current media landscape”. Carl’s talk can be seen on YouTube (below).
I’ve noticed lately that the quality of science writing in newspapers has declined, even in The New York Times, which used to have some really good writing, especially by Carl Zimmer, who doesn’t seem to appear in its pages so often.
CORRECTION: Zimmer is still writing prolifically in the NYT, but covering a beat—vaccination—that I’d missed, (mis)leading me to believe that he was engaged in activities other than writing for the NYT. He’s asked me to correct this in a comment below, so I’ll just add his comment here:
If you had bothered to look at my author page at the Times, you’d see that I have been busier than ever there as I help cover the science of the pandemic. Over the past 10 months, I’ve written 93 stories about Covid-19, which comes to about two articles a week. Please correct your post. You are misleading your readers about my work. https://www.nytimes.com/by/carl-zimmer
I guess he was peeved. The misstatement was my fault, of course, and I’ve fixed it, but I have to say that this is a rather splenetic reply from someone whose work I’ve always praised.
Rather, in place of long-form biology and physics, a variety of people now write for the Times‘s biological “Trilobite” column, and seem to take a more gee-whiz approach to science, producing short columns that are also short on information.
Part of the problem may be that many of these columns are written by freelancers who haven’t spent most of their writing career dealing with biology. My general impression is that the NYT is starting to reduce its coverage of science. That would be a damn shame since it was the only major paper to have a full science section (I don’t get the paper issues any longer, so I don’t know if they still have the Tuesday science section I’d read first).
The sloppy writing seems to be the case with this week’s column, a column reporting a new genome-sequencing study in Nature of monotremes: the platypus and the echidna (“spiny anteater”). I have only scanned the paper briefly, and will read it thoroughly, but on reading the NYT’s short summary I spotted two errors—not outright misstatements of fact, but statements that are incomplete descriptions of the truth, and where an extra word or two would have made the column not only more accurate, but more interesting.
Here’s the article (click on the screenshot):
Maybe I’m being petulant, but here are two quasi-misstatements in the piece. First, this one (emphases are mine):
When the British zoologist George Shaw first encountered a platypus specimen in 1799, he was so befuddled that he checked for stitches, thinking someone might be trying to trick him with a Frankencreature. It’s hard to blame him: What other animal has a rubbery bill, ankle spikes full of venom, luxurious fur that glows under black light and a tendency to lay eggs?
The facts: Only the males have ankle spurs, and of course only the males have venom. (This probably shows that the trait is used not for defense against predators, but for male-male competition during mating.) Females have no venom and have rudimentary spur nubs that drop off before maturing. Of course, females have the genes for producing ankle spurs and venom, as those genes don’t know which sex they’ll wind up in—just like human males have genes for vaginas and breasts and human females carry genes for penises. But the sex-development pathway prevents the expression of venom and spurs in females, just as it prevented me from developing a vagina.
The sex-limitation of the spurs isn’t mentioned in the Nature piece, but every biologist who knows their platypuses also knows that only the males have venom spurs. And, by the way, the echidna has some genes that used to produce venom, but they’re non-expressed “pseudogenes” that have become inactivated. That shows that the ancestral monotreme was almost certainly venomous (this isn’t mentioned in the NYT piece, either).
About those egg-yolk genes:
For instance, many birds and insects have multiple copies of a gene called vitellogenin, which is involved in the production of egg yolks.
Most mammals don’t have the vitellogenin gene, said Dr. Zhang. But the new genomes reveal that platypuses and echidnas have one copy of it, helping to explain their anomalous egg-laying — and suggesting that this gene (and perhaps the reproductive strategy itself) may have been something the rest of us lost, rather than an innovation of the monotremes.
Well, yes, mammals do have the vitellogenin gene. In fact, our own species has three of them, but, as in other mammals they’re pseudogenes—genes that are there in the genome but are broken and not expressed. Humans and other placental mammals don’t require egg yolk because we’re nourished through the placenta, not yolks in shells. The platypus has two vitellogenin genes (described in the Nature paper as “genes”, so the statement that platypuses and echnidas have “one copy” is misleading)—they’re just not “functional” genes.
Now you may say this is quibbling, but it’s not. First of all, the statement that playtpuses have one copy of the egg yolk gene is wrong. They have two, but one doesn’t function. More important, the statement that there are nonfunctional yolk genes in all mammals says something powerful about evolution, something that I discuss in my book Why Evolution is True. Those “vestigial” and nonfunctional genes are evolutionary remnants of our ancestors who did produce egg yolk. Why else would they be there in our genome, doing nothing? Chickens, who of course evolved from reptiles, as we did, have all three vitellogenin genes in working order.
Another error, then, is the statement “suggesting that this genes. . . may have been something the rest of us lost.” No, we didn’t lose it; it’s still there in our genomes. And there’s no “suggestion” about it: it’s sitting there in our DNA, has been sequenced, and has been shown to be nonfunctional. Finally, we KNOW that this gene is NOT an innovation of the monotremes, and have known that for a long time (e.g., see here). It was inherited from their reptilian ancestors.
This isn’t flat out erroneous science reporting, but it’s incomplete science reporting—the summary of a paper phoned in to the NYT. (I also find the Time’s summary curiously devoid of what’s really new in the paper; at least half of it reprises what we already knew.) More important, the reporter missed a good chance to give some powerful evidence for evolution, both in ourselves and in monotremes, whose genomes harbor some dead egg-yolk genes that are active in our avian and reptilian relatives. And yes, those echidnas have dead genes for venom.
Reader Jim Batterson sent me this 25-minute video with the comment:
I know you prefer to read rather than watch a video, but I wanted to make you aware of a 24-minute YouTube video from Vince Racaniello, a virologist at Columbia University who leads a cast of virology geezers and one younger immunologist in a weekly zoomcast production of “This Week in Virology”. He did this standalone presentation to rant a bit on the way that this latest variant in the UK is being hyped to the world. I think he does a pretty good job for any viewer who has had a biology course in the past five or so years.
The point is that viruses are mutating constantly, and yet none the coronavirus mutations have yielded a new “strain”—that is, a mutant type that has new biological properties. The property touted for the new virus is its purportedly increased “spreadability”, but, as Racaniello notes repeatedly, that simply hasn’t been demonstrated. As he shows, you can get some variants spreading more widely than others simply by accident: the variant may not have any effect on spreadability itself but can increase in frequency as a byproduct of “superspreader events”—the main way the virus spreads—because only a small subset of all viruses get passed to other humans.
Racaniello then shows the changes in the new mutant “strain”, noting that only one of the several mutants in the spike protein is even a candidate for a change in spreadability, but there is not an iota of evidence that any of those mutations actually make the strain more spreadable. Nevertheless, all of us are inundated with media scare stories about this “superspreader virus”.
Racaniello’s point is that though there are epidemiological data showing a correlation between the presence of the mutant in some areas and a greater spread of the virus, that’s just a correlation without evidence of causation. And there could be several causes, including accidents. To show this mutant is a “super virus”, you simply have to do lab experiments; epidemiological correlations show nothing.
Racaniello doesn’t rule out that this mutant spreads faster than its ancestors, but he’s not convinced it is, and doesn’t think that we yet have a reason to be concerned. In fact, he suggests that the changes in the new strain may make it less spreadable. Let me add that Racaniello knows what he’s talking about, as he’s co-author on a well known textbook of virology.
Like all good scientists, Racaniello isn’t declaring that this virus is “neutral” compared to its competitors—he’s simply saying that we don’t have any data suggesting it’s more nefarious. In fact, the same story happened earlier with a different mutant that spread widely, but nothing ever came of that. We need experimental cell-culture data from the lab on viral shedding, and that doesn’t exist.
His final comment:
“We should move on from the scary headlines, and get ahead with vaccination programs, which are underway—and that is going to be the way we get away from this pandemic.”
Anyway, this is a good and clear mini-lecture, and listening to it should calm you down a bit if the media have gotten you worried.
Genetic drift is the random change in frequencies of alleles (forms of a gene, like the A, B, and O alleles of the Landsteiner blood-group gene) due to random assortment of genes during meiosis and the fact that populations are limited in size. It is one of only a handful of evolutionary “forces” that can cause evolution—if you conceive of “evolution,” as many of us do, as “changes in allele frequencies over time” (“allele frequencies” are sometimes called “gene frequencies”). Other forces that can cause evolutionary change are natural selection and meiotic drive.
Genetic drift certainly operates in populations, for it must given that populations are finite and alleles assort randomly when sperm (or pollen) and eggs are formed. The question that evolutionists have been most concerned with is this: “How important is genetic drift in evolution?” We know that, if populations are sufficiently small, for instance, drift can actually counteract natural selection, leading to high frequencies of maladaptive genes. This is what has happened in small human isolates, such as religious communities like the Amish and Dunkers. It’s not clear, though, that this has happened with any appreciable frequency in other species.
Drift was once implicated by Sewall Wright, a famous evolutionist, in his well-known “shifting balance theory of evolution“, which maintained that drift was essential in producing many adaptations in nature. That theory was once influential, but has now fallen out of favor, and I take credit for some of that (see my collaborative critiques here and here).
Related to this are various theories that see genetic drift and its maladaptive effects as crucial in forming new species (e.g., the “founder-flush” theory of speciation). In my book with Allen Orr, Speciation, we analyze these ideas in chapter 11 and conclude that drift has been of minimal importance in speciation compared to natural selection.
Finally, genetic drift was an important part of Steve Gould’s theory of punctuated equilibrium, for it was the force that allowed isolated populations to undergo random phenotypic change, tumbling them from one face of “Galton’s polyhedron” to another. This was one of the explanations for why change in the fossil record was jerky. Well, the fossil record may well be punctuated, but Gould’s theoretical explanation was pretty soundly dismantled by population geneticists, including several of my Chicago colleagues (see this important critique).
While one can cite examples of genetic drift operating in nature, like the expected loss of genetic variation in very small populations, in my view it hasn’t been of much importance in speciation, morphological and physiological evolution, or in facilitating adaptive evolution by pushing populations through “adaptive valleys.” Even the view that it has made species vulnerable to extinction by reducing the pool of genetic variation needed to adapt to environmental change has been exaggerated. I know of no extinctions caused by genetic drift, though I haven’t checked on the cheetah example lately (they were said to be highly inbred because of small populations, but I’m not sure that this is what makes them vulnerable to extinction). In fact, for conservation purposes, I believe the importance of loss of genetic variation through drift has been much less than the importance of reduced population size itself that makes populations vulnerable to extinction because individuals can’t find mates or overgraze their environment, or simply because if you’re a small population, random fluctuations in numbers are more likely to make you go extinct. This is demographic rather than genetically based extinction.
But drift has been important in molecular evolution, causing a turnover of gene variants over long periods of time. If those variants are “neutral”—that is, they are equivalent in their response to natural selection—then they will turn over at a roughly linear rate with time, and the changes can be used as a sort of “molecular clock” to estimate divergence times between species. This kind of molecular divergence has been used to construct family trees of species as well as to estimate the times when species diverged. This is a fairly new usage, for such molecular tools and estimates have been available only since the 1960s.
On to the New Scientist bit about drift in its latest issue, a special on evolution.
The 13-point section about how new findings will expand our understanding of evolution includes section 9 about drift, called “Survival of the luckiest.” It first recounts, accurately, how drift operates, but then exaggerates its importance by mentioning two studies of urban populations of animals, populations that in principle should show more drift than wild populations because populations living in cities are small and fragmented. The section says nothing about any of the things I just told you, which is what evolutionists have really been concerned about with respect to genetic drift.
Here’s the entirety of how New Scientist says drift is revising our view of evolution (the author of this section is Colin Barass):
Biologists have known about genetic drift for a century, but in recent years they realised that it could be especially common in urban settings where roads and buildings tend to isolate organisms into small populations. A 2016 study of the white-footed mouse, Peromyscus leucopus, in New York supported the idea. Jason Munshi-South at Fordham University, New York, and his colleagues discovered that urban populations have lost as much as half of their genetic diversity compared with rural populations.
Last year, Lindsay Miles at the University of Toronto Mississauga, Canada, and her colleagues published a review of evidence from about 160 studies of evolution in urban environments, in organisms ranging from mammals and birds to insects and plants. Almost two-thirds of the studies reported reduced genetic diversity compared with rural counterparts, leading the researchers to conclude that genetic drift must have played a role. “Genetic drift can definitely be a significant driver of evolution,” says Miles.
These findings have big implications, because populations lose their ability to adapt and thrive if they lack genetic diversity for natural selection to work on. Of course, genetic drift isn’t confined to urban settings, but given how much urbanisation is expected to grow, the extra threat it poses to wildlife is concerning. It highlights the need to create green corridors so that animals and plants don’t become isolated into ever-smaller populations.
I don’t think those findings do have “big implications”, because the important of reduced genetic variation in urban environments is unclear, particularly when the genes assayed have no clear connection with natural selection. And the import of losing half of your genetic diversity is also questionable: after all, a single fertilize female contains half of the “heritability” of an entire population. Everything rests on whether evolution by natural selection depends on very low-frequency genetic variants, present only in big populations, and we don’t really know if this is the case. And the above study is in white-footed mice, only one species among millions, and only for populations in urban environments. That’s not to denigrate it, just to point out that its relevance to nonurban nature is unclear and its relevance to evolution is equally unclear.
You can read the Miles et al. study at the link (here), and having read it, I wasn’t impressed, since the authors themselves don’t come to nearly as strong a conclusion as does New Scientist. Here’s from the paper’s conclusions:
Although our review of the literature with quantitative analyses of published urban population genetic data sets demonstrates trends towards increased genetic drift and reduced gene flow, these patterns were not significant and were not universally seen across taxa. In fact, over a third of published studies show no negative effects of urbanization on genetic diversity and differentiation, including studies supporting urban facilitation models at a much higher proportion than previously realized. How populations and species respond to urbanization clearly depends on the natural history of the taxa investigated, the number and location of cities being sampled, and the molecular techniques used to characterize population genetic structure.
In other words, although two-thirds of the studies showed reduced variation or increased inter-population differentiation, these patterns were not significantly different from non-urban populations. And if those differences were not significant, you needn’t start speculating about genetic drift. The authors conclude simply that different species show different genetic patterns when living in urban environments.
Miles’s statement that “genetic drift can definitely be a significant driver of evolution” is ambiguous, because she doesn’t say what she means by “significant” or by “evolution” (is she talking just about patterns of molecular evolution, like genetic diversity, or other types of evolution?)
New Scientist, in other words, fails to make the case that genetic drift has changed our view of how evolution operates, much less that it’s modified the modern synthetic theory of evolution. We already knew that small populations lose genetic variation because of genetic drift, and that’s been standard lore for decades. The real novel claims about drift—that it facilitates adaptive evolution, that it’s an important driver of speciation, and that it explains punctuated patterns in the fossil record—have disappeared because of the absence of both data and theory supporting those claims.
I am weary of going after New Scientist, and this may be my last critique of that issue. But be aware that virtually every one of the other nine points is exaggerated as well. Move along folks—nothing to see here.
I’ll continue on with New Scientist‘s 13-section claim that the modern theory of evolution needs a reboot (see previous posts here and here), though I don’t know how much longer I can stand their uninformed palaver written by incurious journalists. Today we’l take up section 4: “There is more to inheritance than just genes”, which emphasizes the importance of epigenetic changes in evolution. The article appeared in this special issue of the rag magazine:
As I’ve written many times before, epigenetic changes are not good candidates for an inherited basis for evolutionary change, mainly because the vast majority of epigenetic modifications of DNA—usually via methylating DNA bases—disappear within one generation, as the DNA effaces the epigenetic markers during sexual reproduction. A few epigenetically produced traits can persist for a few generations, but that’s not a good basis for permanent evolutionary change, and certainly not a general explanation of adaptation. In fact, we know the genetic basis of adaptation in many cases, and it’s nearly 100% due to changes in the DNA sequence, not to epigenetic modification of the DNA sequence. (Lactose tolerance in pastoral human populations is one example.)
To support the claim that epigenetics is important in evolution, author Carrie Arnold mentions the shopworn example of pregnant Dutch women, deprived of food by the Nazis, giving birth to children who became unhealthy adults, with high levels of obesity, diabetes, and so on. Besides this not being an example of adaptive evolutionary change, it’s still not certain that the changes in the kids were produced by epigenetic modification of the DNA. The pregnant mothers were the ones who passed on the traits, and the fetuses could have been affected by the mother’s physiology, not by changes in her DNA. (It’s telling that the children of undernourished fathers alone didn’t show the changes.) There may have been some epigenetic changes, or maternal effects, in that the grandchildren seem to be affected too, but that’s where the train of changes comes to a stop.
Then Arnold mentions an experiment with which I wasn’t familiar, but supposedly demonstrated epigenetic changes that persisted for many generation—25, to be precise:
Subsequent studies in plants and animals suggest that epigenetic inheritance is more common than anyone had expected. What’s more, compared with genetic inheritance, it has some big advantages. Environments can change rapidly and dramatically, but genetic mutations are random, so often require generations to take hold. Epigenetic marks, by contrast, are created in minutes or hours. And because they result from environmental change, they are often adaptive, boosting the survival of subsequent generations.
Take the pea aphid. It is capable of both sexual and asexual reproduction, and comes in two varieties: winged and wingless. When scientists exposed a group of genetically identical pea aphids to ladybirds, the proportion of winged aphids increased from a quarter to a half. This adaptation, which helped them escape the predatory ladybirds, persisted for 25 generations. The aphid DNA didn’t mutate, the only change was epigenetic.
So I “took” the pea aphid, reading the paper that supposedly showed persistent epigenetic variation over 25 generations. Click on the screenshot below to get the paper (from the journal Heredity):
It’s a long and somewhat tedious read, but there are two points to make.
1.) The plastic response to the predator—growing wings (an adaptation that’s genetically encoded)—did not persist for 25 generations on its own. In fact, if you remove the predator, the stimulus for growing wings, the population becomes wingless again within a single generation. So we do not have a case of epigenetic markers persisting on their own for many generations, much less two generations.
2.) There is no evidence that the production of winged forms is caused by epigenetic modification of the DNA, and the authors admit this.
In other words, everything that Arnold says or implies about this experiment is misguided.
The experiment was started with a single clonal population of aphids, that is, parthenogenetically produced individuals from a single female. The population thus lacked genetic variation except for new mutations that could have occurred after the experiment started. One part of the population was the experimental section, exposed to predatory ladybirds. That one produced winged individuals immediately at a proportion of about 50% of the population. This proportion remained stable for 27 generations. Producing wings in the presence of predators is adaptive, of course, as you can flee them, and not producing wings when the predator is absent is also presumably adaptive, as there’s a metabolic and reproductive cost of producing wings you don’t use. Thus the switching between wings and winglessness is an adaptive plasticity, and is presumably coded (not epigenetically!) in the aphids’ DNA.
The control line, lacking ladybirds, stayed at about 25% winged individuals for 25 generations.
At three intervals, the authors took aphids from the experimental line and put them in an environment without predators. If the epigenetic markers persisted in the absence of the predator, and through meiosis, you’d expect these “reversion” lines to still show a higher frequency of winged individuals. They didn’t. They basically reverted to the control level of winglessness within a single generation, presumably because the switch for growing wings (ladybirds) wasn’t there.
So what we see is that to get the adaptive trait, wings, to persist, you need the stimulus to be there constantly. The presence of the predator somehow induces the aphids to grow wings, just as the presence of fish in a pond causes some rotifers to grow fish-repelling spines. And when you take the predator away, the aphids switch back to the wingless form. Here’s a plot showing the frequency of wings in the experimental population (red line), in the control predator-less population, (black line) and the reverted population in which predators were removed (blue line):
Unlike the Dutch situation, or others that report persistence of environmentally induced changes for a few generations, in this case the induced change, the presence of wings, reverts to control levels within a generation. We do not see the kind of trait persistence here that epigenetics advocates tout as important in making the phenomenon important in evolution.
And indeed, we don’t even know if the switch from winglessness to wings is an epigenetic change, as opposed to some chemical change that occurs in the aphids when they sense the presence of predators that turns on “wing-making genes”. (That’s how it works in rotifers: when a fish eats a rotifer, it releases chemicals into the water that induce the other rotifers to produce spines. That’s not an epigenetic modification of the DNA.) If you think that any environmental change is “epigenetic”, then yes, this one could be, but that’s not the way the cool kids construe “epigenetic” these days. It’s taken to mean “alterations of the DNA structure”, which is what journalist Arnold means by mentioning “epigenetic marks [that] are created in minutes or hours.”
There’s one twist in the experiment as well: in the lines subject to predators, the plasticity of individuals became reduced; that is, they were less likely to respond to changes in predators with changes in wings. The paper’s authors impute this to epigenetics, but it could well be due to selection occurring on mutations that arose in the predator lines. That is, since predation was omnipresent, there was less selection pressure to maintain a “switching system,” and your plasticity could erode. To maintain a switch between wings and winglessness, the lineage has to experience periodic bouts of predation alternated with bouts of no predation. So the loss of plasticity itself also says nothing about whether epigenetic markers were accumulating in the DNA.
And, at the end, the paper’s authors admit that we don’t know whether this switch is due to epigenetic modification of the DNA, as the New Scientists reporter claims. From the Heredity paper:
We can thus tentatively attribute the decline in plasticity observed in lines that were exposed to predators for many generations to the action of some non-genetically transmitted information (i.e. information not encoded in the DNA sequence). The hypothesis that observed phenotypic changes were caused by reversible epigenetic changes is thereby more likely but in order to be confirmed, this hypothesis would require to be backed up by molecular analyses.
I can find nothing in this paper that even suggests that epigenetic changes were happening to the aphids’ DNA, much less any kind of inherited changes that persist for more than one generation. This paper is certainly not an example of what New Scientist says it is.
This is the third buzzwordy phenomenon tendered by New Scientist as an exciting new finding that can modify the Modern Evolutionary Synthesis. And it’s the third one that is wrong. I am growing weary, and will see if I need to persist in debunking further claims in the article. Rest assured, though, that most of them are even weaker than the three I’ve discussed. But what does New Scientist care? They want clicks, not accuracy, and I fear that I’m wasting my time. I’d rather write about the new paper on consciousness in crows.
At least the New Scientist article admits that epigenetics is controversial:
The extent of epigenetic inheritance is contested. Some sceptics point out that, during mammalian reproduction, the creation of sperm and egg cells involves erasing epigenetic markers. Others argue that epigenetic transmission across generations is extremely widespread and useful. In plants, for example, it can account for differences in fruit size, flowering time and many other survival-boosting traits.
Yes, but it’s because the transmission across generations lasts about two or three generations at most that is why epigenetic modification by itself is not a good candidate for the “replicator” that produces adaptive evolution.
Yesterday I began “deconstructing” (as the cool kids say) the claims in the new issue of New Scientist, below, stating that evolutionary theory needs a reboot. I don’t intend to go through all 13 “novelties” that supposedly call for an “Extended Evolutionary Synthesis”, but I’ll tackle just a few this week, for “unpacking” (as the cool kids say) all the errors and distortions of the entire article would wear me out. And the rag magazine probably enjoys these posts as all they care about are clicks, not scientific accuracy.
Yesterday I criticized the magazine’s claim that “genetic plasticity”—the observation that the expression of genes and the traits they produce depend on the internal and external environment—is something novel that was just discovered recently, and that it refutes the widespread idea of genetic determinism. Well, this kind of plasticity isn’t new (it’s been around for a century), it doesn’t refute “genetic determinism” construed in some ways, and almost no biologists accept the form of genetic determinism that New Scientist claims is widespread. Today we take up an area I know something more about: speciation.
Point 5 of their article is the assertion, in caps, “SPECIES DON’T REALLY EXIST.” That will be news to the many of us who already see Homo sapiens as a species that’s different from gorillas, orangs, and the two chimp species. It will also surprise those of us who can instantly recognize a local bird as a robin, a starling, a pigeon, a mallard, and so on. Field guides, after all, would be useless if species weren’t distinct.
For, as Ernst Mayr and Theodosius Dobzhansky recognized in the 1930s, nature is not a continuum in which one form blends imperceptibly into another. Rather, nature is “lumpy” if inspected in a single area, and the lumps correspond to species. (This and the other issues below are all discussed in the first chapter and Appendix of my book Speciation with H. Allen Orr.)
The issue is then not to define species a priori, forcing the lumps in nature into the Procrustean bed of that definition, but rather to conceptialize species: describe in words what they represent. In the first paragraph, then, author Colin Barras gets it wrong:
FOR most of history, we have had little trouble defining species. There was a general assumption that a finite number of distinct forms of life had existed unchanged since creation, each sitting in a clearly defined pigeonhole: human, housefly, hawthorn and so on. Within the past few centuries, and particularly after Darwin, evolutionary theory has emerged as a more satisfactory way to explain how species came into existence. Yet in doing so, it has made species far harder to define.
Well, the issue isn’t how to define species but to find out how to recognize them. And yes, evolutionary theory since the 1930s has provided not only a good criterion for recognition, but also a good explanation of how species come into existence: how the process of speciation works. The explanation is, contra New Scientist, intimately connected with how we conceptualize species, for if we don’t know what these discrete units of nature are, how can we possibly understand how they came into being? Yes, there are lots of new species “definitions” that have arisen in the last several decades, but only one has stood the test of time, and is recognized as an accurate conceptualization of nature’s lumpiness by evolutionists. It’s called the “biological species concept” (BSC), and is roughly this:
A species is a group of populations whose individuals have the ability to exchange genes with other members of the group where they coexist in nature. In contrast, individuals belonging to different species cannot exchange genes in nature: they are reproductively isolated from each other.
Thus the key to understanding why you have no trouble telling birds or insects apart in one plot of land is because they remain genetically distinct from one another, with the reproductive barriers (mate discrimination, hybrid inviability, and so on) preserving the differences that accumulate within each species as it adapts to its environment. In other words the species is the thing that evolves. Now of course some populations of a single species can evolve differently from others, and some species show a limited amount of gene exchange with other species: I deal with these complications in my book, which I urge you to consult for further information.
Things go really haywire in the next paragraph:
There are several aspects to the problem. One is that if we accept the idea of species evolving from other species, then we must allow that an ancestral species can gradually morph into one or more descendants. We would still like to place organisms in discrete categories, but doing so is difficult if species blur into one another through time. “As we have come to terms with evolution, it has highlighted a problem with the machinery in our heads we use for classifying,” says Frank Zachos at the Natural History Museum of Vienna in Austria.
Change in a single lineage over time is a non-problem. Of course lineages slowly transform over time, as ours did. If we evolved, for example, from Homo erectus, it becomes a purely arbitrary matter when to give the later segment of that lineage the name Homo sapiens. Everyone recognizes that this is a matter of naming, not of making a crucial and meaningful biological decision. As for the splitting of one species into several, which occurs via (usually) gradual differentiation of geographically isolated populations to the point where they can’t interbreed, it’s also arbitrary when you call the descend moieties “different species”. We know that when no gene exchange can occur, good biological species have come about, but at intermediate stages of the process, I prefer to say that populations are “becoming more and more species-like.” What New Scientist sees as problems here have been dealt with amply in the last 80 years.
Here’s another non-problem:
For Jody Hey at Temple University in Philadelphia, the more important problem is that biologists often have two objectives in mind when they define species: one is the traditional desire to divide nature into easily recognisable packages; the second is to explain, in evolutionary terms, how those species came into existence. “Humans have conflicting motivations towards species,” he says.
Some researchers argue that these two objectives can never be achieved simultaneously. Down the decades, biologists have come up with a few dozen clever ways to define species. Some make it easy to classify the organisms we encounter – by their physical appearance, for example – but tell us little about the evolutionary process itself (see “Sadistic cladistics”, page 49). Other definitions get to the heart of how species come to exist, but can be difficult to use in the real world.
But other researchers, including me and other evolutionists, do think these objectives can be achieved simultaneously. Are we mentioned, and our reasons given? Nope.
I’m a friend of Jody’s, and he’s a terrific scientist (and a reader here), but I disagree with him on this issue. If you read Speciation, you’ll see that the BSC in fact fuses these two objectives. You first conceptualize species as units of nature that have limited or no gene exchange between them where they co-occur. Then the second problem arises immediately, and comes with a built-in research program: “how do the reproductive barriers arise in the first place?” That is the problem of speciation, and the problem that Darwin, despite the title of his 1859 book, couldn’t solve, for he had no notion of species as reproductively isolated units. In fact, the two objectives have already been achieved simultaneously by evolutionists who accept the BSC. Somehow Colin Barras seems to have missed this. No species concept other than the BSC can explain the palpable lumpiness of nature, and also how it comes about.
The third issue, which comes up often, is that gene exchange between apparently distinct species occurs more often than we used to think. (We know this because we have DNA-based ways of detecting such exchange—”introgression”—that we didn’t have a few decades ago. So here’s the supposed problem of “hybrid bonanza”:
In principle, advances in genetic sequencing could have helped by indicating how genetically distinct different groups of organisms are and how long ago lineages diverged. But sequencing has arguably made the problem worse by revealing that interbreeding – more technically, introgression – between closely related “species” is common across the tree of life. “It does seem to be the rule, not the exception,” says Michael Arnold at the University of Georgia in Athens. Indeed, evidence of introgression stretches right to our front door: our ancestors interbred with various ancient hominins that might, in the eyes of some, count as distinct species.
Well, interbreeding is not ubiquitous (humans and orangs, for instance, don’t exchange genes with any other species), and even when hybrids are formed they sometimes are sterile or don’t mate back to one parental species, necessary for introgression. Hybrid ducks, for example, can be fertile, but introgression is limited because the hybrids look weird and aren’t seen as acceptable mates. Yes, introgression is more common than we thought, but often it occurred in the distant past or, if it occurred more recently, is limited. Yes, we had gene exchange with Neandertals and Denisovans, and it appears to have been more than rare, so I tend to see these groups as subspecies of H. sapiens rather than separate species. When there’s that kind of gene exchange, the problem becomes a judgment call. But this problem hasn’t persisted: now all H. sapiens belong to the same species, and there’s no question of an other species of hominin existing now.
In fact, if gene exchange were pervasive and ubiquitous, we couldn’t make family trees of plants and animals very easily: the gene exchange would blur out the twigs. But it hasn’t.
This is a non-problem as well. If you insist on calling geographically isolated populations, like giraffes, as “different species” if they have a certain amount of genetic or morphological differentiation, then that’s also a judgment call, for one can never be sure what degree of genetic differences (usually judged by DNA differences) would correspond to reproductive isolation. If you don’t care about reproductive isolation, then you have no threshhold degree of genetic difference that is biologically meaningful.
The one sure criterion for species delimitation is this: “do the forms interbreed fairly extensively where they co-occur in nature?” If yes, then they’re members of the same species. If not, they’re members of different species. (One other way to demarcate separate species is that if you cross the forms in captivity and the hybrids are completely sterile or inviable, they are separate species, for hybrids would also be sterile and inviable in nature. But if two forms hybridize in zoos and produce fertile offspring, as lions and tigers sometimes do, then it’s a judgment call. In fact, lions and tigers co-occurred in the Middle East in historical times and there are no records of hybrids. Hybridization is an artifact of captivity, as it breaks down the reproductive barriers that kept these cats isolated in nature. Lions and tigers are different species because they don’t exchange genes where they cooccurred in nature.)
The giraffes, living in different parts of Africa, can’t be tested this way because they don’t co-occur, so calling them four different species on the basis of DNA differentiation is a purely subjective exercise (see my post on the giraffes here).
There is one way that looking at genes can help us find new species that aren’t “subjectively described.” This is when you find what seems to be a single species in one area, but then genetic analysis shows that there are actually two forms that each are “fixed” for a different set of genes or chromosome patterns. This is prima facie evidence of non-interbreeding, and we have what biologists call sibling species. Two of the species I worked with, Drosophila pseudoobscura and D. persimilis, for example, were originally thought to be a single species (you can’t tell them apart by looking at them), but research showed that each group is “fixed” for a different set of chromosome arrangements, and you don’t find both arrangements in any individual, so there are no hybrids.
The last bit:
To help add more rigour to the business of defining new species, earlier this year Zachos and other biologists proposed establishing the first single authoritative list of the world’s species. “Species” itself will remain a slippery concept, but at least we could all agree on where to draw the lines.
No, we won’t all agree on where to draw the lines. The giraffe is merely one out of many, many cases in which biologists will quibble about which populations are different species.
To summarize, New Scientist is wrong: species do exist, regardless of some introgression, and we understand not just what they represent—that is, why nature is lumpy rather than continuous—but also how the lumps come to be.
As I reported the other day, New Scientist has a special issue on evolution (photo below), which apparently consists of their admission that Darwin was right after all, along with a “feature special” described as follows:
Our modern conception of evolution started with Charles Darwin and his idea of natural selection – “survival of the fittest” – to explain why certain individuals thrive while others fail to leave a legacy. Then came genetics to explain the underlying mechanism: changes in organisms caused by random mutations of genes. Now this powerful picture is changing once more, as discoveries in genetics, epigenetics, developmental biology and other fields lend a new complexity and richness to our greatest theory of nature. Find out more in this 12-page feature special.
The article, which you can’t access online—though judicious inquiry will yield you a copy—consists of 13 numbered scientific areas that are supposedly prompting a reboot of modern evolutionary theory. I’m not going to reprise all of them, as I’ve done so already about many of the “buzzwordy” areas, including epigenetics and niche construction, but I will single out, over the next week, several of the areas that are, to my mind, exaggerated or grossly misrepresented. For readers who’ve said that New Scientist isn’t so bad, my response is, “Well, its coverage of evolution, at least, is dreadful if you know things about modern evolutionary biology.”
True, in some of these areas the article pays lip service to the fact that they’re “controversial”, but the impression one gets is that evolutionary biology is teeming not just with new ideas, but with new ideas that are non-Darwinian and promise a dramatic revision of the theory. The problem is that most of these new areas are either mistakenly conceived or don’t constitute much of a change in evolutionary theory. In fact, none of them do more than put a new duckling under the wing of Darwinism, and none of them replace the mother duck.
Today’s target is GENETIC PLASTICITY, the first of the supposedly “new” areas of evolutionary biology. It’s described under the clickbait-y title “Genes Aren’t Destiny.”
My immediate response is that we’ve known about genetic plasticity for over a century. But let’s back up: what is genetic plasticity?
It’s simple: it’s the observation that for many genes, their expression depends on the environments in which the organism that carries them (and hence the genes themselves) develops or experiences. There are a gazillion examples. For some genes, you get a permanent effect depending on the environment obtaining during the organism’s growth. One example, which I and two colleagues used in an experiment on the temperature flies encounter in the wild, is the mutant allele white-blood, which affects eye color. The expression of the mutation is sensitive to temperature during just a narrow window of time when eye color forms in the pupal stage. If the temperature is high, the eye can turn out very light yellow or even white, but if the temperature is lower, the eye is darker, down to dark purple. After this sensitive period, the eye color stays the same for the fly’s life. The color is said to be “plastic with respect to temperature.”
Likewise, if you don’t get enough food as a kid, you’ll be permanently small after puberty. That’s because the genes involved in creating “height” are sensitive to the amount of nutrition the organism gets, making “human height” a plastic trait. There are a gazillion genes that are plastic in related ways; in fact, I know of very few genes whose expression isn’t affected by the environment (perhaps genes for polydactyly in humans and cats are examples of the latter).
Some genes can vary their expression over an organism’s lifetime. Cats get thicker coats in winter and revert to shorter coats in summer: the genes producing hair are reversibly plastic to temperature. Snowshoe hare become white in winter and brown in summer, a reversible case of pigment genes sensitive to temperature.
The fact is that since the advent of Mendlian genetics at the beginning of the 20th century, geneticists have recognized the plasticity of genes and the traits to which they contribute. The terms back then were that genes had “variable expressivity” or “variable penetrance” depending on the environment. (White-blood was described in 1945.) The idea of plasticity is not at all new, and was featured in the founding works of the Modern Evolutionary Synthesis in the 1930s and 1940s. It was an integral part of our modern view of development, which has long recognized that almost no traits are produced as invariant by genes acting independently of the environment, while the expression of most genes and traits involve an interaction between genes and environment.
I give you this primer because New Scientist, in #1 of its litany, pretends this idea and its instantiation in organisms is something new and exciting. In fact, they say, citing the Human Genome Project, that we now realize that this kind of interaction refutes genetic determinism:
The more we learn about genetics, the clearer it becomes that “genetic determinism” – the idea that genes and genes alone fix our destiny – is a myth. A given set of genes has the potential to produce a variety of observable characteristics, known as phenotypes, depending on the environment. An Arctic fox changes its coat colour with the seasons. The presence of predators causes water flea Daphnia longicephala to grow a protective helmet and spines.
The power of flexibility
Even a change in social environment can prompt a shift. In the European paper wasp (Polistes dominula), for example, when the queen dies, the oldest worker transforms herself into a new queen. But she isn’t the only one to respond. Seirian Sumner at University College London and her colleagues found that the death of a colony’s queen results in temporary changes in the expression of genes in all workers, as though they are jostling genetically for succession. This flexibility is key to the survival of the colony and the species, says Sumner.
The power of genetic plasticity can be seen in the humble house finch. In the past 50 years, it has colonised the eastern half of North America, moving into habitats ranging from pine forests near the Canadian border to swampland in the Gulf of Mexico. The finch’s underlying developmental plasticity provided the raw material from which novel features evolved, including a range of new colourings and other physical and behavioural traits, says David Pfennig at the University of North Carolina at Chapel Hill. “Stop thinking about this as being like genes or environment, because it’s a combination of the two,” he says.
That’s all she wrote (the author of this section is Carrie Arnold).
Let us note that some plasticity, like hair growth in mammals during winter and coat color in snowshoe hares, has evolved: the changeability of the genes in new environments is an adaptive phenomenon (creating more warmth with longer hair and better camouflage in winter). Plasticity is not always a given and inherent characteristic of genes and traits, but in many cases has evolved as organisms have experienced different environments during their species’ evolutionary history, making lability an advantage over fixity.
Further, one can construe “genetic determinism” in two ways, which the article conflates. First, one can see it the proportion of variation in one trait in one population of organisms that’s caused by the variation among the genetic endowment of individuals. The proportion of variation among individuals in a population due to variation in their genes is called the heritability of that trait, and ranges from 0% to 100%. In humans, for example, the heritability of height in many populations is about 80%, meaning that about 80% of the variation in human tallness that we see in a given population is due to variation in genes. This does not mean that height itself cannot be affected by the environment, for it clearly can (I used the example of nutrition above). But under the existing conditions in a population, one can construe the heritability as an index of genetic determinism in a given population under existing environments.
The important thing, though, is what I said above: THIS IS NOT NEW AT ALL!. It is simply either ignorant or mendacious of New Scientist to pretend that genetic plasticity is both a recent discovery and one that has revised neo-Darwinism. Genetic plasticity was recognized well before neo-Darwinism was formulated in the 1930s as a fusion of genetics, natural history, and evolution, because genetic plasticity was known since the very early days of genetics—almost since Mendel’s work was rediscovered in 1900.
So, if you are masochistic enough to read the entire New Scientist article, you can just move along when you get to point 1; nothing to see here. It’s almost as if the authors touted the claim that the idea of natural selection (which really wasn’t widely accepted until the 1920s) is a new and exciting addition to Darwinism.
The termites are dining well in the world of science, for the two most prestigious science journals in the world, Nature and Science, are both going woke. And by that I mean that they’re buying into tenets of Critical Theory Wokeness that are palpably unscientific.
There are two scientific conclusions denied by ideologues because they’re politically inconvenient. The first is that there are behavioral differences between males and females that are both partly genetic and the result of natural selection. The second is that sex is “binary.” Both of these factual statements are denied on the mistaken grounds that, if they be true, they would mandate sexism and transphobia. That’s not true, of course. As I’ve written many times, human culture has often involved overcoming our evolved biological features in the service of morality and equality. Recognizing that biological sex is binary, for example, shouldn’t fuel transphobia, and scientists should work to make sure it doesn’t. Nevertheless, the idea that sex is nonbinary and men and women are, on average, identical in their behaviors and preferences have become conventional views in progressive politics. If you deny them, you’re toast.
I won’t reiterate why biological sex (defined in animals as males having small gametes and females large ones) is binary in most animals; you can see my defense of this claim here, here, here, here and here. And if it weren’t true, biology would be in deep trouble: every paper that looks at differences between the sexes would have to be scrapped because “sexes” are now seen by the Woke as a social construct, not a biological reality. Indeed, all science journals, including Nature (as we see below) tacitly accept the binary nature of sex.
Gender is a bit less binary, as there are individuals who identify as neither male nor female, even though their biological sex is clear. But gender is still strongly bimodal, as the vast majority of individuals identify as either male or female. But let’s leave gender aside and talk about sex, which is the issue when we come to biology.
As the tweets below show, and as discussed in the Quackometer article below the tweets, Nature is starting to put disclaimers in its reportorial section about both sex and gender being nonbinary. Meanwhile, in the refereed scientific reports that have made the journal selective and famous, the researchers blithely talk about sex as a binary. The two departments of the journal really need to get their act together.
The reason for the waffling, as the article from Quackometer speculates, is “ideological capture”. But more on that later. Let me just add that the denial of the binary in animal (and human) sex has also been promulgated by three evolution societies, as I wrote about here. It’s truly shameful when scientific organizations have to deny truth so as not to anger easily offended ideologues. And it’s equally shameful for Nature to do this.
The kerfuffle was brought to my attention by Matthew, who simply sent me the following tweets. They tell the tale. The first tweet, from writer Jesse Singal, links to the Quackometer article that summarizes Nature‘s confused wokeness:
What's going on at Nature is worrisome. It is INCREDIBLY creepy that whenever sex comes up, the publication feels the need to print that parenthetical, like some sort of mantra to ward off wrongthink. This is not normal.https://t.co/GoIehi6R9h
Now the summary and analysis from Quackometer in an article written by Andy Lewis (click on screenshot). This is a very good piece that captures the insanity of Nature’s behavior.
Here’s the disclaimer Nature puts in its news articles (quotes from Quackometer are indented). The journal not only “recognizes” that neither sex nor gender are binary, but doesn’t even define gender. I’ve put the disclaimers in bold:
In July 2020, a news item reported on “The gender gap in cystic fibrosis”. The article noted how women appear to have poorer outcomes than men, and die earlier,
A comprehensive analysis in 1997 of more than 21,000 people with cystic fibrosis in the United States showed a median life expectancy of 25.3 years for women and 28.4 for men1. The bacteria associated with lung decline and early death were also found to be present in women earlier than in men.
It then declared “(Nature recognizes that sex and gender are not the same, and are neither fixed nor binary.)”
Why it has put this odd disclaimer is not made clear. It makes no sense. The article is about differences in outcomes for people with different sexes (male and female). The article is quite clear about this. It talks of how “females could have a poorer response to  treatment”, and talks of genetic differences between the sexes. The article makes sense if you accept the common use of the word gender in the article title as a synonym for sex – maybe to assuage the more squeamish American audience.
But the odd disclaimer wants to make it clear that sex and gender are not the same. What the meaning of ‘gender’ is in the article then is not made clear. And it goes on to say that neither sex or gender are not binary, despite the whole article being based on the binary differential experience of women and men, boy and girls, males and females to the course of cystic fibrosis and its treatments.
An article published in August 2020 declares, “Sex differences in immune responses that underlie COVID-19 disease outcomes”. An editorial on this paper noted, “The researchers noticed that male participants’ typical immune response to infection differed from that of female participants, which could explain the more severe disease often observed in men.”
It then went on to add a similar disclaimer, ”(Nature recognizes that sex and gender are neither binary nor fixed.)”.
Who, exactly, is Nature here? The scientific papers treat sex as a binary, while the editorials make these ludicrous disclaimers.
Well, you know why the editors are doing this. Andy calls it “ideological capture”:
The only explanation for these strange and incorrect statements is ideological capture. These sentences are mantras of gender ideology – an ideology that claims that sex is not a reliable classification for humans. It is too vague, mutable and subjective to talk about reliably. The only reliable classification is ‘gender identity’ – whatever that is. This fashionable nonsense arose out of postmodernist inspired philosophies in ‘gender studies’ and sociology. As with much of these philosophies, it seeks to undermine meaning in words, to break apart and deny objective knowledge and classifications in an attempt to undermine ‘oppressive power structures’. It is a strictly political philosophy with activist aims that denies science can obtain reliable and objective knowledge and any such claim to knowledge is merely the speech of a dominant and oppressive class – usually white, heterosexual men.
But sex is, of course, fundamental to biology. No peer reviewed biology paper would characterise sex (at least in oogamous organisms like us) as not being ‘binary’, not being a material fact, and being mutable (except in sequential hermaphrodites). We cannot understand reproduction except in terms of its strict binary nature based on the fusion of two highly asymmetric haploid gametes. It is startling that Nature feels it needs to deny these things.
But Nature has form. Indeed. an opinion article published in Nature is an ideological favourite and a classic of this pseudoscientific genre.
In 2015, Claire Ainsworth published an article “Sex Redefined – The idea of two sexes is simplistic. Biologists now think there is a wider spectrum than that.” It is an exemplar of the ideological and denialist approach to sex.
I can’t tell you how annoying that I, as an erstwhile researcher in organismal biology, find this. It’s the denial of science to further ideology. And it’s the same madness we saw in the Lysenko episode, in which classical genetics was denied by a Russian charlatan in the service of Soviet ideology. Lysenko’s bogus theory of “vernalization”—really a “blank slate” idea in which inherited changes in crop production were influenced not by genes, but by environmental treatment—resulted in the death of millions by famine, both in Russia and in China, which also adopted Lysenko’s bogus theories.
Nobody is going to die from Nature‘s risible position on sex, but it will have consequences, as Andy notes:
This Nature article did not redefine sex as the title promised, but stripped it of meaning and rendered it entirely subjective.
Once you have done this, then you can dismantle women’s rights, sports and spaces (as sex is not meaningful), reject sexuality (because a person’s sex is not a reliable object of your desire) and dismantle protections and measurements to ensure fairness and representation for women in business and politics.
You also remove the ability for science to understand how your sex might have material and significant impact on your health and medical treatments.
And that is why this ideological capture of Nature is so worrying and depressing.
How can this be stopped? I don’t know if it can, but scientists can certainly speak out against this nonsense. For if it continues, every paper that separates organisms by sex will have to carry caveats. And it can’t just be humans, as sex is no less binary in humans than in other animals, for sex has to do not with how one “identifies”, but with biology. If Nature were true to its own editorial position, there would be no more mention of sex anywhere in the journal without the ridiculous caveats we saw above.
I’d heard about this kerfuffle, and wrote it off as a tempest in a petri dish until I saw this article in the Daily Beast. Surprisingly, the Beast, which I thought was on the liberal side of the spectrum, took sides against the Perpetually Offended, as it should have given the ridiculous nature of the fracas.
You can read about it at the website below or just peruse my short take her (click on screenshot):
The ignition: Michael Eisen, a well known professor of genetics at UC Berkeley, an advocate for “open” science publishing, and editor of the respected journal e-Life, answered a Twitter question about the most overhyped animal. He was clearly joking, as you can see below (Eisen’s also known for his sense of humor). Eisen suggested Caenorhabditis elegans, a roundworm that has been immensely useful in unraveling the genetics of development. It’s a “model organism,” which means that it’s studied in the lab rather than the wild.
This kind of mock dissing is applied to other “model organisms”, like the Drosophila I work on. That species, too, has taught us an immense amount about genetics and development, but throughout my career I’ve had to endure jokes about it not being a “real” species. I always laughed these off because a). it is a real species found in nature (it’s now a human commensal) and b). starting with T. H. Morgan in the early 1900s, it’s been the insect species used to study classical genetics, molecular genetics, and now evolutionary developmental biology (“evo devo”). From that species we’ve learned, for instance, about sex chromosomes, about gene duplication, about the linkage of genes on chromosomes, and so on—and that’s just the classical-genetics stuff.
I don’t think Eisen knew what he was getting into with his humorous response. (The worm is also a self-fertilizing hermaphrodite, which is what he means by “occasionally they fuck themselves”.)
C. elegans. They wiggle forward. They wiggle backwards. And occasionally they fuck themselves. That’s it. https://t.co/wYyXXViciJ
But he had to clarify himself again, for one clarification only leads to another if you’re facing the Woke. Although scientists have previously not been that immersed in Wokeness, they’re starting to become that way big time, buffeted by the winds of social change and perhaps a bit peevish and restive from the pandemic.
Something can be both an amazing model system and an incredibly boring creature – one might even say the latter is an advantage for the former.
Eisen even got faulted for using the word “fuck,” for his “frat boy humor” and for having a bit of fun on the Internet:
It’s like people forget Twitter is a public platform that reflects also on their professional life. This is something a frat boy would say and he doubled down, wondering why people are complaining he swore 🤦🏻♂️.
Some people, like Coleen Murphy, took umbrage because they had “grants and paper rejected based on *exactly* this reason.” I seriously doubt that this is literally true. Perhaps the rejections were based on a perceived lack of generality from results in C. elegans to other metazoan species, but they could have been rejected for other reasons. At any rate, that’s no reason to dump on Eisen. What we see here is animus aimed at editors and reviewers directed instead at Eisen:
Look, I'm sure he thinks this is all hilarious. But many of us have had grants and papers rejected based on *exactly* this reason (and you can't win- if it's conserved it's the same, and if not, it's just a worm thing) – all from a dude with HHMI funding and head of a journal.
The Beast gives a bit more information. (Ahna Skop’s tweets are now hidden.) The invocation of marginalized people is the new version of an old rule—I can’t remember its name—which said something like “Any Internet argument will eventually devolve to comparisons with Hitler.” Now it’s “systemic racism” instead of Hitler.
By far the most prolific poster in this vein was Ahna Skop, associate professor of genetics at the University of Wisconsin-Madison and previous recipient of a Diversity, Equality and Inclusion-based award in 2018. Dr. Skop—who did not respond to a request for comment by The Daily Beast—argued extensively that making jokes about worms was merely the tip of the iceberg when it came to making jokes about marginalized identities, or an example of a ‘bystander effect’, a psychological theory arguing that individuals are less likely to offer help to a victim in a crowd. (For is it not said: First they came for the worm people, and I said nothing, as I was not a worm person?)
In the resulting threads, Dr. Skop—who identifies as “part Eastern Band Cherokee” and “disabled with EDS”—and others consistently failed to publicly respond to Black scientists like herpetologist Chelsea Connor, who tried to point out that this was a ridiculous conflation. In a private communication Connor shared with The Daily Beast, Skop doubled down, arguing that as she had previously been harmed by entrenched sexism, her concerns regarding the worm joke were justified.
Oy! But sensible people like Dr. Berg tried to defuse the crisis with the correct claim “it was only a joke”. She included screenshots of Skop’s tweets:
Let us bring this ludicrous squabble to an end with a quote from the Beast (criticizing the Offended) and a cartoon encapsulating the gist of the battle:
In falsely equating the real oppression of people belonging to marginalized groups to a Twitter joke about a roundworm, Wormageddon 2020 offers a clear example of how white and white-passing women misuse the language of diversity, equality and inclusion, with little accountability and self-awareness, and without any interest in the hurt that such frivolous invocations cause the people they’re theoretically defending. Someone who took the struggles that marginalized people face in academia seriously, after all, would not invoke them to win a Twitter argument about whether a worm joke is rude. “That comparison should never have been the knee-jerk reaction for them,” Connor said. “And then the response [to criticism] should have been better… The harm done stays with us and they get to log out and forget that this ever happened and let it ‘blow over’ meanwhile we have to work to fix what they did.”
My take: Eisen and Connor 42, Offended Worm People 0. In this case Eisen properly refused to be mobbed, and the attempts to demonize him backfired, so that people like Skop have come off looking ridiculous. I’m just wondering if this episode shows a pushback against cancel culture, as did Trader Joe’s refusal to eliminate the brand names of its ethnic foods.
Two days ago I analyzed an article about hybrid parrots that had just appeared in the Washington Post. It was grossly misleading in assuming that two parrots of different “species” (they weren’t—one was a hybrid) had mated and produced, lo, a parrot of another “new species” (also wrong). I tweeted my correction to the Washington Post, but, to be sure they saw it, I also contacted the author of the post and her editor through another editor, pointing them to my correction.
In the meantime, I made a bet with a reader (you know who you are!) that they would not correct the errors. The reader said that they would.
I figured I’d let two days go by before looking for a correction or update, and that is now. And there is no correction, as you can see by clicking on the screenshot below.
Now granted, the story was by a local-issues journalist with no apparent scientific training, but it still contains scientific claims—claims that are wrong. And their responsibility is to correct them. As it is now, many readers think that a hybrid is the same thing as a new species, even though a single individual cannot be a new species (later there were two, but of course both were hybrids in an aviary).
What’s heartening is that many of the article’s 265 comments so far point out to reporter Vargas that the parrot chicks are not a new species but simply hybrids, and that breeders regularly produce hybrid parrots that they call “hybrids” and not “new species.” But even all those comments on top of a post by a petulant biologist won’t force the Post to admit its errors. FAKE NEWS, FOLKS!