Well, I’ll be! IFL Science highlighted the presence in Antarctica of the only melanistic penguin I’ve ever heard of. We’ve all seen or heard of melanistic squirrels and jaguars or leopards (both called “black panthers”); it’s a genetic trait and can be either dominant (one gene copy and you’re black) or recessive (two copies required). But penguins?
For a panoply of melanistic species, go here, and click on the screenshot to read the article:
The one-minute BBC video is below, and though I worried this penguin may be subject to predation or lack of potential mates, the IFL Science article (and the video) says it’s doing fine:
Adult emperors have black heads and wings, gray backs, and white bellies, with their distinctive yellow-orange markings around the neck. This particular penguin spotted when the Dynasties team were filming the Emperor episode in Antarctica, is almost entirely black, but does have the odd patch of white on its chest and wing tips, and a splash of yellow around its neck.
Sometimes, sadly, it’s not good to stand out in a crowd, though. The mutation can make animals with melanism more easy to spot by predators. In this penguin’s case, not just because it may be more visible on the ice, but because penguins’ white bellies make them look invisible to predators swimming below by helping them blend in with the light from the surface.
Though, as the BBC points out, this one isn’t doing too badly, having survived into adulthood.
In fact, according to the BBC the penguin is doing just fine. Filmed amongst hundreds of its besuited brethren and looking healthy, it appeared to show signs of looking for a mate while huddling for warmth with the other penguins.
It looks lonely to me, but maybe I’m just anthropomorphizing.
UPDATE: Reader Bill Turner sent this photo, taken by his wife Yvette, and added the caption,
“Your post today on a melanistic Emperor penguin prompted me to send the attached photos of a leucistic gentoo, taken at the Chilean Captain Arturo Prat Base on Greenwich Island on 24 December 2018. The bird was, apparently, quite a familiar sight around the island.”
Mark your calendar for tomorrow: Matthew Cobb, sponsored by the groups indicated below, will be talking about the scientific contributions of Rosalind Franklin, and will, I’m sure, dispel many misconceptions that have accreted around her life. He’s kicking off a series of talks on women in science.
This talk will be virtual, but you have to register in advance to see it (it’s free), and then test your connection, as there are two ways to connect. (The site walks you through it.) Registration is here, or you can click on the screenshot below. And. . . you can even ask questions.
Note that it’s at 11 a.m. Eastern time or 5 p.m. Central European Time.
Here’s Matthew’s own summary:
It’s a 40 minute talk (already recorded), followed by live Q&A that might go on for some time. It’s about Franklin’s life, not simply the DNA years. It puts particular emphasis on her post-DNA work on viruses, and casts a rather different light on people’s impressions of what the double helix meant at the time. It doesn’t go into her love life nor do I call her ‘Rosalind’. She is ‘Franklin’ throughout. It was fascinating working on this and helped clarify my views of her – which are even more positive than they were before I began. Includes lots of photos, extracts from her letters to Watson, etc etc.
And here’s the official blurb for the talk:
If you’ve registered, you can go here and click on the “Already registered? Click here” button, or click on the screenshot below. Note on the webinar page there’s a button for asking questions. Put Matthew in the hot seat!
The newly banded Rose-breasted Grosbeak is a gynandromorph, meaning that it is part male and part female. This particular Grosbeak is male on the right side and female on the left, making it a bilateral gynandromorph.
Researchers at the Carnegie Museum of Natural History said less than 10 bilateral gynandromorph birds have been documented in the reserve’s 64-year bird banding history. The reserve’s only other documented Rose-breasted Grosbeak bilateral gynandromorph was banded in 2005.
Annie Lindsay, Powdermill’s bird banding program manager, said finding the gynandromorph is a “once-in-a-lifetime experience.”
“One [of the banding team members] described it as ‘seeing a unicorn’ and another described the adrenaline rush of seeing something so remarkable. They all are incredibly grateful to be part of such a noteworthy and interesting banding record,” said Lindsay in a press release.
The fact the bird is a gynandromorph is discernible [sic] to the naked eye as it has physical traits of both male and female Grosbeaks. On the right, male side of its body, it has ruby wing pits and a ruby breast spot, along with black wing feathers. On the left it has yellow wing pits and a brownish, speckled wing.
At first, the color appears split down the middle insofar as the “wingpits” and breast color are concerned (see photos below of normal male and female), but the head of the bird shows no black on the male side, which it should if this was a truly “split” gynandromorph like the cardinal. Even young males have darker heads, but this bird has a full female head. Ergo, it appears to be a “more-than-half female” grosbeak. Researchers are waiting to see if it acts like a female or male; that is, can it produce eggs? Will it sing a male song? My prediction is that if the head is female, the chances are higher that the brain is female, and it will act like a female—if it can find a mate.
How do these part-male/part-female birds form? I discuss possibilities on the gynandromorph cardinal post, and, in the comments, readers suggest some other possibilities, but we don’t know for sure. It could involve chromosome loss, a non-genetic developmental accident, fertilization by “unreduced” sperm, and so on. Looking at the chromosomes on the male versus female parts of the bird might give a hint.
This year’s Nobel Prize in Chemistry was long anticipated, for the CRISPR/Cas9 system of gene editing was a tremendous accomplishment in biology and chemistry. It promises a lot, including curing human genetic disease (see the first five posts here). Remember, Nobel Prizes in science are designed to reward those who made discoveries potentially helping humanity, not those who just made general scientific advances.
A prize for developing the editing system was, then, almost inevitable. The only question was “who would get it?”, since several people contributed to the work that led to CRISPR/Cas9. It turns out that the Prize—in Chemistry—went to the two frontrunners, Jennifer Doudna of UC Berkeley and Emmanuelle Charpentier at the Max Planck Institute for Infection Biology in Berlin. Other serious contenders were George Church of Harvard, Virginijus Šikšnys at the Vilnius University of Biotechnology, Francisco Mojica of the University of Alicante, and Feng Zhang of the Broad Institute (the dispute was largely over whether those who developed ways to use the method in human cells also deserved the Prize). There will be a lot of kvetching today, but if I had had to pick two to get the prize, given that only three can get it au maximum, it would be Doudna and Charpentier. (They could have awarded up to six prizes if they’d split the CRISPR award between Physiology or Medicine and Chemistry.)
The press release from the Nobel Foundation says this:
Genetic scissors: a tool for rewriting the code of life
Emmanuelle Charpentier and Jennifer A. Doudna have discovered one of gene technology’s sharpest tools: the CRISPR/Cas9 genetic scissors. Using these, researchers can change the DNA of animals, plants and microorganisms with extremely high precision. This technology has had a revolutionary impact on the life sciences, is contributing to new cancer therapies and may make the dream of curing inherited diseases come true.
Researchers need to modify genes in cells if they are to find out about life’s inner workings. This used to be time-consuming, difficult and sometimes impossible work. Using the CRISPR/Cas9 genetic scissors, it is now possible to change the code of life over the course of a few weeks.
“There is enormous power in this genetic tool, which affects us all. It has not only revolutionised basic science, but also resulted in innovative crops and will lead to ground-breaking new medical treatments,” says Claes Gustafsson, chair of the Nobel Committee for Chemistry.
As so often in science, the discovery of these genetic scissors was unexpected. During Emmanuelle Charpentier’s studies of Streptococcus pyogenes, one of the bacteria that cause the most harm to humanity, she discovered a previously unknown molecule, tracrRNA. Her work showed that tracrRNA is part of bacteria’s ancient immune system, CRISPR/Cas, that disarms viruses by cleaving their DNA.
Charpentier published her discovery in 2011. The same year, she initiated a collaboration with Jennifer Doudna, an experienced biochemist with vast knowledge of RNA. Together, they succeeded in recreating the bacteria’s genetic scissors in a test tube and simplifying the scissors’ molecular components so they were easier to use.
In an epoch-making experiment, they then reprogrammed the genetic scissors. In their natural form, the scissors recognise DNA from viruses, but Charpentier and Doudna proved that they could be controlled so that they can cut any DNA molecule at a predetermined site. Where the DNA is cut it is then easy to rewrite the code of life.
Since Charpentier and Doudna discovered the CRISPR/Cas9 genetic scissors in 2012 their use has exploded. This tool has contributed to many important discoveries in basic research, and plant researchers have been able to develop crops that withstand mould, pests and drought. In medicine, clinical trials of new cancer therapies are underway, and the dream of being able to cure inherited diseases is about to come true. These genetic scissors have taken the life sciences into a new epoch and, in many ways, are bringing the greatest benefit to humankind.
I haven’t looked it up, but I think this is the first time that two women have been the sole recipients of any Nobel prize.(Correction: I should have said “Prize for Science”, for, as a reader pointed out below, two women shared the 1976 Nobel Peace Prize: Betty Williams and Mairead Corrigan. Their achievement was organizing to suppress sectarian violence during the Troubles in Northern Ireland.
Here’s the live stream of the announcement from Stockholm. The action begins at 11:45 with the announcement in English and Swedish, and the scientific explanation starts at 19:10.
Once again, although seven people, including Matthew, guessed the winners in our Nobel Prize contest (here and here), nobody got the Chemistry or Physics prizes. Given your miserable failures, I may have to have contest for the literature prize alone.
Matthew was also prescient in his book, Life’s Greatest Secret (2015), which includes this sentence:
“Whatever happens next, I bet that Doudna and Charpentier—and maybe Zhang and Church—will get that phone call from Stockholm.”
In 2017, I reviewed (favorably) Jennifer Doudna’s new book on CRISPR, A Crack in Creation, for the Washington Post. (Samuel Sternberg was the book’s co-author). The book is well worth reading, but I did have one beef connected not with the narrative, but with where the dosh goes for this discovery. Here’s what I wrote then:
. . . this brings us to an issue conspicuously missing from the book. Much of the research on CRISPR, including Doudna’s and Zhang’s, was funded by the federal government — by American taxpayers. Yet both scientists have started biotechnology companies that have the potential to make them and their universities fabulously wealthy from licensing CRISPR for use in medicine and beyond. So if we value ethics, transparency and the democratization of CRISPR technology, as do Doudna and Sternberg, let us also consider the ethics of scientists enriching themselves on the taxpayer’s dime. The fight over patents and credit impedes the free exchange among scientists that promotes progress, and companies created from taxpayer-funded research make us pay twice to use their products.
. . . . Finally, let us remember that it was not so long ago that university scientists refused to enrich themselves in this way, freely giving discoveries such as X-rays, the polio vaccine and the Internet to the public. The satisfaction of scientific curiosity should be its primary reward.
I’m not sure how the legal battle between the participants (via Berkeley and MIT) has shaken out, and can’t be arsed to look it up, but surely a reader or two will know
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.
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.
Occasionally in some species—mostly insects—we see the phenomenon of gynandromorphs: individuals that, through a genetic or developmental accident, have parts of the body that are male, and other parts that are female. They are patchworks of sex. These are most easily spotted in insects, but may have been missed in other species (alternatively, gynandromorph insects may be more viable than, say, gynandromorph mammals or birds, though I have posted on a gynandromorph cardinal). The various posts I’ve done on gynandromorphs are collected here.
Five years ago Matthew and I wrote a post about how gynandromorphs are formed, something well known genetically in our fruit flies (Drosophila). Using special genetic tools, we can also produce gynandromorphs at will. This involves a special X chromosome that gets lost easily during cell division. If you put one special X in females (XX), the tissues in which the X gets lost become XO, which happens to be male tissue, though XO males are sterile. The chromosome loss can happen at various stages of development, so you can get flies split straight down the middle (if the X gets lost at the first cell division), or flies with various-sized patches of male and female tissue.
Here are a few examples from flies (white bits are XO male parts and shaded are XX female parts). Note that the upper-left fly is split straight down the middle. I’ve seen a few of these in my time.
Finding gynandromorphs in nature is rarer, as wild insects are small, mobile, and not easily inspected. But the researchers on the paper below, published in The Science of Nature, found a gynandromorph jumping spider whose right half was male and left half was female. This is easily seen (given that the spiders are tiny: 4-6 mm, or 0.15-0.25 inches), for the spiders are sexually dimorphic, with the males having much larger fangs and chelicerae (mouthparts) than females, as well as different pedipalps (“palps”), distal segments of the legs that serve not only for sensory detection, but also for courtship display and sperm transfer in males.
Having a live spider whose right half is male and whose left half is female immediately gives you the chance to answer a question: “Does this weirdo spider behave as a male, as a female, or both?” This is the question that the researchers answered in the paper below.
You might be able to access the article by clicking on the screenshot, as it’s free with the legal UnPaywall app. The pdf is here and the full reference is at the bottom of this post. If you can’t get the pdf, make a judicious inquiry.
The jumping spider Myrmarachne formicaria is palearctic, and has been introduced in the U.S. The authors found one gynandromorph in Japan in October of 2016, as well as a bunch of normal males and females, which could be used to test the sexual/antagonistic behavior of the gynandromoprph. Here’s what it looked like (see caption below). The very large fangs and chelicerae can be seen on the spider’s right—the male side, as they’re much larger in males than in females. (We don’t know how this individual came about, though I suggest one way below.)
And the palps were also different on the two sides, for the male palps—the spider equivalent of a penis—differ from those of females. (a) shows the ventral view of the right palp in the gynandromorph, and (b) the ventral right palp of a normal male. As you see, the right palp is male, designed to hold sperm. The left palp of the gynandromorph (c) is identical to a normal female palp (d). Females receive sperm in the genital area (“epigyne”), put there by the male’s palps.
The genitals were also split down the middle, with the gynandromorph having a normal female epigyne (the female genital opening that receives sperm) on the left side (e), with a normal female shown in (f), while the right side of the gynandromorphs (arrow) is screwed up, as males don’t have epigynes.
So we have a spider split straight down the middle, from fore to aft. This may have involved the loss of a chromosome in an original female zygote, as normal female spiders are XX and males X0, lacking a Y chromosome. If an XX female zygote lost one X chromosome at the first cell division, one half of the spider would be female (XX) and the other half male (X0), and it could be split down the middle, as this one is. There are other explanations, but this seems the most likely.
So how did this gynandromorph behave—as a male or a female?
The results can be stated briefly: the spider behaved as a male and was perceived as a male by other males. In the (a) part below, you can see the behavior of normal males, who, when they recognize each other, bend their abdomens, move from side to side, open their legs and raise their chelicerae, and, occasionally, engage in battle, trying to topple each other with their chelicerae. (The numbers show the number of pairs in which different behaviors were seen; the one fight is at the bottom.)
(c) shows the gynandromorph male pitted against other males (four trials). The red spider is the gynandromorph; the black one a normal male. The same bending of the abdomen and moving from side to side (“pre-fighting behavior”) was seen in both spiders, indicating that the gynandromorph was not only perceived as a male, but itself behaved as a male. The arrow shows that all four antagonistic interactions terminated without a fight.
What about the gyandromorph faced with a female? Normal male-female courtship behavior is shown in (b). Males approach the female from the front, stretch their legs out to touch the female, and sometimes the female stretches out her legs, too. Neither of the two regular courtships resulted in a mating, which isn’t surprising. (Females are picky.)
Finally (d) shows the gynandromorph (red) encountering a female (black); there were two trials. The gynandromorph male approached the female and reached out his front legs to touch her, just like “normal” males. In these cases, though, the females ran away when this happened, so we don’t know if the females perceive the gynandromrph as male or as some kind of weirdo.
The paper also has videos of the mating and antagonistic behavior here.
The upshot: The gynandromorph, though morphologically half male and half female, behaves as a male, both in interactions with other males and with females. Further, it’s perceived as male by other males, while we don’t know how the female perceived its sex (she might even be confused). This shows that although morphology is split down the middle, behavior seems to be male-specific.
Why is this? We don’t know if the brain, presumably the seat of behavioral repertoires, is split down the middle, which might cause muddled behaviors. The inside of the spider might not show the same pattern as the outside. Alternatively, even though the brain might be half male and half female, the hormones and other chemicals that militate behavior might show male dominance, effacing any female behaviors. It’s interesting that the authors list seven other cases of gynandromorphs in spiders and insects, and in six of these the piecemeal individual behaved as male (the exception was a bee that didn’t show male-specific behavior towards a queen).
This experiment needs to be tried with Drosophila, and I don’t think it has been yet. For in flies we have far more sophisticated ways of changing very small parts of the fly from one sex to the other, and it would be better to use those methods than to use the relatively crude method of manipulating the parts of the fly visible only from the outside. With these techniques in flies, we could determine what parts of a fly must be male to show male behaviors, and what parts female to show female behaviors. That’s a really good question but, as Matthew said, “the cool kids aren’t interested in it.”
Suzuki, Y., Kuramitsu, K. & Yokoi, T. 2019. Morphology and sex-specific behavior of a gynandromorphic Myrmarachne formicaria (Araneae: Salticidae) spider. Sci Nat106, 34.. https://doi.org/10.1007/s00114-019-1625-x
Andrew Sullivan has devoted a lot of the last two editions of The Weekly Dish to the genetics of intelligence, perhaps because he’s taken a lot of flak for supposedly touting The Bell Curve and the genetic underpinnings of IQ. Now I haven’t read The Bell Curve, nor the many posts Sullivan’s devoted to the genetics of intelligence (see the long list here), but he’s clearly been on the defensive about his record which, as far as I can see, does emphasize the genetic component to intelligence. But there’s nothing all that wrong with that: a big genetic component of IQ is something that all geneticists save Very Woke Ones accept. But as I haven’t read his posts, I can neither defend nor attack him on his specific conclusions.
I can, however, briefly discuss this week’s post, which is an explication and defense of a new book by Freddie DeBoer, The Cult of Smart. (Note: I haven’t read the book, either, as it’s just out.) You can read Sullivan’s piece by clicking on the screenshot below (I think it’s still free for the time being):
The Amazon summary of the book pretty much mirrors what Sullivan says about it:
. . . no one acknowledges a scientifically-proven fact that we all understand intuitively: academic potential varies between individuals, and cannot be dramatically improved. In The Cult of Smart, educator and outspoken leftist Fredrik deBoer exposes this omission as the central flaw of our entire society, which has created and perpetuated an unjust class structure based on intellectual ability.
Since cognitive talent varies from person to person, our education system can never create equal opportunity for all. Instead, it teaches our children that hierarchy and competition are natural, and that human value should be based on intelligence. These ideas are counter to everything that the left believes, but until they acknowledge the existence of individual cognitive differences, progressives remain complicit in keeping the status quo in place.
There are several points to “unpack” here, as the PoMos say. Here is what Sullivan takes from the book, and appears to agree with:
1.) Intelligence is largely genetic.
2.) Because of that, intellectual abilities “cannot be dramatically improved”.
3.) Because high intelligence is rewarded in American society, people who are smarter are better off, yet they don’t deserve to be because, after all, they are simply the winners in a random Mendelian lottery of genes fostering high IQ (I will take IQ as the relevant measure of intelligence, which it seems to be for most people, including Sullivan).
4.) The meritocracy is thus unfair, and we need to fix it.
5.) We can do that by adopting a version of communism, whereby those who benefit from the genetic lottery get taxed at a very high rate, redistributing the wealth that accrues to them from their smarts. According to DeBoer via Sullivan,
For DeBoer, that means ending meritocracy — for “what could be crueler than an actual meritocracy, a meritocracy fulfilled?” It means a revolutionary transformation in which there are no social or cultural rewards for higher intelligence, no higher after-tax income for the brainy, and in which education, with looser standards, is provided for everyone on demand — for the sake of nothing but itself. DeBoer believes the smart will do fine under any system, and don’t need to be incentivized — and their disproportionate gains in our increasingly knowledge-based economy can simply be redistributed to everyone else. In fact, the transformation in the economic rewards of intelligence — they keep increasing at an alarming rate as we leave physical labor behind — is not just not a problem, it is, in fact, what will make human happiness finally possible.
If early 20th Century Russia was insufficiently developed for communism, in other words, America today is ideal. . .
Sullivan adds that the moral worth of smart people is no higher than that of people like supermarket cashiers, trash collectors, or nurses. (I agree, but I’m not sure that smart people are really seen as being more morally worthy. They are seen as being more deserving of financial rewards.)
6.) Sullivan says that his own admitted high intelligence hasn’t been that good for him, and he doesn’t see it as a virtue:
For me, intelligence is a curse as well as a blessing — and it has as much salience to my own sense of moral worth as my blood-type. In many ways, I revere those with less of it, whose different skills — practical, human, imaginative — make the world every day a tangibly better place for others, where mine do not. Being smart doesn’t make you happy; it can inhibit your sociability; it can cut you off from others; it can generate a lifetime of insecurity; it is correlated with mood disorders and anxiety. And yet the system we live in was almost designed for someone like me.
This smacks a bit of humblebragging, but I’ll take it on face value. It’s still quite odd, though, to see a centrist like Sullivan, once a conservative, come out in favor of communism and radical redistribution of wealth. So be it. But do his arguments make sense?
Now Sullivan’s emphasis on the genetic basis of intelligence is clearly part of his attack on the extreme Left, which dismisses hereditarianism because it’s said to imply (falsely) that differences between groups, like blacks and whites, are based on genetic differences. It also implies (falsely) that traits like intellectual achievement cannot be affected by environmental effects or environmental intervention (like learning). Here Andrew is right: Blank-Slateism is the philosophy of the extreme left, and it’s misguided in several ways. Read Pinker’s book The Blank Slate if you want a long and cogent argument about the importance of genetics.
But there are some flaws, or potential flaws, in Sullivan’s argument, which I take to be point 1-5 above.
First, intelligence is largely genetic, but not completely genetic. There is no way for a given person to determine what proportion of their IQ is attributable to genes and how much to environment or to the interaction between the two: that question doesn’t even make sense. But what we can estimate is the proportion of variation of IQ among people in a population that is due to variation in their genes. This figure is known as the heritability of IQ, and can be calculated (if you have the right data) for any trait. Heritability ranges from 0 (all variation we see in the trait is environmental, with no component due to genetics) to 1 (or 100%), with all the observed variation in the trait being due to variation in genes. (Eye color is largely at this end of the scale.)
A reasonable value for the heritability of IQ in a white population is around 0.6, so about 60% of the variation we see in that population is due to variation in genes, and the other 40% to different environments experienced by different people as well as to the differential interaction between their genes and their environments. That means, first of all, that an appreciable proportion of variation in intelligence is due to variations in people’s environments. And that means that while the IQ of a person doesn’t change much over time, if you let people develop in different environments you can change their IQ in different ways—up or down. IQ is not something that is unaffected by the environment.
Related to that is the idea that a person’s IQ is not fixed at birth by their genes, but can be changed by rearing them in different environments, so it’s not really valid to conclude (at least from the summary above) that “academic potential cannot be dramatically improved”. Indeed, Sullivan’s summary of DeBoer’s thesis is that the difference in IQ between blacks and whites (an average of 15 points, or one standard deviation) is not due to genes, but to different environments faced by blacks and whites:
DeBoer doesn’t explain it as a factor of class — he notes the IQ racial gap persists even when removing socio-economic status from the equation. Nor does he ascribe it to differences in family structure — because parenting is not that important. He cites rather exposure to lead, greater disciplinary punishment for black kids, the higher likelihood of being arrested, the stress of living in a crime-dominated environment, the deep and deadening psychological toll of pervasive racism, and so on: “white supremacy touches on so many aspects of American life that it’s irresponsible to believe we have adequately controlled for it in our investigations of the racial achievement gap.”
Every factor cited here is an environmental factor, not a genetic one. And if those factors can add up to lowering your IQ by 15 points, on what basis does DeBoer conclude (with Sullivan, I think), that you cannot improve IQ or academic performance by environmental intervention? Fifteen points is indeed a “dramatic improvement”, which according to DeBoer, we’d get by simply letting black kids grow up in the environment of white people. (I note here that I don’t know how much, if any, of that 15-point difference reflects genetic versus environmental differences; what I’m doing is simply asserting that even DeBoer notes that you can change IQ a lot by changing environments.)
Further, what you do with your intelligence can be further affected by the environment. If you’re lazy, and don’t want to apply yourself, a big IQ isn’t necessarily going to make you successful in society. So there is room for further improvement of people by proper education and instilling people with motivation. This doesn’t mean that IQ isn’t important as a correlate of “success” (however it’s measured) in American society—just that environmental factors, including education and upbringing, are also quite important.
What about genetic determinism and the meritocracy? It’s likely that many other factors that lead to success in the U.S. have a high heritability as well. Musical ability may be one of these, and therefore those who get rich not because they have high IQs, but can make good music that sells, also have an “unfair advantage”. What about good looks? Facial characteristic are highly heritable, and insofar as good looks can give you a leg up as a model or an actor, that too is an unfair genetic win. (I think there are data that better-looking people are on average more successful.) In fact, since nobody is “responsible” for either their genes or their environments, as a determinist I think that nobody really “deserves” what they get, since nobody chooses to be successful or a failure. Society simply rewards those people who have certain traits, and punishes those who have other traits. With that I don’t have much quarrel, except about the traits that are deemed reward-worthy (viz., the Kardashians).
This means, if you take Sullivan and DeBoer seriously, we must eliminate not just the meritocracy for intelligence, but for anything: musical ability, good looks, athletic ability, and so on. In other words, everybody who is successful should be taxed to the extent that, after redistribution, everyone in society gets the same amount of money and the same goods. (It’s not clear from Sullivan’s piece to what extent things should be equalized, but if you’re a determinist and buy his argument, everyone should be on the same level playing field.)
After all, if “the smart don’t need to be incentivized”, why does anybody? The answer, of course, is that the smart do need to be incentivized, as does everyone else. The failure of purely communist societies to achieve parity with capitalistic ones already shows that. (I’m not pushing here for pure capitalism: I like a capitalistic/socialistic hybrid, as in Scandinavia.) And I wonder how much of Sullivan’s $500,000 income he’d be willing to redistribute.
If you think I’m exaggerating Sullivan’s approbation of communism, at least in theory, here’s how he ends his piece, referring to his uneducated grandmother who cleaned houses for a living.
My big brain, I realized, was as much an impediment to living well as it was an advantage. It was a bane and a blessing. It simply never occurred to me that higher intelligence was in any way connected to moral worth or happiness.
In fact, I saw the opposite. I still do. I don’t believe that a communist revolution will bring forward the day when someone like my grandmother could be valued in society and rewarded as deeply as she should have been. But I believe a moral revolution in this materialist, competitive, emptying rat-race of smarts is long overdue. It could come from the left or the right. Or it could come from a spiritual and religious revival. Either way, Freddie DeBoer and this little book are part of the solution to the unfairness and cruelty of it all. If, of course, there is one.
Let’s forget about the “spiritual and religious revival” (I wrote about that before), and realize that what we have here is a call for material equality, even if people aren’t morally valued as the same. And why should we empty the rat-race just of smarts? Why not empty it of everything that brings differential rewards, like writing a well-remunerated blog? In the end, Sullivan’s dislike of extreme leftism and its blank-slate ideology has, ironically, driven him to propose a society very like communism.
Yesterday I wrote about Angela Saini’s misguided claim that human populations and races (I prefer “ethnic groups” rather than “races”) are basically genetically identical. So identical, in fact, that, as Saini argued, it’s entirely possible (or even likely) that the genomes of a South Asian and a white Canadian could be more similar than the genomes of two South Asians. That is wrong, but plays into Saini’s ideological bias that there are no appreciable or meaningful difference between biological races.
As I indicated, we now have sufficient data to show that the chances that her assertion is true is close to zero. Looking at the whole genome, you’re not going to find many South Indians whose DNA is more similar to that of a white Canadian than to that of another South Asian.
In trying to understand why Saini would make such a statement, I speculated that she had bought into the “Lewontin fallacy“: the claim by my ex Ph.D. advisor that the vast bulk of genetic variation segregating in our species occurs among individuals within populations, rather than among populations within a classically-defined “race” or among races.
From his mathematical analysis, Lewontin concluded that the term “race” has no biological reality. The error of Lewontin’s claim was pointed out by geneticist A.W.F. Edwards, who noted that Lewontin was treating each gene as independent. But they’re not, because the constraints of history, geographic separation, and evolution ensures that differences among populations and races at different genes are correlated. Taking these correlations into account, Edwards concluded this (characterized in Wikipedia):
In Edwards’ words, “most of the information that distinguishes populations is hidden in the correlation structure of the data.” These relationships can be extracted using commonly used ordination and cluster analysis techniques. Edwards argued that, even if the probability of misclassifying an individual based on the frequency of alleles at a single locus is as high as 30 percent (as Lewontin reported in 1972), the misclassification probability becomes close to zero if enough loci are studied.
And the use of cluster analysis is in fact the way that population-genetic studies are able to describe evolutionary history and ancestry from DNA data. I cited cluster analysis of the genetic structure of the British Isles as an example of how well one can deduce someone’s ancestry and geographic origin from looking at half a million base pairs—a small fraction of the total DNA in the human genome (about 0.02%).
I stand by my claim that Saini was wrong, but I did err on one count, one that doesn’t affect my conclusions but that I wanted to point out to be scientifically accurate.
And that is this: Lewontin’s original claim about the apportionment of genetic variation among individuals, populations, and races was incorrect. This was pointed out to me by reader, biologist, and polymath Lou Jost, who works at a field station in Ecuador. I vaguely remembered that Lou had done some work on this, but had forgotten, as he just reminded me, that work completely invalidates Lewontin’s method.
Lou has written several papers on this error, one of which you can access for free. (I have the other papers if you want the pdfs.) Click on the screenshot:
The math behind Lou’s arguments is above the pay grade of many of us (including me), but I, at least, am convinced that Lewontin was wrong for reasons beyond Edwards’s claim: he was wrong because, as Lou showed, he “used a measure of ‘differentiation’ that doesn’t really measure differentiation.” Lou presented an alternative diversity-based model that will allow you to compare differentiation within and among groups (this holds for species diversity in ecology as well as genetic diversity in and among populations), but he didn’t apply it to Lewontin’s data, because those data are outmoded now (they were based on electrophoretically derived allele frequencies).
The take-home lesson is that Lewontin’s conclusion is wrong not only because it applies to single loci assumed to be uncorrelated, but also because he used the wrong metric to compare within- versus between-group diversity. As Lou noted, the take-home lesson of Lewontin’s paper—that most of the genetic diversity in our species is present in any population of our species, with only smaller amounts added by looking at different populations or races—may still be right. But until Lou’s metrics are applied to the new and better data we have, we just won’t know.
Again, this correction affects an idea that I thought Saini might have been erroneously pondering when she made her misleading statement. It does not affect the fact that her statement is misleading, and that we really can distinguish populations and ethnic groups very well using genetic data—the more data the better. And it doesn’t affect my claim that Saini is either deliberately misleading people or is ignorant about the data on population differentiation in our species, and that her ignorance, willful or not, plays into her ideological narrative about “races.”
I stand corrected on the Lewontin issue, and thank to Lou Jost for setting me straight about the “Lewontin fallacy.”
Angela Saini is a British science writer who belongs to what I call the Cordelia Fine School of Science Journalism (CFSSJ): a school whose members have an explicit ideological bias that colors all of their popular writing. In the case of Fine, her ideology is that there is essentially no evolutionary/genetic difference between the brains and neurology of men and women, and so any behavioral differences we see are of purely social origin. Further, hormones play little or no role in behavioral differences between the sexes. Fine’s motive is good—to reduce sexism and bias—but her modus operandus is not, for it involves misrepresenting science.
In other words, the CFSSJ is characterized by tendentious science writing and confirmation bias, with the bias occurring in how studies are discussed. In the case of Angela Saini, her ideological bias is that all races are equal in any important aspect of biology, and that investigation of differences between races (or, as I call them, “populations” or “ethnic groups”) is liable to play into what she calls “scientific racism”. Ignore the fact that scientists have been trying for decades to debunk the misuse of science in buttressing racism, and most journalists, particularly those with little knowledge of genetics, haven’t been particularly helpful. Some, like Carl Zimmer, know their onions, while others, like Saini, apparently can’t grasp the fundamentals.
I’ve been struck, especially in the CBC interview with Saini shown below, by her willingness to make insupportable statements about differences between groups. I haven’t yet read her book on the topic, Superior: The Return of Race Science, as our library is closed and I don’t want to pay to support ideologically-based biology. But I’ve read other writings of hers, reviews of her books, both pro and con, as well as listened to YouTube videos and lectures. None of this has disabused me of the notion that she’s a member in good standing of the CFSSJ. Further, as we’ve discussed here, she’s misrepresented the situation at University College London by asserting that the scientists there have papered over the college’s history of eugenics and racism.
I’ll give you just one example of how Saini misrepresents the truth in the service of ideology. I was especially concerned about this one because the misrepresentation crops up frequently in discussion of genetics and “race”, and it’s time that people get the issue clear.
The error comes from an interview Saini did for the CBC’s “Quirks and Quarks” show, which you can hear by clicking on the link below. There’s also a partial transcript:
Here’s just one Q&A from that show, but it’s an important one:
Let’s move into the modern era then. Biologists have come up with a really strong scientific critique of the idea of race. Can you take me through that?
Well, for 70 years since this consensus after the Second World War, all that biology has done is reinforce the fact that we are so similar. We imagine the genetic differences between racial groups.
For example, I am of Indian origin. My parents [were] born in India. But if I were to randomly pick a South Asian person on the street and randomly pick a white, Canadian person on the street and test their genomes, it’s perfectly statistically possible for my genome to have more in common with a white person than with the Indian person. That’s how almost complete that overlap is. So we are incredibly similar as a species, and the vast majority of difference that we see is accounted for by individual difference.
Now I’ve tried to parse her statement in a way that it would be correct, but I can’t. In fact, the only way you can say that there’s any validity to her claim of no difference between the South Asians/white Canadians and South Asians/South Asians comparison is to construe “perfectly statistically possible” to mean that you might be able to find one or a couple of South Asians who, throughout their genomes, were more similar to some Canadians than they were to other South Asians. But you will almost never find that. We know this from the genetic data that already exist. You could equally well assert that it’s “perfectly statistically possible” for all the oxygen molecules in your room to move to the other side of the room at once, suffocating you. The error is taking what is possible and making people think that this is what’s common or probable.
In fact, all the genetic data we have shows that Saini’s implications about genetic similarity are wrong. If you want to validate her claim, you would have to look at gazillions of nucleotide bases in the DNA sequences of white Canadians and South Asians (I presume Saini means Indians, as she’s of Indian descent), and show that, on average, the proportion of DNA sites that had identical bases in Canadians vs. South Asians was about the same as the proportion of DNA sites that had identical bases in two randomly selected South Asians.
And that, according to the data we have, is not the case. Because of genetic similarities between populations that are spatially (and historically) contiguous, if you find identical bases at one DNA site, it becomes more likely that you’ll have identical bases at other sites. This is easily shown by combining DNA data from different regions of the genome (different “genes” or “SNPs”) to conduct a cluster analysis of overall similarity. And when you do that, you find that populations cluster based on history and geography. Assuming that, say, you’re not sampling a recent Indian immigrant to Canada as a “white Canadian”, or a Candian who lives in Mumbai as a South Asian, you can pretty well diagnose someone’s geographic ancestry—their “population”—from their genes. Here’s an example from 2015 on a very small scale, showing clustering within the British Isles (click on screenshot to access the paper):
Heres a diagram of the clustering, showing how easily someone’s population can be diagnosed from a large sample of DNA bases. Look, for example, at the demarcation between Devon and Cornwall—populations separated only by a river!
What this shows is that if you use information from the whole genome, people’s origins can be largely diagnosed, even on this small scale that used half a million DNA sites—a small fraction of all the DNA sites, which number 3 billion in humans). If you looked at South Asia versus white Canadians, you’d get even more differentiation. Saini’s claim that it’s likely or probable that you could find more similarity between a Canadian and South Asian than between two South Asians is palpably false.
I think where Saini went wrong is that she committed what’s known as “Lewontin’s fallacy,” named after my Ph.D. advisor and discussed in a paper by the geneticist A. W. F. Edwards. What Lewontin originally asserted, correctly, was that if you take all the genetic variation present in the human species, and apportioned it among individuals, among populations within a so-called “race”, and then among “races” (defined as the classical “races”), you find that of all the variation, 85% can be found among individuals within a population, 8% among populations within a “race”, and only about 6% between “races”. In other words, individuals within a population contain nearly all of the existing genetic variation of our species, and when you add different populations or different races, you don’t beef up the variation much more.
Lewontin took this to mean that there are no such thing as genetically differentiated races (as I said, I prefer, because of the historical freighting of “race”, to use “ethnic groups” or “geographically differentiated populations”). And that’s where he made his error. Lewontin is right if you look at each gene separately and then average the apportionment of variation among different genes. But genes among populations are not independent. As I said, if you’re different at one gene among ethnic groups, you’re more likely to be different at other genes as well. In other words, the structure of genetic variation, because of history and evolution, is correlated. I quote Wikipedia on Edwards’s refutation of Lewontin’s conclusion:
Edwards argued that while Lewontin’s statements on variability are correct when examining the frequency of different alleles (variants of a particular gene) at an individual locus (the location of a particular gene) between individuals, it is nonetheless possible to classify individuals into different racial groups with an accuracy that approaches 100 percent when one takes into account the frequency of the alleles at several loci at the same time. This happens because differences in the frequency of alleles at different loci are correlated across populations—the alleles that are more frequent in a population at two or more loci are correlated when we consider the two populations simultaneously. Or in other words, the frequency of the alleles tends to cluster differently for different populations
In Edwards’ words, “most of the information that distinguishes populations is hidden in the correlation structure of the data.” These relationships can be extracted using commonly used ordination and cluster analysis techniques. Edwards argued that, even if the probability of misclassifying an individual based on the frequency of alleles at a single locus is as high as 30 percent (as Lewontin reported in 1972), the misclassification probability becomes close to zero if enough loci are studied.
The cluster analysis mentioned by Edwards was used in the analysis of the British populations given above.
And if the misclassification probability of an individual becomes close to zero when you add more bits of DNA, as it does, then Saini is simply wrong. Yes, races are not nearly as genetically differentiated as early biologists thought they were, and yes, most of the variation in genes can be found in single populations and not among populations or “races”. But you can still genetically diagnose people as to ethnicity by looking at a big chunk of their DNA. South Asians will be more similar to other South Asians than to a white Canadian.
Most of the bits of genome used in these analyses don’t really do much, or have no functional significance in geographic differences in behavior, morphology, or physiology. But populations also differ in meaningful “adaptive” ways because of natural selection. Lactose tolerance and oxygen-carrying ability of the blood are two famous traits, and this paper by Sarah Tishkoff gives many more. Here’s a figure from that paper. It clearly shows that different populations differ in adaptive traits:
Now just because you can diagnose someone’s ethnicity or geographic origin from their genes does not in any sense buttress racism. All it shows is that our genomes reflect our historical and evolutionary ancestry. Saini, in her desire to show that there are no differences, doesn’t seem to realize that the genetic differences used to diagnose people do not place any races above others—there’s no support for any inherent superiority or inferiority of groups. But rather than admit the truth about genetic difference and then say it doesn’t matter morally or politically, Saini would rather throw out the inconvenient data. This is the hallmark of the CFSSJ: if the data go against your ideology, either ignore them or deny them. Or misrepresent them.
This has already gone on too long, but I’ll support my thesis about Saini’s ideologically based science by directing you to another review of Superior: The Return of Race Science, as well as to an Amazon review which is remarkably thorough. Both reviews discuss Saini’s insupportable and misleading claims about genetics. Looking over her claims (another is that there is no genetic variation within populations affecting cognition; see quote from Amazon review below), I can only conclude that in many places crucial to her thesis, she doesn’t know what she’s talking about.
The first requirement for writing sgood cience journalism or popular science books should be this: be sure you understand the science. Or, as Davy Crockett said, “Be sure you’re right first, and then go ahead.”
From the Amazon review of Superior:
On page 221, Saini says, “The question of whether cognition, like skin colour or height, has a genetic basis is one of the most controversial in human biology.” To be clear, this sentence is referring to the causes of individual variation in cognition, not the causes of differences between group averages. The question of whether or not group differences have a genetic basis is indeed controversial, but in 2019, making such a statement about the heritability of individual variation is equivalent to saying that it’s controversial whether or not global warming exists. Ideas such as the existence of global warming or the heritability of cognitive ability are controversial among some political activists, but among professionals in the relevant fields, these questions have been regarded as settled for more than twenty years.
If she really says that on page 221, it’s a howler. The heritability of IQ, for instance, is around 50%, which means that of the variation of IQ scores within a population, half of that variation is due to variation in genes.