Change the language of ecology and evolutionary biology! An example from sickle-cell anemia.

March 8, 2023 • 9:00 am

I may have mentioned this article from Trends in Ecology & Evolution before, as it outlines all the possible harms that the language of ecology and evolutionary biology (EEB) can cause. Click to read:

Here’s one bit:

In recent years, events such as the coronavirus disease 2019 (COVID-19) pandemic and waves of anti-Black violence have highlighted the need for leaders in EEB to adopt inclusive and equitable practices in research, collaboration, teaching, and mentoring.

As we plan for a more inclusive future, we must also grapple with the exclusionary history of EEB. Much of Western science is rooted in colonialism, white supremacy, and patriarchy, and these power structures continue to permeate our scientific culture.

Here, we discuss one crucial way to address this history and make EEB more inclusive for marginalized communities: our choice of scientific terminology.

By now you should be familiar with this kind of writing, which can be simply copied from one ~~scientific field~~ practicum to another. Chemistry and physics have their own papers calling for a new inclusive terminology, too.

And once again we see the unproven assertion that the “colonialist, white supremacist, and patriarchal” nature of EEB has excluded minorities, and also that the language of the ~~field~~ practicum has been partly responsible for that exclusion.

This is doubly fallacious. It is neither the nature nor the language of science that has kept minorities out of the EEB pipeline, but racism in the past, bigotry whose effects have never been repaired, creating a longstanding underclass. It is change in the nature of society, not in the nature of science, that will create the equal opportunity allowing oppressed people access to careers in science.

And frankly, I consider the claim that the language of our field has contributed to that exclusion a risible proposition. “Field”, for example, which refers to an area of study, has been deemed racist because it harkens back to the days of the plantation. The folks at Stanford have decreed that it’s to be replaced by “practicum.” Thus the age-old ecological tradition of “fieldwork” is now supposed to be “my practicum of studying ecology in the outdoors.” That suggestion would be hilarious if it weren’t true.

Further, the journal American Naturalist has suggested that EEB is ridden with ableist terms, including the population-genetic concept of “fitness”. (By the way, that is my most-viewed post of all time, with nearly 150,000 views.) If any disabled person has been kept out of EEB by this term, or any others, I’d like to know about it, for of course this article gives no such instances.

The article above links to a fill-in form in which you can suggest your own inclusive or innocuous term to replace harmful ones. Go to this page by clicking on the screenshot:

This is part of “The EEB Language Project,” which aims to increase equity in the ~~field~~ practicum by changing words. You are invited to note your own “harmful term”, suggest a more inclusive replacement term, and then give comments. In this way the language of EEB will be Newspeaked into equity.

Now despite the patronizing nature of this project, much less its futility, it’s amusing for those of us in EEB to think of such terms. A colleague and I came up with half a dozen in just five minutes. Here’s one that, I’m sure, has stifled diversity in the field greatly. But to explain it, I must give a biology lesson.

Harmful term: “Heterozyote advantage”.

What it means: This is an example of where the genetic constitution at a single locus (chromosome site) is such that the heterozygote, containing two different gene forms, has a “fitness advantage” (substitute your own less ableist language) over either of the two homozygotes. The classic example (and one of the few we know of) involves the genetic disease sickle-cell anemia.

There are two forms at this gene, which produces the beta chain of hemoglobin: “S“, the so-called “normal allele” (substitute more inclusive language), and the mutant form (you can say “alternative allele”) s, responsible for causing the debilitating disease sickle-cell anemia.

The “s” allele arose when a mutation in the DNA coding for the beta chain (in the genetic code, GAG—>GTG), changed the amino acid in position six of the Hb β chain from glutamic acid to valine. That changes the charge of the hemoglobin molecule, affecting its behavior in the presence of the parasite. If you have only one copy of the mutant form (allele), ergo are a heterozygote with the genetic constitution Ss, you produce half normal and half abnormal hemoglobin, but half is good enough to allow you good health. And if you have two copies of the normal allele (SS), you’re of course also fine.

But if you have two copies of the sickle-cell allele (ss); you get sickle-cell disease, and will have a painful illness and in all probability die young.

The twist in this story is that if you are a heterozygote in West Africa, where malaria is prevalent and often fatal, the heterozygote has both good health and protection against malaria compared to the normal and abnormal “homozygotes”, SS and ss. We’re not sure why this is, but the presence of the single sickle-cell allele in a carrier makes its blood cells break open prematurely when infected by the malarial parasite. This impedes reproduction of the sporozoan parasite that causes malaria so Ss “carriers” gain some protection against the infectious disease. Normal homozygotes (SS) have blood cells that rupture on schedule, so if you’re SS, you can get malaria and die.

Thus we have a situation, but only in areas with malaria, where the normal homozygote is healthy but prone to malaria, the sickle-cell homozygote (ss) gets the genetic disease and dies young, but the heterozygote (Ss) is protected from both malaria and from sickle-cell disease. This is the classic case of heterozygote advantage (also called “heterosis”, “balanced polymorphism,” or “overdominance”).

If you measure the relative reproductive output of the three genotypes, giving the fittest one (Ss) a fitness of 1.0, you get these figures

SS = 0.85 (they produce 15% fewer offspring than Ss genotypes because of malaria)

Ss = 1.0. (genotype with highest production of offspring)

ss = about 0 (they don’t survive to produce any offspring).

Geneticists love this case because when the heterozygotes have the highest fitness, it actually maintains both alleles at stable frequencies in the population. Heterozygote advantage is a way to keep genetic variation in a malaria-ridden population. You can show that this fitness scheme will result in stable equilibrium allele frequencies of S = 0.87 and s = 0.13. As I said, this is a stable frequency, and if the gene frequencies deviate from it, they will return to the equilibrium.

In west Africa, the frequencies of the two alleles in fact match these predicted frequencies very well, supporting the value of mathematical population genetics. The frequency of homozygous ss individuals is the square of the frequency of the s allele, or about 1.7%. It is a sad but ineluctable result of population genetics that because heterozygotes are the fittest genotypes, roughly 2% of the offspring will be born with a fatal disease, and this is simply because the individual with two different alleles has the highest fitness. There is no single allele whose homozygote has the highest fitness, and so, generation after generation, this fitness scheme above produces a large number of doomed infants. (One could take the absence of such an allele as evidence against God, who could have created one. Apparently the death of genetically diseased infants serves some purpose in the deity’s scheme.)

In the U.S., where malaria is almost unknown, the fitness scheme above reverts to one in which the SS genotype has the highest fitness, Ss is a tiny bit lower (Ss individuals can have occasional sickling “crises”), and that of ss remains zero. Eventually, in areas lacking malaria, every individual will become SS and the “s” allele will be eliminated.

It is because of the ancestry of many American blacks from West Africa that one sees sickle-cell anemia almost exclusively in the offspring of two individuals descended from that area (Ss X Ss, one-quarter of whose offspring will have the disease). But in the U.S., lacking malaria, natural selection will eventually eliminate the “s” allele. It will, however, be very slow.

One last note: sickle-cell anemia was the first “molecular disease” ever discovered: a disease caused by a mutation in a single gene that alters the protein it produces. And it was discovered by none other than Linus Pauling and his colleagues, who published this famous paper in Science in 1949 (click screenshot to read, or go here if you’re paywalled).

Now, on to the language issue:

Why the term “heterozygote advantage” is harmful. You notice in the above discussion I’ve used several verboten terms in EEB, including “normal allele”, “mutant allele”, and “fitness.”

To that I will add the term “heterozygote advantage” itself, which is harmful in two ways. First, the term “hetero” privileges heterosexual individuals over other LGBTQ+ individuals. And the idea that Ss individuals have a “fitness advantage” is doubly harmful, for it not only incorporates the ableist term “fitness,” but suggests that one genotype has an “advantage” over the other two. In reality, the SS and ss individuals are to be seen as “differently abled”, although I can’t manage to find a way that ss individuals with sickle-cell disease are “abled”. Some deep thought may suggest a way.

What the term should be replaced with. This is dead obvious: “diversity advantage“. The Ss genotype is best because it has the most diverse allelic constitution, possessing two alleles instead of one. It privileges diversity over boring homogeneity, a result that is also a bonus.

From now on I suggest that my new term, which is mine, replace “balanced polymorphism,” “heterozygote advantage” (ableist), “overdominance” (that’s wholly offensive, conjuring up eugenics and superiority), and “heterosis” (again with the offensive “hetero”).

This is my contribution to inclusive language in EEB, which is mine. Lest you think the suggestion is dumb, remember that it’s no dumber than the notions of “relative fitness” and “fieldwork”, all slated for erasure in the new woke dictionary of EEB.

The coronavirus and some basic evolutionary genetics

February 7, 2021 • 9:15 am

by Greg Mayer

Jerry and I were both working independently on posts about the coronavirus. When we realized this, we conferred and decided to continue our efforts, but with some coordination and cross-fertilization. Jerry’s piece was posted on Friday.

[JAC: Greg has a “technical notes” section at the end which clarifies terms in the text that might confuse nonbiologists.]

1). Getting people vaccinated will impede the origin of new variants, because adaptive evolution is faster in larger populations. Widespread vaccination, by reducing the number of cases, will reduce the population size of the virus. Adaptive evolution is faster in large populations because selection is more effective in large populations; this is a well-known population-genetical result. And it’s also faster because large populations, by having a greater total number of mutations, explore more of the total mutational space—including the possibility of favorable double (or more) mutations in which the component single mutations are not favored but the combinations are. This is, in part, the principle behind the AIDS “cocktail” treatments: by attacking HIV in multiple ways at once, no single resistance-conferring mutation will allow the virus to escape, because if one drug doesn’t get it, another one will. Only having multiple mutations will confer resistance to the whole “cocktail”, but this is very improbable because the individual mutations, not being favored, will not accumulate. But in a very large sample (i.e., a large population), improbable things can happen.

There are also interesting issues of components of fitness or levels of selection in the evolution of viruses (or any disease-causing micro-organism, for that matter). Jerry discussed this in his piece, contrasting the evolution of virulence within an infected host versus transmissibility between hosts. These can be viewed as two components of reproductive fitness: competition to reproduce within the host, and competition to move to new hosts. Or it can be viewed as different levels of selection—individual selection among virus particles within hosts, and group selection between the populations of viruses between the hosts—they all get sneezed out to the next host as a group. The evolution of myxoma virus in rabbits in Australia, which Jerry discusses, has been interpreted from both points of view. The interest comes from the potential conflict between what’s “good” within the host (reproducing very rapidly), and getting to the next host. If you are too good at “taking over” the host, you might kill off the host before you can spread to the next host. And if you don’t spread, you go extinct. So, what’s good in the host may not be good for getting to the next host.

There’s also an interesting issue of what is the proper estimate of population size for the virus. Is it the number of viral particles? The number of hosts? For within-host selection, it would be the number of viral particles in that host. For selection between host populations, it might be nearer to the number of hosts. (I would guess that the theory for this has already been developed in the context of group selection theory.) Either way, fewer hosts, with lower viral loads within hosts, lowers the rate of adaptive evolution of the virus.

2.) By a *very* crude analysis, the UK variant does not show evidence of selection on its protein sequences. The ratio of Nonsynonymous (N) to Synonymous (S) mutations is 13/6 = 2.17, which is very close to the expected ratio of 2.66 for neutral (i.e., unselected) mutation in a completely *random* genome. The defect of this analysis is that the virus’s genome is of course not random. I would expect that someone with the genomic sequence and the right software is already carrying out a proper analysis using the actual nucleotide and codon distribution of the virus. (In fact, I wouldn’t be surprised if it’s already been done; not being a virologist, I don’t follow that literature.) A second, and perhaps more important defect, which would apply even to a proper analysis, is that nonsynonymous/synonmymous ratios average over sites for a whole protein or genomic sequence, so even strong selection at one or a few sites in a protein can be lost in a sea of neutral change in the rest of the protein. (See Technical note below for more details.)

There are other ways of inferring selection, and Jerry stressed one of those: if the virus evolves in parallel in multiple locations, that suggests the action of selection. We seem to be seeing that, independently, in several different locations, the same variant is spreading widely and increasing in frequency. If the variants were neutral, their frequencies would change only due to chances of sampling and which variant happened to get somewhere first, so we wouldn’t expect the same variant to “get lucky” and take over all the time.

Another hint of selection would be if substitutions affecting function (such as nonsynonymous mutations and deletions) are concentrated in a part of the genome known to be of adaptive significance, such as the spike protein. That protein is a highly functional part of the virus, for it’s the part it uses to stick to host cells. The UK variant shows at least two nonsynonymous mutations and one deletion in the spike protein, but without full data, I can’t say if this is a greater than expected number for the spike protein (which forms ca. 10% of the genome).

3). The variants are differentiated strains, not “mutations”. The identified variants differ by multiple substitutions, and thus are not a mutation, but the accumulation of multiple mutations. Some substitutions in a strain may be subject to selection, but others will not be. If we think of the virus as a “species” (which, being a collection of asexual lineages, is not quite what the virus is), then the variants or strains are like “subspecies”: differentiated descendants of a common ancestor, differing in a number of ways, some of which may be adaptive, while others may not be. (In biological species, subspecies interbreed, and thus are a form of geographical variation; in viruses, however, the variants can exist without interbreeding in the same geographic area, including inside the same host, so the analogy to subspecies is inexact.)

4). Some of the media, or at least reporter Apoorva Mandavilli of the NY Times, are grasping that virus evolution is key to the course of the pandemic. Words and phrases in her article include: “selection pressure”, “evolve” (4 times!), “evolving”, “evolutionary biologist”, “adaptation”, and “coronavirus can evolve to avoid recognition”. And here’s a statement in the article of the distinction between genetic drift and selection:

Some variants become more common in a population simply by luck, not because the changes somehow supercharge the virus. But as it becomes more difficult for the pathogen to survive — because of vaccinations and growing immunity in human populations — researchers also expect the virus to gain useful mutations enabling it to spread more easily or to escape detection by the immune system.

This article is a pretty direct affirmation of the importance of understanding how evolution works when dealing with viral diseases.

5). After the AIDS epidemic, we all should have learned the importance of evolutionary biology for transmissible diseases. The lessons learned during the spread, evolution, and control of HIV and other viruses are so clear that they have become textbook examples of evolutionary principles, from elementary grades to college texts. Epidemics are all about evolution.

6.) You should call it the “UK variant”. The article at Ars Technica from which I got the (limited) genomic data I used above, falls over itself trying not to use geographic terms because they cause “stigma”. This is stupid. One of the oldest practices in taxonomy is to name species after the place they are found. The native anole of the southern United States is named Anolis carolinensis, because the description was based on lizards supposed to be from Carolina. It was later found to occur all over the southeastern United States, with closely related forms (sometimes considered conspecific) on a number of West Indian islands. It has also been introduced all over the world, from California to Hawaii to Japan. It is still Anolis carolinensis. Stability of names is important, and names related to place are a useful mnemonic, since they require no knowledge of Latin or an arcane numbering system. (The article refers to the UK variant as “B.1.1.7”. If there’s only one variant this might do, but with multiple ones it becomes an exercise in memorization.)

Technical note. “Nonsynonymous” mutations are mutations of the DNA sequence which change the amino acid structure of the resulting protein. Because the genetic code is redundant (DNA codes for the same amino acid in more than one way), some mutations are “synonymous”, resulting in an unchanged protein. There are 549 possible mutations of the 61 amino acid coding codons (61 codons X 3 nucleotides per codon X 3 possible nucleotides to change into). Of these possible mutations, 399 are nonsynonymous and 150 are synonymous. (I couldn’t find these numbers anywhere, so I counted them up myself from the table in Muse and Gaut (1994); my count could be off, but, I hope, not by much.) If a protein coding DNA sequence has a completely random sequence (i.e. all 61 protein coding codons are equally represented), then mutations occurring at random will occur with a nonsynonymous to synoymous ratio of

N/S = 399/150 = 2.66

and, if the mutations are neutral, will be fixed (i.e. will reach a frequency of 100%) in the same ratio, which is where I got the expected N/S ratio of 2.66 for evolution by neutral mutation.

However, the DNA sequence is not random, so we usually express the nonsynonymous/synonymous ratio by looking at the rate of substitution per site. Thus, we divide the the number of nonsynonymous mutations by the number of nonsynonymous sites (i.e. the number of nucleotide positions which would give rise to a nonsynonymous amino acid if mutated), and similarly for synonymous mutations. This gives us the dN/dS ratio, which is expected to be 1 under neutrality, because we have normalized by the expected rates of each type of mutation. It is greater than 1 when there is positive selection in favor of new mutations. In calculating dN/dS, adjustments can be made for known biases in the process of mutation (e.g. the different rates at which mutations which change the ring structure of the nucleotides occur).

dN/dS ratios are subject to some of the same limitations as raw N/S ratios, including the averaging effect noted above. Yang and Bielawski (2000) is a modestly readable introduction to using rates of nonsynonymous versus synonymous substitution to detect selection.

Charlesworth, B. and D. Charlesworth. 2010. Elements of Evolutionary Genetics. Roberts, Greenwood Village Colorado. An upper level text, but not as daunting as some. Amazon

Diamond, J., ed. Virus and the Whale: Exploring Evolution in Creatures Small and Large. NSTA Press, Arlington, Va. Uses HIV as an example of viral evolution. Amazon

Emlen, D. J. and C. Zimmer. 2020. Evolution: Making Sense of Life. 3rd ed. Macmillan, New York. Uses influenza as an example of viral evolution. Amazon

Herron, J.C. and S. Freeman. 2014. Evolutionary Analysis. 5th ed. Pearson. Uses HIV as an example of viral evolution. publisher

Muse, S.V. and B.S. Gaut. 1994. A likelihood approach for comparing synonymous and nonsynonymous nucleotide substitution rates, with application to the chloroplast genome. Molecular Biology and Evolution 11:715-724. pdf

Yang, Z. and J.P. Bielawski. 2000. Statistical methods for detecting molecular adaptation. Trends in Ecology and Evolution 15:496-503. pdf

h/t Brian Leiter for the Ars Technica piece.

Genetic ignorance in the service of ideology

April 22, 2020 • 12:00 pm

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.

To buttress Fine’s ideology, her books aim at debunking every study that contradicts her preconceived thesis, even though there is now convincing indication of not only genetically based behavioral and morphological differences based on hormones, but also of differences in the brain. In contrast, Fine goes easy on studies that support her thesis.

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.

R.J. “Sam” Berry, 1934-2018

July 6, 2018 • 10:00 am

by Greg Mayer

Robert James ‘Sam’ Berry, Emeritus Professor of Genetics in the Genetics, Evolution and Environment Department at University College London, died on March 29 of this year, following a stroke the previous summer. For decades, Berry had been a major figure in population and ecological genetics. Announcing his death on the UCL website, department head Prof Andrew Pomiankowski wrote

With sadness we note the passing of Professor R J (Sam) Berry, who was the Professor of Genetics at UCL (from 1974) and an active member of the Genetics, Evolution and Environment Department up to the present, and a massive figure in evolutionary and ecological genetics, biodiversity and conservation biology. He was also a leading Christian and wrote extensively on science and religion. We will miss him greatly.

R.J. Berry at Callanish standing stones, Lewis, Outer Hebrides, ca. 2016. Courtesy A. Berry.

Born in Lancashire, he attended Shrewsbury School (Darwin’s alma mater), and did his undergraduate work at Cambridge under R. A. Fisher (whose mathematics, he confessed, was rather over his head). He then went to UCL, where he spent most of his career, receiving there his PhD, and, later, a DSc. In a brief history of his department, he noted its early Darwinian connection, and long affiliation with biological conservation. He did his PhD under the supervision of the mouse developmental geneticist Hans Grüneberg, but, under the influence of Oxonian Bernard Kettlewell, he quickly realized the importance of field work for understanding the genetics and evolution of populations in nature, and he became a lifelong field biologist. He later wrote of Kettlewell, in the preface to Inheritance and Natural History,

More especially, I would like to pay tribute to Bernard Kettlewell, who first taught me to understand and investigate genetical problems in natural populations, and to whom I shall always remain grateful for demonstrating so clearly that true science is vastly greater than the absurd reductionism that too often goes on in laboratories.

R.J. Berry and colleague in the field, ca. 1970s. Courtesy of A. Berry.

His scientific work centered on the nature, distribution, and causes of variation in natural populations, often involving populations on islands, especially the small islands of northwestern Europe, including the British Isles. His choice of study organism was usually a mammal of some sort, often voles, wood mice, and, especially, house mice. In doing so he expanded ecological genetics beyond the realm of the snails, butterflies, and other insects that had long been its focus. In his work on house mice he also expanded his geographic focus, encompassing the study of populations from around the world. This commensal species, carried by humanity all around the globe, found itself newly arrived in places as physically and biotically disparate as tropical Pacific atolls and Antarctic islands. Berry strove to understand the evolutionary underpinnings and consequences of the species’ remarkable geographic and ecological diaspora.

R.J. Berry on Deception Island, South Shetlands, in the far south Atlantic, austral summer 1999-2000; note the shorts. Courtesy of A. Berry.

In much of his mouse work, Berry studied non-metrical skeletal variations– not the lengths or shapes of bones, but the presence or absence of qualitative states, such as a foramen or ossicle being present or not. Such traits, being the result of both genetic and environmental factors during development, he aptly named “epigenetic polymorphisms”, explicitly using the term in its original (and useful) Waddingtonian sense. (C.H. Waddington was his PhD examiner.) One of his uses of these traits was to affirm that the Orkney vole was introduced from the Continent, a conclusion confirmed by later molecular work. An exhibit at UCL’s Grant Museum of Zoology last year highlighted some of Berry’s work, including 4000 house mouse skeletons used in his studies of evolution on islands.

A closeup of some house mouse skeletons at the Grant Museum. Note the skeletons from the Welsh islands of Skokholm and Skomer. Courtesy of A. Berry.

I was early attracted to his work, since my own interests also centered on the phenomena of island life, and I have been drawn to consult it again and again. Most recently, his work on island races and founder effects in wood mice has seemed relevant to my own interest in these phenomena in New Guinean birds, while his synthetic works on island faunas have proven very interesting for looking at the factors influencing island species diversity.

The latter works of Berry just mentioned– his syntheses of island faunas and natural history– reveal another major part of his contribution. Besides his technical papers, he was a superb synthesizer and presenter to the general public of the results of his and others’ studies. This is reflected most clearly in his four volumes in Collins’ New Naturalist series: The Natural History of Shetland (with J.L. Johnston); The Natural History of Orkney (with a revised edition in the Poyser Natural History series); Islands; and Inheritance and Natural History. In the latter, he summarizes and presents clearly not only his own work on British island mammals, but also the voluminous work carried out in Britain on snails, butterflies, grasshoppers, spittle bugs, etc.

The cover of Berry’s last New Naturalist. A St. Kilda wren (*Troglodytes troglodytes hirtensis*), an endemic subspecies produced by insular evolution, overlooks Village Bay on St. Kilda, while puffins and gannets, for which St. Kilda is an essential breeding stronghold, wheel overhead. It illustrates two of Berry’s greatest interests: the importance of islands for studies of evolution, and for conservation.

His interest in natural history led naturally to a strong interest in the promotion of conservation, and in this work he promoted and recognized the importance of dedicated amateurs to understanding biodiversity– what is now sometimes called ‘citizen science’. His New Naturalist books on Shetland and Orkney depended heavily on the contributions of local and amateur naturalists to achieve their comprehensive coverage, which he freely acknowledged. His conservation work was recognized by the National Biodiversity Network Trust, which awarded him Honorary Membership in 2009.

Berry was also active in scientific societies, being elected a Fellow of the Royal Society of Edinburgh in 1981, and being influential in the creation of the Biological Journal of the Linnean Society in its present form (as well as being President of the Society). He was the second editor of the Journal, and edited a number of important issues, including one on evolution in the Galapagos, for which he wrote the introductory essay “Darwin was astonished” (one of my favorite paper titles). In celebration of his many contributions, the Linnean Society has issued a virtual issue of many of his most important papers in the Journal. These articles are open access, and will give a good feel for the depth and range of Berry’s research.

R.J. Berry and colleague with a house mouse in front of a corn rick; ricks are fertile ground for collecting house mice; ca. 1970s. Courtesy of A. Berry.

He was an engaged member of the Church of England, and wrote a number of books arguing the essential compatibility of science and religion, and he was the Gifford Lecturer on natural theology in 1997-98. There have been notices and appreciations by a number of Church related organizations, including Christianity Today and The Faraday Institute for Science and Religion. Joining his religious convictions with one of his secular interests, he was a leading advocate of Christian environmentalism, and was a founder of A Rocha International and the John Ray Initiative, both prominent Christian environmental organizations.

As a prominent accommodationist, his views were in strong contrast to Jerry’s frequently expressed view, epitomized in Faith vs. Fact, that science and religion are incompatible. I can find no evidence that Berry’s work, in lab or field, was influenced by his religious commitments– in all of it he was a thoroughgoing participant in the mainstream of Darwinism. Indeed, I read his work for decades before appreciating his religious views. As John Maynard Smith said of Dick Lewontin‘s Marxism, Berry’s Christianity is not a readily evident determinant of his scientific conclusions.

The British Library interviewed Prof Berry for their Voices in Science project. You can listen to a few clips here, or to the full interview here.

R.J. Berry, showing off a vole for the camera. Courtesy of A. Berry.

I am grateful to my colleague Andrew Berry, Sam Berry’s son and lecturer on organismic and evolutionary biology at Harvard, for answering queries, providing photos, and commenting on an earlier draft of this post.

There is no listing of all Berry’s publications that I am aware of. I include here just a few works that I have read or own.

Berry, R.J. 1964 The Evolution of an island population of the house mouse. Evolution 18:468-483.

Berry, R.J. 1969. History in the evolution of Apodemus sylvaticus (Mammalia) at one edge of its range J. Zool. London 159:311-328.

Berry, R.J. 1977. Inheritance and Natural History. Collins, London.

Berry, R.J. 2000. Orkney Nature. T & AD Poyser, London.

Berry, R.J., T.J. Crawford and J.M. Hewitt, eds. 1992. Genes in Ecology. Blackwell, Oxford.

Berry, R.J. and F.E.N. Rose. 1975. Islands and the evolution of Microtus arvalis (Microtinae). J. Zool. London 177:395-409.

Berry, R.J. and H.N. Southern, eds. 1970. Variation in Mammalian Populations. Zoological Society of London Symposia 26. Academic Press, London.

Berry, R.J., F.H. Tattersall, and J. Hurst. 2008. House mouse. pp. 141-149 in Harris, S. and D.W. Yalden, eds. Mammal of the British Isles: Handbook. 4th ed. Mammal Society, Southampton.

Maynard Smith, J. 1985. Molecules are not enough (review of The Dialectical Biologist by Richard Levins and Richard Lewontin). London Review of Books.

Searle, J.B. … R.J. Berry, … and F. Johannesdottir. 2009. Of mice and (Viking?) men: phylogeography of British and Irish house mice. Proc. Roy. Soc. B 276: 201-207.

Richard Levins, 1930-2016

February 12, 2016 • 11:00 am

by Greg Mayer

Richard ‘Dick’ Levins, the John Rock Professor of Population Sciences at the Harvard School of Public Health, died on January 19 of this year. He was one of the most influential population biologists of the 20th century, and a close colleague and associate of Dick Lewontin, Jerry’s doctoral advisor.

Levins was an early and active participant in the group of biologists that, in the early 1960s, worked to unite ecology, evolutionary biology, and genetics into a unified and theoretically-rich science of the biology of populations. Included among this group was Dick Lewontin, Larry Slobodkin, E.O. Wilson, and, perhaps most saliently for Levins, Robert MacArthur.

Both Levins and MacArthur were skilled in mathematical theory, and both wanted to develop a unified, general, and realistic theory of ecology and evolution. They collaborated on a number of seminal papers, and Levins (1966) wrote an important exposition and defense of the style of modeling that he and MacArthur favored, and which proliferated throughout population biology. The self-conscious unification of ecology and evolutionary biology in which Levins participated was an important event in the history of the field, but it has received little attention from historians. Sharon Kingsland touches on it in her Modeling Nature, but the most extensive treatment I know of is in E.O. Wilson’s memoir, Naturalist (though see note below.)

Wilson had a spectacular falling out with Levins and Lewontin in the 70s, so other accounts would be welcome. Some flavor of the movement, its goals, and participants, can be found in the 1968 symposium volume Population Biology and Evolution, edited by Lewontin, which included contributions by Levins, MacArthur, and Slobodkin, and which was favorably reviewed by Wilson in Science.

Though both Levins and MacArthur were accomplished theoreticians, both also had a natural-historical side (MacArthur, famously, “really knew his warblers“), and it is in fact Levins’ empirical side that first attracted my attention. Levins had a farm in Puerto Rico, and later was professor at the University of Puerto Rico. While there, he had a collaboration of many years with Harold Heatwole, documenting the biogeography of the biota of Puerto Rico and the nearby Virgin Islands, which involved substantial field work.

Levins was most interested in the insects, while Heatwole is a herpetologist. As Heatwole put it, this field work taught Dick “to love ants for themselves.” (There is no good online list of Levins’ papers, but those written with Heatwole are listed at the latter’s website.)Their 1981 paper with Michael Byer is rich in data and modestly synthetic, with a good bibliography. Their work was of great interest to me, as my dissertation field work was concentrated in the Virgin Islands, and my 2012 paper cited below is basically an update of the herpetological data parts of their 1981 paper.

But there was also one important theoretical paper, “On the distribution of organisms on islands”, that came out of their island collaboration. Published in 1963 in the Caribbean Journal of Science, it contains, in capsule form, the equilibrium theory of island biogeography, deriving the species species richness of an island biota from the balance of extinction and colonization.

This is of course, the theory made famous by, and now universally associated with, MacArthur and Wilson, who also first published on it in 1963, but in the more prestigious journal Evolution. The Levins and Heatwole paper has been almost universally overlooked. (Ilkka Hanski and I have cited it.) This could be a lesson in choosing your publication outlets wisely, but, in fairness to MacArthur and Wilson, their paper was more comprehensive, and explored more ramifications. Given the close connections among Levins and the latter two, it would be interesting to know how the ideas developed so as to result in near simultaneous publication of the same basic idea.

Levins did later develop some of the theory from his and Heatwole’s paper into the theory of metapopulations, which looks at a species’ distribution over a region as a “population of populations”– some populations going extinct, while new ones form by colonization, leading to a dynamic landscape of the species’ presence and absence. In fact, the basic metapopualtion model is to this day called the “Levins Model”.

When I was a graduate student, including doing some work in Lewontin’s lab in the Museum of Comparative Zoology, Levins had students based with Lewontin at the MCZ, but, being across the Charles River at the School of Public Health himself, I rarely saw him, and never discussed with him either his field work in Puerto Rico and the Virgin Islands, or the circumstances surrounding the development and publication of his and Heatwole’s version of the equilibrium theory of island biogeography, a failing which, to this day, I regret.

Levins was a lifelong communist, which was evident in his activities with groups such as Science for the People, and his affinity for Cuba and North Vietnam. I could not detect any hint of his political philosophy in his biological work, but John Maynard Smith, perhaps the greatest British evolutionary biologist of the second half of the 20th century, and himself an ex-Marxist who became disillusioned by communism, thought otherwise:

Levins was a Marxist before he was a biologist, and all his work shows it. His book Evolution in a Changing Environment, although it avoids the usual jargon, is the work of a conscious Marxist. I also think that it was a major contribution to ecology…. It is perhaps ironic that he made extensive use of mathematical techniques borrowed from capitalist economic theory: I cannot criticise because I have done the same. Since that time, he has worked more on applications of ecological theory. The essays in this book [The Dialectical Biologist] on pesticides, on Latin community health, and on applied biology in the Third World, reflect these interests. They illustrate the power of Marxism in the right hands. I have long thought of Levins as a rare example of a scientist whose work has been strengthened by adherence to a philosophy – Marxism or any other – and this book has confirmed that view.

Like Ernst Mayr before him– a synthesist of an earlier generation– Levins was able to participate in a symposium and celebration of his life’s achievements– “The Truth is the Whole”– organized at Harvard by his colleagues and students in the year before his death. Reminiscences by a number of his colleagues have been posted at the symposium website.

Richard Levins in Maricao, Puerto Rico, in the early 1950s (from radicalismojudio.org). — Dick Levins in Maricao, Puerto Rico, in the early 1950s (from radicalismojudio.org).

Heatwole, H. R. Levins and M.D. Byer. 1981. Biogeography of the Puerto Rican Bank. Atoll Research Bulletin 251. pdf

Kingsland, S. 1985. Modeling Nature. University of Chicago Press, Chicago.

Levins, R. 1966. The strategy of model building in population biology. American Scientist 54:421-431. pdf

Levins, R. 1968. Evolution in Changing Environments. Princeton University Press, Princeton, N.J.

Levins, R. and H. Heatwole. 1963. On the distribution of organisms on islands. Caribbean Journal of Science 3:173-177.

Levins, R. and R.C. Lewontin. 1985. The Dialectical Biologist. Harvard University press, Cambridge, Mass.

Levins, R., and R.H. MacArthur. 1966. The maintenance of genetic polymorphism in a spatially heterogeneous environment: variations on a theme by Howard Levene. American Naturalist 100:585–589.

Lewontin, R.C., ed. 1968. Population Biology and Evolution. Syracuse University Press, Syracuse, N.Y.

MacArthur, R.H., and R. Levins. 1967. The limiting similarity, convergence and divergence of coexisting species. American Naturalist 101:377–385.

Mayer, G.C. 2012. Island lists of West Indian amphibians and reptiles. Puerto Rico and the Virgin Islands. Bulletin of the Florida Museum of Natural History 51:136-147. pdf

Maynard Smith, J. 1986. Molecules are not enough [review of The Dialectical Biologist]. London Review of Books 8(2):8-9. link

Wilson, E.O. 1994. Naturalist. Warner Books, New York.

Wilson, E.O. 1969. The new population biology [review of Population Biology and Evolution]. Science 163:1184-1185.

* N.B. This book– Slack, N.G. 2010. G. Evelyn Hutchinson and the Invention of Modern Ecology. Yale University Press, New Haven, Conn.– may treat this important episode: Hutchinson was MacArthur’s thesis advisor, but I have not read it.

Will Provine died

September 3, 2015 • 12:00 pm

I’m saddened to report that historian of science and population geneticist Will Provine, a professor at Cornell, died on September 1 at 73. His wife has posted an unbearably sad memoriam on her Facebook page, and Casey Bergman, one of our Chicago Ph.D. students and now a professor at Manchester, reported the news on his website An Assembly of Fragments.

Will was a student of my own Ph.D. advisor, Dick Lewontin—Dick’s first student who was a historian rather than a working scientist. (Dick went on to work with and mentor many other students of the history and philosophy of science.) Will’s Ph.D. thesis became a short book, The Origins of Theoretical Population Genetics (1971), that was (and remains) essential reading for students in population genetics.

Will was a delightful guy, but those who knew him quickly learned that he pulled no punches. He was, as they say, “strident”: strident about creationism and intelligent design, which he detested, strident about religion (he was a diehard atheist, although, as I recall, his father was a preacher), and strident in his later-life opposition to genetic drift, which he viewed—erroneously, I think—as a misguided concept. Religionists often quoted with disdain his remark about the incompatibility of science and religion, “You have to check your brains at the church-house door if you take modern evolutionary biology seriously.”

But opinionated as he was, he was a pleasure to talk to, ever friendly and helpful. As Casey wrote on his site:

I’m moved by his death to recall my experience of having Provine as a lecturer during my undergrad days at Cornell 20 years ago, where his dramatic and entertaining style drew me fully into evolutionary biology, both as a philosophy and as a profession. I can’t say I knew Provine well, but I can say our interactions left a deep impression on me. He was an incredibly kind and engaging, pulling you onto what he called the “slippery slope” where religious belief must yield to rationalism.

And that is my impression, too.

A long time ago Will developed brain cancer—a glioma, as I recall, which is a deadly form of the disease. He spoke openly about it and gave the impression that he didn’t have long to live. But he beat the odds, and must have survived for at least 15 or 20 years after diagnosis.

I remember that when we held a retirement symposium for Dick Lewontin at Harvard, Will gave the opening talk, and was wearing on each side of his head a metal disk with a target on it—a target for the radiation therapy aimed at his tumor. At that time we thought he would die soon, and that, combined with his deeply moving tribute to Lewontin, brought many of us to tears. It was the only time in my life that I saw Dick in tears as well: he had to put his head in his hands.

But it is a great mercy that Will lived so long after that talk—which was years ago—and remained active to the last. I, and many others, will miss him.

William-Provine — Will Provine (1943-2015)

Exclusive pictures: the Crafoord Prize in Biosciences

August 28, 2015 • 12:00 pm

On January 15 I announced that the prestigious Crafoord Prize in Biosciences was awarded jointly to my Ph.D. advisor Dick Lewontin and Tomoka Ohta for their work on genetic variation in natural populations. (See the press release here.) I am pleased to present the photographs of the May 6 ceremony in Stockholm, in which the King of Sweden (who of course also hands out the Nobel Prizes), gave the pricey gold medal to Ohta and to Lewontin’s representative, my friend Andrew Berry (Lewontin couldn’t make it). There’s also a handsome check: about $500,000. A few details about the Prize from Wikipedia:

According to the Academy, “these disciplines are chosen so as to complement those for which the Nobel Prizes are awarded”. Only one award is given each year, according to a rotating scheme – astronomy and mathematics; then geosciences; then biosciences. A Crafoord Prize is only awarded when a special committee decides that substantial progress in the field has been made.

The King gives the prize to Berry:

Berry then conveys the prize to Lewontin at Harvard, with Dick showing proper humility:

The King gives the prize to Ohta:

Ohta and Berry; as Andrew said, “between us Ohta and I are a pretty good embodiment of human polymorphism”:

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