The evolution of Cavalli-Sforza. Part IV

Walter Bodmer and Richard Lewontin at a conference, December 1965.
American Philosophical Society collection

The early 1970s saw two papers move the goalposts on race, first in academia and then throughout society. One was by Walter Bodmer and L.L. Cavalli-Sforza. The other was by a third geneticist, Richard Lewontin.

Bodmer and Cavalli-Sforza (1970) conceded that human races exist while denying that they differ statistically in intellectual capacity, at least on the basis of current evidence. Lewontin (1972) took a different tact: human races don’t exist. Period. No races, no race differences.

He came to this conclusion after analyzing the way various genes vary among human populations, specifically genes whose variants (‘alleles’) produce different blood groups, serum proteins, or red blood cell enzymes. Surprisingly, only 6.3% of this variation was accounted for by large continental races (i.e., ‘Caucasoids’, ‘Mongoloids’, and ‘Negroids’). Another 8.3% was accounted for by sub-racial populations. The rest—over 85% of human genetic variation—existed only among individuals of the same population.

This pattern had been known for some time with respect to blood groups. But researchers had assumed that some kind of balanced polymorphism was inflating within-population variation, perhaps one that hinders the spread of contagious diseases (1). By the early 1970s, however, the same pattern was appearing with other ‘structural’ proteins. The building blocks of flesh and blood were turning out to be remarkably the same in all humans. As Lewontin concluded:

It is clear that our perception of relatively large differences between human races and subgroups, as compared to the variation within these groups, is indeed a biased perception and that, based on randomly chosen genetic differences, human races and populations are remarkably similar to teach other, with the largest part by far of human variation being accounted for by the differences between individuals.

Human racial classification is of no social value and is positively destructive of social and human relations. Since such racial classification is now seen to be of virtually no genetic or taxonomic significance either, no justification can be offered for its
continuance.(Lewontin 1972, p. 397)

How did Cavalli-Sforza react? According to a recent interview, he saw this paper as a turning point in human genetics:

The between-population genetic variation observed with 650,000 SNPs on the 52 populations of the HGDP is 11% (Li et al. 2008) with a very small standard error. It becomes 16% for the X chromosome, as is expected if nearly all the genetic variation is due to drift—that is, the role of natural selection is very limited. The ca. 30-year-old estimate by Lewontin (1972) of this quantity (15%) was based on other markers and populations and was a reason to encourage banning the use of the word race in humans. In any case the new value is even more supportive of dropping the word race.(Manni 2010).

Yet back in the 1970s, and even long after, his reaction was …. silence. From 1972 to 1989, Google Scholar lists 426 publications for which Cavalli-Sforza was an author or co-author (2). None of them cited Lewontin’s 1972 paper. He first commented on it in 1993, some twenty years after the fact (3).

Why the two-decade silence? If Lewontin’s paper had been so important in human genetics, why did Cavalli-Sforza take so long to acknowledge this importance?

It is hard to enter a silent person’s mind. A better approach would be to ask whether any thinking person had reasons for rejecting Lewontin’s finding, or rather the way he spun it. Such reasons fall under three headings:

1. A small genetic difference can make a big cultural difference
Even if human populations differ only slightly in certain genetic predispositions, these slight differences can have big effects.

For instance, the historical economist Gregory Clark has argued that the slow but steady demographic expansion of the English middle class from the 12th century onward gradually raised the population mean for predispositions to non-violence, deferment of pleasure, and other future-oriented behavior. Although the embryonic middle class was initially a small minority in medieval England, its descendants grew in number and gradually replaced the lower class through downward mobility. By the 1800s, its lineages accounted for most of the English population (Clark 2007, pp. 124-129, 182-183; Clark 2009).

The 1800s also saw the triumph of Victorian morality in England. This triumph was due not to a massive change in the gene pool, but rather to a slow incremental change that had finally reached a critical mass. The English middle class could now impose its behavioral norms on the whole population, thereby abandoning the ‘two-tier morality’ of other class-stratified societies.

2. Lewontin’s finding is true only if you look at one gene at a time
Genes vary much more within than between human populations only if we take one gene at a time. This pattern reverses if we aggregate variation at several gene loci. The more we aggregate, the more this genetic variation will exist between populations and not within them.

This fact was known to Cavalli-Sforza back in 1966 when he was constructing his first phylogenies of human populations: “it is desired that the number of genes considered be as high as possible in order to increase the reliability of the conclusions.” (Cavalli-Sforza 1966). When he and another colleague later aggregated data from 75 gene loci of 144 individuals belonging to 12 human groups in Africa, Asia, Europe, and Oceania, he found very little genetic overlap among the groups. Most individuals clustered with other members of their regional group (Mountain & Cavalli-Sforza 1997). This point has also been made by Mitton (1977, 1978), Edwards (2003), and Sesardic (2010).

Clearly, two groups are easier to tell apart with several criteria than with one. With enough criteria, any overlap will shrink to zero and all individuals can be unambiguously assigned to either group. This is basic logic. But all this proves is that human populations are identifiable. It doesn’t prove that the differences between them are greater than the differences within them.

3. The way a gene varies within and between populations will itself vary as a function of the gene’s selective value
When genes vary between populations, they do so usually because the population boundary separates different environments with different sets of selection pressures. Genes that differ across this boundary are necessarily genes that make a difference, i.e., that have high selective value.

In contrast, selective value is necessarily low for genes that differ within a population despite similar selection pressures (unless the different variants form a balanced polymorphism).

The two kinds of genetic variation are therefore not comparable.

And this leads to another problem. Yes, we have a lot of data on the way genes differ between populations, but that data comes largely from genes with little or no selective value—the ones that are most likely to differ within populations! When population geneticists look for a gene worth studying, they tend to choose one that responds weakly to natural selection. This choice is deliberate. They want the gene to be as close to selective neutrality as possible so that it changes at a predictable rate (i.e., only through random mutations). It thus provides a reliable ‘clock’ of population history.

Population geneticists also prefer to study genes whose protein products are easy to find and measure in body tissues. Such ‘structural proteins’ are similar in different species or even different genera. Humans and chimps, for instance, look very much alike if we compare the protein building blocks of their body tissues. These two species have diverged from each other largely through evolutionary changes at a higher level, particularly regulatory genes that control the pace and timing of development.

This point was grasped by Stephen J. Gould (1977, 406). He explained how such genes provide a misleading picture of genetic variation:

The most important event in evolutionary biology during the past decade has been the development of electrophoretic techniques for the routine measurement of genetic variation in natural populations. Yet this imposing edifice of new data and interpretation rests upon the shaky foundation of its concentration on structural genes alone (faute de mieux, to be sure; it is notoriously difficult to measure differences in genes that vary only in the timing and amount of their products in ontogeny, while genes that code for stable proteins are easily assessed).

I remember telling a geneticist that Lewontin’s finding applied only to genes with low selective value. He laconically replied that there was no evidence that things would be any different for genes with higher selective value.

Actually, there is real-world evidence. The same genetic overlap that Lewontin found between human populations also occurs between many species that are nonetheless distinct in anatomy, physiology, and behavior (see previous post).

And Cavalli-Sforza in all this?

He was certainly aware that culture can amplify slight genetic differences. This was, in fact, part of his dual transmission theory—now known as gene-culture co-evolution (Stone & Lurquin 2005, p. 104-108).

He had also been aware since the mid-1960s that the genetic overlap among human populations is a function of the number of genes under consideration. In addition to his 1997 article with Joanna Mountain, this principle has been implicit in most of his work on human populations.

When questioned directly on this subject, with reference to Edwards’ reply to Lewontin (Edwards 2003; Khan 2006a), he diplomatically answered that both were right:

Edwards and Lewontin are both right. Lewontin said that the between populations fraction of variance is very small in humans, and this is true, as it should be on the basis of present knowledge from archeology and genetics alike, that the human species is very young. It has in fact been shown later that it is one of the smallest among mammals. Lewontin probably hoped, for political reasons, that it is TRIVIALLY small, and he has never shown to my knowledge any interest for evolutionary trees, at least of humans, so he did not care about their reconstruction. In essence, Edwards has objected that it is NOT trivially small, because it is enough for reconstructing the tree of human evolution, as we did, and he is obviously right.(Khan 2006b)

What about the third counter-argument? Was Cavalli-Sforza aware that genetic variation within populations is not comparable to genetic variation between populations? We see some awareness in his 1971 textbook, where he argues that most polymorphic genes have little selective advantage. Only in two cases are they subject to strong selection pressures. One case involves balanced polymorphisms. The other involves “transient polymorphisms”—genes quickly moving to fixation in those populations where they are advantageous (Cavalli-Sforza & Bodmer 1971, pp. 732-735). Such genes are thus more likely to vary between than within populations.

So perhaps he was aware. Or perhaps not. Even less clear is what he was thinking during his long silence on Lewontin’s 1972 paper. This paper was, after all, in Cavalli-Sforza’s own field of study. It was also widely commented on by other human geneticists. So why the silence?

One reason was his tenuous professorship at Stanford. It was this position that had propelled him to academic stardom, and he may have decided that discretion is the better part of valor. His pragmatism is recounted by a former colleague, Anthony Edwards:

When in the 1960s I started working on the problem of reconstructing the course of human evolution from data on the frequencies of blood-group genes my colleague Luca Cavalli-Sforza and I sometimes unconsciously used the word ‘race’ interchangeably with ‘population’ in our publications. In one popular account, I wrote naturally of ‘the present races of man’. Quite recently I quoted the passage in an Italian publication, so it needed translating. Sensitive to the modern misgivings over the use of the word ‘race’, Cavalli-Sforza suggested I change it to ‘population’. At first I was reluctant to do so on the grounds that quotations should be accurate and not altered to meet contemporary sensibilities. But he pointed out that, as the original author, I was the only person who could possibly object.(Sesardic 2010).

And the others in all this?

Lewontin’s paper met with either enthusiasm or silence. Two attempts at rebuttal were published in 1977 and 1978 by Jeffrey Mitton, a zoologist at a second-tier university. Another one was made much later, in 2003, by Anthony Edwards, a geneticist who no longer held an academic position. All three papers used the second counter-argument, i.e., within-population diversity exceeds between-population diversity only if you consider one gene at a time. Although I know several zoologists who are aware of the third counter-argument, none of them has ever written it up for publication.

Why did Lewontin’s paper meet with so little opposition? First, there was the wave of attacks on “racist” professors during the early 1970s, and the chill that subsequently spread through academic life. Many felt it best to be prudent. Second, there was the tenure-track system, which compelled untenured professors to ingratiate themselves with key members of academia. This system had always existed but was now being manipulated to advance an ideological agenda.

Thus began the soft totalitarianism of the late 20th century, not with a bang but with a whimper—or rather a silent acquiescence.

Notes

1. If your surface proteins differ from your neighbors’, you are less likely to be infected by contagious pathogens. There is thus selection for variability in surface proteins within each population.

2. In some cases, several references actually refer to a single paper (because of errors or variations in transcription). This overcount would not lead to an undercount of references to Lewontin’s 1972 paper.

3. He first cited Lewontin’s 1972 paper in 1990. His first substantive comments came three years later, when he cited it to show that genetic variation occurs mainly within human populations whereas cultural variation occurs mainly between them (Cavalli-Sforza 1993). This seems to be the only one of his publications that discusses the implications of Lewontin’s 1972 paper. All in all, he cited it three times in the 1990s and once in the 2000s.

References
Bodmer, W.F. and L.L. Cavalli-Sforza. (1970). Intelligence and race, Scientific American, 223(4), 19-29.

Cavalli-Sforza, L.L. (1966). Population Structure and Human Evolution, Proceedings of the Royal Society of London. Series B, Biological Sciences, 164, 362-379.

Cavalli-Sforza, L.L. (1993). “How are values transmitted?” in M. Hechter, L. Nadel, and R.E. Michod (eds), The Origin of Values, New York: Aldine de Gruyter, pp. 305-317.

Cavalli-Sforza, L.L. and W.F. Bodmer. (1971). The Genetics of Human Populations, San Francisco: W.H. Freeman and Co.

Cavalli-Sforza, L.L. and F. Cavalli-Sforza (2008). La génétique des populations : histoire d'une découverte, Paris: Odile Jacob. (translation of Perché la scienza : L’aventura di un ricercatore).

Clark, G. (2007). A Farewell to Alms. A Brief Economic History of the World, Princeton University Press, Princeton and Oxford.

Clark, G. (n.d.). The indicted and the wealthy: surnames, reproductive success, genetic selection and social class in pre-industrial England,

http://www.econ.ucdavis.edu/faculty/gclark/Farewell%20to%20Alms/Clark%20-Surnames.pdf

Edwards, A.W.F. (2003). Human genetic diversity: Lewontin’s fallacy. BioEssays, 25, 798-801.

Gould, S.J. (1977). Ontogeny and Phylogeny. Belknap Press: Cambridge (Mass.)

Khan, R. (2006a). 10 questions for A.W.F. Edwards, Gene Expression, August 28, 2006.
http://www.gnxp.com/blog/2006/08/10-questions-for-awf-edwards.php

Khan, R. (2006b). 10 questions for Luigi Luca Cavalli-Sforza, Gene Expression, August 24, 2006.
http://www.gnxp.com/blog/2006/08/10-questions-for-luigi-luca-cavalli.php

Lewontin, R. (1972). The apportionment of human diversity, Evolutionary Biology, 6, 381-398.

Manni, F. (2010). Interview with Luigi Luca Cavalli-Sforza: Past research and directions for future investigations in human population genetics, Human Biology, 82, 245–266.

Mitton, J.B. (1977). Genetic differentiation of races of man as judged by single-locus and multilocus analyses, American Naturalist, 111, 203-212.

Mitton, J.B. (1978). Measurement of differentiation: reply to Lewontin, Powell, and Taylor, American Naturalist, 112, 1142-1144.

Mountain, J.L. and L.L. Cavalli-Sforza (1997). Multilocus genotypes, a tree of individuals, and human evolutionary history, American Journal of Human Genetics, 61, 705-718.

Sesardic, N. (2010). Race: a social destruction of a biological concept, Biology and Philosophy, 25, 143-162.

Stone, L. and P.F. Lurquin. (2005). A Genetic and Cultural Odyssey. The Life and Work of L. Luca Cavalli-Sforza. New York: Columbia University Press.

The evolution of Cavalli-Sforza. Part III

Sir Walter Bodmer in 1977. He wanted to shut down research on race and IQ but had no academic credibility in human genetics. Cavalli-Sforza supplied the missing credibility.

The mid-1950s saw Cavalli-Sforza shift from bacteria to human subjects, with his studies of genetic drift in the villages of Italy’s Parma valley. In the mid-1960s, his scope of interest broadened as he used blood-group data to trace the ancestry of human populations, thus showing how they had progressively broken up to form the ones we know today.

What were Cavalli-Sforza’s views on race during this period? He seems to have been silent. In this, he followed the example of other postwar geneticists who were all too aware of the cloud of suspicion that hung over their heads. Cultural anthropologists were mostly the ones who talked about race, and they downplayed its importance.

The silence was broken in the late 1960s by two academics: a physicist, William Shockley, and a psychologist, Arthur Jensen. In 1969, Jensen argued in the Harvard Educational Review that African-American children had lower IQs for genetic reasons and that efforts to close the IQ gap, like Head Start, were doomed to failure.

This issue was already making waves in academia when Cavalli-Sforza came to Stanford University for a trial year in 1968-69. In Stanford’s genetics department, a close friend and colleague, Joshua Lederberg, had written a letter attacking attempts to link race to IQ. One of its signatories was another colleague, Sir Walter Bodmer (Stone & Lurquin 2005, p. 98).

Bodmer had experienced racism as a child (1). He wanted to refute this new racism in a high-profile journal, with a view to shutting down research on race and IQ. Unfortunately, he had no credibility in the field of human genetics, as Cavalli-Sforza would later discover when the two of them began writing The Genetics of Human Populations:

W. Bodmer spent several months in Italy, and a year in the United States for this collaboration. He was much stronger than me in mathematics, but he did not know human genetics and had only worked with the genetics of bacteria and fungi.
(Cavalli-Sforza & Cavalli-Sforza 2008, p. 169)

Bodmer asked Cavalli-Sforza to co-author a manuscript on race and IQ to be published in Scientific American. It is doubtful that Cavalli-Sforza had much to offer on the subject, having never written on it before.

But it would have been harder for him to refuse Bodmer’s request. He had no tenure at Stanford and his only friends there were Bodmer and Lederberg. The latter, in particular, had helped Cavalli-Sforza rebuild his career during the difficult postwar years and had been instrumental in getting him a position at Stanford. There was thus an implicit exchange of services. In return for past and future favors, Cavalli-Sforza lent credibility to an article that might otherwise have attracted less attention or, perhaps, never been published. It certainly allowed Bodmer to write the following ‘expert opinion’:

As geneticists we can state with certainty that there is no a priori reason why genes affecting I.Q., which differ in the gene pools of blacks and whites, should be such that on the average whites have significantly more genes increasing I.Q. than blacks do.
(Bodmer & Cavalli-Sforza 1970, p. 28)

According to Bodmer, such a statistical difference would be unexpected for two reasons. First, it could not result from chance events (e.g., genetic drift, founder effects, etc.) because intelligence is a polygenic trait. The laws of chance would thus prevent the many different genes from having, on balance, more intelligence-boosting variants in one human population than in another. Second, natural selection could not have created the black-white IQ difference because black Americans have been in the United States for only two hundred years. This is far too recent for their IQ to have diverged from that of white Americans, even with strong differences in natural selection.

The first argument is wrong. Stature is a polygenic trait, yet it will differ significantly among random samples taken from a single population. Although many genes are involved in stature, some have a much stronger effect than others, with the result that variation at such gene loci is not drowned out by other genetic variation. The phenotypic variation is therefore noticeable.

The second argument is also wrong. It assumes that the black-white IQ difference is limited to the United States. Yet no one has ever made this assumption, other than Bodmer.

After being published in 1970, the article was incorporated the following year into a textbook by the same two authors, The Genetics of Human Populations. Both publications presented several counter-arguments to the idea that IQ varies with racial background:

1. Although IQ seems to be highly heritable, with estimates ranging from 40 to 80%, it doesn’t follow that the black-white difference in IQ is 40-80% genetic. The difference could be entirely due to environmental causes. Heritability studies are based on twins who share a common social environment. In contrast, black and white Americans inhabit very different social environments.

2. Because of their unusual in utero environment, twins may provide inaccurate estimates of heritability.

3. Black Americans reportedly have higher IQs when the testers are black American. Thus, cultural factors, including the design of the IQ test itself, might account for the black-white IQ difference.

4. Other contributing factors might include maternal malnutrition and/or a deficient home environment.

5. Even if the black-white IQ difference is proven to be mainly genetic, this knowledge has no practical applications in a free and democratic society. In contrast, a putative environmental cause does have practical applications (e.g., improvements to schooling and nutrition, elimination of barriers to economic advancement, breaking down of cultural barriers, etc.). Even if these applications fail to deliver their promised outcomes, the negative impacts will be minor.

As for Bodmer’s natural selection argument, it was quietly dropped from The Genetics of Human Populations.

The two authors nonetheless acknowledged the possibility that the black-white IQ difference could be genetic:

In summary, therefore, we do not exclude the possibility that there could be a genetic component to the mean difference in IQ between black and white Americans, but simply maintain that presently available data are inadequate to resolve this question in either direction. (Cavalli-Sforza & Bodmer 1971, p. 799)

This position was surprisingly moderate and already trending toward reactionary. The early 1970s saw the beginning of efforts to purge academia of ‘racist’ professors. After Jensen’s 1969 article, students and faculty staged large protests outside his U.C. Berkeley office. He was denied reprints by his publisher and not permitted to reply to letters of criticism. Similar harassment was directed at other academics, such as psychologist Richard Herrnstein and sociologist Edward Banfield.

As a concession to this antiracist movement, Cavalli-Sforza and Bodmer added the following caveat:

We are, of course, aware of the dangers of either overt or implicit political control over scientific inquiry. The suppression of Galileo and the success of Lysenko are two notorious examples of the evils of such control. Most scientists, however, do submit to certain controls over research on human beings such as, for example, the right of an individual to be experimented on, and the confidentiality of the information collected by the census bureau. These controls are imposed to protect the individual from possible direct detrimental effects of scientific investigations. The treatment of the Jews in Nazi concentration camps is a testimonial never to be forgotten to the needs for such controls. There can be no doubt that in the present racial climate of the United States, studies on racial differences in IQ, however well intentioned, could easily be misinterpreted as a form of racism and lead to unnecessary accentuation of racial tensions. Since we believe that no good case can, at present, be made for such studies on scientific or practical grounds, it follows naturally that we do not see the point in particularly encouraging the use of government or other funds for their support […] (Cavalli-Sforza & Bodmer 1977, pp. 801-802)

This reasoning is more than a bit disingenuous. The existing controls concerned only how research was to be carried out. Here, the two authors were arguing for controls on the aims of research, the why.

It is also a bit silly to suggest that the Holocaust happened because the victims weren’t given consent forms. Many deportees had in fact signed forms promising that they would be sent to labor camps. Evidently, such documents were not worth the paper they were printed on. They were a lie. But how do you fight a lie in a society that criminalizes the mere fact of saying what you think? Nazi Germany practiced too much control, not too little.

Cavalli-Sforza himself knew about life in a controlled society, particularly during his wartime research with Dr. Prigge.

Professor Prigge was in no way a Nazi, but of course we spoke about the government with much precaution, whereas in Italy the criticisms against fascism were frequent and overt. Among all the people we met in Germany, none had heard about the Shoah or the concentration camps. We learned about their existence, in Italy, only after the war.
(Cavalli-Sforza & Cavalli-Sforza 2008, p. 35)

Of course, bad things can also happen in a free and democratic society. And they can happen just as often. The difference, however, is that their worst effects can be curtailed—by protesting against them, by denouncing those who are responsible, or simply by pointing out their existence. During the last war, the American and Canadian governments interned people of Japanese origin on the west coast. This was an injustice and was denounced as such at the time. But it did not lead to mass murder. Elsewhere, similar internments did.

Ironically, by endorsing controls on research, Cavalli-Sforza may have been acting on fears he had earlier acquired in a less free world. Today Jensen, tomorrow … who knows? Who will be next? Perhaps someone warned him against sitting on the fence. And then there was his wartime past ... Yes, a fearful mind is the devil’s playground.

By co-authoring the 1970 Scientific American article, Cavalli-Sforza helped initiate a process with long-lasting consequences. As an expert on human genetics, and as someone less politicized than other academics, Cavalli-Sforza gave key support at a key time to the soft totalitarianism that would overrun much of academia. The following decades would see increasing control of the marketplace of ideas (2).

Notes

1. "Walter Bodmer was born in Germany, in the city of Frankfurt am Main which Cavalli had coincidentally visited during World War II. […] Sir Walter’s early infancy had been deeply disrupted by events unfolding in Nazi Germany. His father was a Jewish medical doctor (his mother was a Gentile) with aspirations to academia. However, years before the Nazis took power in Germany, during the period known as the Weimar Republic, Bodmer’s father had already been told that his hopes of becoming a university professor were futile, given his “racial” background. In 1938, threatened by the Nazi political regime, he left Germany under the pretext of taking a vacation. He went to England, where he was soon followed by his wife and young son, who was then only two and a half years old."
(Stone & Lurquin 2005, p. 79)

2. Bodmer is perceived as being one of Cavalli-Sforza’s close associates. He was certainly the closest one during the 1970s, when they jointly wrote two textbooks and a number of articles. Bodmer is given nine mentions in the index to Stone and Lurquin’s biography of Cavalli-Sforza, many of which are lengthy. Strangely enough, he receives only three mentions in the autobiography, two of which are single sentences. It is also odd that the autobiography says nothing about the 1970 Scientific American article, which was Cavalli-Sforza’s first high-profile publication.

References

Bodmer, W.F. and L.L. Cavalli-Sforza. (1970). Intelligence and race, Scientific American, 223(4), 19-29.

Cavalli-Sforza, L.L. and W.F. Bodmer. (1971). The Genetics of Human Populations, San Francisco: W.H. Freeman and Co.

Cavalli-Sforza, L.L. and F. Cavalli-Sforza (2008). La génétique des populations : histoire d'une découverte, Paris: Odile Jacob. (translation of Perché la scienza : L’aventura di un ricercatore).

Jensen, A.R. (1969). How much can we boost IQ and scholastic achievement? Harvard Educational Review, 39, 1-123.

Stone, L. and P.F. Lurquin. (2005). A Genetic and Cultural Odyssey. The Life and Work of L.Luca Cavalli-Sforza. New York: Columbia University Press.

The evolution of Cavalli-Sforza. Part II

Guido Orefice (Roberto Benigni) explaining Italian race science to a class of schoolchildren. La vita è bella

What were Cavalli-Sforza’s initial views on race? The question does not come up in his publications before the 1960s, so we can only presume that his beliefs were like those of his peers, particularly Italian anthropologists.

But just what were those beliefs? A Latin version of Nazi racism? This seems to be the premise of the film Life is Beautiful (La vita è bella). The hero visits a local school and ridicules “racist Italian scientists” by posing as the perfect Italian:

Our race is superior. I've just come from Rome, right this minute... to come and tell you in order that you'll know, children... that our race is a superior one. I was... chosen, I was, by racist Italian scientists... in order to demonstrate... how superior our race is. Why did they pick me, children? Must I tell you? Where can you find… someone more handsome than me? (link)

In reality, wartime Italian anthropologists did not consider the Italian people to be a race, let alone a superior one. Nor did they conceptualize ‘race’ in sharply defined terms. Renato Biasutti (1878-1965), Raffaello Battaglia (1896-1958), and others promoted the view that human populations are dynamic, variable, and evolving. Meanwhile, Adriano Buzzati-Traverso (1913-1983) was contributing to the new field of population genetics.

Their world view actually differed little from that of most postwar anthropologists. If we take “the most important single work produced during the war period” (Cooper 1946), Le razze e i popoli della terra, initially published by Biasutti in 1941, we find that it was republished several times in the 1950s and 1960s. In 1959, it earned a favorable review from American Anthropologist, the harshest comments being: “The theoretical positions […] are often uncongenial to those reared in the epigonous Boasian tradition. […] Social structure is inadequately handled, and in contrast, minor racial differences are lavishly presented” (Hewes 1959, pp. 618, 620).

This is not to say that Cavalli-Sforza’s peers were antiracist. Clearly, they endorsed the race concept and accepted that human populations differ statistically not only in anatomical traits but also in mental ones. In this respect they were like many British and American anthropologists of the same time period. Race denialism, as we know it today, did not become predominant until the 1970s.

Such was the reality of ‘race science’ in fascist Italy. But reality is not everything. There is also mythology—the popular narratives that help us make sense of reality. In the years after World War II, this conflict would become a founding myth for the postwar era—the triumph of Good over Evil and the advent of a freer, fairer world... As such, it would energize the quest for social justice on many fronts: the Civil Rights movement in the U.S.; the struggle against colonialism; the peace movement, and so on. The terms ‘racist’ and ‘fascist’ would be used far more often after 1945 than during the war itself.

Thus, in pursuing his postwar career, Cavalli-Sforza soon realized that his past was a handicap. There were others like him: Kurt Waldheim, François Mitterand, Pierre Elliot Trudeau ... For such people, fascism was not the god that failed. It was the god that died. The world had irrevocably changed, and the time had come to bury the past.

After 1947, he would no longer cite his wartime publications. Later on, he changed his name from L.L. Cavalli to L.L. Cavalli-Sforza. The reason appears in his autobiography:

My father, Pio Cavalli, had died (while we were at Cambridge, in 1949), and Francesco Sforza, the second husband of my maternal grandmother, Maria Fumagalli, widow Manacorda, wanted to adopt me, in order to join his name to my family name.
(Cavalli-Sforza & Cavalli-Sforza 2008, p. 107)

The autobiography places the name change in 1950 (1). In that year, he would have been 28, was already married, and had children of his own. Such circumstances were not normally a basis for adoption, either under Italian law or by custom. Even more inexplicably, he was still publishing under his old name as late as 1953—four years after his father’s death. Google Scholar lists three publications by L.L. Cavalli in 1950, one in 1951, five in 1952, and two in 1953 (2).

Notes

1. Stone and Lurquin (2005, p. 27) state that he changed his name at the age of 27, hence in 1949 (date of birth = Jan. 25, 1922). This is impossible, since it was not until the summer of 1950 that he returned to Italy after two years of research abroad.

2. Sometimes more than a year will elapse between the submission of a manuscript and its publication. Perhaps this explains the 3-year lag in “implementing” his name change. On the other hand, one can easily make minor changes to a manuscript before it goes to press, particularly when one gets the galley proofs.

References

Biasutti, R. (1941). Le razze e i popoli della terra. Torino: Unione Tipografico/Editrice Torinese

Cavalli-Sforza, L.L. and F. Cavalli-Sforza (2008). La génétique des populations : histoire d'une découverte, Odile Jacob.

Cooper, J.M. (1946). Anthropology during the war III. Italy, American Anthropologist, 48, 299-301.

Hewes, G.W. (1959). World ethnographies and culture-historical syntheses, American Anthropologist, 61, 615-630.

Life is Beautiful - script
http://www.script-o-rama.com/movie_scripts/l/life-is-beautiful-script-transcript.html

Stone, L. and P.F. Lurquin. (2005). A Genetic and Cultural Odyssey. The Life and Work of L.Luca Cavalli-Sforza. New York: Columbia University Press.

The evolution of Cavalli-Sforza. Part I

Germ warfare was a priority for both Allied and Axis scientists. Was one of them a young L.L. Cavalli-Sforza?

With an academic life spanning almost half a century, L.L. Cavalli-Sforza has become perhaps the foremost authority on human population genetics.

He first entered this field in the early 1940s. As a medical student at the University of Pavia, he encountered Emilio Veratti, who lectured on Italian genetics, and Adriano Buzzati-Traverso, who specialized in fruit fly genetics. He went on to study the genetics of bacteria, specifically how to select strains that can better resist radiation and nitrogen mustard (mustard gas):

Starting in 1941, bacteria had become my major interest and in 1948 I gave a paper at the International Congress of Genetics in Stockholm on cross resistance to radiation and nitrogen mustard in E. coli based on work done earlier in Milan with Niccolo Visconti (Cavalli-Sforza 1992).

This account, written forty years after the facts, is consistent with a description he gave in 1950:

Nitrogen mustard resistance was found to be gradual or abrupt in increase in different experiments, only a moderate degree of resistance being acquired, which made a detailed analysis difficult. In E. coli K-12 nitrogen mustard resistance is not accompanied by higher resistance to radiations, as in the case of E. coli B. (Cavalli & Maccacaro 1950)

In the same article, he also described experiments to make E. coli more resistant to chloromycetin, an antibiotic. It is not clear where, when, or for whom this work was done, although some of this research could have been postwar (or early war, i.e., before the U.S. entry in Dec. 1941). The co-author, G.A. Maccacaro, had been supported by a grant from the Rockefeller Foundation, and the K-12 strain had been supplied by an American researcher.

In an earlier article, however, Cavalli-Sforza reported findings from another research project. These findings were the mean death times (i.e., time to death) of mice in response to progressively higher doses of anthrax and pneumococci (Cavalli & Magni 1947). This research was novel in that it measured time to death, as opposed to the percentage killed.

To learn more about this period of Cavalli-Sforza’s life, we can turn to his recent autobiography. Among other things, his research work took him to Germany:

I went to see him [Emilio Veratti] to ask him for advice about certain bacteriological research that I had conducted with Giovanni Magni, my college and faculty classmate. It had to do with a study on bacterial virulence using a mathematical method. Veratti told me that to his knowledge the only person who could help us was a German professor, Richard Prigge. We later discovered he was right.

[…] With Magni, in Como, we studied anthrax, which is still talked about today because it is one of the most fearsome bacteriological weapons

[…] it was not so difficult to measure bacterial virulence [in mice] and we continued our research because we really wished to study this mechanism with a view to creating possible vaccines.

At this point, the advice of Veratti, who had suggested that we try to obtain a scholarship to study at Frankfurt am Main with Prof. Prigge, the only European scientist who could understand the worth of our experiments, proved to be useful. We had the luck of getting a scholarship to spend the summer [of 1942] in Germany. (Cavalli-Sforza & Cavalli-Sforza 2008, pp. 31-34)

The autobiography mentions another stay in Germany, this time with the renowned geneticist Timofeeff-Ressovsky:

Buzzati asked us, Magni and me, to join him in Berlin, in August 1942, at the Berlin-Buch Kaiser-Wilhelm Institute of Genetics (now the Max-Planck Institute). It was a bit before our research stay in Frankfurt with Prigge.

At the time, the Institute was run by the famous Russian geneticist Nikolai Wladimirovich Timofeeff-Ressovsky, a man of an extraordinary personality, intelligent, likeable, and enthusiastic; in sum, very Russian.

[…] After my meeting with N.W. Timofeef, I decided that I would devote my career to genetics research. (Cavalli-Sforza & Cavalli-Sforza 2008, pp. 39)

One gets the impression that the meeting with Timoffeef in Berlin happened during a short stay, perhaps a single visit. Yet when Cavalli-Sforza dedicated his genetics textbook to Timoffeef in 1947, he called him “a friend and teacher, with the wishes that he will be able to continue his work” (Cavalli & Buzzati-Traverso 1947). These words suggest a longer working relationship.

Cavalli-Sforza’s autobiography provides the best account of his wartime research, but certain details contradict those in his earlier accounts. For one thing, the earlier ones (with one exception) have him studying E. coli, and not anthrax, although this contradiction may be more apparent than real. He could have been working with E. coli as a prelude to riskier work with anthrax. Alternatively, the E. coli work may have been postwar.

But the contradiction is more fundamental when it comes to his research aims. The earlier accounts have him seeking to create more resistant strains of bacteria, and not better vaccines. These two aims are contradictory because vaccines are normally made from weaker, not stronger strains. Perhaps he also wished to study drug resistance—a legitimate subject of medical enquiry. But why was he also interested in bacterial resistance to radiation and mustard gas?

This sounds more like germ warfare research. More precisely, he seemed to be working on ways to combine anthrax with chemical and radioactive agents, presumably as part of a single warhead.

We’ll probably never know the whole story. Perhaps even Cavalli-Sforza didn’t know. And does it matter? Neither side used germ warfare in WWII, out of fear that the other side would retaliate in kind. (Yes, our side had its own germ warfare program).

Still, it does matter. It certainly did to Cavalli-Sforza. He apparently dreaded having his wartime record brought up, and this dread would guide his behavior later in life ...

Note

During the war years and the immediate postwar era, Cavalli-Sforza published under the name of Cavalli. To date, I have been unable to locate his four wartime articles or even their titles.

References

Bonezzi, G, L.L. Cavalli, and G. Magni. (1943). Zentralbl Bakteriol, I Orig, 150, 17–25.

Cavalli, L. L., and G. Magni. (1947). Methods of analysing the virulence of bacteria and viruses for genetical purposes, Heredity, 1, 127–132; doi:10.1038/hdy.1947.8
http://www.nature.com/hdy/journal/v1/n1/abs/hdy19478a.html

Cavalli, L. L., and G. Magni. (1943). Zentralbl Bakteriol, I Orig, 150, 25–32.

Cavalli, L.L., and G. Magni. (1943). Zentralbl Bakteriol, I Orig, 150, 353–371.

Cavalli, L.L., and G. Magni. (1942). Boll d Soc Med Chir Pavia, 20, 609–624.

Cavalli, L.L. and G.A. Maccacaro (1950). Chloromycetin resistance in E. coli, a case of quantitative inheritance in bacteria, Nature, 4232, 991-992.

Cavalli, L.L. and A. Buzzati-Traverso (1947). Teoria dell'urto ed unità biologiche elementari, Milan, Longanesi.

Cavalli-Sforza (1992). Forty years ago in genetics: The unorthodox mating behavior of bacteria, in J.F. Crow and W.F. Dove (eds). Anecdotal, Historical and Critical Commentaries on Genetics, Genetics Society of America.http://profiles.nlm.nih.gov/BB/B/C/C/Z/_/bbbccz.ocr

Cavalli-Sforza, L.L. and F. Cavalli-Sforza (2008). La génétique des populations : histoire d'une découverte, Odile Jacob.