Category: human biology

Finally: a sensible discussion of “race”

March 23, 2018 • 11:15 am

And by “sensible,” of course, I mean a discussion that aligns with my own views. I’ve often written that while there are no finite and strongly genetically demarcated human “races”, there are meaningful and statistically diagnostic differences between populations, ethnic groups, or whatever you want to call them. This is in opposition to the common Left-wing view that races are purely “social constructs” having no biological reality.

Well, there aren’t a finite number of groups whose members are 100% genetically differentiated from other groups. But when you take all genes together, there are sufficient average frequency differences that one can discern statistical clusters that, in turn, allow you to use lots of genes to pretty much diagnose where somebody’s from and who their ancestors were. These “statistical clusters” are real, not social constructs, for they fall out regardless of the politics or biases of the investigator.

Recognizing their existence by no means justifies bigotry or stereotyping, but we shouldn’t dismiss the existence of those clusters simply because, in the past, people with an incorrect idea of “race” have used differences to justify segregation and prejudice. Yet all too often, as with genetic differences among ethnic groups, behavioral differences between the sexes, and evolutionary psychology, those on the Left simply dismiss entire fields because of a fear that scientific research will justify discrimination. And in theory it could, as it did in the past, but it’s better to know the facts and at the same time absorb the idea that the moral and legal equality of all humans, and the equality of opportunity they deserve, does not depend on evolutionary or genetic details. For if it did, then scientific findings could be used to justify prejudice—something that all humanists reject. Asserting that entire fields, like genetic analysis of human ethnic groups, are simply parsing “social constructs” is a form of anti-intellectualism that will stifle scientific progress. If some Leftists had their way, for instance, there would be no evolutionary psychology, no attempt to understand the evolutionary roots of modern human behavior. Do we really want to impose a moratorium on such work?

The recognition of genetic clusters as meaningful entities is the point that David Reich makes in the article given below. Reich, as you may know, is an accomplished professor of genetics at Harvard who’s done a lot of work on DNA-based human and primate phylogenies, human disease genes, interbreeding among ancient lineages of hominins (e.g., Denisovans, Neanderthals, etc.), and mapping human ancestry by looking at statistical grouping. (There’s a big NYT article about his work here.)

I highly recommend you read his essay in the New York Times‘s Sunday Review (click on screenshot):

I’ll give just two quotes from Reich: one about the scientific data and the other about its moral implications—or lack thereof. But read the article!

The data:

[After the 1972 paper of my advisor Dick Lewontin], a consensus was established that among human populations there are no differences large enough to support the concept of “biological race.” Instead, it was argued, race is a “social construct,” a way of categorizing people that changes over time and across countries.

It is true that race is a social construct. It is also true, as Dr. Lewontin wrote, that human populations “are remarkably similar to each other” from a genetic point of view.

But over the years this consensus has morphed, seemingly without questioning, into an orthodoxy. The orthodoxy maintains that the average genetic differences among people grouped according to today’s racial terms are so trivial when it comes to any meaningful biological traits that those differences can be ignored.

The orthodoxy goes further, holding that we should be anxious about any research into genetic differences among populations. The concern is that such research, no matter how well-intentioned, is located on a slippery slope that leads to the kinds of pseudoscientific arguments about biological difference that were used in the past to try to justify the slave trade, the eugenics movement and the Nazis’ murder of six million Jews.

I have deep sympathy for the concern that genetic discoveries could be misused to justify racism. But as a geneticist I also know that it is simply no longer possible to ignore average genetic differences among “races.”

Groundbreaking advances in DNA sequencing technology have been made over the last two decades. These advances enable us to measure with exquisite accuracy what fraction of an individual’s genetic ancestry traces back to, say, West Africa 500 years ago — before the mixing in the Americas of the West African and European gene pools that were almost completely isolated for the last 70,000 years. With the help of these tools, we are learning that while race may be a social construct, differences in genetic ancestry that happen to correlate to many of today’s racial constructs are real.

Recent genetic studies have demonstrated differences across populations not just in the genetic determinants of simple traits such as skin color, but also in more complex traits like bodily dimensions and susceptibility to diseases. For example, we now know that genetic factors help explain why northern Europeans are taller on average than southern Europeans, why multiple sclerosis is more common in European-Americans than in African-Americans, and why the reverse is true for end-stage kidney disease.

I am worried that well-meaning people who deny the possibility of substantial biological differences among human populations are digging themselves into an indefensible position, one that will not survive the onslaught of science. I am also worried that whatever discoveries are made — and we truly have no idea yet what they will be — will be cited as “scientific proof” that racist prejudices and agendas have been correct all along, and that those well-meaning people will not understand the science well enough to push back against these claims.

And how we should handle the future discoveries of genetics:

For me, a natural response to the challenge is to learn from the example of the biological differences that exist between males and females. The differences between the sexes are far more profound than those that exist among human populations, reflecting more than 100 million years of evolution and adaptation. Males and females differ by huge tracts of genetic material — a Y chromosome that males have and that females don’t, and a second X chromosome that females have and males don’t. [JAC: I find this statement somewhat misleading, because he’s talking about “biological” differences, not differences in genetic content, and the Y chromosome doesn’t have many genes.]

Most everyone accepts that the biological differences between males and females are profound [JAC: Again, it’s not clear what he means by “profound,” but I’d agree that they are there and that they do explain differences between the sexes in both morphology and behavior.] In addition to anatomical differences, men and women exhibit average differences in size and physical strength. (There are also average differences in temperament and behavior, though there are important unresolved questions about the extent to which these differences are influenced by social expectations and upbringing.)

How do we accommodate the biological differences between men and women? I think the answer is obvious: We should both recognize that genetic differences between males and females exist and we should accord each sex the same freedoms and opportunities regardless of those differences.

It is clear from the inequities that persist between women and men in our society that fulfilling these aspirations in practice is a challenge. Yet conceptually it is straightforward. And if this is the case with men and women, then it is surely the case with whatever differences we may find among human populations, the great majority of which will be far less profound.

An abiding challenge for our civilization is to treat each human being as an individual and to empower all people, regardless of what hand they are dealt from the deck of life. Compared with the enormous differences that exist among individuals, differences among populations are on average many times smaller, so it should be only a modest challenge to accommodate a reality in which the average genetic contributions to human traits differ.

It is important to face whatever science will reveal without prejudging the outcome and with the confidence that we can be mature enough to handle any findings. Arguing that no substantial differences among human populations are possible will only invite the racist misuse of genetics that we wish to avoid.

Between the unwarranted pseudoscientific statements of Nicholas Wade and James Watson on one hand (both criticized in Reich’s article) and the genetic blank-slateism of various ideologically-biased scientists and cultural anthropologists (who don’t act like scientists) on the other, lies the reasonable position—the one limned by Reich.

Greg’s Take on Reich’s Article

by Greg Mayer

I also like Reich’s article, but if he hopes to be able to talk about genetic differentiation, he’s going to have to stop accepting the “race is a social construction” fallacy, because that means everyone who thinks race is a social construction, or been convinced it is because they keep getting told it is, will ignore everything else he says. As he points out, there is measurable genetic variation; that that variation can be important (clinically, cognitively, etc.); and that that variation allows the identification of the geographic origin of individuals– and the latter is what race means. (As always, I use the zoological definition of a geographic race or subspecies. Subspecies may be described when it is the case that if you show me a specimen I can tell you where it is from, and, conversely, if you tell me where it is from I can tell you what it looks like.) The mass of genetic data on humans now allows us to divide indigenous populations  (i.e. pre-Columbian) into so many races that fit the zoological definition of a race that one of the chief arguments against recognizing races is that there are too many recognizable races– 23 and Me is selling microracial identification on television! Very fine scale genetic data make recognition of geographic groupings so easy that the problem with subspecies isn’t that you can’t tell them apart, but rather you can tell everything apart, even local populations.  Nomenclaturally, subspecies are optional, and there could be reasons, both practical and social, not to name them.

Reich cites Dick Lewontin‘s 1972 apportionment of diversity finding (which, of course, is true), but then doesn’t mention (or perhaps even realize) that that finding  says nothing about whether there are recognizable races. What Reich does do, although more indirectly than I would, is to argue that human moral equality must not rest upon an empirical finding of no genetic differences, because then the finding of genetic differences will undermine the argument for moral equality. I 100% endorse him on the principle that human moral equality should NOT depend on an empirical argument about genetic differentiation. The problem with basing human moral and civil equality on empirical claims about human biological similarity is that such claims may prove to be mistaken. Anthony Tony Edwards, in his commentary on Dick’s 1972 paper, says it quite nicely:

“But it is a dangerous mistake to premise the moral equality of human beings on biological similarity because dissimilarity, once revealed, then becomes an argument for moral inequality.”

[Also, Reich seems terribly naive if he thinks “Most everyone accepts that the biological differences between males and females are profound.” I predict he will be assailed from the left on this point. And, Jerry and I wrote our commentaries independently of one another.]

h/t: Rodney, Greg

A human chimera

March 4, 2018 • 10:45 am

Reader Tom Alves called my attention to the singer Taylor Muhl, a human chimera. Chimerism is the situation in which an individual results from the fusion of two early-stage fertilized eggs (zygotes), and thus has the genetic constitution of two separate individuals. This is a very rare condition: geneticists estimate that there are fewer than 100 people on Earth known to have it. That’s probably a big underestimate, though, as it’s often hard to diagnose. As Live Science explains:

Muhl has a type of chimerism called tetragametic chimerism. This can happen in cases of fraternal twins, where there are two separate eggs fertilized by two separate sperm, and the two zygotes “merge and form one human being with two different cell lines,” said Dr. Brocha Tarshish, a clinical geneticist at Nicklaus Children’s Hospital, in Miami, who is not involved in Muhl’s case. This happens very early in embryonic development, Tarshish said.

Most of the time, people with chimerism probably go undiagnosed, Tarshish said. Indeed, without specific biomedical tests (such as genetic testing), it’s impossible for doctors to tell that a patient is a chimera, according to a 2009 paper about the condition. But there may be subtle clues to this condition: Some people with chimerism have “patchy” skin coloration (like Muhl does) or different-colored eyes, the paper said. In some cases, chimerism is diagnosed when a person is found to have two different blood types.

Muhl discovered her condition when she noticed a difference in pigmentation on her torso that runs right down the middle, as shown in this picture from her Instagram site:

She also noticed, and you can see this on some pictures on the internet, that features on her left side are larger than those on the right. This suggests that the twins differed in genes affecting body size. (She also has a double tooth on the left side of her mouth.) I see that in her eyes and nose:

Finally, she’s been ill most of her life. That’s explained by the fact that she’s a fusion of two different people with genetically different tissues (since she’s fused with her sister’s embryo, the two sides share only half of their genes), so her immune system from one twin is constantly trying to reject the foreign tissue of the other—and there are also two immune systems.  Apparently Muhl has an allergic reaction to some metals on one side of her body but not the other.

Further, Live Science, the Independent, and The Daily Mail (actually, the Mail‘s story is decent), report that Muhl has two different lymphatic systems and “two bloodstreams”. The circulatory system thing I don’t understand, for Muhl has only one heart, and that has to pump all the blood through her body. That means that the circulatory systems, if they are genetically different, still have to be fused into one functional system. She’s also reported to have two blood types.

Sometimes human chimeras are detected through paternity tests: a woman’s somatic cells, which are sampled to get her genotype, might be from one zygote, while her ovaries, which produce the eggs, could be from another. That means that her children would share only 1/4 of her genes instead of 1/2, something that could be detected genetically. The American woman Lydia Fairchild is one of these cases. She separated from her husband, and having had three children with him, had to take a paternity test when she and her ex-husband were dealing with child support. The tests showed that while her ex-husband was the father of all the kids, she didn’t seem to be. Although her kids were almost removed from her, they eventually found out that Ms. Fairchild was a chimera: her skin and hair cells didn’t match the genotype of her kids to the required degree, but her cervical cells did. Fairchild was a woman with two different genotypes.

One wonders if a male twin could fuse with a female, and produce a double-sex person. I know of no such cases, though male cells from a woman’s own fetus can be incorporated in parts of a woman’s body—a phenomenon called “microchimerism.” As Scientific American reported:

A 2015 study suggested that this happens in almost all pregnant women, at least temporarily. The researchers tested tissue samples from the kidneys, livers, spleens, lungs, hearts, and brains of 26 women who tragically died while pregnant or within one month of giving birth. The study found that the women had fetal cells in all of these tissues. The researchers knew that the cells were from the fetus, and not from the mother, because the cells contained a Y chromosome (found only in males) and the women had all been carrying sons.

Here’s a video of Muhl from a television show that tells a little bit more of her story.

 

In an article on race and medicine, New York Times does its best to ignore and denigrate race

December 11, 2017 • 10:15 am

Furthering my claim that the New York Times is becoming more regressive in its Leftism, we have a long article in the science section on race and medicine. The thing is, the author of the piece does his very best to pretend that there’s no such thing as “race”, even while investigating—and buttressing, to some extent—the connection between race (or ethnicity, if you will) and illness.  But the ideological petticoat of author Moses Velasquez-Manoff shows throughout, particularly at the end. Valasquez-Manoff, a science writer, lacks science degrees, which may explain his cluelessness about how scientists conceive of “race,” but, given that I tried to explain it to him in a long phone interview, I doubt it.

I’ve explained my take on “race” many times before, and you can search for it on this site. (If you want just one article, go here, which summarizes and glosses a like-minded piece from Quillette by Bo Winegard, Ben Winegard, and Brian Boutwell). Like virtually all geneticists, I don’t see a finite and absolutely discrete number of easily identifiable “races”—that’s a strawman that people like Velasquez-Manoff attack. Maybe the general public thinks this, but Velasquez-Manoff is talking to scientists and about accepted science here.  “Race” (or “ethnicity”, if you like that word better) is simply a term for human “ecotypes”: groups of different evolutionary ancestry that have evolved different traits.

Like many animal species, humans, especially during our evolution after we left Africa, were divided into relatively discrete groups that were geographically isolated from other groups. In the absence of frequent migration between areas (such as we have now), these groups differentiated genetically, and generally along lines of geography. (Barriers like oceans and mountains are formidable obstacles to inter-group mating!) That differentiation was due to either divergent forms of natural or sexual selection, or to random genetic drift.

You can see these differences using either DNA sequencing or morphology (physical traits). Although, as is well known, there is more genetic differentiation among individuals among one ethnic group or population than among different groups, you can nevertheless pick out these groups by using combinations of genes, for differences at one gene tend to be correlated with differences in other genes. So, for example, we can see clustering of genes among people from the Americas, Oceania, native Australians, Europe/Middle East, and East Asia, and this clustering enables their recognition as groups that evolved semi-independently.

The Winegard et al. paper gives several examples of how “ethnicity” is correlated with genetic clustering; here’s one quote:

Empirical studies bear this logic out. The geneticist Hua Tang and her colleagues, for instance, found that self-reported ethnicity corresponded almost perfectly with genetic clusters from 326 microsatellite markers  (a microsatellite marker is a piece of repetitive DNA in which a series of DNA base pairs are repeated). Other studies have demonstrated even more power to identify people’s ancestry accurately. These studies illustrate that, whatever the meaning of the claim that there is much more variation within than among races, researchers can, if they use the appropriate procedures, distinguish human ancestral groups from each other with remarkable accuracy. The significance of these genetic differences among groups is entirely an empirical question.

And my own words, which quote the Tang et al. paper:

Here’s a quote from the abstract of the Tang et al. paper, published in The American Journal of Human Genetics, an excellent journal. The article is free online:

Of 3,636 subjects of varying race/ethnicity, only 5 (0.14%) showed genetic cluster membership different from their self-identified race/ethnicity. On the other hand, we detected only modest genetic differentiation between different current geographic locales within each race/ethnicity group. Thus, ancient geographic ancestry, which is highly correlated with self-identified race/ethnicity—as opposed to current residence—is the major determinant of genetic structure in the U.S. population.

Despite the clear evidence that human populations are genetically different and differentiable—although the presence of clusters within clusters precludes us from picking out discrete “races” having sharp boundaries—ideologues pretend that these differences don’t exist or aren’t meaningful. That’s because they fear that recognizing different groups will lead to discrimination against those groups, for the very same reason that biological ideologues won’t consider the possibility that there are genetically based differences between the behavior and neurology of men and women. Recognizing differences, they fear, will lead to institutionalizing bigotry based on those differences: to racism and sexism. The article by Winegard et al. dismantles this idea handily. The truth is the truth, regardless of whether it fits your ideological biases. And we can and should promote equality on moral rather than biological grounds.

But Velasquez-Manoff doesn’t like the idea of race, and so when he’s trying to discuss whether we should base some medical decisions or treatment on ancestry or ethnic background, he gets all antsy. You can read the article for yourself:

Here are a few quotes from the piece that shows the author’s lack of understanding of a more sophisticated concept of “race”, and his attempt to dismiss the importance of geographic differences between human populations:

Professor Yudell belongs to a growing chorus of scholars and researchers who argue that in science at least, we need to push past the race concept and, where possible, scrap it entirely. Professor Yudell and others contend that instead of talking about race, we should talk about ancestry (which, unlike “race,” refers to one’s genetic heritage, not innate qualities); or the specific gene variants that, like the sickle cell trait, affect disease risk; or environmental factors like poverty or diet that affect some groups more than others.

Ummm. . . race and ancestry are pretty much the same thing, and if genetic differences aren’t innate qualities, I don’t know what they are. What Velasquez-Manoff means by “innate qualities” is probably stuff like IQ or behavior, controversial topics about which we have little firm knowledge with respect to ancestry. What we’re talking about here are genetic differences that may have an effect on the incidence of diseases like sickle-cell anemia and Tay-Sachs, (Valasquez-Manoff’s tortuous attempt to avoid concluding that sickle-cell anemia is more frequent in populations descended from West Africa then from other populations is amusing.)

Here’s more:

What’s new today is that modern genetic science has revealed just how arbitrary the old race categories — Negroid, Caucasoid, Mongoloid and so on — really are. Yes, there is variation in the human family, but there are few sharp divides where one set of traits ends and another begins. Rather, traits exist in gradients, reaching high frequency in some populations and lower frequency in others. As the geneticist Sarah Tishkoff of the University of Pennsylvania reminded me, human beings are too young as a species, too promiscuous and full of wanderlust, always moving and mixing, for the kind of separation and differentiation that would cause true speciation to have occurred.

Well, these categories are not completely arbitrary: they just don’t pick out the totality of genetically recognizable groups. And yes, there aren’t sharp divides between groups and traits (or genes), for we see groupings within groupings—exactly what you’d expect if humans formed populations that were semi-isolated after they left Africa.  And who on earth even claims that there are “true species” in humans? No scientist I know! We’re not reproductively incompatible or isolated, which is the criterion for true species. We simply differ in our traits and genes, which is what we call “subspecies” or “ecotypes.” Remember, genetic differences among ethnic groups are correlated, for groups became genetically differentiated as semi-isolated populations.

Velasquez-Manoff prefers medical diagnostics based on genes rather than ancestry, apparently not realizing that these are correlated. Yes, we’d like to know everyone’s full DNA sequence for the best medical treatment, but sometimes an ancestry-based approach is better, simply because some diseases are clearly correlated with ancestry (and I recognize that there’s a conflating issue of culture, which isn’t genetic), and because in most cases we don’t know which genes are involved in disease and which variants are associated with which conditions. So these paragraphs, for instance, are confused:

The takeaway from studies like this is that rather than relying on race, doctors should focus on the genes important to whatever puzzle they face — an approach often called “precision” or “personalized” medicine. The idea is that tailoring treatment to the patient’s genotype, not to skin color or hair texture, would improve outcomes.

Consider the case of kidney disease. Scientists have found that African-Americans fare worse than whites when it comes to this illness. The assumption had long been that some environmental factor explained the difference. But in recent years, scientists have linked certain variants of a gene called APOL1 to worse kidney-related outcomes. Those variants are enriched in people of African ancestry. Girish N. Nadkarni, a kidney specialist at Icahn School of Medicine at Mount Sinai in New York City, explained to me that scientists think this may be because those variants protect against the sleeping sickness endemic to some parts of Africa.

Yes, it would be good to have the APOL1 genotype of all patients, but look: here the author admits that there are genetic differences between groups that correlate with their ancestry. They just don’t show a perfect correlation. Further, there may be other genetic differences between groups beyond APOL1 that affect kidney disease, but we don’t yet know about them, and so might be able to use self-identified ancestry as a correlate of those unknown differences. This is why my own doctor, Alex Lickerman, uses “race” as a guide to diagnosing prostate cancer. He’s quoted in the article:

Alex Lickerman, founder of ImagineMD, a medical concierge service in Chicago, cites the example of prostate cancer. For unclear reasons, African-Americans have a higher risk than whites. One test for the cancer, which looks at prostate-specific antigen, is controversial because it can yield false positives. Some recommend against using it at all.

But Dr. Lickerman says that merely being aware that African-Americans have a higher disease risk impels him to order the test more often for African-American patients. To his mind, the elevated risk of cancer outweighs the risk of a false positive. “Race is a crude marker, but it’s a usable marker,” he said. In that respect, it is no different from other factors doctors consider, most of which are based on imperfect studies of limited size and scope, and need to be weighed carefully.

Note that Lickerman recognizes race as a sign of ancestry that is correlated with genetic differences—and the genes for prostate cancer probably haven’t all been identified. It’s better in this case to partly base tests on race than to do nothing in the absence of genotypic data. What Lickerman is doing here, which seems sensible, involves recognizing the reality of “race”.

When discussing the higher incidence of hypertension in African-Americans than in white Americans, Velasquez implicates racism. He doesn’t seem to recognize two things: that hypertension in American blacks might be due to other cultural differences, like diet, or that it might be due to an interaction between evolved black/white genetic differences with factors like diet. The author simply wants to flaunt his virtue by singling out racism as the likely cause:

African-Americans, who on average have about 20 percent European ancestry, suffer from high blood pressure more often than whites do. Some studies indicate that among African-Americans, the darker one’s skin, the greater the risk of high blood pressure. The pattern could indicate that African ancestry is responsible.

Yet Africans in Africa don’t generally have high blood pressure. So some argue that the experience of having dark skin in the United States — of experiencing racism — is what’s raising blood pressure. In this case, Dr. Burchard says, even though race is a social construct, the best way to talk about the associated disease risk may be to use the labels, since the societal baggage that comes with them may be causing the problem.

Note that Velasquez-Manoff fails to present alternative but even more credible hypotheses (I don’t think that experiencing racism is a more likely explanation for hypertension than is diet, for instance). At any rate, he fails to lay out both genetic and interactive explanations. And the notion that “race is a social construct” is simply ridiculous. If it were, Lickerman’s ministrations would be futile. If race were purely a social construct, ancestry and ethnicity wouldn’t be correlated with any biological factors.

Of course we’d like to have the DNA profile of all patients, but we’d also like more research on exactly which genes are associated with disease. Such genes, though, may be hard to identify because they have tiny effects. In the meantime, there are occasions, as with sickle-cell anemia and prostate cancer, that ethnicity, or “race”, or “self-identified race”, can be used meaningfully in a medical way. And that, of course, means that ethnicity is not a “social construct”, for it has biological meaning. That’s the point that the Winegard et al. article tries to make.

Velasquez-Manoff’s virtue signaling and distaste for any concept of race is most evident in his last paragraph:

Science seeks to categorize nature, to sort it into discrete groupings to better understand it. That is one way to comprehend the race concept: as an honest scientific attempt at understanding human variation. The problem is, the concept is imprecise. It has repeatedly slid toward pseudoscience and has become a major divider of humanity. Now, at a time when we desperately need ways to come together, there are scientists — intellectual descendants of the very people who helped give us the race concept—who want to retire it.

It’s pretty clear that he doesn’t like race because it “divides humanity.”  Well, it partitions humanity on the basis of genetic difference, but that’s not what he means. He means that genetic differences cause friction between people. The solution to that is not to pretend that the genetic differences don’t exist, but to stop them from creating bigotry and hatred.

And if you want, discard the word “race”—but let’s keep “ancestry,” shall we?. No biggie, since “ancestry” is a term that enlightened biologists see as closely associated with “race”. Should we retire the concept of “ancestry”, too? If so, then why does Velasquez-Manoff mention it repeatedly?

I have to say that when I talked to Velasquez-Manoff and tried to tell him about the more modern concept of “fuzzy” race that encompasses a variety of nested populations that differ genetically, I could sense that he didn’t like what I was saying. And at the time I got a bad feeling about what he was going to write, as I could sense him ignoring what I was trying to tell him. In fact, I’ll go so far as to say that he was determined at the outset to downplay the significance of genetic differences between ethnic groups. And that is surely reflected in his piece, which I found notably unenlightening and genetically ignorant, even if it was politically correct.

A lovely graph that tells our story

October 9, 2017 • 8:00 am

by Matthew Cobb

I came across this beautiful graph in an article in the journal Cell this week. It shows declining levels of genetic variability among 51 populations of humans across the planet, plotted against the distance of each population from East Africa:

The data in the figure are from a 2008 paper in Science by Jun Li and co-workers [JAC: reference at bottom; free access] looking at human genetic variation. They studied 938 unrelated people and  650,000 genetic variants, measuring the levels of heterozygosity in each population – this the frequency with which individuals had different copies of a each genetic variant.

This striking result is additional evidence that we originated in Africa and gradually moved around the planet, losing genetic variability as we went. The last places we reached in this survey – the Americas, show the smallest levels of variability.

This is exactly what you would expect: in species that have spread geographically, the ancestral populations have the highest levels of genetic variability. Populations that have moved into new areas tend to lose variability for two reasons. First, they initially contain just a subset of the variability present in the original population. This is probably the explanation for most of the effect on this figure, as many of the genetic variants they have studied will be in ‘junk’ DNA that has no effect on the phenotype. Where the variants are in genes that have an effect, variability can be lost again as the population is subject to new selection pressures in their new environment, which further reduces heterozygosity. Or, as the authors put it:

This trend is consistent with a serial founder effect, a scenario in which population expansion involves successive migration of a small fraction of individuals out of the previous location, starting from a single origin in sub-Saharan Africa.

The final reason why this figure is so pleasing is that it gives a straight line—that doesn’t happen very often in biology!

However, if we look closely, it’s not totally linear – in particular, African populations can show varying levels of variability that do not appear to be related to geographical distance from East Africa (in fact, from Addis Ababa). If you plotted only the African data, you wouldn’t be very impressed. This African variability may be for a number of reasons: the origin of humans may not have been precisely in East Africa, or humans have lived for far longer in Africa than anywhere else on the planet, and may have been subject to particular selection pressures reducing their variability (for example, in an isolated group). An explanation of those four African points at the top, which show essentially identically high levels of variability, may be that there were consistently high levels of gene flow between these groups, maintaining the variability.

Whatever the case, this figure underlines that we are a global species, spanning out across the planet, adapting and losing genetic variability as we traveled.

____________

Li, J. Z., D. M. Absher, H. Tang, A. M. Southwick, A. M. Casto, S. Ramachandran, H. M. Cann, G. S. Barsh, M. Feldman, L. L. Cavalli-Sforza, and R. M. Myers. 2008. Worldwide Human Relationships Inferred from Genome-Wide Patterns of Variation. Science 319:1100-1104.

Researcher: Human sense of smell better than everyone thinks; may rival that of dogs!

May 16, 2017 • 8:30 am

John P. McGann of the Department of Psychology at Rutgers University has spent fourteen years looking at the olfactory (smelling) system of mammals, and has published a new paper in Science suggesting that what we think we know about our own sniffing ability, compared to the reputed Super Sniffers of dogs and rodents, is wrong. McGann suggests, to a fanfare of publicity in various venues, that we’re not that bad: in fact, he notes that humans may be just as good as dogs and mice at detecting odors.

His paper is referenced below, and access is free if you have the free and legal Unpaywall extension (get it!).

McGann suggests that the presumed olfactory inferiority of humans is based on observations of the relatively small size of human olfactory lobes in the brain—observations made by Broca and other early neuroanatomists, and promulgated by Freud, who said that the absence of an acute sense of smell in humans led to sexual repression, since sex was partly based on odors.  After reviewing the historical evidence, McGann gives his biological evidence. Here are his main points:

  • Although the relative size of olfactory lobes compared to brain size as a whole is smaller in humans than in rodents, the absolute size if the lobes is much larger.

This shows the relative sizes of human and mouse olfactory lobes; the mouse lobe is much larger relative to its whole brain:

(From paper): Gross anatomy of the olfactory bulbs of human and mouse. (A) Ventral aspect of human brain, with meninges removed from the cortex. Area indicated by dotted rectangle is enlarged in (B). (B) View of left and right olfactory bulbs and olfactory tracts from (A). (C) Ventral aspect of mouse brain, with olfactory bulbs visible at the top. Up is anterior in all three panels. Dashed lines denote the approximate border between bulb and tract.

But the absolute size of the human bulb, which McGann sees as one key to good olfaction, is much larger than that of the mouse:

(From paper): Comparison of the mouse and human olfactory bulb. View is of the ventral aspect of the left olfactory bulb. Both bulbs are at the same scale.
  • Further, the absolute number of neurons in mammalian olfactory bulbs is relatively constant (McGann sees that as an indicator of smelling ability as well).

This graph shows that the number of neurons in the olfactory regions varies among mammal species by less than a factor of ten, regardless of the much larger variation in body size—and humans aren’t particularly low:

(From paper): ig. 3 Comparison of olfactory bulb neuronal numbers across mammalian species. The number of putative neurons per olfactory bulb for each species, as measured by isotropic fractionation. Numbers are drawn from Ribeiro et al. (48) and Oliveira-Pinto et al.
  • Data showing a larger number of inactivated olfactory genes in humans compared to dogs and mice is questionable. 

In Why Evolution is True, I noted that many human “olfactory receptor genes”, each binding to a separate molecule and allowing us to smell it, have been inactivated by mutations: they’re dead “pseudogenes”. As McGann reports, humans have 1000 such genes, but “only” (his quotes) 390 of them code for receptor proteins. In contrast, mice have 1300 such genes, of which 1000 code for proteins. This has been taken as evidence that mice can smell a lot more acutely than can humans. But McGann points out that 60% of the human pseudogenes are transcribed into messenger RNA in the nose.

But that’s weak evidence, as we already know that many pseudogenes are transcribed into RNA but not translated into proteins, so this says nothing about the number of OR proteins made in humans versus mice. Besides, even if every transcribed pseudogene in humans was made into an active, odor-receptive protein, there would still be 1000 active genes in mice versus about 750 in humans.  Further, McGann didn’t do the comparison for pseudogenes in dogs or mice.

Here’s a table from a 2007 PLoS paper by Nimura and Nei showing those three species. If McGann wants to make the pseudiogene argument for human sniffing, he has to take into account the data below, and the possibility that many dog, mouse, and rat pseudogenes may also produce receptor proteins. Thus, I’m not convinced by his pseudogene evidence. (Note that every olfactory gene in cetaceans like whales is a pseudogene, suggesting they really aren’t used to smell, as those genes aren’t functional underwater.)

  • The structure of the olfactory system differs between humans and other mammals. 

These difference include a larger number of glomeruli (cluster of nerve receptors) in the human olfactory bulb compared to rodents, and the observation that the bits of human cortex used for processing olfaction is more “elaborate” (i.e., has more neural connections) than in other species. To me, this says little about the relative abilities of humans vs. other mammals to detect odors.

The most crucial question, however, involves not just neurons or pseudogenes but is this: “How many different odors can humans detect compared to, say, dogs and mice, and do we detect them at different thresholds?” It’s classically assumed that dogs and mice are better sniffers than are humans, but McGann said the data are not convincing, are based on anecdotes, and also rely on tests of molecules that humans wouldn’t have been selected during their evolution to smell anyway. Here are a few quotes (my emphasis if you want just the high spots):

Human olfaction is excellent and impactful

Historical and anatomical expectations aside, is the human olfactory sense actually impoverished? No, the human olfactory system is excellent, although it depends on the criteria employed. For instance, dogs may be better than humans at discriminating the urines on a fire hydrant and humans may be better than dogs at discriminating the odors of fine wine, but few such comparisons have actual experimental support. When properly tested, the primate olfactory system is highly sensitive to many odors and can exert strong influences on behavior, physiology, and emotions.

Humans with intact olfactory systems can detect virtually all volatile chemicals larger than an atom or two, to the point that it has been a matter of scientific interest to document the few odorants that some people cannot smell (i.e., specific anosmias). A prominent recent study calculated that we could also tell virtually all odors apart, with an estimated ability to discriminate more than 1 trillion potential compounds . Although this exact number is highly sensitive to the assumptions made, it is clear that the human olfactory system is excellent at odor discrimination, far better even than the putative 10,000 odors claimed by folk wisdom and poorly sourced introductory psychology textbooks.

One key insight in comparing the olfactory system of primates and other animals has been that different species have different sensitivities to different odorants. . . . A recent experiment tested olfactory thresholds for six sulfur-containing odors in mice, spider monkeys, and humans. Relative olfactory sensitivity varied with odorant : Humans were three orders of magnitude more sensitive than mice or monkeys to 3-mercapto-3-methylbuytl-formate, with all 12 human subjects outperforming all of the individual animals, yet all 12 humans were worse than all of the mice (and comparable to the spider monkeys) on 3-mercapto-3-methylbutan-3-ol. Overall, the humans were most sensitive to two of the six odorants, whereas the mice were most sensitive to four of the odorants. This finding complements older literature. . .

Human behavior is strongly influenced by olfaction. Environmental odors can prime specific memories and emotions, influence autonomic nervous system activation, shape perceptions of stress and affect, and prompt approach and avoidance behavior . Humans can follow outdoor scent trails and even exhibit dog-like casting behavior when trails change direction . The human olfactory system also plays a major, sometimes unconscious, role in communication between individuals. Each person produces a distinct odor that reflects not only dietary and environmental factors but also interacts with the immune system’s “self/non-self” histocompatibility markers to incorporate genetic information that permits the discrimination of kin from non-kin . The contents of this “body odor cocktail” are interpreted in parallel with environmental odors in the brain and can drive mate and food choice, as well as communicating information about anxiety and aggression in other people. We even appear to unconsciously smell our hands after shaking hands with strangers [JAC: Not me!], suggesting an unexpected olfactory component to this common social interaction. Although many of these olfactory experiences do not recruit attentional resources, they can be exceptionally salient in traumatic circumstances . When such circumstances result in posttraumatic stress disorder, olfactory hallucinations frequently become part of the symptomology.

Well. it’s clear from this (assuming McGann is right) that we need good comparative tests involving a variety of different molecules—not just molecules that would have been important in species’ evolutionary past—before we can say that the bloodhound is a better tracker by odor than is a human. But statements like “human behavior is strongly influenced by olfaction” says nothing about our relative sniffability compared to other species. This kind of writing is, I think, a bit tendentious.

The Guardian has a summary article about this paper, and shows that our own Matthew Cobb, who studies olfaction in flies for a living, thought the paper was great:

Matthew Cobb, professor of zoology at Manchester University, said the review had altered his own perspective on a study that he has focused on for much of his career. “We have this myth that humans can’t smell very much,” he said. “McGann’s exploring the actual evidence for that, which it turns out is fairly poor. It’s going to change my teaching next year.”

But others disagree:

Alexandra Horowitz, a scientist at Barnard College in New York, whose work focusses on canine olfaction, notes that while dogs track scents, find drugs and detect ovarian cancer in plasma samples, humans merely “notice if there is a bad smell on the train or someone has been cooking when we come home.”

“That there are olfactory specialists, such as perfumers or animal trackers indicates that with attention, we can get much better,” she added. “But not dog-level.”

While I’m not an expert like Matthew or Alexandra, my own take is that this paper is provocative and convinces me that more experiments need to be done, especially involving the ability of different species to detect different odors. Perhaps we’ve been too cavalier in our claims that humans are an auditory and visual species while dogs and mice depend more on olfaction. Old assumptions may be wrong, and McGann’s paper is useful for re-examining a famous set of such assumptions. He may be right, but I’m not convinced that his data show that. At best they show that we need to provisionally withdraw the common claim that we can’t smell as well as mice and dogs. (One thing I can say, though, is that humans smell better than dogs, especially wet dogs! I’ll be here all week, folks.)

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McGann, J. P. 2017. Poor human olfaction is a 19th-century myth. Science Vol. 356, Issue 6338,DOI: 10.1126/science.aam7263

The evolution of sexual dimorphism in humans: Part 2

December 21, 2016 • 11:00 am

In a post one week ago, “The ideological opposition to biological truth,” I argued that sexual dimorphism for body size (difference between men and women) in humans is most likely explained by sexual selection, and that it also reflects behavioral differences between males and females: males compete for females, and greater size and strength give males an advantage. That competition results from females—in many species, not just ours—being a “scarce” resource for males, since the number of males capable of breeding far exceeds the number of females who cannot breed because they’re tending offspring or in gestation. This disparity can be categorized in two ways:

  • The behavioral operational sex ratio: the ratio of sexually active males to fertilizable females at a given time. This is about 11.7 in humans!
  • The physiological operational sex ratio, the same ratio but for all individuals capable of reproducing (rather than those actually engaged in mate-hunting). This is about 8.6 in humans.

The ratios are greater in some primates (gorillas have values of about 84!), but if they’re greater than 1, there’s room for sexual selection, since there are more males seeking females than there are females available as mates. This itself is one bit of evidence for the operation of sexual selection in humans.

Now how the sexual selection actually operated in our ancestors is not perfectly clear. Some of it, as the data suggest, involves male-male competition: fights between males to control females, as we witness in gorillas, deer, and elephant seals. Females are more or less constrained to mate with the winning males. Or females may prefer to mate with the biggest and strongest males, for those males may protect their offspring—and hence the female’s genes—better than do smaller, weaker males. (This gives an evolutionary advantage to those females who can discern and choose the best males.)

Both of these factors can, of course, work at the same time, and there are other more arcane forms of sexual selection I won’t mention, including other signs in males of “good genes”. But any sexual-selection scenario goes along with a difference in sexual behavior, explaining why, even today, males are more promiscuous and willing to mate than are the choosier females.

A further possibility is that there could be an ecological distinction between males and females, with males hunting, and thus needing size and strength, while females do gathering (presumably females don’t have time to hunt because they’re rearing children). That doesn’t involve sexual selection, but it also fails to explain all the data, like the correlation between sexual dimorphism and polygyny within humans, and the fact that in our primate relatives there’s not only the same correlation among species, but no palpable division of labor among males and females. It also doesn’t explain the existence of traits like beards, lower voices, or same-sex aggression among human males but not females. Nevertheless, there’s no reason why several forces couldn’t work together to cause men to have evolved larger body size and increased musculature (as well as other features) in our ancestors. But surely sexual selection is one, for the evidence below fits no other hypothesis.

As I noted, these relatively uncontroversial ideas about sexual selection (not mine, actually; they’re the conventional wisdom among evolutionists beginning with Darwin), was challenged by Holly Dunsworth, an associate professor of anthropology at the University of Rhode Island, on her website. Dunsworth, who called my theory (supported by lots of data cited in my original post) a “story”, offers her own speculations, which really are a story because they lack empirical support and don’t explain a lot of observations. Here’s what she said:

It’s not that Jerry Coyne’s facts aren’t necessarily facts, or whatever. It’s that this point of view is too simple and is obviously biased toward some stories, ignoring others. And this particular one he shares in this post has been the same old story for a long long time.

What about the other side of the body size sexual dimorphism story?

What about the women?

Selection could well be the reason they stop growing before men and why they end up having smaller bodies than men, on average.

Perhaps men can make babies while growing, but perhaps women can’t. Energetically, metabolically. So reproduction wins over growth. We reach sexual maturity and stop growing. Is that just a coincidence?

Why doesn’t this (and other tales) fit alongside the big-aggressive-males-take-all explanation for sexual dimorphism? #evolution

But as I noted in the piece she criticized, selection on females—through either evolution of female preference or on differential ecological roles between the sexes—could affect sexual dimorphism. But Dunsworth conveniently ignored that bit. Her criticisms were echoed by an article by Jesse Singal in New York Magazine, which claimed, as did Dunsworth, that I was offering mere “stories”—unevidenced speculation. Singal said this:

In Dunsworth’s view, all she is asking for is some nuance and, well, skepticism. “People love to boil complex processes down to their preferred (intentional or not) story,” she wrote, “with some in leading roles and others completely absent, and we don’t have to take that anymore.” Her tweeted example about growth nicely captures this: It could be that Coyne’s aggressiveness story leaves out important details about why men are bigger than women, or fails to explain certain aspects about that differences. Overall, it certainly seems like people are quicker to latch onto evo-psych stories that reinforce certain views of men and women.

That last sentence is a veiled accusation that my piece was sexist. I reject that completely.

As I noted in part I of this response, neither Singal nor Dunsworth appreciated that I have a long published history of criticizing “just-so” stories in evolutionary psychology. I don’t like unevidenced speculation when it’s promoted as truth. But the sexual selection theory for human sexual dimorphism is supported by a lot of evidence. It is manifestly not a mere “just-so” story.  In my original piece I adduced this evidence (revised slightly):

  • In human societies studied by Richard Alexander, those societies that are more polygynous (in which males compete more intensively for females) show greater sexual size dimorphism than societies that are more monogamous. This was a prediction made before the data were acquired—a prediction derived from sexual selection theory. And it was fulfilled. UPDATE: I see now that Alexander’s finding wasn’t reproduced in another experiment, so consider this conclusion questionable.
  • Among species of primates, there’s a good correlation between the polygyny of a species and sexual dimorphism: those species in which males have a higher variance in offspring number, and in which males thus compete more intensely for females, also show a greater ratio of male/female body size, even when corrected for phylogeny. (Too, in primate species in which males fight each other over females, the relative size of the canine teeth, used in battle, is larger than in species showing less direct male-male competition.)
  • In humans, as in many other species in which males compete for females, the sex ratio at birth favors males. They then die off at a higher rate due to higher risk-taking and exploratory behavior, and also senesce faster, which is why among older humans there are so many more females than males. (Check out any Gray Line tourbus.) This is predicted by sexual selction theory.
  • In line with the above, in humans and other primates, males show from the outset great exploratory and risk-taking behaviors, and as adults show many other behaviors that differ from those of females, such as greater dispersal. Is this due to the Primate Patriarchy? Probably not, given that these differences in behavior are shown in many species besides ours and make evolutionary sense.

There’s more evidence, too, which I’ll mention shortly.

But what’s the evidence for Dunsworth’s theory? As far as I can see, there isn’t any. Her theory claims that 1) females can’t reproduce while growing, while males can. 2) There’s a tradeoff between growth and reproduction, so if you stop growing as a female, you can start reproducing earlier. Conclusion: females stop growing before males because reproduction is all-important, and therefore they’re smaller than males as adults.

But the data don’t even support her theory. Puberty begins in females at about ages 10 and 11, and in males between 11 and 12.  (The age of both appears to be decreasing in recent years.) Yet males keep growing this whole period and well beyond, as do females. There’s no indication that females stop growing when they become reproductively competent. Here are growth curves (stature and weight) for both males and females. Stature begins tapering off at about ages 14-15 in both sexes (a slower taper in males), but both sexes continue to grow until age 20.

Females:

growth-2-20-girls

Males:growth-2-20-boys

Now we don’t know about body sizes and ages of puberty in our ancestors, which is the really important information, and I doubt we’ll have that given that it’s virtually impossible to ascertain the age of puberty in fossils. But clearly there’s no support in any data for Dunsworth’s hypothesis that “perhaps men can make babies while growing, but perhaps women can’t. Energetically, metabolically.” Both men and women can make babies while they’re still growing. But men continue to grow not only faster but also bit longer than do women (see above), something which explains sexual dimorphism. But since men are reproductively competent when they hit puberty, why do they keep getting bigger? Dunsworth doesn’t tell us, but sexual selection theory does. Men achieve greater stature and muscle mass by both growing faster than females, and tapering off a bit later.

So Dunsworth’s hypothesis is not only unsupported by data, but fails to explain the growth data that do exist.

More important, her theory doesn’t explain the four points given above—points that are well explained by sexual selection theory.  She and New York Magazine fail to realize that the sexual-selection explanation for human sexual dimorphism is not a “story”, but makes supported predictions and clarifies previously obscure observations. How irritating to see these people distort what we know about evolutionary theory and human biology!

As I mentioned in earlier posts, I think Dunsworth is blinkered by her ideology, because she thinks that sexual selection theory ignores females. Well, straight male-male competition without female choice does involve evolution mainly in males, but there are forms of sexual selection that involve female choice, too, and that has surely happened in species like birds and fish. In those groups, and others, males show ornaments and colors not useful in male-male competition, but are the object of female choice. And some of that process may have happened in our own lineage. The competing theories are not zero-sum, so that only one can be right. All these processes can work together. But surely one is sexual selection.

Regardless, sexual selection as an explanation implies that there are also sexual differences in behavior: differences we see in modern experiments and are probably not purely cultural because a. they’re predicted by the differences in body size and b. we see the same difference in mate choosiness in many other species—and not just primates. It’s an ineluctable consequence of the difference in reproductive investment between males and females.

I’ll now list some other observations about human mating and morphology that are explained by sexual selection theory but not explained at all by Dunsworth’s theory. Some of these come from the references given at the bottom of the post.

  • In other sexually dimorphic primates, including chimpanzees and gorillas, direct contests between males can be observed, and probably existed in our ancestors since paleoanthropological data show that many more males were killed by violence than females, possibly reflecting inter-group battles, which in modern hunter-gatherer societies are often over females. Many societies also show “bride theft”, capture of females by bands of males—common in Amazonian hunter-gatherer societies.
  • Male humans have more robust skulls than do females, including mandibles and brow ridges. This may reflect evolution to withstand blows to the head. (Males also have a higher tolerance for pain.)
  • Men are not only taller and heavier than women, but are stronger, particularly in the upper body. While size differences are about 8%, and body mass about 15-20%, women’s bodies have a higher percentage of fat, so that when you look at fat-free body mass, men are 40% heavier, have 60% more lean muscle mass, 80% greater arm muscle mass, 75% more upper-body muscle mass, and 50% more lower body mass. This difference in relative amount of muscle mass cannot be explained by Dunsworth’s theory, which is purely about growth, but is explained by male-male competition under sexual selection—and perhaps by female preference as well. This is reflected in differential athletic performance, and is why men and women usually compete separately in athletics. Even for men and women of equal sizes, men are far stronger; as Hill et al. note, “the average man is stronger than 99.9% of women (some of this, of course, may be because men work out; I haven’t checked the references.)
  • In every society studied, men are physically more aggressive than women, both in play as kids and as adults. The vast majority of murderers are men, and this aggressive activity peaks during men’s peak reproductive years, when they would be competing for mates most strongly. These data do not include killings in war.
  • Traits like beards and lower voices in men (men’s vocal folds are 60% longer than women’s, giving them lower voices) have been shown to act as indicators of dominance; both are evolved morphological traits. (The evidence supporting all these claims can be found in the papers cited below.) Women also prefer larger men and deeper voices, so there may have been an element of female choice in sexual selection, though of course the observations we make are on modern rather than ancient hominins.
  • Sexual dimorphism is also seen in our ancestors like Australopithecus and H. erectus, implying that it’s been acting on our lineage a long time. But there’s also some evidence, cited by Plavcan, that the degree of sexual dimorphism has waxed and waned as females got either bigger or smaller over time, implying that there may have been some separate natural selection in females that could increase or decrease sexual dimorphism (but never effaced it).
  • Finally, Buss’s article and others not cited outline the psychological and behavioral differences between males and females that make sense under sexual selection. These not only include the greater promiscuity of males than females, but also the greater sexual jealousy of males toward women than vice versa (our male ancestors weren’t always sure who the father of their mate’s children was, while women were far more certain). There is also a big difference between males and females in their attitudes towards casual sexual experiences (guess in which direction), and in how exacting their standards are for a short-term mate (guess again). Men have lower psychological thresholds for risk-taking. And so on. As Buss wrote, “Large sex differences appear reliably for precisely the aspects of sexuality and mating predicted by evolutionary theories of sexual strategies.”

I’ve adduced about a dozen pieces of evidence supporting the sexual selection explanation for human morphological and behavioral dimorphism—none of which can be explained by Dunsworth’s hypothesis. (And that hypothesis was dead in the water anyway, contradicted by the known data.) Since all hypotheses must, at bottom, be supported by the weight of accumulated scientific evidence, it is clear that sexual selection, and male-male contest competition in particular, is a compelling explanation for human sexual dimorphism. In contrast, Dunsworth’s hypothesis isn’t in the least compelling. That doesn’t mean we shouldn’t keep evaluating the evidence or suggesting new hypotheses, but simply that these should be supported by data rather than ideological preference.

I urge readers to look at the papers below, and use the data (and that from other papers) to evaluate theories about human behavioral and sexual dimorphism. I don’t propose to engage in a dialogue with Dr. Dunsworth about this, but I would like to know how her theory can explain the dozen-odd observations given above.

Dunsworth must have emitted something like twenty tweets about her piece, impugning me; and she even issued this over-the-top pronouncement:

Well, there’s fighting material above, but I’ve had my say. Still, I can’t believe that simply my writing a post on human sexual dimorphism and its implications would drive anybody away from studying human evolution. After all, the give-and-take of hypotheses, critical thinking, and data are the very meat of science, and if you disagree with somebody, you don’t simply walk away from a field. I sure as hell am not leaving evolutionary biology because Dunsworth and New York Magazine took out after me!

2028_4_16

UPDATE: Things are getting worse: Peter Boghossian is arguing with Dunsworth on Twitter (I’m not involved, as I avoid Twitter Wars), but now we’re getting lumped with some rather unsavory types (except for the “evolutionists”):

h/t: Steve, David

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Buss, D. M. 1995. Psychological sex differences. Amer. Psychologist 50:164-168.

Hill, A. K., D. H. Bailey, and D. A. Puts. 2017. Gorillas in our midst? Human sexual dimorphism and contest competition in men. pp. 235-249 in: On Human Nature: Biology, Psychology, Ethics, Politics, and Religion. in M. Tibayrencand F. J. Ayala (eds.) .On Human Nature, M.  Tibayrenc and F. J. Ayala, eds. Academic Press.

Puts, D. A. 2010. Beauty and the beast: mechanisms of sexual selection in humans. Evolution and Human Behavior 31:157-175.

Plavcan, J. M. 2012. Sexual size dimorphism, canine dimorphism, and male-male competition in primates. Where do humans fit in? Human Nature 23:45-67.

The world’s oldest woman, and only living person born in the 19th century

December 16, 2016 • 12:45 pm

Meet Emma Morano of Italy, who was born in 1899 and has attained the status of both “oldest living person” and “only person born in the 19th century”. She turned 117 on November 29.

Click on the screenshot below to go to a video of the world’s oldest woman. Be sure to turn the sound on.

screen-shot-2016-12-16-at-12-16-33-pm

The New York Times also documents her life, which was tough. But thanks to her diet of three eggs per day (according to the video, two raw and one fried), she’s still here. Times writer Elisabetta Polvoledo says this:

I wrote about Ms. Morano two years ago, when she was only 115, and she told me she believed that her secret to longevity was eating three raw eggs a day and remaining single.

Ms. Morano has no doubts about how she made it this long: Her elixir for longevity consists of raw eggs, which she has been eating — three per day [JAC: note disparity between Reuters video and this piece] — since her teens when a doctor recommended them to counter anemia. Assuming she has been true to her word, Ms. Morano would have consumed around 100,000 eggs in her lifetime, give or take a thousand, cholesterol be damned.

She is also convinced that being single for most of her life, after an unhappy marriage that ended in 1938 following the death of an infant son, has kept her kicking. Separation was rare then, and divorce became legal in Italy only in 1970. She said she had plenty of suitors after that, but never chose another partner. “I didn’t want to be dominated by anyone,” she said.

Ms. Morano, who has cut back to two eggs a day, lives a very simple life. She has been homebound for some years, and her diet remains Spartan, if unorthodox: In addition to eggs, she eats bananas and ladyfinger cookies.

Of course when all these people are asked the “secret of longevity”, they say the same thing, which is basically “do what I did.” Still there’s some wisdom in the following:

Ms. Morano’s doctor of nearly two decades, Carlo Bava, said that despite her age, his patient was still in excellent health, and her memory sharp. “She’s in great form,” he said. “And I think she’s happy to have made it to this birthday.”

Diet aside, Dr. Bava said he thought Ms. Morano had lived such a long life because she was cared for. “The secret is in growing old with people who love you, which is different from growing old and being put up with,” he said.

But maybe there’s something to eggs after all. I just remember that the world’s oldest cat, Creme Puff, who lived to be 38 years and 3 days old (!!!!), was fed on a diet of asparagus, coffee with heavy cream, broccoli, and bacon and eggs.