health

I blame Harold Dibble. Oh, sure, all these "paleo diet" people point the figure at Loren Cordain, but Dibble was the first to give them a cookbook!

So now, it's a "movement" and it's in the New York Times:

Mr. Durant, 26, who works in online advertising, is part of a small New York subculture whose members seek good health through a selective return to the habits of their Paleolithic ancestors.

Or as he and some of his friends describe themselves, they are cavemen.

Oh sweet mercy. Give me a break.

This guy grows a "cheerful Jim Morrison" beard and installs a small chest freezer in his apartment (there's a photo of the "meat locker" that's supposed to "spook a female guest"), and we're supposed to think he's a weirdo survivalist of some kind? Hasn't this reporter, Joseph Goldstein, ever been outside the city? If he'd gone out to flyover country -- say, New Jersey -- he'd discover bigger deep freezes in the homes of most hunters. The only thing strange about this guy is that he doesn't have a basement to put it in.

Well, how's it working out for them?

Most of the cavemen at Mr. Durant’s gatherings are lean and well-muscled, and have glowing skin. A few wear trim beards. Some claim that they no longer get sick. Several identify themselves as libertarians.

OMG, they're LIBERTARIANS! It's like Manhattan has finally fallen to those "rewilding" people! Come on baby, light my fire!

There's a typical kind of "lifestyle" article in the NY Times, where a reporter interviews three or four people who all do some weird thing, as if they were part of a trend sweeping the nation. But it always turns out that these three or four people all know each other, are all twenty-somethings, all live in some fashionably bohemian area of Manhattan, and (often) just happen to be acquaintances of the reporter.

Now this could be because the NY Times only hires reporters plugged into hot new trends, which are all started by twenty-somethings in Chelsea. Or it could be that twenty-something reporters on deadline tend to "run home to mama" when they can't think of any other ideas.

You tell me which this is:

Another caveman trick involves donating blood frequently. The idea is that various hardships might have occasionally left ancient humans a pint short. Asked when he last gave blood, Andrew Sanocki said it had been three months. He and his brother looked at each other. “We’re due,” Andrew said.

The article itself is pretty deep in snark, and with all its talk of fasting and blood donation, it's like a flashback to 1994. Which I admit is kind of entertaining. The article's lead photograph, posing three of the "cavemen" dressed all in black in front of the Cro-Magnon diorama at the American Museum of Natural History, makes them look like the cast of Pleistocene Twilight.

The only reason I'm really incensed is its promotion of a self-proclaimed guru (whom I won't name), whose website (which I won't link) promotes some of this quackery. Some of the resulting advice seems to be dangerous. For example, a current entry encourages people not to carry or drink water during workouts -- I suppose because cavemen didn't have water bottles? It's a good way to get yourself hospitalized or worse.

I'm the last person to promote gatekeeping in science. But a piece of free advice: Don't get your information about human evolution from non-anthropologists who charge you money for subscriptions and seminars!

Meanwhile, on the Upper East Side we hear from a doctor who prescribes his patients Cordain's Paleo Diet. Supposedly that shows the trend is spreading into the mainstream -- although The Paleo Diet is now eight years running.

I don't think there's anything harmful about adopting a hunter-gatherer-like diet. I do doubt whether it's the most healthful diet for some people -- the point of "adaptation" is to increase offspring number, not longevity! Besides, some populations have been adapting to agricultural diets for ten thousand years. The most healthful diet for you might be the diet of your recent ancestors, not your Paleolithic ones.

But to be honest, the best food is the food that brings you nearer the ones you love. And if frozen venison ribs in your living room can make you "a chieftain of sorts among 10 or so other cavemen", well more power to you. Maybe it will bring you a Wilma Flintstone, too.

Where did leprosy come from as a human pathogen, and how did it spread through the world? Two years ago, this new research would have merited a whole book. Now it's all packed into a single Nature Genetics paper by Marc Monot and coworkers.

I mean, there's a lot in here:

1. They used next-gen sequencing platforms to get three additional whole-genome sequences for the pathogen that causes leprosy, Mycotuberculum leprae.

2. By comparing the different strains together with an already-available one, representing patients in four countries, they measured the genome diversity and found SNPs between strains.

3. They then genotyped the resulting SNPs in 400 isolates, building a phylogeny of worldwide strains of M. leprae today.

4. They did a phylogeographic analysis of the strains, testing hypotheses about past transfers of the bacterium among regions.

5. And then, on top of all that, they recovered skeletal remains from "leprosy graveyards" in six countries, diagnosed the skeletal correlates of leprosy in 13 cases and genotyped the resulting extracts for M. leprae, placing them on the global phylogenetic tree.

Whew!

Well, I assume that the skeletal work was done separately, with samples being sent to the lab folks to do their DNA extraction.

This would be a really good topic for a documentary. There's all the historical information about leprosy to draw upon, including of course its prominent appearance in the Bible and Father Damien. There's the triumph of effective treatments in developed parts of the world -- an aspect that this paper emphasizes, as it attempted to find out whether regions of the world that now lack M. leprae once had the strains expected from their geographic placement. And there's the continuing tragedy of the disease in many less developed parts of the world, with the need to deliver treatment more effectively. Meanwhile, the phylogeographic aspects of this paper provide another historical angle, about the spread of leprosy around the world on human trade routes.

Plus there's the whole mystery of how it got into humans in the first place:

Finally, it is worth discussing the enormous discrepancy between the period at which pseudogene formation is thought to have arisen and the origin of early humans. It has been estimated recently that the bulk of the pseudogenes in M. leprae arose no earlier than 9 million years ago. Pseudogene formation is an indicator of radical change in the lifestyle of the host bacterium, such as from the free-living to pathogenic state or of adaptation to life within a particular tissue or cell type. In the case of M. leprae, obligate parasitism of humans or another primate species would represent such a change. Although modern humans represented by H. sapiens have existed only since approximately 250,000 years ago and left Africa within the last 100,000 years to settle other regions, earlier hominids are thought to have diverged from chimpanzees over 5 million years ago. Reconciliation of the estimated time of pseudogene formation with human evolution could be achieved if an ancestor of M. leprae infected an early primate and then underwent genome decay and was subsequently transmitted vertically—although this seems unlikely, given that more genetic diversity among M. leprae isolates would be expected if this were true. Alternatively, the genome decay could well be ancient, but M. leprae may only recently have become a human pathogen. For instance, it is conceivable that an ancestral form of M. leprae infected an invertebrate host such as an insect, which later acted as a vector for transmitting the bacillus to humans. Support for the latter scenario is provided by studies of the related pathogen Mycobacterium ulcerans, which is at an early stage of reductive evolution and appears to be transmitted to humans by water bugs and/or mosquitoes. Further insight into the timing of pseudogene formation in M. leprae will be provided by microbiology and paleomicrobiology and by deeper genome sequence analysis.

In rough outline, you "date" a pseudogene by counting the number of nonsynonymous substitutions in comparison to some other species where the gene is functional. When the gene was functional, most substitutions of nonsynonymous mutations would have been prevented by purifying selection. You generally apply more detailed assumptions, but that's the basic process. I raise the point because dating a 9-million-year-old event in a bacterial species on the basis of nonsynonymous mutations is probably not going to give a very tight confidence interval, to put it charitably. Maybe 9 million is 4 million?

In any event, leprosy is one more addition to a growing story about the coevolution of pathogens with Homo. It may have a long history with us, like its congener, tuberculosis. It apparently doesn't have a long history of coevolution within different regionally variable human populations -- tuberculosis does. Possibly it is a relatively recent invasion from another species, which would make it maybe more like the evolutionary dynamics of vivax malaria.

We don't lack for examples, and tabulating the histories of all of these pathogens may give us a better picture of the population ecology of Homo in Pleistocene times.

References:

Monot M and many others. 2009. Comparative genomic and phylogeographic analysis of Mycobacterium leprae. Nat Genet 41:1282-1289. doi:10.1038/ng.477

Will the swine flu lead to the next big evolutionary change for humans? No. But it has already begun to affect the way people interact with each other. I wandered onto campus a couple of weeks ago and saw people wearing face masks! We've been asked to plan for our "essential" classes in the event of a pandemic.

It's a good time to be on leave. But my kids' school has been closed the rest of the week. It's the flu -- more than a third of the whole school was out sick yesterday.

In the August Smithsonian magazine, writer Rob Dunn discussed a hypothesis that tries to relate cultural diversity and xenophobia (fear of the other) to the rate of infectious disease ("The culture of being rude"):

In a series of high-profile papers, Corey Fincher and Randy Thornhill, both at the University of New Mexico, and Mark Schaller and Damian Murray of the University of British Columbia argue that one factor, disease, ultimately determines much of who we are and how we behave.

Their theory is simple. Where diseases are common, individuals are mean to strangers. Strangers may carry new diseases and so one would do best to avoid them. When people avoid strangers—those outside the tribe—communication among tribes breaks down. That breakdown allows peoples, through time, to become more different.

Differences accumulate until in places with more diseases, for example Nigeria or Brazil, there are more cultures and languages. Sweden, for example, has few diseases and only 15 languages; Ghana, which is a similar size, has many diseases and 89 languages. Cultural diversity is, in this view, a consequence of disease.

On the surface, this seems a poor example -- the population has been thin in Sweden relative to Ghana for most of the last 6000 years, until the rise of the Swedish state. It's no surprise that a recent population expansion coupled with political centralization would result in a relatively uniform language and culture area.

But as the article goes on to explain, some of the theorists think that the rise of states is itself a dependent variable. They would propose that the growth of polities was limited in Ghana because of a high disease load, retaining and fostering a cultural diversity that would have been wiped out by natural political consolidation in a less-disease-prone region of the world.

That's the logic, at least.

This kind of topic is interesting but endlessly frustrating. The frustration -- at least for me -- comes from the ready confusion of biological and cultural processes of change. Dunn's article says as much:

As a rule, it is good to be skeptical of biologists who, like Fincher and Thornhill, propose to explain a whole bunch of things with one simple theory. More so when those biologists are dabbling in questions long reserved for cultural anthropologists, who devote their careers to documenting and understanding differences among cultures and their great richness of particulars. Biologists, and I am no exception, seem to have a willingness–or even need—to see generalities in particulars. Fincher’s new theory would offer an example of these desires (and a little hubris) run amok, of biologists seeing the entire history of human culture through one narrow lens. It would offer such an example, if it didn’t also seem, quite possibly, right.

As a rule, I'm skeptical of everything. "Wary of strangers" wouldn't keep our school open -- those kids are all catching the flu from their friends. It doesn't take very many contacts between groups of people to spread an epidemic far and wide.

In that respect, it's a problem for percolation theory. You've got a network of people through which the flu can be transmitted. If the people tend to be highly interconnected, with each other, the flu spreads widely. But even if links between groups are rare, the strong interconnections within a group can keep the epidemic alive long enough to make it to the next hop. At some critical level, the links are no longer enough, and the pathogen can't propagate.

So does it do you personally much good to be wary of strangers, if you have a few cosmopolitan friends? Everything can make a little difference to the percolation network, but it seems to me that people carrying the "xenophobia" gene would still maintain large social networks including a few people who interacted far and wide with strangers. It's not that the direction of the effect is wrong; it's that a wholesale elimination of stranger contact by an individual may have little effect on her probability of infection, since friends may have gotten the pathogen from strangers.

It's awful hard for a "xenophobia" gene to get going in that scenario.