But many subjects are not like that. Understanding, to the extent that it is possible at all,  requires mastery of many facts.  Consider Barbarossa, the invasion of the Soviet Union.  More than three million Germans invaded, with hundreds of thousands of motor vehicles and even more horses.  The Germans had the initiative and were tactically superior: the Russians had greater numbers and resources, if they could survive long enough to bring them into play.  The Germans had to win quickly, if they were to win at all.

Modern armies require enormous amounts of supply, mostly gas and ammo. In those days, supply mainly meant railroads. In Germany, and in most of Europe, the separation between the rails, the rail gauge,  was 1,435 mm (4ft 8 1/2 in).   So when the Germans invaded France, they could immediately make use of the French railnet.  In Russia, the Germans faced a problem: the gauge was different, 1528 mm (5 ft).  German locomotives could not use those tracks until they had been converted.  As Pravda used to say, this was no coincidence:  it is thought that the Czarist government made this choice for defensive reasons.

It was difficult for a WWII-style army to operate for any length of time when more than 100 km from a rail head or port.   After the initial lunge, the Germans could not advance faster than the rate of gauge conversion.  Maybe they  couldn’t find enough railway engineers. Maybe Hitler thought his unconquerable will could trump mere logistics.  Maybe the Wehrmacht high command underestimated the difficulty of working in the rasputitsa and the Russian winter.  Whatever the reason, they couldn’t rebuild the railroads fast enough to take Moscow in 1941.

You can’t really understand the War in the East without understanding rail gauges -  assuming a spherical Soviet Union is not the way to go.

Anyhow, it strikes me that a certain amount of knowledge  may lead to useful insights. In particular, it may help us find low-hanging-fruit, technical innovations that are tasty and relatively easy – the sort of thing that seems obvious after someone thinks of it.

If we look at cases where an innovation or discovery was possible – even easy – for a long time before it was actually developed, we might be able to find patterns that would help us detect the low-hanging fruit  dangling right in front of us today.

For now, one example.  We know that gastric and duodenal ulcer, and most cases of stomach cancer, are caused by an infectious organism, helicobacter pylori.  It apparently causes amnesia as well. This organism was first seen in 1875 – nobody paid any attention.

Letulle showed that it induced gastritis in guinea pigs, 1888. Walery Jaworski rediscovered it in 1889, and suspected that it might cause gastric disease. Nobody paid any attention.  Krienitz associated it with gastric cancer in 1906.  Who cares?

Around 1940, some American researchers rediscovered it, found it more common in ulcerated stomachs,  and published their results.  Some of them thought that this might be the cause of ulcers – but Palmer, a famous pathologist,  couldn’t find it when he looked in the early 50s, so it officially disappeared again. He had used the wrong stain.  John Lykoudis, a Greek country doctor noticed that a heavy dose of antibiotics coincided with his ulcer’s disappearance, and started treating patients with antibiotics – successfully.   He tried to interest pharmaceutical companies – wrote to Geigy, Hoechst, Bayer, etc.  No joy.   JAMA rejected his article. The local medical society referred him for disciplinary action and fined him

The Chinese noticed that antibiotics could cure ulcers in the early 70s, but they were Commies, so it didn’t count.

Think about it: peptic and duodenal ulcer were fairly common, and so were effective antibiotics, starting in the mid-40s. . Every internist in the world – every surgeon – every GP was accidentally curing ulcers  – not just one or twice,  but again and again.  For decades. Almost none of them noticed it, even though it was happening over and over, right in front of their eyes.  Those who did notice were ignored until the mid-80s, when Robin Warren and Barry Marshall finally made the discovery stick. Even then,  it took something like 10 years for antibiotic treatment of ulcers to become common, even though it was cheap and effective. Or perhaps because it was cheap and effective.

This illustrates an important point: doctors are lousy scientists, lousy researchers.  They’re memorizers, not puzzle solvers.  Considering that Western medicine was an ineffective pseudoscience – actually, closer to a malignant pseudoscience  – for its first two thousand years, we shouldn’t be surprised.    Since we’re looking for low-hanging fruit,  this is good news.  It means that the great discoveries in medicine are probably not mined out. From our point of view, past incompetence predicts future progress.  The worse, the better!

Here, for example is a simulation of 100 histories, i.e. parallel worlds, in which a single mutation causing lactase persistence appears in an adequately mixed population of 50,000 reproducing adults who are dairying people. The mutation is dominant, so both carriers and homozygotes enjoy a 5% fitness advantage due to the ability to digest lactose and hence obtain 40% more calories from the same diet as people without the mutation: see here for the details. We don’t imagine this advantage to be important every year, but in times of stress lactase persistents (LPs) would have been more likely to survive and, perhaps, avoid slaughtering their herds to eat them.

Evolution of Advantageous Mutant in 100 Worlds

In twelve (the expected number is ten) of the one hundred worlds the mutant persisted long enough that deterministic forces took over and it increased in frequency just as theory predicts. In the other 88 worlds the mutation may have hung around a while at low frequency but was eventually lost to drift. Since the time until determinism takes over is random, even where the mutant eventually won the time is highly variable. In the green world it took about four thousand years to reach a frequency of one half while in the tardy red and dark blue worlds it took about six thousand years.

This may provide some quantitative understanding of history. A figure tossed about for the age of the west Eurasian mutation is eight thousand years. With a five percent advantage it only reaches a frequency of seventy to eighty percent in that time while the frequency in northern Europe today approaches fixation. The advantage must have been greater than five percent.

On the other hand there are grounds for sorry pessimism here. I have the naive human idea that history makes sense while this exercise shows that it is worse than a crapshoot. An extremely rare random accident, the mutation, caused one of the greatest population blooms we know about, if our theory of the Indo-European tie in with LP is correct.

When we teach population genetics we study gene frequency change, usually with the assumption that population size is held constant. In this case we can’t defend such an assumption since the 5% advantage of LP is huge. In this Malthusian dairying environment the advantage would lead immediately to explosive population growth, which is almost certainly what did happen.

This figure is from the same simulation program as the figure above but the outcome is slightly different (randomness). Only five of the one hundred mutations persisted and the simulation only goes to five thousand rather than ten thousand years (drawing a million binomial samples of size two slows my poor desktop to a crawl so I stop things early).

LP causes population growth

In the five rare cases where the new mutant persists it leads to population growth, but how much? In one history, the right red one, the population has risen to about seventy thousand people, while at the other extreme it has risen to nearly eight hundred thousand people because it happened to become common faster. With the more realistic advantage of ten percent these number would be much higher. The full figure is not shown because my poor desktop begged me to give it a rest.

Are these simulated population numbers implausible? I think not, recalling that the Indo-European expansion is like the explosion of a huge inkball in western Eurasia from the perspective of history. Toward the end of the five thousand year interval people at the center must have been moving away as fast as they could to avoid being trampled.

There are several recent papers on the genetic basis of human adaptation to high altitude-, and they clearly show that natural selection has taken a different path in each of these populations. This was obvious even before the sequencing started: Andean Amerindians are barrel-chested and have high levels of hemoglobin, while Tibetans pant at the drop of a hat but don’t have particularly high levels of hemoglobin.  Moreover, the Tibetan adaptive response works better.  Very few Tibetans get chronic mountain sickness, but a significant fraction of Andean  highlander do, especially with increasing age.  Tibetan babies are significantly plumper than Andean babies.  There are hints that the Ethiopian pattern may also be more effective than the Andean, but that hasn’t been studied as much.

Overall, as Cynthia Beall has pointed out, the  Tibetan pattern is closer to that seen in animal species that have lived at high altitude for long periods of time.

Rasmus Nielsen concluded the changes in Tibetans happened over about 3,000 years. I  doubt that.  People have probably been in the altiplano longer than that, and yet their adaptations are substantially less effective.

Hominids have lived in or near Ethiopia and Tibet for much, much longer than anyone has lived in the New World – something like 100 times longer.  It is possible that  the populations of modern humans living in those  areas picked up some altitude-friendly alleles from archaic humans that had lived at high altitude for a very long time – and naturally had more effective adaptations. It only takes a tiny bit of admixture to transmit  beneficial alleles.  We now have some probable examples of such transmission: it looks as if some archaic HLA alleles (Neanderthal and Denisovan) have reached high frequency in Eurasians, while a very divergent Denisovan version of OAS1, a innate immune gene, is common in Melanesians.

We can be sure that the Andean Indians did not have this opportunity, since humans have only been in the New World for 15,000 years or so.  No llama jokes, please.

As for Freudian explanations, exotic-becomes-erotic, etc: just reading the social-science literature on the subject is enough to make you wonder if the human brain really does exist to cool the blood.

A fair number of the smarter people interested in the subject agree with me.  Not that they think it proven, but they agree that it is the only theory out there that makes any evolutionary sense.  Bill Hamilton thought it made sense. So does Alan Grafen.  Mike Bailey thinks it more likely than any other explanation tendered thus far.

My model – not the only possible  model based on a pathogen,  but reasonable  – leans on a couple of natural examples.  One is narcolepsy.  We now know that narcolepsy happens when a particular kind of neuron, concentrated in a little region in the hypothalamus, somehow gets zapped.   99% of narcolepsy cases happen in the 25% of the population that has a particular HLA type – which suggests that something, probably a virus, triggers an overenthusiastic immune response that zaps a neuron subpopulation that produce a particular neurotransmitter (called hypocretin or orexin) that regulates appetite and sleep patterns.  And it doesn’t do anything else: narcoleptics aren’t stupid. You can compare narcolepsy to type I diabetes or Parkinson’s disease. Suppose there’s a neuron subpopulation that  performs a key function in male sexual desire:  wipe out that subpopulation, and Bob’s your uncle.

Another is toxoplasma, which we now know changes mouse behavior in ways that increase a mouse’s chance of being devoured by a cat, the definitive host for toxo.  Infected mice are attracted to cat urine, while uninfected mice avoid it.  In fact, in infected mice,  cat urine apparently triggers activity in neural pathways involved in sexual arousal. Microorganisms can reprogram sexual attraction in mammals.

I have had people complain that I’m neglecting the social aspects  of homosexuality, what it means, how people think of it.  Let me tell you a story.  In certain parts of west Africa,  boys are expected to start menstruating around age 14.  And they do,  sort of:  you  start seeing blood in their urine.  When that happens, there’s a big ceremony, everyone says ‘today you are a man’.  Whatever.  The thing is, that’s about the time they put the boys into the flooded rice fields, where they’re exposed to schistosoma haematobium, which causes urinary schistosomiasis.  It’s bad for you: it can impair growth and cognitive development in  children, reduces productivity,  and is a potent cause of bladder cancer over the long term.

Our explanation of male menstruation as urinary schistosomiasis must undermine these people’s traditional culture. Eliminating schistosomiasis would undermine it even further,  just as the rubella vaccine dealt a heavy blow to deaf culture by cutting the number of congenitally deaf children in half. .

Isn’t that just too damn bad.

P.S.  The title comes from the coolest response to this hypothesis I’ve ever received, from some inspired fool in New Zealand: “And descending into the most disturbing depths of madness and the most depraved abuse of science yet conceived, we will even be told that homosexuality is caused by a virus or a bacterium. “

Indian elephants, although not truly domesticated, are routinely tamed and used for work in Southern Asia. The locals in Sub-Saharan Africa seem never to have done this with African elephants – but it is possible. The Belgians, in the Congo, hired Indian mahouts to tame African elephants, with success. It’s still done in the Congo, on a very limited scale, and elephants have recently been tamed in other parts of sub-Saharan Africa, such as the Okavango delta. Elephants have long generations, which makes true domestication difficult, but people have made domestication attempts with eland, African buffalo, and oryx.  They’re all tameable, and eland have actually been domesticated to some extent.  If a species is tameable, economically useful upon taming, and has a reasonable reproductive schedule, domestication is possible: selection for even a few generations can change their behavior enough to make dealing with them a lot easier.

As for the Americas – have you ever had a deer eating out of your hand?  Bison seem too wild and scary to have ever been domesticated, but then I’m sure you would have said the same thing about the aurochs, the wild ancestor of cattle.

In fact, in my mind the real question is not why various peoples didn’t domesticate animals that we know were domesticable, but rather how anyone ever managed to domesticate the aurochs. At least twice. Imagine a longhorn on roids: they were big and aggressive, favorites in the Roman arena.

Let me throw out an idea originated by an old friend, Ivy Smith. Consider mice, cats, and toxoplasma. Toxoplasma is a protozoan with a two stage life cycle: one in an intermediate host (mice and rats, among others) and a definitive host (some feline).  Toxoplasma only reproduces sexually in the definitive host, and it ‘wants’ to end up there. It manipulates the behavior of the intermediate host in ways that increase the probability of transmission to the definitive host. For one thing, it makes mice like the smell of cat urine, which elicits fear in uninfected mice. In fact, it seems that toxoplasma-infected mice are sexually excited by cat urine. How weird – a parasite rechanneling sexual interest…

The idea is that at least some individual aurochs were not as hostile and fearful of humans as they ought to have been, because they were being manipulated by some parasite. The parasite might have  caused a general reduction of fear or aggression without infecting or aiming at humans – or, maybe, humans really were the definitive host, and the parasite knew exactly what it was doing. The beef tape worm – which we originally acquired from lions or hyenas back in Africa a couple of million years ago – might have gained from making infected bovines quiet, passive, maybe even overly friendly in the presence of humans. This would have made domestication a hell of a lot easier.

Parenthetically, such host manipulation may play a really important ecological role.  For all we know, if canids and felids had to rely purely on their own abilities, they’d starve.

The beef tape worm may not have made it through Beringia.  More generally, there were probably no parasites in the Americas that had some large mammal as intermediate host and Amerindians as the traditional definite host. Amerindians simply hadn’t been there very long. Domesticating bison may have too hard for unaided humans, back in the day.

There’s a cluster of Y-chromosomes found in inner Eurasia that vary only slightly, and thus must have a recent common ancestor. They are surprisingly common: there are something like 16 million carriers.  The analysts who discovered this (Zerjal et al) concluded the men with these Y-chromosomes are the direct male-line descendants of Genghis Khan,  the Master of Thrones and Crowns.  They have to be right: no one else conquered such a vast empire and had his sons (and their sons, and so on) rule and enjoy their harems for centuries.  More than that, the Golden Family continued to have high social status long after the fall of the dynasties,  even into recent times.

Since power descended through the male line, you don’t expect to see the same thing happen with autosomal genes. Genghis accounts for about 25% of Mongolia’s Y-chromosomes, but the general ancestry fraction attributable to him must be a lot lower.  Still, what if the average Mongol today is 0.5% Genghis? Upon sequencing lots of typical  contemporary Mongols, you would notice certain chromosomal segments showing up again and again: not just in one family but in the whole country,  and in other parts of inner Asia as well.  If you started keeping track of those segments, you would eventually be able to make a partial reconstruction of Genghis’s genome.  It would be incomplete, since any given region of the genome might have missed being transmitted to any of his four legitimate sons (Jochi, Chagatai, Ogedei, and Tolui).  They certainly didn’t carry his X-chromosome.  You might be able to distinguish the autosomal genes of Genghis and his wife Borte by looking at descendants of his by-blows, if you could find them.  Still, even if you managed to retrieve 75% of his genome, that’s not enough to make a clone.  It would however,  allow sure identification if we found his tomb.

And since he’s likely buried in permafrost,  his DNA could be in good shape.  Then we could clone him (assuming reasonable continuing progress in genetics) and of course some damn fool would. Will.

Back around the time I was born, anthropologists sometimes talked about some cultures being more advanced than others.  This was before they decided that all cultures are equal,  except that some are more equal than others.

Anyhow, that kind of comparison can be interesting.  In the Old World, civilization arose first in the Middle East, and that heavily influenced later starts such as European and Chinese civilization.  Civilization in the Americas seems to have arisen completely or almost completely independently: there may have been some pre-Columbian contacts, but it looks as if the Amerindians developed agriculture and technology on their own.

I’ve been trying to estimate the gap between  Eurasian and Amerindian civilization.  The Conquistadors were, in a sense, invaders from the future: but just how far in the future?  What point in the history of the Middle East is most similar to the state of the Amerindian civilizations of 1500 AD ?

I would argue that the Amerindian civilizations were less advanced than the Akkadian Empire,  circa 2300 BC.   The Mayans had writing, but were latecomers in metallurgy.  The Inca had tin and arsenical bronze, but didn’t have written records.   The Akkadians had both – as well as draft animals and the wheel. You can maybe push the time as far back as 2600 BC, since Sumerian cuneiform was in pretty full swing by then. So the Amerindians were around four thousand years behind.