Bugs Versus Drift

For a while now we have seen occasional articles about how people outside of sub-Saharan Africa may have more genetic load, generated by drift over a population history in which Eurasians generally had a smaller effective population size. This is related to those recent papers with similar but stronger conclusions about Eurasian archaic humans like Neanderthals and Denisovans.

As I mentioned, I kind of doubt that that Neanderthals and Denisovans were all that screwed up – partly because a more complete theory indicates that salvage mutations get easier as you drift away from the optimum and ameliorate the effects of low population size to a surprising degree, but even more because the Neanderthals obviously weren’t all that screwed up, didn’t have their fitness depressed by tens of percent, because they stood off anatomically modern humans for something like 70,000 years after first encounter. Results count. The mechanism makes a lot more sense for Flores hobbits because their population was much smaller, but even more because they actually were screwed up: it shows in their skeletons.

So, just how screwed up do Eurasians look, compared to Africans? I mean, if we’re going to be busy explaining a phenomenon, shouldn’t we bother to make a cursory check to see whether it even exists? I know that probably sounds radical…

Of course there’s no bloody sign of any such thing. Sub-Saharan Africans have shorter lifespans and lower IQs than most Eurasian populations. East Asia has lower genetic diversity than Europeans – so has had lower effective population size over the past few tens of thousands of years – yet those populations have higher average IQs and longer lifespans than Europeans.

On the other hand, it is also the case that strong selection for any particular trait tends to mess up other traits – logical, considering trade-offs. So strong selection for resistance to falciparum malaria has made lots of deleterious variants common in the tropical and subtropical parts of the Old World. We know many that are strongly, obviously bad for you – even lethal – but there are surely many others with milder (but still negative) effects. We know that selection for resistance to sleeping sickness has selected for APOL1 variants that greatly increase the risk of kidney failure, so that African-Americans develop end-stage renal disease (ESRD) about 3.5 times more often than people of European ancestry. Those APOL1 variants also exacerbate kidney disease caused by sickle cell, and there’s an AIDs-related kidney-wrecking syndrome (HIVAN: HIV-associated collapsing glomerulopathy) (while AIDs is of course much more common in blacks) that seems to require those African APOL1 variants – HIVAN is up to 50 times more common in blacks than whites. Those social constructs can sure seem real when they’re shoveling the dirt over your face.

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91 Responses to Bugs Versus Drift

  1. Sandgroper says:

    The only ones I can guess at are greatly heightened risk for nasopharyngeal cancer in Cantonese (for which salted dried fish may also be an environmental trigger), and heightened risk for stomach cancer in Japanese (for which pickled vegetables might be an environmental trigger).

    I suspect some malaria resistance in at least some southern Chinese rice farmers, but have no idea what the downside might be – in the very early days of Hong Kong as a British colony, the Brits built a military barracks in an area where the local Chinese farmers were wet-farming rice, in an area of swamp at the mouth of a large freshwater stream which then drained into the sea. So many of the Brit. soldiers stationed at the barracks died of malaria in a period of only a few years (literally hundreds of them) that the barracks were abandoned, the stream was entrained and had a concrete roof built over it, and the whole swampy area was filled in to make a horse racing track (whereupon the malaria disappeared, because there was no stagnant fresh water for the mosquitoes to breed in any more).

    • another fred says:

      “The only ones I can guess at are greatly heightened risk for nasopharyngeal cancer in Cantonese (for which salted dried fish may also be an environmental trigger)…”

      I recall reading where that was traced to some local dish made from moldy bread.

  2. MawBTS says:

    East Asia has lower genetic diversity than Europeans – so has had lower effective population size over the past few tens of thousands of years – yet those populations have higher average IQs and longer lifespans than Europeans.

    I have heard people claim that Africans have more genetic diversity than the rest of the world put together, so Africans can’t possibly score behind Europeans on any standardised trait.

    Can’t argue with that logic. Also, insects vary in size more than elephants, so there’s probably insects bigger than elephants out there. Somewhere.

    • Tim says:

      Can’t argue with that logic.

      But the African American population on the other hand has much of the genetic diversity of Africa AND most of the genetic diversity of western Europeans. Yet, as individuals, they still they score behind Europeans on many standardised traits.

      How could that possibly be true if it was solely due to genetics? (BTW, this is not the case with physical attributes such as height, weight, and speed, where test results are more difficult to be skewed due to test design).

      • MawBTS says:

        Here’s an example of what I mean, someone attributing Kenyan/Jamaican athletic prowess to their genetic “diversity” instead of fast-twitch muscle fibres.

        Noting that X has more variety than Y tells you nothing about where they stand in absolute numbers. 10C-30C degree weather is more variable than 35C-40C degree weather. It’s clearly not hotter.

        Tolstoy said “All happy families are alike; each unhappy family is unhappy in its own way”. I think of genetic diversity in similar terms: there’s an infinite number of ways you can suck.

        • Bla says:

          Well, fast-twitch muscle fibers indeed have nothing to do with Kenyan athletic prowess.

          • Sandgroper says:

            He’s getting his east and west mixed up. The sprinters with all the quick twitch muscle came from West Africa, where the slaves came from. Selective breeding of slaves didn’t hurt.

            The middle and long distance runners come from Kenya and Ethiopia on the eastern side of Africa and above a certain altitude – not much quick twitch tissue, but high altitude adaptation.

          • Bla says:

            Sandgroper, is there any proof of selective breeding of slaves? Especially with better sprinting times as a result? If anything, higher percentage of fast-twitch muscle fibers might have had deleterious effects on ability to do work they were doing. Short bursts of energy and faster tiring are not necessarily what you look for in your agricultural manual workers.

          • Sandgroper says:

            I’m told by someone I trust that slaves were bred because it was cheaper than importing new ones. Selective breeding for strength would have the effect of increasing quick twitch muscle.

          • engleberg says:

            Any proof of selective breeding of slaves?

            A very small needle buried in a giant avalanching mountainous haystack of Use the Prettiest Girls For Sex Slaves.

          • ziel says:

            Sandgroper – don’t think so. Importing slaves was outlawed in the U.S. in the early 19th century. But I don’t think there was much ‘breeding’ of slaves – the “work ’em to death and keep importing new ones” seemed to be the prevailing model in most of the New World.

            In the U.S., the scaling-up of cotton production mostly occurred after the slave trade was outlawed, so there probably was some effort to keep slaves alive and reproducing. But I would think selective breeding would have been a pretty daunting proposition for even the most determined slaver.

          • Bla says:

            Cheaper? Sure. Especially since the British decided to abolish the trade…
            It’s certain most of the slaves in the US were born there. Just compare numbers of brought slaves http://www.slaverysite.com/Body/facts%20and%20figures.htm with demographic data for CSA https://en.wikipedia.org/wiki/Confederate_States_of_America#Demographics
            Now, were the slaves purposely bred, or it is just a natural (most people would do breeding without any outside pressure) result of fertility being higher than mortality (Caribbean case was the opposite, so was the climate and agriculture) rates (which certainly made slave owners happy)? Was there any selective breeding (where? how often? for how long? would the effect last past the abolition era?) and even if there was, why would anyone breed for strength if that meant less efficient worker (I guess they would have noticed that)?
            And if there already is a higher average percentage of fast-twitch muscle fibers in (some?) West African populations, why complicate explanation (unless the evidence for that is quite clear)?

          • MawBTS says:

            Yeah, sorry, I screwed up.

          • MawBTS says:

            Sandgroper, is there any proof of selective breeding of slaves?

            Magic eightball says “cautious yes”.

            There’s antebellum accounts of slaves who say they were forcibly mated by their owners. There’s occasional references in trade materials to “breeding” and “stock” etc. I’m sure some of these guys had an idea of what they were doing.

            But could this have affected the frequency of alleles in any meaningful way? Almost certainly not. Too sporadic, and over too brief a period.

            My understanding is that nobody really bred slaves until the Atlantic Slave Trade was abolished in 1807. Like Ikea furniture pieces, it was cheaper to buy new ones.

          • J says:

            Doesn’t it also have to do with narrower hips?

          • Sandgroper says:

            No – they thought it did, but then they reviewed it and decided it doesn’t.

          • Sandgroper says:

            OK, forget the slave breeding. That wasn’t the main point anyway. The main point is the world’s best sprinters have West African ancestry, and the world’s best distance runners come from the Ethiopian and Kenyan Highlands in eastern Africa, where they have high altitude adaptation – I suspect by introgression of archaic alleles, as seems to be the case with Tibetans.

          • John Hostetler says:

            Any reason to think slaves had any greater sprinting potential than the population from which they came, adjusting for malnutrition and other environmental disease? And if they had, slave women were capable of doing plenty of selection all by themselves, amplifying the existing African trend toward choosing the most muscular men to father their children. Or do the pretty girls like physicists best? I forget.

          • Bla says:

            Sandgroper, Epstein argued “not really” in Sports Gene. According to him, Oromos and Kalenjins looked more like altitude responders than fully adopted peoples (who may lose the effect beneficial to results as they fully adopt). He might be wrong though, I can’t really tell.
            He also writes about the running economy, with narrower hips (could you explain if that was disproven, and how?) and thinner lover legs being especially important.

          • Bla says:

            MawBTS, makes sense. Although I would guess slave population in (what was to become) US was increasing naturally long before British abolished the trade.

          • Sandgroper says:

            Bla, sorry for the slow response. All I can say is that I recall reading an article that said further research had shown that narrow hips did not give any advantage, but I can’t give you a reference, and forget where I saw it.

            As for lower legs, all of the top middle distance runners now are ‘front foot’ runners, which puts a lot of stress on the lower leg muscles, particularly the calf muscles. You can’t see it in this clip of Genzebe destroying yet another world record (she now has a swag of them), but if you look closely at her feet in other clips of her, her heels never touch the ground when she is running. And, OK, sample of one, But I would not say she has thin lower legs. Fairly narrow hipped, I guess, but not excessively. She’s Oromo, from a whole family of elite runners, so although she trains hard at altitude, she is obviously genetically gifted.

            I am willing to predict that, barring injury or illness, Genzebe is on track for a certain gold medal at the Rio Olympics, and possibly 2 or 3 of them. She was on track for a gold in the London Olympics, but tore a hamstring in one of the heats and had to be carried off the track in agony. She’s recovered well from that, and over the past two years she has been collecting world records and world championship gold medals like crazy. Over 1,500m or 3,000m, no one can stay anywhere near her. Watch and enjoy – poetry in motion. She’s the one in the blue top, obviously.

          • Bla says:

            Well, I didn’t jump at my response either. 🙂
            Since men and women differ on average on limb length, hips width… we could guess extremes would be less pronounced in top female athletes.
            Of course all have to have strong calf muscles, but, their length ( with Achilles tendons length being the opposite) vary.
            To use the extreme because it is easy to see, try googling Dorian Yates and Ronnie Coleman and notice the difference in their calf muscles length (it is sure to say none of them would make top medium and long distance runner, and have no connection with either Oromos or Kalenjins, but they make lower leg difference easily demonstrable).

            Here is a quote from Sports Gene about lower legs:
            As expected from their latitudes of ancestry, though, the Kalenjin and Danish boys did display bodytype differences. A greater portion of the body length of the Kalenjin boys was composed of legs. The Kalenjin boys were, on average, two inches shorter than the Danish boys, but had legs that were about three quarters of an inch longer.
            The scientists’ most unique finding, though, was not the length of the legs, but their girth. The volume and average thickness of the lower legs of the Kalenjin boys was 15 to 17 percent less than in the Danish boys. The finding is substantial because the leg is akin to a pendulum, and the greater the weight at the end of the pendulum, the more energy is required to swing it.* Biologists have demonstrated this in humans in controlled conditions.
            In one particularly well-controlled study, researchers experimented with adding weights onto different parts of runners’ bodies: the waist, the upper thigh, the upper shin, and around the ankle. Even when the weight stayed the same, the farther down the leg it was placed the greater the energetic cost to the runners. In one phase, each runner had to wear eight pounds around his waist, which required about 4 percent more energy to run at a given pace compared with when he wasn’t wearing eight pounds of weights. But when the runners were subsequently equipped with a four-pound weight on each ankle they burned energy 24 percent more rapidly while running at the same pace,
            even though their total weight had not changed one ounce from the previous condition.

            Weight that is far out on the limbs is called “distal weight,” and the less of it a distance runner has, the better (i.e., if you have thick calves and ankles, you won’t be winning the New York City Marathon). A separate research team calculated that adding just one tenth of one pound to the ankle increases oxygen consumption during running by about 1 percent. (Engineers at Adidas replicated that finding in the process of constructing lighter shoes.)
            Compared with the Danish runners, the Kalenjin runners tested by the Danish scientists had nearly a pound less weight in their lower legs. The scientists calculated the energy savings at 8 percent per kilometer.

            Plus this footnote:
            A small 2012 study in the European Journal of Applied Physiology found that a group of Kenyan runners had Achilles tendons that are 2.7 inches longer than nonrunner white control subjects of the same height. That is to be expected, given the Kenyans’
            proportionally longer lower limbs. Longer Achilles tendons can store more elastic energy. (Recall: world champion high jumper Donald Thomas.) The next question for scientists: How much do those long tendons influence running ability?

      • RCB says:

        Imagine a trait that is affected additively by a 100 loci. Each locus is segregating for 2 alleles, one of which (the “smart” allele) makes you slightly smarter – say, it adds 1 point to some measure called Intelligence.

        Now imagine two populations. Population 1 has allele frequency 0.5 at each locus. This means that they have maximum possible heterozygosity (0.5 at each locus). The mean Intelligence is 100 (100 loci * 2 alleles per loci * 1 Intelligence point per smart allele * 1/2 probability of the smart allele), with a standard deviation of sqrt(2000.5(1-0.5)) = 7.07. A person with Intelligence of 130 is one in a hundred thousand.

        Population 2, through a history of drift and selection for intelligence, has a rather different distribution. All of these loci have gone to fixation. But 65 of the loci are fixed for the smart variant, and 35 for the dumb. Notice that this population has 0 heterozygosity and 0 standard deviation in intelligence (at least genetically). Every smart allele that is present in Population 2 is also in Population 1; indeed, Population 1 actually has more kinds of smart alleles than Population 2. For any particular locus, each genotype in Population 2 is also contained in Population 1, and then some. But the mean intelligence of Population 2 is 130, meaning that everyone in Population 2 is smarter than the vast majority of Population 1.

        To address your particular point, it is clear that a hybrid population of these two populations will be intermediate in Intelligence: a hybrid gets a guaranteed 65 smart points from his Population 2 parent, and an average of 50 from the Population 1 parent, yielding an average right between the two.

        Obviously this is an extreme example, but you get the point.

        Read about Lewontin’s fallacy.

        • gcochran9 says:

          Assuming that Lewontin was actually a geneticist,’fallacy’ is probably the wrong word. More like ‘hoax’.

        • Fourth doorman of the apocalypse says:

          with a standard deviation of sqrt(2000.5(1-0.5)) = 7.07.

          Assuming you are using sqrt(Npq) that should be sqrt(2000.5(1-0.5)) which comes out to 7.07 on my calculator.

          Strangely, that was the calculation I tried to do a while ago and never came up with the correct numbers.

          • Fourth doorman of the apocalypse says:

            Oh, shit. I see what went wrong. WordPress ate the * characters in the formula.

            It should have been sqrt(200*0.5*(1-0.5))

            Let’s see if this works.

            450 loci seems to produce an interesting result under that model.

      • gcochran9 says:

        It is not diversity that matters, rather the frequency of variants that influence the trait. If some population has higher frequencies of the variants that push the trait higher – possibly even 100% freqeuncy of those plus variants – it has a higher average value of the trait.

        Thoroughbred horses don’t have much genetic variety: Mongolian and Tuva ponies have a lot more. But Thoroughbreds are faster.

        • Tim says:

          Thoroughbred horses don’t have much genetic variety, and they are unlikely to get much faster in the future. If they were allowed introduce Mongolian and Tuva genetics into their gene pool, they would have much more potential.

          The hybrids would have to go through an intense selection process, but they would likely result in faster horses.

          • RCB says:

            Probably yes, actually. Fisher said the same thing in regard to interracial marriage, I believe.

            The details matter, in practice. You’d want a very large breeding population, and weak selection, to ensure that no beneficial variants are lost by chance.

          • TWS says:

            If you open the stud books to faster horses then you will get faster horses. That’s how the Quarter Horse associations ran things for a long time open stud books.

            If you hope to speed up the Thoroughbred horse by adding ponies you will have to ruthlessly cull the results and will wind up with much slower horses until you winnow down the gene pool until you are right back at the Thoroughbred genome.

            Might as well try mixing with Shetland ponies or Belgium draft horses. You’ll have as much success adding chihuahuas to the GSD line to get better schutzhund dogs.

          • Rick says:

            It may not match intuition, but it is actually true. Just because they are ponies doesn’t mean they don’t carry alleles for faster running that are not present in other breeds.

            This has been proven numerous times in crop improvement. (Not with running, though, except maybe in beans).

        • RCB says:

          I agree that, in practice, interbreeding with a slower/dumber/whatever population is not the most practical way to get faster/smarter/whatever. The pony hybrid population would require lots (hundreds?) of generations of selection to surpass the speed of the original quarter horses, if ever. You’d need to select slowly so that you give time for recombination to produce novel gene combinations, which is the point of the whole exercise. Selecting too quickly would indeed just lead to inferior stock (fast genes would be lost by chance). Maybe, at the end, when your grandchildren finish the experiment, they’d find that ponies had virtually nothing to offer, making the whole thing moot. Still, it’s plausible that Mongolian ponies have a handful of alleles that, if bred into quarter horses, would make them even faster. Sorry if you don’t get that.

          • TWS says:

            I get it. I think it is as difficult a way to try to improve the speed of the race horse as I have ever read. You’d do better by simply shooting the slow horses. I can think of a dozen easier ways to improve the speed rather than waiting hundreds or thousands of years on the off chance you might pick up something missing from the Thoroughbred line. Then get their speed up again after through ruthless culling to fix the lost alleles

            I’m sure it’s possible. Just not practical.

            • gcochran9 says:

              Already we only breed the fastest thoroughbreds: their effective population size is something like 100 !. And yet there hasn’t been any improvement in speed in some decades. Conceivably they’ve gone as far as they can with the cards they were dealt.

          • Rick says:

            Fast genes will never be lost because you can always backcross to the original strain.

            When my grandchildren have their pony enriched race horses, they will be faster than your grandchildren’s thoroughbreds (which will still be stuck running 1.25 miles in 2:02.25 +/- 3 seconds, just like they have for the last 65 years).

          • TWS says:

            The thoroughbred stud books are closed and they only have three founding studs. It would be much quicker to open the stud books to any horse that could run the course in x-time. Make it a test of function rather than heredity and form.

            My horses would be spanking the ass off your limping ponies. Long before your umpty great grandchildren received any benefit. How long do you think the breeding cycle is for horses? It’s not like we’re talking dogs where you get at a minimum one or two breeding cycles a year per female.

            Also any benefits might be missed in a particular generation because of lack of conformation/phenotype. One of the most famous founding studs for cavalry horses in the east had everything wrong with him in conformation. It was by chance that he bred and his progeny was found to be a good cavalry horse. With horses it is a bare minimum of three years before you really know what you are getting. More like three generations before you are even sure that line is one you want to pursue.

            Thoroughbreds aren’t improving because they’ve maxed out what they’ve got. Big gains are seen in weird mutations like the bigger heart through Eclipse’s line. If there are other alleles for speed out there that don’t cause some problem with the current conformation of the horse. Eclipse’s trait for an enlarged heart was passed down through his female offspring and it was only discovered after he was dead.

            I guess because I was brought up in a family that raised Quarter Horses for stock work and racing I can see that it would be possible. I can also see the decades of useless, slower, and expensive generations of horses you’d have to feed and care for before you might get any benefits.

          • Rick says:

            Sometimes I forget what gcochran is talking about when he says that some people are just stupid. But then, I am reminded again by people like yourself. Or… maybe this is just a misunderstanding and you are just not seeing the big picture because you want to be right.

            I understand you have experience breeding horses. I have had over 40 years of experience breeding rodents and plants. Both of these are small and have very short generation times.

            Unless the species involved is rare and has limitations successfully breeding (like a giant panda), breeding for improvement or trait transfer has nothing to do with generation time. It has to do with money.

            With annual plants, you can easily cross and grow and select millions of individuals per year. With mice, you could do the same, if you had the funds. With horses, you could also do the same. It is only about money.

            With the fastest 20 studs, you could impregnate many thousands of ponies or even every mare you could buy.

            The fact is that genetic diversity and selection are the only two ingredients to improving any trait.

            By only breeding your thoroughbreds with other selected horses with already lower genetic diversity, you are missing out on a lot of the possibilities. Some of those possibilities will be very rare genes that contribute to faster running.

            The major impedance to faster horses is that they don’t allow the introduction of new genes.

            You are literally arguing with yourself here.

            • TWS says:

              You willfully missed what I said, then compared horses to rodents. Horses are not like rodents, how many generations do you get in a year? How long before full maturity?

              I said it would take a metric load of time and effort on a human scale. Money? Money is trivial compared to the time. Sometimes you don’t know for generations what you’ve got.

              I thought the idea utterly silly not impossible given unlimited resources and time. If you’re Bill Gates rich go for it. It would be as useful an allocation of his ‘charity’ money as what he does now.

  3. Peter Lund says:

    “for for”

  4. n/a says:

    Great post. Thanks for the insights

  5. marcel proust says:

    For those of us less fluent/knowledgeable, what is a “salvage mutation?” Neither google nor wikipedia is helpful. Thx.

    • gcochran9 says:

      Imagine that an organism with a fair number of slightly mutated genes that produce slightly suboptimal proteins. That’s the sort of thing that might happen in a population that was small for a long time: selection in such a population is not very effective at eliminating slightly deleterious mutations, those whose damage is on the order of the inverse of the population size.

      Maybe those proteins aren’t folding in the proper way as reliably as they should. A mutation that increased the production of, or the activity of, a chaperone protein would be favored: it would reverse some of the damage.

  6. Race can be treated as a social construct on a college campus, especially as the bulk of the population is young, healthy, IQ 90 and above, active, etc. That’s the environment that matters, isn’t it? I’m not sure those other people you are talking about even exist.

    I mean, I went on junior year abroad and those people looked pretty much the same, too.

    • gcochran9 says:

      I guess it can if you can’t tell or don’t care whether someone is a lot different in intelligence. I always thought it was pretty easy to tell: when your date is disappointed because she thought Close Encounters was going to be a documentary, you get up and run.

      • RCB says:

        Agreed. I thought lots of my college classmates were surprisingly dumb, for being at UCLA. That’s probably due to (1) my natural arrogance and (2) the fact that I was an anthropology major.

        An alternative hypothesis: it’s easy for college students to believe that race is a social construct because they don’t actually encounter many racial minorities on campus (except Asians, of course). I didn’t, anyway…

      • TWS says:

        I was walking across the campus at UW some years ago with my mother. An earnest girl pushed a petition at us ‘to end hunger’. We asked how would it end hunger? The poor dear had no idea. We just laughed and walked on. She was sure there was a magical link between the number of signatures and the growing and distribution of food world wide.

      • Rick says:

        I have always found this tricky because I often meet a lot of very intelligent people in situations where lots of alcohol is involved. Especially at scientific conferences.

        This is why I always suggest and immediately make a followup email. People show their intelligence much better with a few minutes to think abut each word.

  7. pyrrhus says:

    Hmmmm….Since northern and western Europeans have proven to be much more innovative than Asians, but don’t live as long, that seems to indicate that some negative mutations have accumulated from that drive for originality, even outside the Ashkenazi….

  8. RCB says:

    Is there any theory on just how small a population has to be before mutational meltdown really becomes a problem? This is clearly not a linear phenomenon. Dropping in pop size from 100k to 90k is clearly not as bad as dropping from 20k to 10k. Perhaps most archaic human populations never dropped below the threshold for a long enough time (fixation of deleterious mutations by drift takes a while) for this to really be important?

    • Jim says:

      The population of Sentinel Island is estimated to be less than 1k. I read once that when an exploratory visit was made there including some people from other Andaman Islands these other Andaman Islanders could not recognize any words spoken by the Sentinel Islanders. This suggests the Sentinel Islanders have been isolated for quite a long time. In contrast when Captain Cook visited Hawaii he was astonished by how similar the Hawaiian Language was to Tahitian.

    • RCB says:

      Let me put it another way:

      Cochran writes “For a while now we have seen occasional articles about how people outside of sub-Saharan Africa may have more genetic load, generated by drift over a population history in which Eurasians generally had a smaller effective population size.”

      Which suggests that people think like this: “Oh, a population was smaller for a long time, or when through a bottle neck. They must have been fucked up pretty bad by genetic load. Poor folks.”

      But it seems to me that you have to get quite small, and stay quite small for a while, for this effect to be non-negligible. I don’t know how small, but perhaps human populations never really got to a zone where this was a big problem? I’m sure a pro could tell me.

      In contrast, load is approx proportional to mutation rate, as I recall from elementary pop gen. Seems that even small changes in mutation rate (father’s age? environment?) could dominate the picture.

      • gcochran9 says:

        I’m not at all sure that a pro could tell you. When the impact of a mutation is small or zero, it is hard to determine what that impact actually is by looking at the sequence, or indeed by any other procedure other than watching for Ne generations, ideally repeated over and over to eliminate chance effects….

        Truncation selection is the most effective way of removing load, but selection in different populations may be truncation-like to different extents. That too could dominate.

        • Rick says:

          As we’ve seen from maize for quite a long time, the best way to end up with a very robust and productive population is to have an initial population with a ton of genetic diversity.

          But then… you create multiple independent small inbred populations from the starting one, then have them each come back together as pairs, and then get isolated and small again, and then come back together again, etc.

          This is how you can eliminate genetic load and weak alleles. It works in every type of sexually reproducing organism. If any single selective pressure was put on all of the populations involved, then that is where most of the improvement will be when they come back together.

          Maybe this happened to humans in some places. But it would require there being diverse small isolated populations for long periods of time, that then randomly ran into one another.

    • gcochran9 says:

      I think that looking at ecological examples would tell you more than theory.

      • Small human island populations are worth looking at. The problem is they quickly get snuffed out when the big bad world of mankind finds them. One very interesting population that should have been closely looked at by now genetically but have been purposely ignored are the original inhabitants of Tasmania. They are almost undoubtedly a higher percentage Denisovan than their neighbors on the Australian mainland but it is one of those sticky situations where few men dare to tread. Their faces sure as hell are archaic looking. There are plenty of photographs of aboriginal Tasmanians dressed in victorian finery and damned if they don’t look like neanderthals dressed in victorian finery. Who knows if their primitive existence was due to in part to inbreeding or a higher percentage Denisovan. Some folks get a little upset about the racist implications so their genes have never been looked at, for the good of us all no doubt.

        There has been some hubbub lately about what those troublesome Andaman islander genes are doing at a percentage of 2% in the amerinds living in the tropics of South America. Logic would tell you that 1) they got there before the second wave of amerinds from Beringia and 2) they never got the hang of killing big tasty animals that didn’t have enough sense to run away from people because they never saw them before. But down that logic road lies trouble because once again the dirty head of racism rises up, so a it isn’t discussed in polite company. Anyway if logic ruled the land of this particular niche of science then it would have been proposed by now that very few Andaman islanders made all the way across the Pacific ocean and the ones that made it were so very few that they became very inbred. What happens to severely inbred humans? Among other things they get stupid. So the arriving humans from way across the Pacific ocean beat the next wave of amerinds by thousands of years but did not rapidly expand and take over the two continents because damn few of them made it and they were easily brushed aside by the next wave of humans who came in sufficient numbers to not be inbred.

        But anyway these are ecological examples where humans might have been seriously inbred.

  9. MEH 0910 says:

    OT: http://www.nytimes.com/2016/04/12/health/people-who-avoided-illness-could-be-key-in-treating-those-who-didnt.html?_r=0

    “Somewhere in the world are 13 incredibly lucky people. Although they do not know it, each inherited a mutated gene that causes a fatal or terribly debilitating disease in infancy or childhood — but these people are adults, and healthy.

    Their DNA may hold clues to treating others who did not escape the gene’s effects.

    That is the conclusion of a paper, published Monday in the journal Nature Biotechnology, in which researchers searched databases containing genetic sequences from nearly 600,000 healthy adults and found these remarkable 13.”

    • Rick says:

      “Somewhere in the world are 13 incredibly lucky people.”

      Or… everywhere else in the world are more than 7 billion very lucky people without either mutation?

  10. iffen says:

    “I’m told by someone I trust that slaves were bred because it was cheaper than importing new ones.”

    It was cheaper to import new ones to the Islands and South America. They were literally worked to death on the sugar plantations and in the mines. Slave owners in Brazil considered it a stroke of good fortune to have a slave live for ten years.

    From the beginning, conditions were much better in what became the US. The natural increase was substantial and after importation was made illegal it took off. I read (can’t bring up the reference now) that conditions were not as good in Tidewater SC because they used the gang system and worked year round because they grew indigo and rice. Also, I wonder how conditions could have been much better on a sugar plantation in Louisiana as opposed to Cuba. Anyway, just looking at the slave schedules in the censuses is enough to verify a tremendous natural increase in the slave population.

  11. Greying Wanderer says:

    http://www.bbc.co.uk/news/science-environment-17457561

    “He said that during the ice age, the total mammoth population in Eurasia dipped from tens of thousands to very few.

    Dr Dalen added: “The DNA investigations found there was a 30% loss in genetic diversity as the population levels dropped – but that was to be expected.”

    Seems to me there might be two cases:

    1) pop gets very low because of limited space e.g. small island -> low diversity cos inbreeding problems

    2) pop gets very low because of extreme environment -> low diversity cos extreme selection

    so maybe the problem for species who go through (2) only occurs when the environment changes i.e. they are too adapted for one extreme and don’t carry as much spare part DNA to help them transition when the environment changes.

    For example if a trait developed in one environment that conferred a propensity for self-motivating guilt (as opposed to group-motivated shame) it might be very good in one context but very bad in another..

    #

    Also reminds me of a recent thing vis a vis population size and selection.

    If
    – selection pressure for a particular environment is x
    – random mutations y ~ eff. pop. size
    then shouldn’t there be a particular pop size for maximum selection in a particular environment where x > y ?

    For example a duck and a squirrel swim to Australia and initially happen to have the particular pop size (small but not too small) for maximum selection in the new environment -> platypus.

    • Tim says:

      “For example a duck and a squirrel swim to Australia and initially happen to have the particular pop size (small but not too small) for maximum selection in the new environment -> platypus.”

      Exactly. This is a perfect example for something.

  12. Greying Wanderer says:

    medical aspect

    I don’t really know but my gut feel tells me the medical consequences of this will be eventually be penicillin / Star Trek sized – McCoy takes a blood sample from a patient to get their DNA and puts it into a med machine which creates a tailored pill for that person.

  13. Greying Wanderer says:

    “Sandgroper, is there any proof of selective breeding of slaves? Especially with better sprinting times as a result?”

    If twitch muscle was connected to a gene that also gave malaria protection then there wouldn’t need to be selective breeding of slaves (except maybe in the opposite direction to produce more stamina).

    West African dancing effectively displays twitch muscle and there’s probably a reason that way of dancing caught on.

    The Chinese sprinter guy comes from the ex malarial south – has he got it too?

  14. Greying Wanderer says:

    @Rick
    “Unless the species involved is rare and has limitations successfully breeding (like a giant panda), breeding for improvement or trait transfer has nothing to do with generation time. It has to do with money.”

    But that’s the other guy’s point (implicitly) – money has everything to do with generation time.

    humans > horses > plants

    Also with plants there’s also strong artificial selection from outside.

    Say there were 100 fast horse genes in total and thoroughbreds already have 60 of those from previous breeding and other strains of horse/pony between them have the other 40 – but only one each – then crossing thoroughbreds en masse with all the other strains would be a terrible and destructive idea idea would crush the average frequency of all the beneficial genes.

    So yes if you gave over Wyoming to horse breeding, divided it into lots and mixed some thoroughbreds with different strains of pony (and kept one lot with unmixed thoroughbreds) then you could probably do what you say.

    I only mention this because spin about hybrid vigor from plants is sometimes used to bolster PC and it’s obviously a total crock unless the conditions are the same (unless you don’t mind everything being worse for thousands of years while it sorts itself out).

    #

    “Fast genes will never be lost because you can always backcross to the original strain.”

    If you maintain a breeding stock of the original strain.

    #

    Thing is if Africans already have much more genetic diversity than everyone else then clearly that doesn’t help on its own. Higher genetic diversity is only beneficial as an input to the process of selection – so people came out of Africa with a lot of spare part (neutral) DNA and some of it turns out to be positive in some new environment and gets selected to high frequencies (and some gets selected against). The end result of the process is less diversity.

    If other populations have already gone through that process once as they moved out of Africa then they are already partly selected for the best frequencies (at the time) so a 50/50 mix adds diversity but damages the existing frequencies.

    So, seems to me if people are serious about wanting improvement and not harm then the way to do it with humans would be maintain a mostly homogenous majority and add small numbers of people from outside preferably selected on the basis they are unusually good at something.

    Then any negative consequences are limited in scale while – as we’ve seen in other cases – any particularly beneficial genes have an engine of their own.

    #

    long spiel but a serious question

    if one were to devise a eugenic immigration policy for a country like Japan which is both
    a) very homogenous
    and
    b) already well above the human average in functional ability
    and (based on actual genetics not blank slate nonsense) what would it be like?

    If yoiu’re not going to do it in a lab first then my (fail-safe) guess is it would be to maintain high homogeneity while adding small numbers of outsiders who have shown some exceptional ability in something (as long as they were assimilable – no point otherwise).

    • Rick says:

      ““Fast genes will never be lost because you can always backcross to the original strain.”

      If you maintain a breeding stock of the original strain.”

      You can freeze buckets of horse sperm and even clone horses if necessary.

      It all has to with with the strategy. This is actually very well worked out.

      If you want to improve horses or the Japanese for any particular trait, then you make many crosses with as many diverse individuals as possible.

      Then, you make sibling crosses you check for recessive alleles that are either super or terrible.

      Separately you backcross the hybrids to the original breed.

      In the next generation you repeat the sibling crossing and backcrossing.

      You have to make some kind of selection along the way, and this is where money the limiting factor.

      Slower selection at the start is always best. After a few generations, you can be very harsh.

      • Greying Wanderer says:

        Thanks, that’s how i imagined it.

        So if you had Wyoming as a laboratory gulag split into lots of separate camps where you could directly control the prisoner’s breeding then – taking into account the 25 year generation length – it seems likely you could guarantee hybrid vigor after n generations.

        In lieu of that kind of setup though – at least for populations who are already above the human average – I’d say the safe immigration based version would entail having a strict homogenous / endogamous border which only allows in small numbers of outsiders who are exceptional in some way.

        (not just IQ imo could be anything beneficial – for example I read recently about the only copper in Afghan who doesn’t take bribes. that’s what I’d do personally – breed coppers who kill you if you try to bribe them)

        • Rick says:

          “only allows in small numbers of outsiders who are exceptional in some way.”

          The biggest issue here is exactly what the original post was about.

          You will be selecting some super individuals for you population at a low number, but then a terrible virus or other disease could wipe most people out. Diversity for the thing you are not selecting for is also important.

          If you select too stringently, you get either a dead population, or one of 10% quality and 90% parasites.

          • Greying Wanderer says:

            True but exceptional individuals from distant populations will also carry the diverse spare part DNA from their parent population along with whatever makes them exceptional.

            Otherwise yes, unfortunately my experimental iron coppers would prob all die of athlete’s foot.

  15. Matt says:

    On the main blog topic, re: genetic diversity vs bugs for lifespan and IQ, the fortunate thing here is that we have two homo sap populations with high tropical disease load and general adaptation to a tropical climate, one with high diversity, the Africans, and one with low diversity, the Oceanian Papuans.

    So that suggests we can perhaps make a comparison, that can help us quantify the effects the effect of a tropical disease climate independent of genetic diversity. Unless tropical disease load is very, very divergent between Papuans and Africans.

  16. Matt says:

    Btw, any thoughts on this – http://news.discovery.com/human/genetics/humans-infected-neanderthals-with-diseases-160412.htm?

    It would amuse me if the secret to Sapiens’ success in Eurasia was simply that we (the bulk of our ancestry) gave the Neanderthals and the other archaics herpes.

    But I would think the same objection, that the Neanderthals held their own for too long against the early Shkul-Qafzeh type Homo Sapiens, would apply here? That a fatal transfer of disease load from Sapiens to Neanderthal should not take many millennia to effect.

  17. Insightful says:

    Susannah Mushatt Jones is African-American and she is the oldest person in the world. What does Dr. Cochran have to say about this?

  18. Sam says:

    “Sub-Saharan Africans have shorter lifespans and lower IQs than most Eurasian populations.”
    FWIW, adjusting for infant mortality, there isn’t significant difference in lifespan between sub-Saharan African and Eurasians.

    • Jim says:

      That’s remarkable in view of the extreme level of poverty in Sub-Saharan Africa compared to most of Eurasia. I would have thought diseases like malaria would have made a significant difference.

      I wonder how much of the difference in lifespan between whites and blacks in the US is due to much higher rates of homicide?

      • Sam says:

        “I wonder how much of the difference in lifespan between whites and blacks in the US is due to much higher rates of homicide?”

        Homicide along doesn’t account for much – but in combination with heart disease, diabetes, cancer, pre- and -antenatal conditions, you can account for most of the difference in black-white life expectancy difference in the US.

    • gcochran9 says:

      You’re wrong. Perhaps you haven’t heard of AIDs? But to be fair, few (no) countries in sub-Saharan Africa are at the point where senescence-related diseases are by far the main cause of death, as they are in Japan, Europe, or the US. In the US the difference in life expectancy is about 4 years. “Higher death rates due to heart disease, cancer, homicide, diabetes, and perinatal conditions” accounted for 60 percent of the gap.” Genetics is probably the driver of the difference in perinatal conditions – lower birth weight. Heart disease? less clear, I think, but the kidney problems and salt-sensitivity in African-Americans are obviously genetic, although some other cardiovascular problems seem to go up with European ancestry. Diabetes? Probably the differences in risk are due to genetic factors: risk for Type-II goes up with degree of African ancestry. While Type-I is much more common in Europeans.

      • Sam says:

        I should have qualified my statement a bit. Once you adjust for infant mortality, life expectancy differential between sub-Saharan African countries and Eurasia goes away. The AIDS effect matters only for a few countries concentrated in southern Africa: Botswana, Lesotho, Malawi, Mozambique, Namibia, South Africa, Swaziland, Zambia and Zimbabwe. These countries account for only 14% of the SSA’s population. So my claim holds for most of the region.

        • ziel says:

          “Once you adjust for infant mortality, life expectancy differential between sub-Saharan African countries and Eurasia goes away.”

          That’s just not credible.

          • Sam says:

            The relevant data is publicly available. It will only take a few minutes. Try it.

            • gcochran9 says:

              I did. You’re wrong.

              By age 15 you’re past infant mortality. On average a 15-year old in the US makes it to 79.4, China 76.8, Bangladesh 74.1, India 70.9, Nigeria 64.3

              No guarantee that those differences are much caused by differences in senescence, but they exist after you’ve removed infant mortality.

              That’s once.

  19. Fourth doorman of the apocalypse says:

    @RCB: I want to thank you for helping me to understand …

    I liked your example above because I had played around with something like that before but got the numbers wrong. The problem was that the variance was wrong.

    So, I thought maybe restriction of range could help, and then I realized that would reduce the variance even more, and changing it to 1,000 loci each of 0 or 0.1 IQ points does not change the variance.

    So, then I thought about the possibility of two sub populations, and maybe I read it here somewhere.

    It seems that if you have two sub-populations of roughly equal sizes whose means differ by 2SD, then the variance of the whole population will be something like SD^2.

    Of course, that raises the question of a mechanism, but I wonder if assortative mating and female choice and regression to the mean might not drive this.

    I will have to try to find some discussions of this stuff.

    • Fourth doorman of the apocalypse says:

      So, I whipped out R last night after a few beers and demonstrated that I was talking some bullshit.

      The following seems to show it clearly:

       n<-dnorm(x,mean=100,sd=15)
       y<-dnorm(x,mean=115,sd=15.0)
       z<-dnorm(x,mean=85,sd=15.0)
       plot(x,n,type='l',lwd=1)
       points(x,(y+z)/2, type='l', col=2)
      

      It looks like a pretty flattened normal curve … I dunno. Maybe my R-fu is poor.

      • Fourth doorman of the apocalypse says:

        Hmmm, that was the wrong curve … the R should have been:

        n<-dnorm(x,mean=100,sd=15)
        y<-dnorm(x,mean=115,sd=7.07)
        z<-dnorm(x,mean=85,sd=7.07)
        plot(x,n,type=’l’,lwd=1)
        points(x,(y+z)/2, type=’l’, col=2)

        The resulting curve demonstrates the rubbish.

  20. Sean says:

    https://westhunt.wordpress.com/2012/09/09/the-black-white-mortality-crossover/ “Eighty year old Blacks live longer, on average, that 80 year old whites.” (in the US)

    From what I know and have observed from contact with blacks, their commonest anti disease mutations cannot be deleterious to facial structure, teeth, bone density, reflexes, perception, athleticism / dancing.ability or sex drive (in either sex).. The rote memory ability of black Africans compares favorably with the white average . So these dinged genes are lying around doing nothing in the genome until a disease resistance or higher level cognitive function is called on?

  21. Pingback: African-Americans develop end-stage renal disease (ESRD) about 3.5 times more often than people of European ancestry | Neoreactive

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