In popular fiction, mutants are cool. They have special powers and look like Hugh Jackman. In reality, though, mutations that have any effect at all are almost always bad for you. Everybody has a number of mutations of varying severity. Some completely destroy a gene’s function, while others cause lesser degrees of harm. Mutations occur every generation, while selection is always eliminating them. At any given moment, there will be a small percentage of defective copies of each gene in the population.

In a simple model, a given mutant has an equilibrium frequency μ/s, when μ is the mutation rate from good to bad alleles and s is the size of the selective disadvantage. To estimate the total impact of mutation at that locus, you multiply the frequency by the expected harm, s: which means that the fitness decrease (from effects at that locus) is just μ, the mutation rate.  If we assume that these fitness effects are multiplicative, the total fitness decrease (also called ‘mutational load’) is approximately 1 – exp(-U), when U is where U=Σ2μ, the total number of new harmful mutations per diploid individual.

The mutation rate for any particular locus is low: for a typical gene, something like 10-5.  But over the genome as a whole, the total rate is on the order of 1 per generation, or maybe a bit larger than that. Suppose U is 1: then the average person has a fitness that is less than two-thirds that of a mutation-free individual, one with all typos corrected. Some estimates have U as high as 4.2 in humans: in that case, average fitness is only about 1% of a mutation-free individual.  This big change occurs because U is up in the exponent.

Suppose that some human population had their mutation rate increase by 50%?  What would happen? They would immediately experience an increase in genetic disease. The first thing you would notice would be a higher rate of dominant genetic diseases like Marfan syndrome and neurofibromatosis. For the the case of a dominant lethal, the percentage increase in the first generation would be the same as the increase in the mutation rate – because dominant lethals must be generated fresh every generation. Less drastic mutations would increase more slowly, because there is already a substantial background level. Marfan syndrome decreases fitness by about 25% – it would take something like a century to reach the higher equilibrium rate. A mutation that decreased fitness by 1% would require about 2500 years.

Those 2500 years would make the Dark Ages look like a picnic. Things would get worse and worse. After a millenium or two, _nobody_ in this hypothetical population would be as fit as as today’s average. You would expect to see lots of changes, all bad. Lifespan would surely go down. Infant mortality and miscarriage rate would go up.  IQ would decrease, probably more so than many other fitness traits, since more
than half of all genes are expressed in the brain. It’s a a big mutational target – more to go wrong. People would be crazier, too – as if we didn’t have enough trouble already.  In the long run, thousands or tens of  thousands of years, this population would adapt to the consequences of the higher mutation rate, assuming that it didn’t go extinct. Brains would cost just as much as they ever did, but would deliver less fitness per cubic centimeter: under these conditions the fitness-maximizing size would go down. Natural selection would also be reshaping other traits –  you’d still be seeing adaptation to disease and climate and whatnot. But complex adaptations would not work as well.

Innovations, including useful innovations, are generated by a fairly small number of smarter-than-average people.  That fraction would drop dramatically as average IQ decreased, because of the shape of the normal distribution, which decreases more and more rapidly with increasing distance from the mean.  Innovation would probably stop.  At the very least, the rate of innovation we’ve grown to love, fast enough to keep ahead of population growth, would falter. The world would become Malthusian. You’d see cats and dogs living together.

All this assumes reasonably random mating.  It also assumes that the fitness-reducing effects of mutations are multiplicative, which seems reasonable but is not at all certain. It is possible to imagine ways in which certain patterns of selection could limit the increase in mutation load.  For example, suppose that only a certain fraction of people could mate – say the top 30% in fitness – while others never reproduced. That would severely limit the increase in mutational load, since each genetic death would eliminate many bad alleles. This model, truncation selection, is halfway plausible in a dog-eat-dog Malthusian world, but nobody knows how close it is to reality.  Geoffrey Miller would suggest that sexual selection would ameliorate this problem.  Even if some of these optimistic scenarios are correct, people in our hypothetical high-mutation population would be worse off. The question is exactly how much.
What would a spelling-checked person, one with no genetic typos, be like?  Since no such person has ever existed, we have to speculate.  I figure that kind of guy would win the decathlon, steal your shirt and your girl – and  you still couldn’t help liking him.

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43 Responses to Typos

  1. Jim says:

    Cochran – What are the principal causes of mutations? Do we know? Is it background radiation? If it is errors in the replication of DNA do we have any idea of the most likely cause of these or is it that all we can say is “random error”?

    • gcochran9 says:

      I think we don’t know, except in a general sense. We know (probably) that radiation isn’t the main cause, since the mutation-doubling dose in mice is pretty high, a hundred rads or more. Errors happen in DNA replication: they tend to go up with temperature. You wouldn’t think that temperature would matter in mammals, since they regulate their internal temp, but when you look at mammalian sister species, those in higher-temperature environments seems to accumulate mutations faster. Not clear why this is so.

  2. Robert Dole says:

    I understand why random mutation (from a wayward high energy photon or somesuch) is generally bad (although necessary, in the long run). But what if natural selection has arranged the genome so that the regions that undergo the most “self referential” mutations (like duplications, deletions, and palindromic stuff on the Y) also contain genes that are more frequently (than average) beneficial or neutral when repeated or lost? Evolving capacities that promote stable future adaptation (using preexisting, potentially modularized material) would be ideal for parasites or predators that are, I suspect, able to pay a higher metabolic price (or whatever is required to maintain genetic redundancy/robusticity) to stay ahead of their prey/hosts.

    For example:

    A genomic point-of-view on environmental factors influencing the human brain methylome (2011)
    > While some common CNVs are polymorphic and often inherited in humans, a higher frequency of de novo rare CNVs are found in patients with autism and schizophrenia compared to unaffected controls. In addition, individuals affected by neurodevelopmental disorders in general appear to have a greater overall burden of common polymorphic CNVs than unaffected controls. Chromosomal regions that are hotspots for primate specific segmental dups and chimpanzee/human differences frequently coincide with the breakpoints of CNVs found in autism andschizophrenia, including 1q21.1, 15q11.2 and 15q13.3.31

    > The other major challenge to interpreting the genetic relevance of CNVs is understanding how the loss or gain of specific chromosomal loci may cause disease. Since the loss of a gene copy is generally expected to be more pathogenic than a gain, the goal of human CNV disease association studies is often to find genes within small rare CNV deletions. However, this worthy approach may be unjustifiably ignoring the “elephant in the room” of rare CNV duplications associated with autism that are much larger than deletions (>500 kb) and contain more genes implicated in autism than the CNV deletions that are more intensely investigated.

    Autism and schizophrenia are only adaptive when integrated into larger populations:

    Changing perceptions: The power of autism (2011)

    > Most grant proposals, research papers and reviews on autism open with, “Autism is a devastating disorder”. Mine do not.

    > I am a researcher, clinician and lab director concentrating on the cognitive neuroscience of autism. Eight autistic people have been associated with my group: four research assistants, three students and one researcher.

    > Their roles have not been limited to sharing their life experiences or performing mindless data entry. They are there because of their intellectual and personal qualities. I believe that they contribute to science because of their autism, not in spite of it.


  3. R. Right says:

    Are you saying that the only thing that keeps all of us from being superman are replication errors? Or another way, our imperfection is the price to be paid for the ability of the species to evolve? Would a zero mutation population be hyper-fit right up until the point it died off from some change in the environment?

    • gcochran9 says:

      Well, the kind of superman we’re talking about probably couldn’t fly. But the theory of genetic load does suggest that someone with no mutational load would be extraordinary. Assuming that we develop the ability to edit the genome fairly freely, we should actually be able to do this sometime in the next few decades.

      And yes, a population with no ongoing mutations would eventually run into something they couldn’t handle. If nothing else, a new bug of some kind.

  4. Rachelle says:

    In respect for your complaint in the last post that commentators were violating a basic Internet rule by staying on topic, I am going to comment on an earlier post.

    THE 10,000 YEAR EXPLOSION, p. 189 “We believe that the Ashkenazi Jews have a genetic advantage in intelligence that arose from natural selection for success…. Strong selection for intelligence also produced some unpleasant side effects, in the form of alleles that boost IQ in carriers while causing harm to homozygotes.”

    This sounds similar to my suggestion that homosexuality may arise in some individuals because of an unfortunate conjunction of alleles that are generally beneficial in other individuals.

    Of course you may be correct in believing that a pathogen is involved as a cause of homosexuality. However, the argument that because they do not reproduce successfully one can rule out a genetic cause for homosexuality does not seem very much more persuasive than saying that Tay-Sachs or thalassemia cannot be genetic because those diseases interfere with reproductive success. Put simply, saying a condition cannot have genetic origins because it precludes reproductive success is not reasonable. There are too many known instances where nature tolerates a certain level of discards because the advantages to others in the population outweigh the losses. Perhaps homosexuality is one of those.

    • gcochran9 says:

      I was being sarcastic, about the basic rule of the Internet. Maybe you didn’t notice. In the future, I strongly suggested sticking to the subject of the post.

      Tay-Sachs and thalassemia are genetic: the identical twin concordance is 100%. That is not the case for homosexuality, where the twin concordance is 20-25%. There has to be some major non-genetic factor at work in the causation of homosexuality.

      Second, Tay-Sachs, and thalassemia, and sickle-cell disease, are Mendelian. They’re caused by recessive mutations: one copy does something positive (clear for sickle-cell and thalassemia, likely for Tay-Sachs) while two copies are harmful or even lethal. Mendelian diseases have a clear inheritance pattern: homosexuality does not have a Mendelian pattern of inheritance.

      Third, those common Mendelian diseases all seem to be the consequence of strong and recent selection. The mutations themselves are young: the defenses against falciparum malaria all look to be less than 5000 years old.

      Older adaptations generally don’t look like this. They’re more complex, – not one-gene affairs like sickle-cell. They are produced by a set of genes working together. And they don’t have such awful side effects. Here I have to talk about tradeoffs.. There are many cases in which a favorable trait is associated with a negative trait. For example, a big animal may be safer against predation, but it has to find more food. Such a tradeoff is an inevitable result of the laws of physics. Evolution can’t eliminate it.

      But consider twinning in sheep. Usually sheep have just one lamb at a time, and in the past this was probably the best strategy: it was too hard to guard and nurture two. But in favorable modern circumstances, say in New Zealand, twinning actually increases fitness. Several mutations that cause twinning have been increasing in sheep. One fairly common one (a change in the gene BMP15) is found in Inverdale sheep. One copy causes twinning, two cause sterility. Now that increases fitness, when the gene frequency is low, but it does so in a sloppy manner. Surely there is a better way: lots of other animals regularly have twins, without any genetic sterility. And of course there is, but the sheep have just started down this path. The BMP15 mutation is a first-cut adaptation (like sickle-cell), not a well-regulated, complex adaptation. Give it time. There will be modifer mutations that make it happen when it should and not otherwise.

      Common Mendelian mutations in humans are mostly like this – first-cut adaptations to recernt, strong evolutionary pressures. Malaria has generated all the really common ones. It can do so because malaria is such a potent disease: protection against it is worth a lot.

      If homosexuality was Mendelian and found only in populations originating in the malarious belt of the Old World, it would almost certainly be a side effect of a malaria-defense mutation, like sickle-cell or Melanesian ovalocytosis. It certainly doesn’t hurt fitness any more than those mutations in homozygotes – sickle cell homozygotes used to die young (still do in Africa) , while ovalocytosis homozygotes all die in utero.

      But it isn’t Mendelian, and it isn’t found solely in those malaria-belt population. Nor is the problem of focusing your sexual interest on the opposite sex exactly new. You’d think that evolution would have mastered that trick by now. It’s been hundreds of millions of years. Let me emphasize this: the opposite-sex problen has been around for hundreds of millions of years, not 5000 as in the case of falciparum malria, not 1000 years like white-collar jobs in the Ashkenazi Jews, not 50 or 100 like overprotected sheep.

      Birds do it, bees do it, even educated fleas do it – but Noel Coward didn’t. Homosexuality is an anomaly.

      Why would anybody take a genetic explanation as the default when the great majority of common fitness-reducing syndromes in humans are known to have been caused by infectious agents? Look, not so long ago, even now to an extent, there was a tremendous amount of sterility and reduced fertility (tens of percent) in central Africa, to the point where the regon was caused the ‘sterility belt’. Why didn’t people start out with the assumption that those infertile women wre executing a genetic strategy – one in which they skipped personal reproduction and helped their sister have more kids, like worker bees? I mean, they actually _did_ help their sisters raise kids. You could see it happening every day, in contrast to all the models in which homosexual men do something useful for their kin or clan that has somehow never, ever been observed. Just as well that nobody argued this, because it wasn’t true.

      It was the clap.

      Maybe I’ll hear soon about how deafness is an adaptation.

      • jb says:

        Here’s a thought. It’s true that evolution has had hundreds of millions of years to perfect opposite sex attraction. But for most mammals this involves scent, which keys into a deep and ancient area of the brain. Great apes are visual, without much sense of smell, so they can’t use the old mechanism. Being visual, one would expect that any new mechanism would involve sight. But this has always kind of puzzled me. Objectively speaking, there really isn’t that much difference between the shapes of men and women — at least nothing comparable to the differences between male and female pheromones. If you raised a bunch of same-sex children on a desert island, with no exposure to the opposite sex, I’d be willing to bet they’d all turn out gay once the hormones kicked in at puberty. What other possibility is there? Visual cues just don’t seem strong enough to prevent that from happening.

        So, what else do apes have to work with? Well, they are really good at learning! Monkey see, monkey do. Young chimpanzees see adults copulating all the time, so when their own hormones kick in they have a pretty clear idea where they might want to direct their energies. Human hunter-gatherers may not see quite as much, but I’ll bet the young ones are much less in the dark than children in more advanced societies where everybody is covered up all the time, and the mechanics of the whole thing are kept as mysterious as possible. I remember being a young boy, and getting little erections, and being very interested in what they were for, but not getting much information from my parents. I did manage to pick up on the fact that it had something to do with girls though, and eventually I went to the encyclopedia and figured it out for myself (any yes, it was pretty interesting!). But…, I didn’t actually feel anything specific until years later, in middle school, when I was thunderstruck by this absolutely perfectly beautiful girl in the grade above me (who I never did manage to talk to 😦 ). Before then it was entirely intellectual, and I just can’t discount the possibility that if I had gotten (or been given!) a wrong idea somewhere along the way, I might have taken a different path, with a beautiful boy at the end of it.

        So that’s my hypothesis: that because we’ve lost the ancient scent cues, human sexuality is partly learned, and that children — who put in a lot of effort trying to figure out what is expected of them! — can get confused as a result of the lack of adequate information. Actually, I think this idea could explain a lot more than homosexuality! There are many other sorts of deviant sexual behavior, and they could all start the same way; a child latching on to some cue — an overheard remark, an image in a movie, or just an oddball thought — and dwelling on it, and being shaped by it, and in the end not even remembering the original cue.

        (Anyway, good idea or bad, I don’t remember reading this anywhere else, so it’s possible it’s original to me, in which case once it has become the orthodoxy I will doff my pseudonym and claim it!)

      • Rachelle says:

        ‘I was being sarcastic about the basic rule of the Internet”

        Perhaps. I thought it was because you recognized that your argument about railroad gauges did not hold water.

        In any event, I do not suggest a genetic explanation as ‘the default’, but only as a possibility. You assume much more than I say.

        Nor did I embrace the model that homosexual men do something useful for kin or clan. My thought was that something that is useful in heterosexual individuals may, in some instances, get misdirected. It could even be a normally useful propensity that is triggered by an external event, not excluding a pathogen.

        If the appearance of homosexuality does not fit typical Mendelian examples, I wonder if it fits known instances of infection. I don’t know the answer to this question, but is it usual for an infectious agent to cause problems with a relatively fixed proportion of the population in almost all instances?

        You gave the example of a time not so long ago in which there was a ‘tremendous amount of sterility….” in Central Africa. Has the homosexuality pathogen ever gotten so infectious that there was a ‘tremendous amount’ of homosexuality in a population?

        On the other hand, have conditions ever improved enough in any society for the rate of infection with the homosexuality pathogen to decline? Certainly that has happened with other infectious agents like polio, cholera and the plague that are still extant.

        If the pathogen for homosexuality has been around for millions of years, why haven’t we evolved a better way of dealing with it other than essentially to sterilize a small but not insignificant percentage of the population?

        By the way, If you hear soon that deafness is an adaption, it will not be from me. I think someone with a disability is disabled…not “differently abled”. Nor do I think that homosexuality is an adaptation. I think that it might be a misfire of something that is an adaptation.

  5. John says:

    A new study suggests diabetes may start in the intestines: http://www.sciencedaily.com/releases/2012/02/120215123352.htm

    Could this be evidence of a possible pathogenic cause of diabetes?

  6. Doug1 says:

    I’m with Rachelle on a possible genetic cause for male homosexuality.

    I’ve heard speculation that it might be a genetic variation that when expressed in females makes them particularly feminine and highly attractive to males, but when expressed in males has a tendency to make them gay.

    • ziel says:

      If I could think of just one example where the sisters of a gay guy were smokin’ hot and hyper-fertile I might be tempted to consider it. But of course it would have to be a lot more than one example – it would have to be true in nearly every case.

      • gcochran9 says:

        Like so many explanations of homosexuality, it relies upon phenomena that have never been observed. I think that the driving impulse behind this is a notion that adaptations are good, and since homosexuality is thought to be good by all right-thinking people, it must be adaptive. Adaptive isn’t quite the same as good, though: consider parasitic wasps.

        Generally speaking, this topic brings out the stupid in people.

    • Rachelle says:

      “I’ve heard speculation that it might be a genetic variation that when expressed in females makes them particularly feminine and highly attractive to males, but when expressed in males has a tendency to make them gay.”

      That is an interesting thought. Losing a male or two might more than be made up for by a female who is exceptionally attractive. Even if it isn’t an actual adaptation, it sounds like it could be a successful adaptation. It would certainly get the genes around. It would be amusing to see how a computer model for an evolving population would run that one.

      • ziel says:

        But, again, have you ever actually observed such a phenomenon – that the gay guys you know typically have really attractive and “active” sisters? I sure haven’t – I don’t even know of one such case. “Us” and “People” aren’t regularly trotting out paparazzi pics of the bimbo siblings of gay celebrities.

        If such a phenomenon were real, it would be well known. Older brothers would be counseling their brothers to “hang out with gay dudes, cuz they got the hottest sisters, trust me”. It’s simply not plausible.

    • saintonge235 says:

              Think carefully.  Do you think that men who had sex with men had as many children, on average and throughout history, as men who didn’t have sex with men?   Because the argument against a genetic cause for men being sexually attracted to men is simple: on average, those with the hypothetical ‘gay gene’ have lower reproductive success than those who don’t have the gene.

              If you answered “Yes, they did have as many children who became succesfully breeding adults,” please show your evidence.

              If you answered no, then a genetic cause for male homosexuality requires either a) a hugely high mutation rate, thus maintaining the 2-3% gay male population, or b) a recent change such that gay men used to have as many children successfully raised to adulthood and breeding as men who only have sex with women, but don’t now, or c) for every gay male who has an average of 2-x children successfully raised to adulthood, a relative has the ‘gay gene’ and raises 2+x children to adulthood and breeding, with the surplus being caused by the gene’s presence or d) a new science to replace population genetics, which must be in error, or e) some combination of the above.  The argument against a genetic cause for female homosexuality is similar,

              Stand and deliver.

  7. Michael 2 says:

    “spelling-checked person, one with no genetic typos, ”

    Assume I could make a spelled check clone of myself. What would be the Fst between myself and my clone?

  8. dave chamberlin says:

    The meek were supposed to inherit the earth
    but they aren’t the ones who most frequently birth
    it’s those without will
    who can’t swallow a pill
    whose love of their children is their source of self worth

    Just thought I’d toss that out there for yuks. I rather doubt that the worst case scenario will happen but rather than run off with my opinions I would like to ask a few questions that are on topic…
    1) Do we see any indications yet of higher spontaneous abortion rates since modern medicine has allowed +99% of children to reach adulthood rather than the pre modern times rate of about 50%.
    2)How high are human spontaneous abortion rates and why are they so high as compared to other species.
    3) We don’t have any real evidence of what causes the high variability in inherited human intellegence yet, do we?

    • gcochran9 says:

      1. Probably not yet.

      2. Weirdly high. The chance of getting a healthy baby out of one ovulatory cycle is maybe 25%. Nobody knows why.

      3. We know it’s largely genetic. In the populations examined so far, no single gene has a major effect. Variations in mutational load are probably part of the story.

      • whatever says:

        “2. Weirdly high. The chance of getting a healthy baby out of one ovulatory cycle is maybe 25%. Nobody knows why.”
        Haldane’s rule?
        It postulates reduced fertility / low reproductive success in hybrid species. We are human -neanderthal hybrids.
        If, only if, some of the sex specific chromosomes (I know that this is not the case), let say Y, in some of the human populations, now or in the past, was actually inherited from the neanderthal line, that would have made the fertility rates even worse.
        Still, we are hybrids between at least two species. Or more. That counts in terms of fertility.

  9. jb says:

    It’s interesting that a mere 50% increase in the base mutation rate would cause such harm. It takes a much higher increase over the recommend dose before most pharmaceuticals become dangerous, and anything that turned lethal with a 50% increase would be tightly regulated. I’m not quite sure what I am getting at here — I guess I’m just wondering whether it’s just a coincidence that we happen to be skating so close to the edge of disaster, or whether there is some deeper significance.

  10. Jim says:

    Cochran – Is it true as I seem to recall having read somewhere that the reason for mammals having the testes located outside the body cavity is to keep them cooler and so reduce the mutation rate?

  11. Sean says:

    Could a long series of consanguineous matings result in something close to a “spelling-checked person, one with no genetic typos”, in genes that make a difference, at least.

    • gcochran9 says:

      Yes, but the inbred population tends to do very poorly for a quite a while, because individuals have a much increased chance of having two copies of bad recessives. Moreover, chance would probably fix some of the less-bad deleterious mutations. You can sometimes get higher fitness by first doing this and then outbreeding: this probably has a lot do with the success of hybrid corn.

      Some human populations having practiced inbreeding more than others, for a long time. They probably have fewer bad recessives. It looks as if cousin marriage causes fewer problems in such populations.

      • Sean says:

        Outbreeding shelters the deleterious mutations for higher fitness, but it’s storing up trouble for the future. A highly outbred mating can have a lot of ‘typos’ without it being obvious to a prospective mate. So if you are of mixed ancestry (IE biracial) it is better to backcross to one of the parental stocks than to mate with someone of the same ancestral mix ?

  12. FredR says:

    Are there any environmental factors varying across the space and time of human history that affect mutation rate (besides I guess nuclear accidents)?

  13. gcochran9 says:

    Other than advanced paternal age, I think we don’t know. In two years or less, we probably will know. If environmental factors are at all significant, it will be a health concern, and you’ll see various efforts to do something about it.

  14. The Monster from Polaris says:

    “Suppose U is 1: then the average person has a fitness that is less than two-thirds that of a mutation-free individual, one with all typos corrected.”
    That should be slightly more than one third (36.7%), it’s the fitness decrease that’s nearly two thirds.
    And the fitness for U=4.2 is very close to 1.5%.

    dave chamberlin, there are some religious groups with very high fertility, e..g., Laestadians and Haredim. I fear that they are the ones who will inherit the Earth. See Eric Kaufmann: ‘Shall the Religious Inherit the Earth?’

    whatever & Haldane’s rule: I know nothing about these matters, but it’s something like 1000 generations since we mated with Neandertals, so wouldn’t we have developed some way around that low fertility by now? (Or maybe not, since the low chance per ovulation cycle of getting a healthy baby doesn’t seem to be the main limit on our effective fertility.)

    • Anonymous says:

      We did, did not we. (7 billions). Increased life span, delayed menopause, increase ovarian reserve, increased sex drive would all compensate the high rate of miscarriages;
      we still go on; purifying selection, in -vitro conceptions, free medical help, sponsored programs to fight sterility etc. The age of the clones is near, too. The high energy brains that caused some of the troubles at birth are (still) paying out.
      Or I am wrong, which is more likely.

  15. Bob says:

    How do we measure the typo rate in an individual or group? Now given the known IQ mean shifts between groups can we measure a typo rate difference that correlates?

    • gcochran9 says:

      We can measure the current rate by accurately sequencing parents and children and then comparing. This has been done, recently and to a very limited extent. To estimate the existing genetic load, you could sequence people and then count the number of knocked-out and severely altered genes. Again, we are just getting started on this.

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  17. coldequation6 says:

    It seems that this implies that zero population growth would inevitably lead to death by mutational load, barring custom-made genomes in designer babies. Some people have to die, or at least fail to reproduce, even if you can conquer disease and Malthusian constraints. The number would be higher now, as parental age and therefore mutation rates increase.

    That’s really pretty horrible when you think about it.

  18. albatross says:


    Do pathogens have much of an impact on this? I know there are viruses that end up in the germline from time to time (retroviruses, especially, but other damaged virus genomes are lying around in our DNA). If some pathogens have a noticable impact on rate of mutations passed to offspring, then better sanitation and vaccination and nutrition and such should give us somewhat fewer mutations, and you’d expect successive generations to be smarter and healthier, and to pass that on.

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  22. ehrgeiz0 says:

    Has anyone ever considered transposons (AKA jumping genes)? We’ve got about 100,000 of them in every cell of our body, and they can copy and insert themselves just about anywhere in the genome. Some can even use reverse transcription (retrotransposons), just like retroviruses.

    Speaking of which, we seen to have a few fossil endogenous retroviruses in our genome, and these ancient insertion events led to us producing amylase in our saliva, enabling us to eat starchy foods like rice, wheat and potatoes. Other endoretroviruses fuse the cells formed during embryogenesis into a placenta (a trait shared by all placental mammals). Some may even protect us from other harmful viruses.

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