Evolution is slow–until it’s fast: Genetic Load and the Future of Humanity

Source: Priceonomics

A species may live in relative equilibrium with its environment, hardly changing from generation to generation, for millions of years. Turtles, for example, have barely changed since the Cretaceous, when dinosaurs still roamed the Earth.

But if the environment changes–critically, if selective pressures change–then the species will change, too. This was most famously demonstrated with English moths, which changed color from white-and-black speckled to pure black when pollution darkened the trunks of the trees they lived on. To survive, these moths need to avoid being eaten by birds, so any moth that stands out against the tree trunks tends to get turned into an avian snack. Against light-colored trees, dark-colored moths stood out and were eaten. Against dark-colored trees, light-colored moths stand out.

This change did not require millions of years. Dark-colored moths were virtually unknown in 1810, but by 1895, 98% of the moths were black.

The time it takes for evolution to occur depends simply on A. The frequency of a trait in the population and B. How strongly you are selecting for (or against) it.

Let’s break this down a little bit. Within a species, there exists a great deal of genetic variation. Some of this variation happens because two parents with different genes get together and produce offspring with a combination of their genes. Some of this variation happens because of random errors–mutations–that occur during copying of the genetic code. Much of the “natural variation” we see today started as some kind of error that proved to be useful, or at least not harmful. For example, all humans originally had dark skin similar to modern Africans’, but random mutations in some of the folks who no longer lived in Africa gave them lighter skin, eventually producing “white” and “Asian” skin tones.

(These random mutations also happen in Africa, but there they are harmful and so don’t stick around.)

Natural selection can only act on the traits that are actually present in the population. If we tried to select for “ability to shoot x-ray lasers from our eyes,” we wouldn’t get very far, because no one actually has that mutation. By contrast, albinism is rare, but it definitely exists, and if for some reason we wanted to select for it, we certainly could. (The incidence of albinism among the Hopi Indians is high enough–1 in 200 Hopis vs. 1 in 20,000 Europeans generally and 1 in 30,000 Southern Europeans–for scientists to discuss whether the Hopi have been actively selecting for albinism. This still isn’t a lot of albinism, but since the American Southwest is not a good environment for pale skin, it’s something.)

You will have a much easier time selecting for traits that crop up more frequently in your population than traits that crop up rarely (or never).

Second, we have intensity–and variety–of selective pressure. What % of your population is getting removed by natural selection each year? If 50% of your moths get eaten by birds because they’re too light, you’ll get a much faster change than if only 10% of moths get eaten.

Selection doesn’t have to involve getting eaten, though. Perhaps some of your moths are moth Lotharios, seducing all of the moth ladies with their fuzzy antennae. Over time, the moth population will develop fuzzier antennae as these handsome males out-reproduce their less hirsute cousins.

No matter what kind of selection you have, nor what part of your curve it’s working on, all that ultimately matters is how many offspring each individual has. If white moths have more children than black moths, then you end up with more white moths. If black moths have more babies, then you get more black moths.

Source SUPS.org

So what happens when you completely remove selective pressures from a population?

Back in 1968, ethologist John B. Calhoun set up an experiment popularly called “Mouse Utopia.” Four pairs of mice were given a large, comfortable habitat with no predators and plenty of food and water.

Predictably, the mouse population increased rapidly–once the mice were established in their new homes, their population doubled every 55 days. But after 211 days of explosive growth, reproduction began–mysteriously–to slow. For the next 245 days, the mouse population doubled only once every 145 days.

The birth rate continued to decline. As births and death reached parity, the mouse population stopped growing. Finally the last breeding female died, and the whole colony went extinct.


As I’ve mentioned before Israel is (AFAIK) the only developed country in the world with a TFR above replacement.

It has long been known that overcrowding leads to population stress and reduced reproduction, but overcrowding can only explain why the mouse population began to shrink–not why it died out. Surely by the time there were only a few breeding pairs left, things had become comfortable enough for the remaining mice to resume reproducing. Why did the population not stabilize at some comfortable level?

Professor Bruce Charlton suggests an alternative explanation: the removal of selective pressures on the mouse population resulted in increasing mutational load, until the entire population became too mutated to reproduce.

What is genetic load?

As I mentioned before, every time a cell replicates, a certain number of errors–mutations–occur. Occasionally these mutations are useful, but the vast majority of them are not. About 30-50% of pregnancies end in miscarriage (the percent of miscarriages people recognize is lower because embryos often miscarry before causing any overt signs of pregnancy,) and the majority of those miscarriages are caused by genetic errors.

Unfortunately, randomly changing part of your genetic code is more likely to give you no skin than skintanium armor.

But only the worst genetic problems that never see the light of day. Plenty of mutations merely reduce fitness without actually killing you. Down Syndrome, famously, is caused by an extra copy of chromosome 21.

While a few traits–such as sex or eye color–can be simply modeled as influenced by only one or two genes, many traits–such as height or IQ–appear to be influenced by hundreds or thousands of genes:

Differences in human height is 60–80% heritable, according to several twin studies[19] and has been considered polygenic since the Mendelian-biometrician debate a hundred years ago. A genome-wide association (GWA) study of more than 180,000 individuals has identified hundreds of genetic variants in at least 180 loci associated with adult human height.[20] The number of individuals has since been expanded to 253,288 individuals and the number of genetic variants identified is 697 in 423 genetic loci.[21]

Obviously most of these genes each plays only a small role in determining overall height (and this is of course holding environmental factors constant.) There are a few extreme conditions–gigantism and dwarfism–that are caused by single mutations, but the vast majority of height variation is caused by which particular mix of those 700 or so variants you happen to have.

The situation with IQ is similar:

Intelligence in the normal range is a polygenic trait, meaning it’s influenced by more than one gene.[3][4]

The general figure for the heritability of IQ, according to an authoritative American Psychological Association report, is 0.45 for children, and rises to around 0.75 for late teens and adults.[5][6] In simpler terms, IQ goes from being weakly correlated with genetics, for children, to being strongly correlated with genetics for late teens and adults. … Recent studies suggest that family and parenting characteristics are not significant contributors to variation in IQ scores;[8] however, poor prenatal environment, malnutrition and disease can have deleterious effects.[9][10]

And from a recent article published in Nature Genetics, Genome-wide association meta-analysis of 78,308 individuals identifies new loci and genes influencing human intelligence:

Despite intelligence having substantial heritability2 (0.54) and a confirmed polygenic nature, initial genetic studies were mostly underpowered3, 4, 5. Here we report a meta-analysis for intelligence of 78,308 individuals. We identify 336 associated SNPs (METAL P < 5 × 10−8) in 18 genomic loci, of which 15 are new. Around half of the SNPs are located inside a gene, implicating 22 genes, of which 11 are new findings. Gene-based analyses identified an additional 30 genes (MAGMA P < 2.73 × 10−6), of which all but one had not been implicated previously. We show that the identified genes are predominantly expressed in brain tissue, and pathway analysis indicates the involvement of genes regulating cell development (MAGMA competitive P = 3.5 × 10−6). Despite the well-known difference in twin-based heritability2 for intelligence in childhood (0.45) and adulthood (0.80), we show substantial genetic correlation (rg = 0.89, LD score regression P = 5.4 × 10−29). These findings provide new insight into the genetic architecture of intelligence.

The greater number of genes influence a trait, the harder they are to identify without extremely large studies, because any small group of people might not even have the same set of relevant genes.

High IQ correlates positively with a number of life outcomes, like health and longevity, while low IQ correlates with negative outcomes like disease, mental illness, and early death. Obviously this is in part because dumb people are more likely to make dumb choices which lead to death or disease, but IQ also correlates with choice-free matters like height and your ability to quickly press a button. Our brains are not some mysterious entities floating in a void, but physical parts of our bodies, and anything that affects our overall health and physical functioning is likely to also have an effect on our brains.

Like height, most of the genetic variation in IQ is the combined result of many genes. We’ve definitely found some mutations that result in abnormally low IQ, but so far we have yet (AFAIK) to find any genes that produce the IQ gigantism. In other words, low (genetic) IQ is caused by genetic load–Small Yet Important Genetic Differences Between Highly Intelligent People and General Population:

The study focused, for the first time, on rare, functional SNPs – rare because previous research had only considered common SNPs and functional because these are SNPs that are likely to cause differences in the creation of proteins.

The researchers did not find any individual protein-altering SNPs that met strict criteria for differences between the high-intelligence group and the control group. However, for SNPs that showed some difference between the groups, the rare allele was less frequently observed in the high intelligence group. This observation is consistent with research indicating that rare functional alleles are more often detrimental than beneficial to intelligence.

Maternal mortality rates over time, UK data

Greg Cochran has some interesting Thoughts on Genetic Load. (Currently, the most interesting candidate genes for potentially increasing IQ also have terrible side effects, like autism, Tay Sachs and Torsion Dystonia. The idea is that–perhaps–if you have only a few genes related to the condition, you get an IQ boost, but if you have too many, you get screwed.) Of course, even conventional high-IQ has a cost: increased maternal mortality (larger heads).

Wikipedia defines genetic load as:

the difference between the fitness of an average genotype in a population and the fitness of some reference genotype, which may be either the best present in a population, or may be the theoretically optimal genotype. … Deleterious mutation load is the main contributing factor to genetic load overall.[5] Most mutations are deleterious, and occur at a high rate.

There’s math, if you want it.

Normally, genetic mutations are removed from the population at a rate determined by how bad they are. Really bad mutations kill you instantly, and so are never born. Slightly less bad mutations might survive, but never reproduce. Mutations that are only a little bit deleterious might have no obvious effect, but result in having slightly fewer children than your neighbors. Over many generations, this mutation will eventually disappear.

(Some mutations are more complicated–sickle cell, for example, is protective against malaria if you have only one copy of the mutation, but gives you sickle cell anemia if you have two.)

Jakubany is a town in the Carpathian Mountains

Throughout history, infant mortality was our single biggest killer. For example, here is some data from Jakubany, a town in the Carpathian Mountains:

We can see that, prior to the 1900s, the town’s infant mortality rate stayed consistently above 20%, and often peaked near 80%.

The graph’s creator states:

When I first ran a calculation of the infant mortality rate, I could not believe certain of the intermediate results. I recompiled all of the data and recalculated … with the same astounding result – 50.4% of the children born in Jakubany between the years 1772 and 1890 would diebefore reaching ten years of age! …one out of every two! Further, over the same 118 year period, of the 13306 children who were born, 2958 died (~22 %) before reaching the age of one.

Historical infant mortality rates can be difficult to calculate in part because they were so high, people didn’t always bother to record infant deaths. And since infants are small and their bones delicate, their burials are not as easy to find as adults’. Nevertheless, Wikipedia estimates that Paleolithic man had an average life expectancy of 33 years:

Based on the data from recent hunter-gatherer populations, it is estimated that at 15, life expectancy was an additional 39 years (total 54), with a 0.60 probability of reaching 15.[12]

Priceonomics: Why life expectancy is misleading

In other words, a 40% chance of dying in childhood. (Not exactly the same as infant mortality, but close.)

Wikipedia gives similarly dismal stats for life expectancy in the Neolithic (20-33), Bronze and Iron ages (26), Classical Greece(28 or 25), Classical Rome (20-30), Pre-Columbian Southwest US (25-30), Medieval Islamic Caliphate (35), Late Medieval English Peerage (30), early modern England (33-40), and the whole world in 1900 (31).

Over at ThoughtCo: Surviving Infancy in the Middle Ages, the author reports estimates for between 30 and 50% infant mortality rates. I recall a study on Anasazi nutrition which I sadly can’t locate right now, which found 100% malnutrition rates among adults (based on enamel hypoplasias,) and 50% infant mortality.

As Priceonomics notes, the main driver of increasing global life expectancy–48 years in 1950 and 71.5 years in 2014 (according to Wikipedia)–has been a massive decrease in infant mortality. The average life expectancy of an American newborn back in 1900 was only 47 and a half years, whereas a 60 year old could expect to live to be 75. In 1998, the average infant could expect to live to about 75, and the average 60 year old could expect to live to about 80.

Back in his post on Mousetopia, Charlton writes:

Michael A Woodley suggests that what was going on [in the Mouse experiment] was much more likely to be mutation accumulation; with deleterious (but non-fatal) genes incrementally accumulating with each generation and generating a wide range of increasingly maladaptive behavioural pathologies; this process rapidly overwhelming and destroying the population before any beneficial mutations could emerge to ‘save; the colony from extinction. …

The reason why mouse utopia might produce so rapid and extreme a mutation accumulation is that wild mice naturally suffer very high mortality rates from predation. …

Thus mutation selection balance is in operation among wild mice, with very high mortality rates continually weeding-out the high rate of spontaneously-occurring new mutations (especially among males) – with typically only a small and relatively mutation-free proportion of the (large numbers of) offspring surviving to reproduce; and a minority of the most active and healthy (mutation free) males siring the bulk of each generation.

However, in Mouse Utopia, there is no predation and all the other causes of mortality (eg. Starvation, violence from other mice) are reduced to a minimum – so the frequent mutations just accumulate, generation upon generation – randomly producing all sorts of pathological (maladaptive) behaviours.

Historically speaking, another selective factor operated on humans: while about 67% of women reproduced, only 33% of men did. By contrast, according to Psychology Today, a majority of today’s men have or will have children.

Today, almost everyone in the developed world has plenty of food, a comfortable home, and doesn’t have to worry about dying of bubonic plague. We live in humantopia, where the biggest factor influencing how many kids you have is how many you want to have.


Back in 1930, infant mortality rates were highest among the children of unskilled manual laborers, and lowest among the children of professionals (IIRC, this is Brittish data.) Today, infant mortality is almost non-existent, but voluntary childlessness has now inverted this phenomena:

Yes, the percent of childless women appears to have declined since 1994, but the overall pattern of who is having children still holds. Further, while only 8% of women with post graduate degrees have 4 or more children, 26% of those who never graduated from highschool have 4+ kids. Meanwhile, the age of first-time moms has continued to climb.

In other words, the strongest remover of genetic load–infant mortality–has all but disappeared; populations with higher load (lower IQ) are having more children than populations with lower load; and everyone is having children later, which also increases genetic load.

Take a moment to consider the high-infant mortality situation: an average couple has a dozen children. Four of them, by random good luck, inherit a good combination of the couple’s genes and turn out healthy and smart. Four, by random bad luck, get a less lucky combination of genes and turn out not particularly healthy or smart. And four, by very bad luck, get some unpleasant mutations that render them quite unhealthy and rather dull.

Infant mortality claims half their children, taking the least healthy. They are left with 4 bright children and 2 moderately intelligent children. The three brightest children succeed at life, marry well, and end up with several healthy, surviving children of their own, while the moderately intelligent do okay and end up with a couple of children.

On average, society’s overall health and IQ should hold steady or even increase over time, depending on how strong the selective pressures actually are.

Or consider a consanguineous couple with a high risk of genetic birth defects: perhaps a full 80% of their children die, but 20% turn out healthy and survive.

Today, by contrast, your average couple has two children. One of them is lucky, healthy, and smart. The other is unlucky, unhealthy, and dumb. Both survive. The lucky kid goes to college, majors in underwater intersectionist basket-weaving, and has one kid at age 40. That kid has Down Syndrome and never reproduces. The unlucky kid can’t keep a job, has chronic health problems, and 3 children by three different partners.

Your consanguineous couple migrates from war-torn Somalia to Minnesota. They still have 12 kids, but three of them are autistic with IQs below the official retardation threshold. “We never had this back in Somalia,” they cry. “We don’t even have a word for it.”

People normally think of dysgenics as merely “the dumb outbreed the smart,” but genetic load applies to everyone–men and women, smart and dull, black and white, young and especially old–because we all make random transcription errors when copying our DNA.

I could offer a list of signs of increasing genetic load, but there’s no way to avoid cherry-picking trends I already know are happening, like falling sperm counts or rising (diagnosed) autism rates, so I’ll skip that. You may substitute your own list of “obvious signs society is falling apart at the genes” if you so desire.

Nevertheless, the transition from 30% (or greater) infant mortality to almost 0% is amazing, both on a technical level and because it heralds an unprecedented era in human evolution. The selective pressures on today’s people are massively different from those our ancestors faced, simply because our ancestors’ biggest filter was infant mortality. Unless infant mortality acted completely at random–taking the genetically loaded and unloaded alike–or on factors completely irrelevant to load, the elimination of infant mortality must continuously increase the genetic load in the human population. Over time, if that load is not selected out–say, through more people being too unhealthy to reproduce–then we will end up with an increasing population of physically sick, maladjusted, mentally ill, and low-IQ people.

(Remember, all mental traits are heritable–so genetic load influences everything, not just controversial ones like IQ.)

If all of the above is correct, then I see only 4 ways out:

  1. Do nothing: Genetic load increases until the population is non-functional and collapses, resulting in a return of Malthusian conditions, invasion by stronger neighbors, or extinction.
  2. Sterilization or other weeding out of high-load people, coupled with higher fertility by low-load people
  3. Abortion of high load fetuses
  4. Genetic engineering

#1 sounds unpleasant, and #2 would result in masses of unhappy people. We don’t have the technology for #4, yet. I don’t think the technology is quite there for #2, either, but it’s much closer–we can certainly test for many of the deleterious mutations that we do know of.


45 thoughts on “Evolution is slow–until it’s fast: Genetic Load and the Future of Humanity

  1. >Over time, if that load is not selected out–say, through more people being too unhealthy to reproduce–then we will end up with an increasing population of physically sick, maladjusted, mentally ill, and low-IQ people.

    No, you won’t, because the overall reproductive rate will crater. So you will end up with a shrinking population of those people.

    Surviving plenty is just as much of a filter as is surviving scarcity.


  2. I think 23&me was making baby steps to matching up people, but I think their politics stopped them. At the very least, they have a ‘community manager’ that responds in typically leftist fashion to incoherent cries of racism.

    But just a service like that could help. And in a generation or two, this would be routinely done for newborns, and mothers would probably be working on who is going to marry who long before they hit puberty. This would only become more true if government care broke-down, because then having some smart children would become even more important for old age.

    But for it to really break in the right direction, somebody (by which I mean government) has to want us, and not for the short-term, but inter-generational. A lot of the big cities and big universities are glad to have smart people, but they haven’t thought ahead to when you can no longer pull from the entire globe- or worse, should the entire globe end up doing what the West did.

    I am vaguely remembering maybe a ketogenic diet might help reduce mutational load. It inhibits… something to do with gene expression… I will try to remember, but anyway, I mentioned it because there may be interventions prospective parents could use to improve the chlld’s chances.


  3. β-hydroxybutyrate is an inhibitor of histone deacetylases.

    Not going to solve everything, but it would mitigate some of the problem. Guys could plan ahead- 72 days( I think) is the sperm production cycle. Low carb, stay away from alcohol, etc…

    Dave Asprey and his wife wrote a book along these lines. Knowing Dave, it’s probably overkill. I haven’t read it, but I probably will if the issue comes up.


  4. Would your mind be blown if I told you that heritable morphologic change could occur without a change in gene frequency?


    Physiologic systems are Intelligent and evolution can occur due to the interaction of intelligent physiology with the environment. This leads credence to Eldredge and Gould’s punctuated equilibrium theory.



    This stuff blows my mind! What do you think about this?


    • “…heritable morphologic change could occur without a change in gene frequency…”

      Are you saying that the “expression” or how much a gene is expressed of genes is more important?

      Epigenetics? Jim Penman has a book where he says that wide availability of food causes loss of vigor in animals.


      He has another book,”Biohistory : decline and fall of the West”.

      So what you’re calling “genetic load” may be nothing of sort but a epigenetic loss of fitness. This sort of fits in with what we know about exercise. It’s peak work to exhaustion that causes the best peak over all health and fitness. A few minutes a day at peak is better than an hour of milling around.


  5. Fantastic post. One of the best things I’ve read in months

    1. What do you think about Europe today? If material prosperity results in genetic load, they’ve surely built up a lot. But Cochran seems to say the Middle East and Africa have the highest genetic loads, at least geographically (native Australians high as well).

    If Europe’s gene pool is dirty, will mixing in ME genetics help or exacerbate the problem? Seems like straining social support programs could be a good thing in the long term. But the replacement population is high gene-load already… hybrid vigor?

    2. Wondering if this is “The Great Filter” of the Fermi’s Paradox. We’ve hit the point where gene load is crippling the innovative cores of human civilization (Euro, Japan, Korea). We need to start cleaning up genetic code for new babies, but we aren’t there yet. Will we make it over the hurdle?

    China seems like our only hope now. Apparently rough social conditions, high IQs, not afraid to keep out immigration and gene-edit kids…


    • 1. https://www.unz.com/gnxp/genetic-load-is-higher-outside-of-africa/ Genetic load appears to be higher outside of Africa. (Though I’m not sure this is load so much as drift.)
      I think some folks were hopeful that African and Aboriginal IQs were being artificially depressed via cousin marriage and older men taking multiple wives, resulting in higher load in their offspring, and that therefore IQ could be fairly easily raised in these areas by changing these practices. Which could certainly be true, but has also been historically offset by high infant mortality rates.

      1.b. I don’t know, but I don’t think there’s that much intermarrying going on. Something like 70% of married Pakistanis in Britain are married to their 1st cousins. Hybrid vigor is a fascinating concept, but I haven’t seen any evidence (yet) of it working in humans. So from a genetic standpoint, I’m not expecting much. Now, could the introduction of lots of migrants have physical, political, or psychological effects? Surely. But I don’t know yet what.

      2. I hope not.
      2b. I wouldn’t call China “our” hope, exactly. But otherwise, yes, China has a chance of overcoming these issues. They have their own, of course.


      • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1448064/ in this study it looks like mixed race children have poorer health by most measures.

        After populations separate and genetic drift sets in there may be selection for genes that are beneficial when combined with other genes that happen to be common in the population but may just happen to be detrimental when combined with genes common in other populations. The rest of the genome is part of the selecting environment.


      • Thing is, humans aren’t livestock or corn breeds; no one is saying, “hey, let’s cross this group with that group of human, I think that result would be really interesting.” People have children for normal human reasons, so everything is confounded by factors like “which sorts of people are most likely to pick these pairings.” If the people who marry interracially are, by and large, people who are so super successful they can have their pick of any partner, then their kids’ll be above average for mundane reasons; likewise if people marry interracially because they’re unsuccessful with their own race and so have to “settle” as it were for someone of another race, then their kids should be below average.
        Plus, you know, the mule is go-to example of hybrid vigor, and it’s sterile; donkeys and horses appear to have split 4+ million years ago, whereas the absolute deepest splits in the human family tree are only, at max, about 250,000 years. Two groups like Middle Easterners and Europeans aren’t even different races on this scale; they’re both Caucasians.
        Of course if there’s inbreeding depression going on, a bit of outbreeding can do wonders, but Europe hasn’t had a problem with that in ages.

        I do sometimes wonder what would happen to a person who got some adaptation for really cold environments from one parent and adaptations for heat from the other. Could they stand both environments well? What if they were just never comfortable?


  6. #1 is exactly what will happen and we all know it. We can expect limited application of 2 & 4, probably not 3 anywhere. The very fact that your mind placed the Malthusian dilemma in first place indicates strongest probability: no true skeptic genuinely believes in schemes of human improvement that depend on the overcoming of all sorts of biases and vested personal interests which have never been overcome and because they cannot be — or there’d be no dilemma!

    Frankly, the sooner #1 takes over the better, in my opinion, so one can stop hearing about the wondrous ways in which technology will bail us out yet again, which in reality is just postponing the climax of the dilemma. But even then, of course, as they’re munching on the corpses of their weaker neighbors perhaps, the disingenuous masses will find some way to chirp that “Malthus was wrong!”


    • I was thinking of mules as livestock.
      Siberian huskies and related breeds have a lot of wolf in them and seem pretty strong/healthy.
      There’s a problem that “vigor” doesn’t refer to a specific trait, but any trait that seems enhanced in hybrids–making it hard to search for.


      • Mules have certain advantages but they have their down sides too, like not being able to reproduce themselves. Not replicating yourself seems the opposite of vigor. My cousin switched their operation from random cows to a particular breed and made such better money. Partly becuase the breed was purpose built generations ago for dairy production

        Husky’s are almsot two different breeds these days. One used for pulling and work vs show/ looks/ pets. Don’t know how much wolf is in them but the work dogs are generally healthier. Years of rescuing has lead me to believe mix breed dog’s tend to have more problems, particularly issues between the ears. My Lady Pit so true to form she could be calender girl for pit bulls. She has a good gait, no health issues, can jump a 6 foot fence, run down live stock, chase pigs etc etc. Boy was breed to kill other dogs and is pit mixed with who knows what but suffers from joint pain because he hips don’t match his frame and some things like that.

        When breeding stock and dogs you are looking to create certain traits. Once you do that you back breed to refine them. Random mix breed dogs can be wonderful pets and friends but are unlikely to do work like a critter special breed for it


      • All “siberian” dogs, like Huskies, Eskmo dogs, even the little Shiba Inu, have a bit of wolf in them. Too widespread to just be showdogs–people purposefully crossed them with wolves and then refined them to keep useful wolf traits.


    • I think hybrid vigor only works when you’re talking about line breeding. Where you have two lines with similar characteristics. They eventually get inbreeding depression so you cross the two separate lines to get hybrid vigor. Or at least that’s one way I’ve been told it works.


      • Almost all commercial strawberries are a cross between the wild Virginia strawberry and the wild Chilean strawberry. On their own they weren’t inbred, but they didn’t always even produce fruit and when they did, it was tiny. Together, they produce large, sweet berries.
        But plant genetics can be complicated things.


  7. ”However, in Mouse Utopia, there is no predation and all the other causes of mortality (eg. Starvation, violence from other mice) are reduced to a minimum – so the frequent mutations just accumulate, generation upon generation – randomly producing all sorts of pathological (maladaptive) behaviours.”

    It would be interesting if instead of infinite food and water. Food and water are rationed from the beginning hence ensuring limited carrying capacity. This would ensure competition for resources and selection quite different from predaton.


  8. Would it be OK if I cross-posted this article to WriterBeat.com? There is no fee; I’m simply trying to add more content diversity for our community and I enjoyehd reading your work. I’ll be sure to give you complete credit as the author. If “OK” please let me know via email.



  9. “Currently, the most interesting candidate genes for potentially increasing IQ also have terrible side effects, like autism, Tay Sachs and Torsion Dystonia. The idea is that–perhaps–if you have only a few genes related to the condition, you get an IQ boost, but if you have too many, you get screwed.”

    With autism, it seems to be the case that both (a) it’s largely genetic, and (b) autism severe enough to get a diagnosis seriously reduces evolutionary fitness. Since the genes responsible have managed to survive in our genome for quite a long time (if Somali’s can develop it, that must be a few thousand years at least?), there must be some kind of fitness benefit to having some autistic traits (improved focus at hunting? Hmmm…), otherwise the alleles responsible would have been removed over the many generations that have elapsed since they arose.

    “If all of the above is correct, then I see only 4 ways out”

    As others have touched on, there is a 5th – assortive mating. That would cause a caste system to develop – or rather, as Charles Murray has written about, *is* causing a caste system to develop – but it would work to preserve a low mutational load in a sub-population?

    Alternatively, we could put some average IQ individuals in cryogenic storage and send them into the future, where they can solve the problems that have been caused by low-IQ individuals running things.


    • I’m not convinced that Somali autism is the same thing as regular autism. Very anecdotally, diagnosed autism seems associated with high-math ability families. They also seem to be very good at memorizing lots of data, which seems useful in a world before books were cheap and the internet was easily available. My suspicion is that the underlying condition involves increasing the % of the brain devoted to certain mathematical and memorizing tasks at the expense of certain verbal tasks. In moderation, this lets someone excel at certain skills while still being smart enough to make up for their deficits. In excess, they can’t talk. Autists also tend to be extremely dedicated to whatever their passions are. This aids in the collection of large amounts of data, helping them succeed in a particular field. I remember in Slate Star Codex’s review of Trump’s The Art of the Deal, he compared Trump’s detailed recounting of deals he’s made to an autistic’s recounting of their particular interest. Given two people of equal IQ, the passionate person will have an easier time mastering a particular skill and succeeding in that field. These traits can all work in moderation.


  10. Probably like speaking to a wall, but everybody is putting a lot of weight on a theory (neo-Darwinism) that cannot explain speciation. You think it’s proven with your tree moths. Color me skeptical. Instead, give me a detailed description of how neo-Darwinian processes produce a complex system, such as echo-location in bats. It cannot be done. You are just assuming light skin is the result of “random mutations.” This cannot be found in the fossil record.


    • Speciation is easy to prove. Are dogs and wolves different species? Yes. (You treat a wolf like a dog at your peril.) How did they get to be different species? Humans selected particular traits in the dogs they bred until they had a creature that was sufficiently different from wolves to call them different species.

      Speciation isn’t some magic process. It’s just what happens when two different groups become (for any reason) sufficiently different from each other that it makes sense to call them different species.


      • You’ve proved there are species. You have not done anything to demonstrate you can get a new species from an existing species by neo-Darwinian processes.


      • People have made new species–take the fox experiment in Russia. It’s very easy. Just breed until you get one. Don’t know why you think species is some big barrier we can’t cross.


  11. And “fitness” is a circular concept. How do you determine whether a human is “fit” before he or she reproduces? IQ? Washboard abs? Python delts? All three?


      • Then you’ve admitted it is circular. Gould wrote about an “engineer’s criteria,” such as we would use to judge a car, a plane or a boat. Do you see the problem with using terms created to describe machines made by conscious agents to describe an unguided process? Let’s see some of these criteria for what makes a human fit. In fact, the common complaint is that people who are not “fit” (IQ) are the ones reproducing successfully. How can that be if evolution is “survival of the fittest”?

        I submit to you that “genetic load” does not exist. Humanity may become extinct, but it won’t be some process of accumulating dis-genetic mutations.


      • You asked how to judge fitness before reproducing. Fitness is the ability to reproduce. Ergo, you cannot (though you can make some good guesses based on what has worked previously.)


    • You can determine an individual’s fitness by their phenotypical quality, the absence of bad genes, the absence of neurological disorders, etc. It’s not hard.


  12. […] Nevertheless, the transition from 30% (or greater) infant mortality to almost 0% is amazing, both on a technical level and because it heralds an unprecedented era in human evolution. The selective pressures on today’s people are massively different from those our ancestors faced, simply because our ancestors’ biggest filter was infant mortality. Unless infant mortality acted completely at random–taking the genetically loaded and unloaded alike–or on factors completely irrelevant to load, the elimination of infant mortality must continuously increase the genetic load in the human population. Over time, if that load is not selected out–say, through more people being too unhealthy to reproduce–then we will end up with an increasing population of physically sick, maladjusted, mentally ill, and low-IQ people. […]


  13. Charlton’s thesis is testable: Repeat the mouse experiment using a different species of rodent, like deer mice or field mice, whose mouse-like appearance is due to convergent evolution, not common ancestry. Or use wild-caught specimens of Mus musculus, the true mice.

    If they exhibit the same pathologies as Calhoun’s mice, it’s a psychological reaction to over-crowding. If they suffer different pathologies, it’s mutational load.


  14. There is one problem with this analysis and that is whether infectious diseases like TB and cholera, that used kill many children in olden times killed only the “less fit” or killed more randomly.


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